Tudor Capital Australia Pty Limited v Christensen

1. [1]

   McCOLL JA: Mr Grant Christensen died suddenly and unexpectedly at his home on 8 September 2008 when he suffered ventricular fibrillation [1] leading to cardiac arrest. At the time of his death he was employed as a Portfolio Manager by the appellant, Tudor Capital Australia Pty Limited (Tudor Capital).

2. [2]

   The respondent, Penelope Christensen, Mr Christensen’s widow, commenced proceedings against Tudor Capital in the Workers Compensation Commission (Commission) on 9 August 2011, claiming an entitlement to compensation payments in respect of his death pursuant to s 9 of the Workers Compensation Act 1987 (NSW) (WCA). Arbitrator Wynyard upheld her claim. [2] He held Mr Christensen’s death had been, in substance, caused by viral myocarditis which, in turn, Mr Christensen had contracted by reason of employment stress. On appeal, the Deputy President of the Commission confirmed the Arbitrator’s decision. [3]

3. [3]

   Tudor Capital appeals against the Deputy President’s decision pursuant to s 353(1) of the Workplace Injury Management and Workers Compensation Act 1998 (NSW) (WIM Act). On that appeal, Tudor Capital must establish that it is aggrieved by a decision of the Presidential Member in point of law.

4. [4]

   In my view, for the reasons which follow, Tudor Capital has established that it is so aggrieved. Pursuant to s 353(2), the matter should be remitted to the Commission constituted by a Presidential member for determination by the Commission in accordance with the Court’s decision.

Factual background

1. [5]

   Tudor Capital is a corporate member of an internationally established hedge fund business founded in the United States of America. Mr Christensen commenced employment with Tudor Capital in Melbourne in February 1997. When the Melbourne office closed in July 2000, he relocated to London, where he was employed by Tudor Capital’s sister corporation, Tudor Capital (UK) LP. He remained in London until the end of 2007 at which time he and his family relocated to Sydney. He recommenced employment with Tudor Capital as a Portfolio Manager on approximately 21 January 2008.

2. [6]

   Mr Christensen experienced a number of difficulties during his first few weeks in the Sydney office, many of which related to a unique UNIX-based database system for market closing prices, known as the “TIC Shell”, he had developed by means of an algorithmic system. To operate his program, he required information stored on servers located in the United States. That data was accessible over the internet, but the internet connection speed between the Sydney office and United States office was slow, as was the internet generally in the Sydney office. These technical difficulties caused Mr Christensen frustration in not being able to operate his program efficiently, especially as he had been out of the market and unable to trade for four weeks during the move to Sydney.

3. [7]

   Although Mr Christensen’s technical difficulties were largely resolved by 27 February 2008, they caused delays which amounted to nine weeks in total and compromised his ability to perform. He was subsequently asked by Tudor Capital’s CEO to produce a simulation of results that his program would have produced had he been trading consistently in the period between December 2007 and July 2008, a task which also interfered with his ability to trade fully. Although the simulation outcome was extremely positive, his actual trading results and hence his earnings had fallen well behind his expected results.

4. [8]

   These circumstances led to Mr Christensen being placed on a “watch list” at a meeting of Tudor Capital’s Capital Allocation Committee on 1 July 2008. Placement on the “watch list” meant his performance would be reviewed over the balance of the financial year. Mrs Christensen’s evidence was that Mr Christensen was not advised of his placement on the watch list until around 20 August 2008.

5. [9]

   As Mr Christensen mainly traded in European and US markets, he also experienced difficulties in dealing with the time difference between Sydney and those markets. In addition to working from home between 8am and 9am, and his time at the office between 9:30am and 7pm, Mr Christensen would work between 10pm and 2am in order to watch the US market.

6. [10]

   During this time, Mr Christensen and others in the finance industry were affected by the significant problems facing economies around the world during the course of 2008, ultimately culminating in the Global Financial Crisis (GFC).

7. [11]

   In early September 2008, Mr Christensen developed the flu. On 4 September 2008 he consulted his family doctor for a chest infection and was prescribed an antibiotic. He took sick leave on 5 September 2008. He returned to work on 8 September 2008. On that day he was observed by a colleague, Sharon Easten, to be short of breath when walking to his car.

8. [12]

   That evening, after putting the children to bed, Mr Christensen was sitting on a couch with Mrs Christensen when he suddenly stopped talking, sighed and collapsed unconscious and pulseless. Ambulance officers who were called noted he was in ventricular fibrillation. He was unable to be revived.

9. [13]

   Mr Christensen had no history of collapses, chest pain, shortness of breath (other than as reported on the day of his death) or palpitation. He had been physically active, playing cricket and football, and was a keen cyclist. There was no family history of sudden death. His brother and sisters are alive and in good health. [4]

10. [14]

    The autopsy report by Dr B Elston, pathologist, addressed to the Coroner included, the following:

Legislative framework

1. [15]

   The following provisions of the WCA are those in force at the time Mrs Christensen lodged her s 25 claim. For convenience, I refer to the relevant provisions in present tense.

2. [16]

   Section 9 of the WCA provides:

3. [17]

   Section 25 of the WCA contained in Pt 3 (Compensation – benefits), Div 1 (Compensation payable on death), provides:

4. [18]

   “Injury” is defined in s 4(a) of the WCA relevantly as “mean[ing] personal injury arising out of or in the course of employment.” [6] There was no suggestion that Mr Christensen’s death was caused by a disease as referred to in s 4(b) of the WCA.

5. [19]

   In Pt 2 (Compensation – liability), s 9A provides:

6. [20]

   Section 11A was directed to psychological injury and provided:

Compensation claim

1. [21]

   As I have said, on 9 August 2011 Mrs Christensen submitted a claim for compensation benefits from Tudor Capital pursuant to s 9 of the WCA seeking lump sum compensation and weekly payments of compensation in respect of each dependent child. [8] On 25 July 2012 her claim was declined by Tudor Capital’s workers compensation insurer, Allianz Australia Workers Compensation (NSW) Limited, when it issued a notice pursuant to s 74 of the WIM Act (Insurers to give notice and reasons when liability disputed) in substance, denying any relevant injury. It also relied upon ss 9A and 11A of the WCA in defence of the claim. [9]

2. [22]

   On 2 April 2013 Mrs Christensen filed an application to resolve a dispute (ARD) in relation to the compensation claim. The ARD described the cause of Mr Christensen’s injury and death as:

3. [23]

   Against the requirement to “describe how the injury occurred”, appeared:

4. [24]

   Mrs Christensen’s claim did not discriminate between the two limbs of the s 4 definition of “injury”, that is to say whether the injury she contended Mr Christensen had suffered was one “arising out of or in the course of employment.” [10]

5. [25]

   Tudor Capital filed a reply to the ARD (Reply) on 30 April 2013. It denied that Mr Christensen’s employment in any way caused his death, disputed and denied that his fatality resulted from an injury arising out of or in the course of his employment and submitted that Mr Christensen did not suffer a psychological injury but that, if he did, it was not an injury which arose out of or in the course of his employment as defined by ss 4 and 11A(3) of the WCA. It also disputed for the purposes of s 9A, WCA, that Mr Christensen’s death resulted from an injury to which his employment with Tudor Capital was a substantial contributing factor. The Reply also noted aspects of medical reports and the autopsy report, observed that research undertaken by leading cardiac experts identified that there were over 400 sudden cardiac deaths per year in Australia where post mortem examination identified no specific cause of death and submitted that, based on the medical and factual evidence, the probability was that the injury (albeit that it was disputed and denied) would have happened anyway, or at about the same time, or at about at the same stage of Mr Christensen’s life if he had not been at work or had not worked in his employment with Tudor Capital.

6. [26]

   To the extent that Mrs Christensen asserted that Mr Christensen suffered a work related psychiatric or psychological injury, Tudor Capital also asserted that he did not suffer from such a condition constituting the requisite diagnostic threshold for a psychological injury pursuant to the Diagnostic and Statistical Manual for Mental Disorders, [11] and, as such, disputed that he suffered a psychiatric or psychological condition satisfying the definition of injury in ss 4 and 11A(3) of the WCA. It also contended that, if he did suffer a psychological injury, any such injury was wholly or predominantly caused by reasonable action it took with respect to transfer, performance appraisal and discipline in accordance with s 11A(1) of the WCA. Tudor Capital also raised the point that the claim for compensation was made more than six months following Mr Christensen’s death, and accordingly, disputed liability pursuant to s 261 of the WIM. That basis of opposition to the compensation claim does not appear to have been pursued.

7. [27]

   Mrs Christensen filed an Amended Application to Resolve a Dispute on 4 July 2014 (Amended ARD), it would appear from the Arbitrator’s decision with an application to admit late documents. [12] The Amended ARD amended details in the original ARD concerning cause of injury and death and description of how the injury occurred as follows.

8. [28]

   The description of the cause of injury and death was:

9. [29]

   The description of how the injury occurred was:

The arbitration

1. [30]

   Mrs Christensen’s claim was heard by Arbitrator Wynyard on 23 September 2014, 18 and 19 May 2015 and 16 June 2015. The hearing was limited to Tudor Capital’s liability to pay compensation. Issues of apportionment of any compensation as between members of the family were deferred to permit appropriate submissions to be put on behalf of the children, who were to be separately represented in respect of that aspect of the proceedings should Tudor Capital be found liable to pay compensation. [13]

2. [31]

   Mrs Christensen contended that Mr Christensen’s death was caused by stress associated with his employment, which rendered him susceptible to a viral illness which in turn caused or aggravated his ventricular fibrillation, cardiac arrest and death. [14] She asserted, in reliance upon a report from Associate Professor David Richards, a clinical cardiologist, that the ventricular fibrillation was caused by viral myocarditis. Acute myocarditis is the presence of inflammatory cells (lymphocytes) in the interstitial cells of the myocardium, the middle layer of the heart wall. In a case of acute myocarditis, inflammatory cells are attracted to the heart muscle which is infected by a virus. They indent (bore into) the underlying myocyte, inflicting damage which causes the muscle cell to stop contracting, eventually compromising the heart function and causing arrhythmia. [15] According to counsel for Tudor Capital, the inflammation, which is the result of the body’s defence mechanisms, including T cells, coming in to deal with the virus, is sufficient to cause the heart to go out of rhythm.

3. [32]

   Tudor Capital contended that Mr Christensen’s death did not result from an injury arising out of or in the course of his employment within the meaning of s 4 of the WCA. It further asserted that his death did not result from an injury to which his employment was a substantial contributing factor within the meaning of s 9A of the WCA. Throughout most of the hearing its case was that Mr Christensen’s death was caused by coronary artery disease. However, that case was abandoned towards the end of the hearing. Its case, as ultimately put, was that Mr Christensen was suffering from hypertrophic cardiomyopathy, a disease in which a portion of the heart muscle wall becomes thickened with fibrous (scar) tissue, a condition that is prone to ventricular fibrillation and sudden death. [16]

4. [33]

   The case was fought on two fronts. The first related to the evidence in respect of the temporal events leading up to Mr Christensen’s death (temporal issue). Mrs Christensen asserted that the nature of Mr Christensen’s employment exerted such pressure on his health that it led to his contraction of a viral illness that in turn led to his death. Tudor Capital denied that allegation. The second related to the cause of Mr Christensen’s fatal cardiac arrest, and concerned the conflicting expert medical evidence. [17] Although the medical experts were in agreement that Mr Christensen had suffered ventricular fibrillation which led to cardiac arrest causing his death, there was a factual contest between the parties as to the cause of the ventricular fibrillation.

5. [34]

   There was extensive medical evidence.

6. [35]

   Mrs Christensen called Associate Professor Richards. She also tendered expert reports from Dr David Whalley, also a cardiologist, and Professor William Rawlinson, an infectious diseases physician.

7. [36]

   Tudor Capital called Professor Anne Keogh, a specialist cardiologist at St Vincent’s Hospital, and Dr Rainer. Professor Keogh described herself as the founding cardiologist with Dr Victor Chang of the transplant unit, whose areas of special interest for thirty years were cardiomyopathy and heart failure. Tudor Capital also tendered two expert reports of Associate Professor B J Hudson, a specialist in microbiology and infectious diseases.

8. [37]

   It is important to note at the outset that the arbitration took a somewhat unusual course. As the Deputy President observed, “the hearing … [was] at times, interrupted by adjournments occasioned by reason of the effluxion of hearing time and by the interposition of the evidence of the expert witnesses.” [18] Counsel for Mrs Christensen, Mr Wardell, commenced submissions on 18 May 2015. His submissions on that day were confined, it would appear, to the temporal issue. They were made before Associate Professor Richards was called. On the same day Mr Grant, counsel for Tudor Capital, also made submissions on the temporal issue and Mr Wardell commenced his reply.

9. [38]

   Whereas expert reports were extensively prepared and commented upon by each party’s experts, important evidence was tendered late in the day. Of such evidence, the most significant was tendered on 19 May 2015 when Tudor Capital made an application to admit late documents, an application which included slides of tissue taken on Mr Christensen’s autopsy. According to counsel for Tudor Capital in this Court, the application was made by way of a telephone conference, and, to the extent, if any, there was any debate about the application, it was not recorded. This may be practical, but it is clearly undesirable if the subject of a tender is controversial. It is not apparent that this application fell into that category.

10. [39]

    The application was allowed and Tudor Capital tendered the actual pathology slides created at the autopsy which, for reasons which are not explained, were not the subject of evidence until after most of the expert reports were prepared, and until after Associate Professor Richards gave evidence. They became exhibit 12. Dr Rainer and Professor Keogh were then called and occupied the balance of that day.

11. [40]

    Exhibit 12 depicted slides representing tissue samples taken from various parts of Mr Christensen’s heart (set out on the right hand side of the page in exhibit 12), and, by way of comparison, on the left hand side of some pages, slides captioned as “normal” slides of the same area. In addition, on two pages, the slides on the left hand side of the page depicted heart muscle cells if affected by viral myocarditis, while the slide on the right hand side of one page showed Mr Christensen’s heart was not so affected. Dr Rainer and Professor Keogh gave oral evidence that the slides depicting Mr Christensen’s heart revealed cell pathology and an underlying and pre-existing disorder of the heart muscle (hypertrophic cardiomyopathy), but not viral myocarditis.

12. [41]

    The final hearing day was 16 June 2015 on which date Mrs Christensen made an application to admit late documents, in part to tender a further report from Associate Professor Richards dated 11 June 2015 addressing aspects of Professor Keogh’s oral evidence. Finally, on that day, Mr Grant, at the direction of the Arbitrator, commenced and concluded his submissions in chief before Mr Wardell had completed the submissions he had commenced on 18 May 2015. [19]

13. [42]

    According to Tudor Capital’s submissions, because of the order in which exhibit 12 was tendered, what was depicted by the slides was not specifically put to Associate Professor Richards. However, as is apparent, Mrs Christensen adduced further evidence, none of which addressed the autopsy slides.

14. [43]

    On the first front, Mrs Christensen adduced extensive evidence about the stresses to which she contended Mr Christensen’s workplace had exposed him. That evidence, as the Arbitrator described it “in broad outline was that a number of events during 2008 had adversely affected [Mr Christensen’s] immune system, in consequence of which he developed flu like symptoms in the weeks before his death.” [20]

15. [44]

    The occurrence of these events was not in dispute. It included the circumstances of the family’s move to Sydney from London, the fact that when Mr Christensen started with Tudor Capital in Sydney in January 2008 he had been out of the market for four weeks, and had been unable to trade, that he was unable to operate the TIC Shell efficiently because of the slowness of the computer he had been allocated, the fact that, due to the different time zone in which he was working, he had to readjust his system which entailed a long working day, meaning he usually missed having dinner with the family. As I have said, it took about nine weeks to resolve the technical difficulties but, according to Mrs Christensen, the delay compromised Mr Christensen’s ability to perform, which eventually resulted in him being placed on a “watch list” in June 2008, a fact of which he was, according to Mrs Christensen, apparently not informed until around 20 August 2008. [21] The Arbitrator accepted this evidence.

16. [45]

    Mrs Christensen also adduced evidence concerning what she submitted were physical signs of the stress Mr Christensen was suffering, manifesting in neck pain, gastro-flu and breathlessness on the day he died. [22]

17. [46]

    The Arbitrator concluded:

18. [47]

    The Arbitrator also set out extensive evidence of Mr Christensen’s interaction with a life coach, a facility Tudor Capital offered to all its Portfolio Management. [23] Those notes disclosed, according to the Arbitrator, “that [Mr Christensen] was not coping with the disadvantage he had been placed in by the move.” He regarded the notes as “strong supportive evidence for [Mrs Christensen’s] assertions.” [24]

19. [48]

    Finally, in outlining Mrs Christensen’s case on the first front, the Arbitrator set out a letter of condolence the Chairman of Tudor Capital, Paul Tudor Jones II, wrote to her after Mr Christensen’s death, in which he said:

20. [49]

    The Arbitrator also referred to Tudor Capital’s lay witnesses’ evidence concerning Mr Christensen’s work environment. [26] That evidence included evidence about Mr Christensen’s general performance, technology issues in the Sydney office and the circumstances in which Mr Christensen was placed on the watch list. It is unnecessary to refer to it in any detail. The Arbitrator did not place much weight upon it, save to note that he rejected evidence from Mr Kevin Wulwick, a UK resident who was both Associate General Counsel for Tudor Capital Europe LLP and counsel for Tudor Capital, to the extent he put in issue whether Mr Christensen was suffering from stress, due to his trading model not working. [27]

21. [50]

    Leaving aside the controversy as to whether there was sufficient evidence to found the Arbitrator’s ultimate finding as to the cause of Mr Christensen’s death, there are other issues, which require close attention to be paid to the medical evidence. Those issues include Tudor Capital’s complaints that neither the Arbitrator nor the Deputy President properly analysed that evidence and, too, Mrs Christensen’s complaint that the case Tudor Capital sought to propound in this Court was not put in the Commission. Accordingly, it is necessary to set out extensive passages of the medical evidence, including passages not referred to in the Commission.

22. [51]

    In addition to the passage from the autopsy report set out above, [28] the Arbitrator recorded that Dr Elston also reported that microscopic examination of Mr Christensen’s cardiovascular system showed:

Mrs Christensen’s expert evidence

1. [52]

   Dr Whalley gave the following opinion (which was based in part on the “post mortem result”) as to the cause of Mr Christensen’s death in his report of 11 February 2010:

2. [53]

   Professor Rawlinson gave evidence as to whether there was a relationship between stress and susceptibility to viral illness which the Arbitrator summarised as follows:

3. [54]

   Associate Professor Richards prepared six reports between 5 September 2011 and 11 June 2015. According to counsel for Tudor Capital, Associate Professor Richards’ reports were almost exclusively the source of Mrs Christensen’s medical evidence concerning the existence of viral myocarditis. Of these six reports, the Arbitrator referred only to the first, dated 5 September 2011. In that report, Associate Professor Richards was asked to consider first whether the nature of Mr Christensen’s employment was a substantial contributing factor to his death. He expressed the following opinion:

4. [55]

   Associate Professor Richards discounted the possibility Mr Christensen may have experienced idiopathic ventricular fibrillation because of the presence of the viral illness during the week prior to death. [33] He also discounted the possible effect of pre-existing coronary arterial disease. In his report dated 5 September 2011, he expressed the opinion that:

5. [56]

   In a report of 2 September 2013, Associate Professor Richards wrote in response to Professor Keogh’s report of 14 June 2013: [35]

6. [57]

   In the same report, and in response to Professor Keogh’s report of 8 August 2013 in which she expressed the view, relevantly, that “atherosclerotic coronary artery disease was the primary abnormality”, Associate Professor Richards wrote:

7. [58]

   Associate Professor Richards concluded this report by saying:

8. [59]

   In a report dated 29 April 2014, in response to a report from Associate Professor Hudson of 14 January 2014 and one from Professor Keogh of 11 February 2014, [36] Associate Professor Richards wrote:

9. [60]

   In his report dated 30 April 2015, Associate Professor Richards commented on Dr Rainer’s report of 12 March 2015 in which, among other matters, Dr Rainer reviewed the autopsy slides (exhibit 12), [37] and Professor Keogh’s report of 13 March 2015. [38] Associate Professor Richards did not personally examine the autopsy slides as he said that was outside his area of clinical expertise.

10. [61]

    In his 12 March 2015 report, Dr Rainer expressed the view, in short, that Mr Christensen died from a cardiomyopathy, based in part “on the positive finding [derived from the autopsy slides] and … the lack of any other findings to which a cause of death could be ascribed after a complete and thorough autopsy.”

11. [62]

    In response, Associate Professor Richards reiterated his view that “[i]n the absence of any other precipitating factor to cause acute left ventricular failure soon before death, it is … likely that the viral illness was the precipitating factor which caused sudden death”, and that the absence of histological changes did not disprove a diagnosis of viral myocarditis causing death.

12. [63]

    In response to Professor Keogh’s report of 13 March 2015, noting that “[h]istology remains the gold standard for establishing the diagnosis of myocarditis … there is no non-invasive gold standard”, Associate Professor Richards agreed. However, he commented that he could not ignore the fact that Mr Christensen had a viral illness for two weeks prior to his death, and developed dyspnoea due to acute left ventricular failure, and died suddenly with ventricular fibrillation. In his view, this clinical scenario was most likely due to viral myocarditis, in the absence of any other explanation for these features, the “clinical scenario” being the viral illness for two weeks prior to death, breathlessness and sudden death from ventricular fibrillation was most likely due to viral myocarditis, in the absence of any other explanation for these features”.

13. [64]

    Associate Professor Richards’ final report dated 11 June 2015 post-dated both his oral evidence and that of Dr Rainer and Professor Keogh. As I have said, it was tendered by Mrs Christensen on an application to admit late documents. According to her counsel, it was intended to address a matter never raised in Professor Keogh’s written reports. It is apparent from this report that Associate Professor Richards was asked to comment on Professor Keogh’s evidence before the Commission on 19 May 2015. The precise extent to which he was asked to comment is not apparent as his report doing so refers to only one aspect of Professor Keogh’s oral evidence which was that the “viruses that attack your throat … never go for the myocardium … the bugs that cause the flu and a cough … aren’t the ones that cause … viral myocarditis …”. Associate Professor Richards disagreed with that evidence as he explained in a manner neither party suggested was relevant here. He did not otherwise address Professor Keogh’s oral evidence and made no reference to Dr Rainer’s oral evidence.

14. [65]

    In the same report, Associate Professor Richards also said that a viral infection did not need to affect all of the heart to have a lethal potential. He said localised viral myocarditis may cause ventricular fibrillation which would lead to fibrillation of all ventricular myocardium.

15. [66]

    Associate Professor Richards gave evidence in the proceedings by teleconference on 18 May 2015 which had the unfortunate consequence that some of his responses to questions were apparently too indistinct to be transcribed. He expressed the following view in cross-examination:

16. [67]

    Associate Professor Richards did not agree that the way to diagnose whether Mr Christensen suffered from myocarditis or not was to look at the pathology. He also said:

Tudor Capital’s expert evidence

1. [68]

   In his report of 14 January 2014, Associate Professor Hudson reviewed Professor Rawlinson’s opinion as to the link between psychological stress and infection and he concluded:

2. [69]

   Associate Professor Hudson was of the opinion “that it [was] more likely than not that [Mr Christensen’s] death was due to an arrhythmia relating to coronary artery disease in a patient who [was] suffering from an intercurrent virus infection [and] … that it was more likely than not that death would not have occurred if [Mr Christensen] had not been suffering from a coronary artery disease, ‘a condition unrelated to [his] employment.’” [42]

3. [70]

   Associate Professor Hudson also said:

4. [71]

   Although, as I have said, the coronary artery disease case was abandoned in the course of the hearing, the Arbitrator dealt with it, and rejected it when considering Associate Professor Hudson’s evidence. [43]

5. [72]

   However, the Arbitrator did, it appears, rely in part on Associate Professor Hudson’s evidence that there was likely a relationship as discussed by Professor Rawlinson between psychological stress and an increased risk of developing a viral illness, in inferring that that was evidence which supported the first step in Mrs Christensen’s case that there was a connection between the cause of Mr Christensen’s viral illness and his employment. [44]

6. [73]

   Dr Rainer was the only pathologist who gave evidence. His experience was extensive. He was the main pathologist at St Vincent’s Hospital with responsibility for cardiac, pulmonary and renal pathology. In the 22 years prior to preparation of his first report in 2014, he had examined all diseased hearts removed from patients at transplantation and had been the main pathologist diagnosing rejection and other complications post transplantation. He had also seen all acute cardiac material biopsied from patients presenting at St Vincent’s over the same period.

7. [74]

   In his first report dated 10 February 2014, written before he saw the autopsy slides, Dr Rainer spoke of the pathological concepts of myocarditis and cell and tissue injury. He explained that an acute myocarditis was defined as the presence of inflammatory cells in the interstitial tissues of the myocardium. An international panel of pathologists had produced criteria for its diagnosis known as the “Dallas criteria”. [45] The Dallas criteria govern the microscopic interpretation of myocardial biopsies, the size of biopsies and terminology of the observed processes. In his second report to which I refer below, Dr Rainer described the Dallas criteria as the “gold standard for diagnosing viral myocarditis”, but also explained that cases which did not fulfil the criteria, but where there was clinical evidence of myocardial inflammation, could be monitored and further biopsies taken if the process became diffuse.

8. [75]

   The Dallas criteria included the requirements that in order to make a finding of acute myocarditis, there “must be concordance of T cell infiltration and myocyte damage in the absence of fibrosis and myocyte hypertrophy” and “[t]o exclude acute myocarditis at least five biopsies >2mm [were] required”. Dr Rainer pointed out that the second requirement was to overcome the “potential focal or patchy nature of an acute myocarditis.” He observed that misinterpretation of the term “patchy” was apparent in some of the expert witnesses’ reports. He said five biopsies of two millimetres each were sufficient to overcome any potential sample defect in relation to an acute myocarditis because of “‘patchiness’ of the process”. Dr Rainer explained that using the Dallas criteria separated cases of acute myocarditis from cases of ischaemic damage and cardiomyopathy.

9. [76]

   Dr Rainer disagreed with Dr Whalley’s comments in his 11 February 2010 report that Mr Christensen’s “postmortem was not reported to show any inflammatory infiltrate … but this process can be patchy and may not show up depending on the timing of the postmortem relative to the onset of the viral illness.” In Dr Rainer’s view, the sampling of the myocardium made at the autopsy was sufficient to overcome any potential sample defect because of the possible patchy nature of an acute myocarditis.

10. [77]

    Dr Rainer was of the view that Mr Christensen’s tissue samples revealed fibrosis, myocyte hypertrophy and myocyte disarray which were not those of an acute process, but were evidence of a chronic disease process that was long standing. He explained that the chronic disease process revealed in Mr Christensen’s tissue samples was unlike an acute myocarditis and expressed the opinion that Mr Christensen was not suffering from acute myocarditis at the time of his death. [46]

11. [78]

    In his second report dated 12 March 2015, Dr Rainer expressed the view that at post mortem histological examination of the myocardium would conclusively diagnose acute myocarditis. By the time he wrote this report, the autopsy slides (exhibit 12) had been provided to him. He reviewed the slides and attached to his report photographs of the major cardiac histological changes revealed by the slides, by comparison to slides taken from a “normal heart”. He also expressed the view that Mr Christensen’s heart had been extensively sampled and opined that the size of the sample was sufficient to overcome any potential sample defect. He said that in total 2150 square millimetres had been sampled and referred to an article on the Dallas criteria in which the author asserted that “5 square millimetres of cardiac tissue will diagnose 2/3rds of acute myocarditis cases”.

12. [79]

    Dr Rainer referred to page 8 of exhibit 12 on which there were two slides, on the left hand side of the page, one entitled “[v]iral (lymphocytic) Myo – card – itis = (from Latin) Muscle cells – heart – inflammed [sic, inflamed] with lymphocytes”, captioned as “[h]eart muscle cell death due to lymphocytes with active black nuclei, damaging heart muscle cells and their alignment”. On the right hand side of the page was a slide entitled “Mr Christensen’s heart muscle esp Right ventricle Cardio – myo – pathy Heart – muscle – diseased”, captioned “[m]any heart cells in disarray with scar tissue between them. Highly abnormal and dysfunctional. No lymphocytes. A chronic and non specific process”.

13. [80]

    Dr Rainer expressed the view that Mr Christensen’s myocardium showed myopathic features. He described myopathic changes as non-specific changes that develop in response to myocyte injury which, in the absence of hypertensive, valvular or ischaemic heart disease, are taken to indicate a cardiomyopathy. He said that interstitial fibrosis was the most significant myopathic change as it can lead to myocardial dysfunction and can act as a substrate for an arrhythmia. He observed that in Mr Christensen’s heart, the myopathic features were most prominent in the right ventricle and in the upper part of the interventricular septum. He said that there was no inflammation in any of the slides of Mr Christensen’s heart which were examined.

14. [81]

    Dr Rainer observed that comparison of two of the slides (to which he referred as 4 and 5), [47] which depicted the myocardium from the upper part of the interventricular septum in Mr Christensen’s and a normal heart respectively, illustrated the “abnormality of interstitial fibrosis” that had developed in Mr Christensen’s heart.

15. [82]

    Based on the autopsy report and his examination of the slides, Dr Rainer expressed the opinion that Mr Christensen died from a cardiomyopathy, to which his occupation and employment had not been contributing factors. While he expressed the view that the precise mode of Mr Christensen’s death could not be determined histologically, he said it was highly probable to have been an arrhythmia caused by the interstitial fibrosis developing as a complication of a cardiomyopathy. He opined that other medical specialists would reach a similar opinion “based on the positive finding outlined and based on the lack of any other findings to which a cause of death could be ascribed after a complete and thorough autopsy.”

16. [83]

    In oral evidence, Dr Rainer repeated his opinion that Mr Christensen’s heart had been comprehensively sampled with 28 tissue samples measuring roughly a square centimetre in diameter from various heart walls of the left and right ventricle and the septum in total. [48] He said the “28 blocks of tissue taken really comprehensively examine that heart”, that the sampling “covered the whole heart” and that there was no inflammation apparent. He was critical of Associate Professor Richards’ estimate of how much material was looked at during the autopsy on the basis that he had underestimated the thickness of the 28 tissue samples. Mrs Christensen accepted in the course of the appeal hearing, that the effect of Dr Rainer’s evidence was that the sampling was not patchy.

17. [84]

    Dr Rainer explained the process of ventricular fibrillation he hypothesised having occurred in Mr Christensen’s case by reason of the fibrosis present in his heart by reference to the slides at page 10 of exhibit 12, once again, the left hand slide depicting a normal heart, the right hand slide, Mr Christensen’s. As the Arbitrator recounted his evidence:

18. [85]

    Dr Rainer said that “in a case of acute myocarditis the microscope would reveal some evidence of its presence”. [50] He said the slides revealed no evidence of myocarditis in circumstances where such evidence would have been expected to have been found had Mr Christensen been affected by that condition. Further, the slides revealed fibrosis (or scar tissue) which he said was consistent with longstanding cardiomyopathy and, in his opinion, was the underlying cause of Mr Christensen’s ventricular fibrillation.

19. [86]

    Dr Rainer could not explain what caused the ventricular fibrillation at the moment it happened, [51] however he summarised the situation as follows:

20. [87]

    Dr Rainer agreed that the ventricular fibrillation from which Mr Christensen died could happen at any time, without warning and, subject to the commencement of the irregularity of the heartbeat, which I understand to refer to the commencement of the ventricular fibrillation, without symptoms. He said that once the heart lost its rhythm, there would be virtually immediate loss of consciousness within seconds.

21. [88]

    Dr Rainer described the slide on the left hand side of page 8 of exhibit 12 as depicting a case of acute myocarditis and explained the process it depicted. He said the black dots on the slide were “inflammatory cells specifically lymphocytes”, attracted to the area “via the virus that’s infecting the heart cell, the myocytes”. The slide showed the “lymphocytes … indenting the underlying myocycte … [a]nd at the point that they’re indenting the myocycte they’re inflicting damage … [which] occurs what they’re [sic, as in original] basically doing are [sic] boring a hole in the membrane of those muscle cells.” The consequence was that the “muscle cell … stops contracting … eventually … result[ing] in compromise to the heart function.” He explained that the inflammation symptomatic of viral myocarditis was outside the heart muscle, but was represented by the inflammatory cells pushing into the heart muscle cells.

22. [89]

    The Arbitrator referred to the slide on the left hand side of page 8 of exhibit 12 essentially in terms of Dr Rainer’s evidence, adding, “as I understood Dr Rainer’s evidence, that that inflammation would be expected to be present if a person had contracted myocarditis.”

23. [90]

    Dr Rainer’s evidence as to the slide on the right hand side of page 8 depicting Mr Christensen’s heart muscle was that there was no inflammation present and that the black dots which were visible (which were the nuclei of the myocyte) were not normal, but showed variation in size and shape which were a reflection of Mr Christensen’s cardiomyopathy. He said that the slide did not show any sign of inflammation, in other words, no sign of a virus. He explained that that was because the way a virus manifested itself in the heart was that it entered the heart cells, then altered the membranes of those cells such that they attracted inflammatory cells and it was the inflammatory cells which did the damage. He said that this was not present in the case of Mr Christensen. Although the Arbitrator referred to this slide by summarising its caption, (albeit omitting that part which stated “No lymphocytes. A chronic and non specific process.” [52] ), he did not otherwise discuss its significance.

24. [91]

    Dr Rainer attributed the fibrosis and myocyte disarray observed in the slides of Mr Christensen’s heart to hypertrophic cardiomyopathy which he had concluded was the most likely cause of the arrhythmia (ventricular fibrillation) and Mr Christensen’s death. He described the fibrosis evidence evident in the autopsy slides as significant and as “a severe focal fibrosis in the upper part of the septum” which was significant because the “conducting system of the heart traverses the upper part of the septum”. He agreed that the fibrosis was not so severe that it was highly probable that arrhythmia would occur at the time of Mr Christensen’s death, but that it could have occurred at any point of time.

25. [92]

    Dr Rainer was asked whether it was possible that death could follow so quickly after the development of viral myocarditis that it left no histological trace. He rejected that proposition. He said “there must be some histological cause for the death, that is, if the virus just simply enters the cell, does not have time to attract any inflammatory cells to it, then there will be no damage to the heart.” He also rejected the proposition that viral myocarditis “could … nevertheless cause fibrillation and arrhythmia,” saying “[n]o, that’s dependent upon the damage.”

26. [93]

    Dr Rainer agreed that it was possible that myocarditis could have been missed in the sampling of Mr Christensen’s tissue, albeit he said that he thought it “very unlikely because of the need to show damage.” He accepted, however, the possibility would be greater if there was a relatively short time between the onset of inflammation and the death. [53]

27. [94]

    Dr Rainer accepted in cross-examination that it was possible for long standing hypertrophic cardiomyopathy to be present in a heart and for there to be a subsequent attack by a virus producing viral myocarditis as a separate entity.

28. [95]

    In her first report of 15 June 2012, Professor Keogh stated:

29. [96]

    Professor Keogh considered that each of the features referred to in paragraph [17] of her report were constitutional medical conditions and not related to employment. Having regard to the findings on autopsy, Professor Keogh expressed the opinion that a ventricular fibrillation arrest could have occurred at any stage of Mr Christensen’s life irrespective of his employment. [54]

30. [97]

    In her next report of 14 June 2013 (which was written in response to a request from Tudor Capital’s solicitors to comment on Professor Rawlinson’s report), Professor Keogh disagreed with Professor Rawlinson’s assertion that the autopsy did not find a cause of Mr Christensen’s death.

31. [98]

    Professor Keogh said that the key findings on cardiac microscopy that were clearly abnormal were interstitial fibrosis, myocyte hypertrophy most pronounced in the right ventricle and myocyte disarray. She expressed the opinion that the myocyte hypertrophy most pronounced in the right ventricle may be attributed to Mr Christensen’s exercise regime but it could also be an intrinsic condition, for example a form of hypertrophic cardiomyopathy.

32. [99]

    Professor Keogh expressed the view that interstitial fibrosis and myocyte disarray were distinct histological abnormalities which could not be ignored. She said that interstitial fibrosis was the anatomic substrate which gives rise to ventricular arrhythmias. She observed that even mild interstitial fibrosis could allow an abnormal electrical pathway giving rise to a lethal arrhythmia.

33. [100]

    Professor Keogh also observed that myocyte disarray was not a normal finding and occurred with primary myocardial disease, most usually hypertrophic cardiomyopathy which she described as “an endogenous disease not known to be associated with any environmental factors and taking various forms with courses which range from benign to malignant (meaning resulting in sudden death).

34. [101]

    She also rejected Professor Rawlinson’s diagnosis of viral myocarditis as it was not seen at autopsy, and as there were no histopathological hallmarks for it on post mortem. She noted evidence of Mr Christensen being breathless and lethargic on the day he died, and being found in ventricular fibrillation. She said that those matters constituted circumstantial clinical evidence “consistent with the above”.

35. [102]

    The Arbitrator treated the last phrase as referring to “circumstantial clinical evidence consistent with a diagnosis of myocarditis”. [55] I doubt that that is so as Professor Keogh had already excluded viral myocarditis in the previous paragraph of her report. Rather, in my view it is more probable that Professor Keogh was referring to interstitial fibrosis and hypertrophic cardiomyopathy (the hallmark of which was the myocyte disarray which was present on post mortem) which, as I have said, she had already expressed the opinion were consistent with abnormal findings on cardiac microscopy. [56]

36. [103]

    Professor Keogh agreed with Professor Rawlinson that any relationship between psychological stress and viral illness was unproven. [57] She observed that there was no need to invoke conjecture in the present case, “when the histological diagnosis so clearly points to a primary cardiac cause of death with two contributing histological and pathophysiological pathways being evident.”

37. [104]

    Professor Keogh also opined that premature coronary artery disease and features of hypertrophic cardiomyopathy identified in the Coroner’s autopsy report were “pre-existing conditions [and] were the cause of death [and] it is probable that these would have caused morbidity and/or mortality at some stage in [Mr Christensen’s] life irrespective of his employment with [Tudor Capital].”

38. [105]

    Professor Keogh concluded that Mr Christensen’s death could most accurately be said to be due to a primary ventricular arrhythmia, for which there were two structural causes, one being interstitial fibrosis and the other moderate coronary artery disease, both of which she described as constitutional conditions. She expressed the view that these constitutional factors substantially contributed to his death.

39. [106]

    In her third report dated 8 August 2013 in which she was asked to comment on Associate Professor Richards’ report of 9 September 2011, Professor Keogh disagreed with his conclusion that it was more likely than not that stress at work had caused or aggravated the viral illness which itself caused or aggravated ventricular fibrillation and cardiac arrest. Professor Keogh said that the primary problem was constitutional and that the key abnormality on autopsy – “the key substrate for ventricular fibrillation” – was myocyte disarray and fibrosis, both known to be associated with sudden death. [58]

40. [107]

    Professor Keogh observed that insofar as Associate Professor Richards had considered the findings post mortem were consistent with four possible diagnoses – viral myocarditis, arrhythmogenic RV (right ventricular) dysplasia, arteriosclerotic coronary artery disease and idiopathic ventricular fibrillation – arteriosclerotic coronary artery disease was the primary abnormality and that, combined with fibrosis, this was the “single highly probable cause of the ventricular fibrillation, which led to death”. She added that a hypertrophic cardiomyopathy could not be excluded as the Coroner noted “some myocyte disarray in the right ventricle.”

41. [108]

    Professor Keogh also pointed out that no myocarditis was detected at autopsy, neither was any intermyocyte edema or myocyte necrosis [59] seen on microscopy, they being the histopathological hallmarks of a viral myocarditis. She observed that not all of the heart “would have been studied” but that samples had been taken which showed no features consistent with a myocarditis. [60]

42. [109]

    Professor Keogh accepted that it was possible, but she said “not probable, that the viral illness caused ventricular fibrillation, cardiac arrest and death of [Mr Christensen]” and, again, that it was “possible, but not probable, that ventricular fibrillation or cardiac arrest was aggravated, accelerated, exacerbated, or a deterioration caused by the viral illness.” [61]

43. [110]

    When asked to describe the relationship between non work related matters, conditions and the suspected cardiac event, Professor Keogh observed that “[s]udden death from a primary ventricular arrhythmia due to underlying structural cardiac fibrosis or due to ischemia from moderate coronary artery disease can occur at any time – during sleep, rest, recreation [and does] not require a discernible triggering event.”

44. [111]

    In her report of 11 February 2014, Professor Keogh explained her expertise in reading cardiac biopsies when a pathologist was not available, something she said she had done since 1986 up to 25 times a week under the tutelage of pathologists at St Vincent’s hospital. She was also asked to clarify some statements in her 8 August 2013 report. One of these was her use in that report of the word “possible”. She said that she had used that word in relation to “4 possible diagnoses entertained by A/Prof Richards” when she meant “proposed”. She said she did not mean “possible” because her “view [was] that Mr Christensen died of ventricular fibrillation, due to structural cardiac abnormalities which included coronary artery disease, cardiac fibrosis, right ventricular myocyte hypertrophy and myocyte disarray.”

45. [112]

    Professor Keogh was also asked to clarify in her 11 February 2014 report some statements in her 14 June 2013 report. In the course of this exercise, Professor Keogh stated that “myocarditis is only rarely a cause of heart failure or of sudden death, compared to the far more commonly seen coronary artery disease.” In her opinion “the absence of histological changes of myocarditis (edema, myocyte necrosis, lymphocyte and monocyte infiltrate) rules out myocarditis as a cause of death in Mr Christensen.”

46. [113]

    In her report of 12 August 2014, asked to comment on Associate Professor Richards’ opinion “that a virus, due to stress at work, caused VF [ventricular fibrillation] death”, Professor Keogh said she could not “move away from the logic provided by the pathological changes seen at autopsy. Mr Christensen had coronary artery disease, myocyte disarray and fibrosis, all of which are known substrates for VF [ventricular fibrillation]. Mr Christensen did not have changes of viral myocarditis.” [62]

47. [114]

    In her report dated 13 March 2015 Professor Keogh endorsed the view in the Dallas criteria “that histology was the ‘gold standard’ for establishing a diagnosis of myocarditis. She said that there was only one method to diagnose myocarditis conclusively post mortem which was where histology showed an inflammatory cell infiltrate and cell death. In this present case, “where large pieces of the whole myocardium were available after death for histological examination, they showed no inflammation” which, she opined, meant no myocarditis. [63]

48. [115]

    Like Dr Rainer, Professor Keogh first had access to the autopsy slides in 2015. Asked to comment on them in her 13 March 2015 report, she wrote:

49. [116]

    Professor Keogh also expressed the view in this report that there was far more myocardium shown on the autopsy slides than would be supplied by multiple biopsies, and the size of the sample was large enough to overcome any sampling errors. [64] She was highly certain that the cause of Mr Christensen’s death was an established cardiomyopathy of months to years duration based on the structural changes of the myocytes, a mode of death known to involve ventricular fibrillation. She said that the coronary artery disease, the myocyte disarray and fibrosis (chronic cardiomyopathy) seen at autopsy were all known substrates for ventricular fibrillation. She added that Mr Christensen did not have changes of viral myocarditis.

50. [117]

    In her oral evidence, Professor Keogh described seeing the autopsy slides as “a bit of a defining moment”, rather than simply interpreting Dr Elston’s findings. [65] She also said they were “a bit of a game changer”. [66] She said it was “really important to … work from the source document…which…were the whole heart … which was sliced up and sampled.” She said the slides revealed Mr Christensen to be suffering hypertrophic cardiomyopathy. [67] She said that people with that condition are prone to ventricular fibrillation sudden death, that ventricular fibrillation was an instantaneous event and that in Mr Christensen’s case, sudden death was the first symptom. [68]

51. [118]

    Professor Keogh described the “fibre disarray” apparent on the slides was “very specific for hypertrophic cardiomyopathy”. She also said hypertrophic cardiomyopathy was a genetic disorder which was not stress-related, but was an “innate structural constitutional disease and doesn’t have much to do with the environment at all.” [69] She said that after seeing the slides, she had set aside her view concerning the existence of relevant coronary artery disease, instead preferring the diagnosis of hypertrophic cardiomyopathy as being the relevant abnormality leading to cardiac arrest and death.

52. [119]

    Professor Keogh compared the slides on page 8 of exhibit 12. She described that on the left hand side as “viral myocarditis, show[ing] that the linear muscle cells are broken up and they’re being eaten and damaged by inflammatory cells and … the dark black dots are the nuclei of very active lymphocytes and white cells which have been stimulated by the virus to come in and attack the heart muscle…”. She described the one on the right hand side depicting Mr Christensen’s biopsy as “[not] show[ing] those black nuclei”, but as showing “disarrayed muscle [sic, as in original transcript; should be “myocyte”] cells …all the nuclei are differing sizes which shows how incredibly stirred the myocardium actually is, and no inflammatory cells, very distorted myocytes…no myocarditis”. She said that hypertrophic cardiomyopathy did not need a trigger, rather it was the “abnormal myocytes … the disarray of myocytes that are the whole problem and the propagator of sudden death.”

53. [120]

    Professor Keogh was firm in her evidence that, absent histological evidence of inflammatory cells and lymphocytes with active black nuclei as depicted on the left hand slide on page 8 of exhibit 12, Mr Christensen did not have viral myocarditis. She attributed the breathlessness he experienced in the afternoon to a rhythm disturbance which was not as malignant as the ventricular fibrillation, perhaps atrial fibrillation or ventricular tachycardia, being short runs of ventricular fibrillation not sufficient to kill a person.

54. [121]

    Professor Keogh said that she was unaware whether viral myocarditis started focally or not, but said that by the time it became clinically evident, a person had heart failure, the classic features of which were a thick-walled heart on echocardiogram, breathlessness, fever and the white cell count in their blood. In addition, she said, the microscopy looked as it did in the case of the autopsy slides, looking at page 8 of those slides, on the left hand side where a sample of myocarditis showed “the little black active nuclei.” She thought in Mr Christensen’s case the breathlessness he exhibited in the afternoon may have been a clue, although it is clear from a subsequent answer that she was speaking theoretically.

55. [122]

    Professor Keogh rejected the proposition that there could be an undetected viral myocarditis, saying a viral myocarditis diagnosis “requires inflammatory cells, without inflammation there can be no myocarditis, since it’s against its definition”.

56. [123]

    In the course of cross-examination, Professor Keogh was asked about her first report in which she had not excluded the possibility of a viral myocarditis “since post mortem sampling does not sample the entire of the right and left ventricles.” Professor Keogh said that was written in reliance on the autopsy report which was written by a “generalist pathologist” and that was not the same as seeing the slides of the heart. Professor Keogh accepted that the slides “made it pretty clear that there was no room for a sampling bias that had managed to magically miss myocarditis.” According to Professor Keogh, it would be virtually impossible to miss viral myocarditis on autopsy, although she accepted “[t]here’s no such thing as absolutely or never”. She described this as a “semantic conce[ssion], not really to do with biology, pathology or medicine … that something impossible or hardly probable or highly unlikely can occur.” She said she had never seen a case of an acute viral myocarditis in a patient with an existing hypertrophic cardiomyopathy. She said they were two quite different conditions. Viral myocarditis was very rare, while hypertrophic cardiomyopathy was very common. [70]

57. [124]

    Professor Keogh in due course accepted that in her first report she was prepared to entertain viral myocarditis as a possible diagnosis, until she had “seen the slides of what’s very clearly a hypertrophic cardiomyopathy, not adequately underlined … by the pathologist’s report.”

58. [125]

    The Arbitrator was critical of Professor Keogh’s response to this line of questioning concerning her early view that viral myocarditis was a possible cause of Mr Christensen’s death. He said that, rather than admit that in her first report she had not excluded the possibility of a viral myocarditis, even though the sampling had not shown inflammation, she “gave a discursive answer which was critical of the Coroner’s pathologist”. [71] The Arbitrator set out extensive passages from Professor Keogh’s cross-examination, [72] in the course of which he variously observed that she “was losing patience with” the cross-examiner, becoming “somewhat assertive”, and beginning to “evade the [cross-examiner’s] questions.” [73]

59. [126]

    Although throughout this account, the Arbitrator was critical of what he described as Professor Keogh’s discursive answers, ultimately he did not express a view that this in any way detracted from her evidence that the slides showed Mr Christensen was suffering from hypertrophic cardiomyopathy and that that was the relevant abnormality leading to his cardiac arrest and death.

60. [127]

    Associate Professor Richards was not recalled to respond to the evidence of Dr Rainer or Professor Keogh. Although Mrs Christensen tendered his expert report dated 11 June 2015, in which, as I have said, he was asked to comment on Professor Keogh’s oral evidence, the only question to which it responded related to whether or not viruses which attack the throat or upper respiratory tract can also attack the heart and cause viral myocarditis to which he responded in the affirmative.

Submissions to the Arbitrator

1. [128]

   Because Mrs Christensen contended that the manner in which Tudor Capital advanced its case in this Court on the medical issues was not advanced in the Commission, it is necessary to look at the way the parties’ cases in this respect were put there, the detail of which does not appear in the Arbitrator’s reasons. Although it appears from the transcript that the Arbitrator may have been provided with written submissions from, at least, Mrs Christensen’s counsel, no written submissions to the Arbitrator were included in the appeal books, only those made on the appeal from the Arbitrator to the Presidential Member. Neither party, in particular Tudor Capital, contended it was necessary for this Court to have access to any such submissions.

2. [129]

   Mr Grant who appeared for Tudor Capital before the Arbitrator submitted that the evidence established “overwhelmingly” cardiomyopathy was the most likely cause of Mr Christensen’s ventricular fibrillation and death. He said that the case was one of “two conflicted views as to the cause” of death, and that the issue was which was the more probable. He sought to distinguish Seltsam Pty Ltd v McGuiness [74] on the basis that, having regard to the competing evidence about causation, the case was not one which could be resolved by recourse to circumstantial evidence.

3. [130]

   Mr Grant submitted that there was no evidence which contradicted Dr Rainer’s, he having been the only pathologist who gave evidence. He emphasised that Dr Rainer’s expertise was examining material from the heart, that he had expressed the opinion that the tissues taken at autopsy were sufficient to eliminate sampling error, that the tissues did not demonstrate acute myocarditis and that Mr Christensen was not suffering from that condition when he died. In addition, he drew attention to Dr Rainer’s evidence that the autopsy “made positive pathological findings of a chronic longstanding disease process in the form of histological findings of fibrosis, myocyte hypertrophy and myocyte disarray [which] establish[ed] the presence of a disease process that is chronic and longstanding, not acute.” [75]

4. [131]

   Mr Grant explained the way the case had evolved in terms of the parties having only recently obtained access to the autopsy slides. He took the Arbitrator in detail through Dr Rainer’s second report and his explanation of what was depicted in the autopsy slides, concluding with the submission based on Dr Rainer’s opinion, that Mr Christensen’s death was highly probable to have been caused by an arrhythmia caused by interstitial fibrosis developing as a complication of cardiomyopathy to which his occupation and employment were not contributing factors. Mr Grant submitted that that was a clear cause of death which was not contradicted on the available pathology from the autopsy. He explained that in a case of viral myocarditis the virus attracts the inflammatory cells which inflict the damage and cause the arrhythmia and that there was no evidence of that phenomenon on the autopsy slides.

5. [132]

   Mr Grant also submitted that Professor Keogh’s evidence that Mr Christensen died of hypertrophic cardiomyopathy which was a genetic and constitutional defect and not due to viral myocarditis was not met by Mrs Christensen’s evidence. He pointed out that her evidence was consistent with Dr Rainer’s.

6. [133]

   Mr Grant then took the Arbitrator through Professor Keogh’s evidence concerning Mr Christensen having a hypertrophic cardiomyopathy which was a “highly genetic disorder” and an “innate, structural, constitutional disease” which did not have much to do with the environment.

7. [134]

   Conversely, Mr Grant emphasised that there was no evidence that Mr Christensen suffered from myocarditis. He submitted that Associate Professor Richards was expressing an opinion based upon a set of possibilities in that he thought Mr Christensen’s death was due to myocarditis because that can lead to ventricular fibrillation, even though there was no proof in fact that Mr Christensen suffered from that disorder. He pointed out that Associate Professor Richards had conceded he was not a pathologist and, accordingly, had not looked at the autopsy slides.

8. [135]

   Mr Grant criticised Associate Professor Richards’ theory that Mr Christensen had myocarditis notwithstanding that there was no evidence for that proposition, whereas cardiomyopathy “was a very persuasive basis for why [Mr Christensen] might go into ventricular fibrillation”.

9. [136]

   Mr Grant submitted that the fact Mr Christensen had an upper respiratory tract infection prior to his death had nothing to do with what caused his death, but, rather, was a coincidence. He submitted that it would be to disregard Dr Rainer’s evidence to regard the autopsy sampling as “patchy” and that Mrs Christensen had to persuade the Arbitrator that there was some focal point myocarditis which did not show up in the autopsy which had caused the ventricular fibrillation.

10. [137]

    Mr Wardell, who appeared for Mrs Christensen before the Arbitrator, submitted that Mr Christensen suffered one of two personal injuries, either the entry of the virus into his body, in particular, into his upper respiratory tract, or the entry of the virus into the myocardium causing defibrillation and death.

11. [138]

    Mr Wardell emphasised Dr Rainer’s evidence that there was a possibility that myocarditis could have been missed if there was a relatively short time between the onset of the inflammation and death, albeit he thought in terms of likelihood it to be “very unlikely because of the need to show damage.” He submitted that Dr Rainer’s concession was sufficient for Mrs Christensen’s purposes “to open up the argument that that possibility [became] a probability based on the evidence of Professor Richards.”

12. [139]

    Mr Wardell pointed out that to a large extent Mrs Christensen did not cavil with Dr Rainer’s evidence, accepting that Mr Christensen had fibrosis of long standing present, as demonstrated by the autopsy slides. He accepted the autopsy slides did not show inflammation consistent with myocarditis, but contended that that was not conclusive.

13. [140]

    Mr Wardell submitted that Associate Professor Richards had answered every opinion expressed by Professor Keogh and explained the basis upon which he disagreed with her. He contended that Professor Keogh was an unsatisfactory witness having regard to her general demeanour both in her reports and in her oral evidence.

14. [141]

    Next, Mr Wardell pointed out that Mr Grant had not put to Associate Professor Richards that this was a case of hypertrophic cardiomyopathy. Counsel accepted that the rule in Browne v Dunn [76] did not apply in the Commission but observed that Associate Professor Richards had been cross-examined on the basis that coronary artery disease was a more likely cause of Mr Christensen’s death, whereas the next day Dr Rainer and Professor Keogh had rejected that proposition and said that cardiomyopathy was the cause.

15. [142]

    Mr Wardell emphasised nevertheless that both Dr Rainer and Professor Keogh had accepted the possibility that Mr Christensen’s viral myocarditis was so focal by reason of its recency that it was not picked up on the autopsy slides.

16. [143]

    In reply, Mr Grant submitted that even if Professor Keogh’s evidence was, in effect, ignored, in the absence of any evidence of myocarditis, Mrs Christensen had to establish that was the most likely explanation for Mr Christensen’s death in the face of proven pathological changes with a proven explanation as to why ventricular fibrillation could be set off.

Arbitrator’s determination

1. [144]

   The Arbitrator first dealt with the temporal issue.

2. [145]

   Before the Arbitrator, Tudor Capital submitted that Mrs Christensen’s theory that stress had caused the breakdown of Mr Christensen’s immune system meant that she was advancing a case of psychological stress as demonstrated by the various temporal events upon which she relied. Tudor Capital submitted that the highest the evidence demonstrated was that Mr Christensen had suffered nothing more than from time to time emotional upset and frustration and that these could not constitute injury within the meaning of s 4 of the WCA. [77]

3. [146]

   The Arbitrator rejected that submission. In his view, Mrs Christensen’s case was that the frustrations and emotional upsets were such as to compromise Mr Christensen’s physical state of being and that it was a physical event which caused Mr Christensen’s death, namely the entry into the myocardium of the virus which he acquired because the stress caused him to become run down and susceptible to a viral illness. [78]

4. [147]

   In the Arbitrator’s view, Mrs Christensen’s case was founded on the proposition that the temporal events so weakened Mr Christensen’s immune system that he fell ill with a viral illness which acted on his heart causing him to go into ventricular fibrillation. The Arbitrator accepted that those events weakened Mr Christensen’s immune system so that he contracted a viral illness which, in turn, caused his eventual cardiac arrest. [79]

5. [148]

   After summarising Mrs Christensen’s evidence concerning the stress of the move to Sydney, the Arbitrator found that those stresses were not significant in the onset of Mr Christensen’s viral illness and that the deterioration in his health did not occur until sometime in August after the domestic issues had settled down. [80]

6. [149]

   The Arbitrator then turned to the technical frustrations Mr Christensen experienced at work in adjusting to working in the Sydney office. He found that the “IT difficulties” were relevant matters in the eventual deterioration of his health. [81] He also concluded that being placed on the watch list, and the late notice of that fact, was one of many factors which contributed to the breakdown of Mr Christensen’s health. [82]

7. [150]

   The Arbitrator said the evidence satisfied him that because of the particular stress to which Mr Christensen was subject in 2008, his health suffered. He made the following finding:

8. [151]

   The Arbitrator was also satisfied that the letter of condolence dated 6 November 2008 sent by Mr Jones contained admissions, among other matters, that Mr Christensen and others were experiencing heightened stress and anxiety in 2008 and that the fact that Mr Christensen had been placed on a watch list was not communicated to him until close to his death. [83]

9. [152]

   In respect of the temporal dispute, the Arbitrator concluded:

10. [153]

    The Arbitrator then turned to the medical issue. He described the approach to causation in assessing the medical evidence described in Murray v Shillingsworth [84] and Woolworths Ltd v Christopher-Coates [85] as critical in the determination of the case. [86] He rejected Tudor Capital’s submission that, as a matter of common sense following the causal chain, the most likely explanation for Mr Christensen’s death was that given by Dr Rainer and Professor Keogh, whose evidence was based on a scientific premise, being the post mortem analysis of the histopathology in the tissue samples which exhibited disarray that was indicative of death by cardiomyopathy. He held that “the disarray present post mortem was equally consistent with a cardiac arrest being caused by a viral myocarditis.” [87]

11. [154]

    The Arbitrator noted that although Dr Elston was unable to ascertain the cause of Mr Christensen’s death, his autopsy report allowed for the possibility that a lesion occurred in Mr Christensen’s heart and death occurred so rapidly that no changes could be identified. The Arbitrator also noted that Dr Rainer agreed that there would not be diffuse changes shown where death had followed shortly after the entry of the virus into the myocardium. Dr Rainer also said there must be some histological evidence of the damage thereby caused. He referred to Dr Rainer’s evidence concerning the focal diffuse spread of myocarditis. [88]

12. [155]

    The Arbitrator noted that Dr Whalley was of the opinion that the post mortem process was so “patchy” that it may not show up an inflammatory infiltrate. [89] The Arbitrator also noted Professor Keogh had also held that view in her original report of 15 June 2012 which had allowed for the possibility of a viral myocarditis on the basis that post mortem sampling did not sample the entirety of the right and left ventricles. However Professor Keogh had abandoned that opinion for reasons the Arbitrator did not find persuasive. He referred to Professor Keogh’s evidence describing the late discovered autopsy slides as a “game changer.” He clearly did not accept that view, describing the autopsy slides as no more than the post mortem sampling, the defect in which (that they did not sample the entirety of the right and left ventricles, nor the septum) had been the basis for her original opinion. He concluded that he was not satisfied that the extent of the sample taken was able to “negate that fundamental problem with the post mortem process that is to say, that it sampled only parts of the relevant tissue.” [90] In that respect, the Arbitrator acknowledged the evidence of Dr Rainer who said that because the cause of death had not been ascertained in the sudden death of a young man, a larger sample than usual was taken at post mortem. [91]

13. [156]

    Mrs Christensen accepted Dr Rainer’s evidence that the post mortem tissue sample subjected to histopathological examination did not show any signs of myocarditis. The Arbitrator accepted that Associate Professor Richards was incorrect in his assumption as to the size of the samples taken, however he did not regard that error as significant. He accepted (as indeed he said was conceded by Professor Keogh) that it was possible that nonetheless myocarditis had been the cause of death. He said that whether this (referring to the absence of histopathological evidence) was because, notwithstanding the adequacy of the sampling, somewhere else within the ventricular area or the septum of the heart there may have been the inflammatory signs that would be consistent with myocarditis, or because the viral attack was so sudden that it left little trace, or a combination of both, was a moot point. In any event, in his view, the size of the samples was not critical to Mrs Christensen’s contention. [92]

14. [157]

    The Arbitrator was satisfied that Mr Christensen probably died within hours of the entry of the virus into his heart and that the failure of the tissue samples to reveal any sign of myocarditis was consistent with a recent attack, as the histological evidence “may not have been diffuse, and was accordingly missed.” [93]

15. [158]

    The Arbitrator accepted that the consequence of this finding was that he rejected Professor Keogh and Dr Rainer’s evidence that the cause of death was hypertrophic cardiomyopathy. [94] This appears to have been, in part at least, because he had “considerable difficulty in accepting that the death of [Mr Christensen] at that particular moment was unconnected to the sequence of [temporal] events” he had earlier described. [95]

16. [159]

    The Arbitrator was satisfied that Mrs Christensen had established there was a causal chain of circumstance that resulted in the deterioration of Mr Christensen’s health, allowing the introduction of a viral illness into his body. He accepted the evidence of both Professor Rawlinson and Associate Professor Hudson that there was a “connection, as yet not fully understood, between stress and the risk of viral illness.” He said “[t]he nature of that stress was frustration and emotional upset.” [96]

17. [160]

    The Arbitrator was also satisfied that the viral illness from which Mr Christensen was suffering had “caused the myocarditis by affecting [his] heart when he became breathless earlier in the evening.” In this respect, he accepted the evidence of Associate Professor Richards that it was that episode of breathlessness which was the first involvement of the heart with the viral illness. [97]

18. [161]

    The Arbitrator held that there was “a clear causal link between all these events.” [98] He was satisfied, in so doing he said, paraphrasing Herron CJ in EMI (Aust) Ltd v Bes, that “medical science has been prepared to say that the cause of death may have been by virtue of the intrusion into the myocardium of a virus which caused the ventricular fibrillation and cardiac arrest … [and that] medical science does not say in this individual case that there is no possible connection between the events and the death – either the connection between stress and the breakdown of [Mr Christensen’s] health allowing the entry into his system of a viral illness, or the subsequent entry of the virus by virtue of the T cell lymphocytes into [Mr Christensen’s] myocardium causing ventricular fibrillation and cardiac arrest.” [99]

19. [162]

    After referring to Kooragang Cement Pty Ltd v Bates [100] for the proposition that “whether a condition has resulted from a relevant work injury is a question of fact [and] what is required is a commonsense evaluation of the causal chain,” [101] the Arbitrator concluded:

20. [163]

    Accordingly, the Arbitrator concluded that Tudor Capital was liable to pay compensation pursuant to s 25 of the WCA.

Appeal to Presidential Member

1. [164]

   Tudor Capital appealed against the Arbitrator’s decision pursuant to s 352 of the WIM Act. Such an appeal is not a review or new hearing, but is limited to a determination of whether the decision appealed against was or was not affected by any error of fact, law or discretion, and to the correction of any such error. [103]

2. [165]

   Section 352 in its present form was inserted into the WIM Act by the Workers Compensation Legislation Amendment Act 2010 (NSW) (2010 Act). The amendment was intended to overcome the decision in Sapina v Coles Myer Limited. [104] In that decision, according to the Parliamentary Secretary, Mr Michael Veitch, who delivered the Second Reading Speech to the Bill which became the 2010 Act, “the Court of Appeal extended the scope of appeal rights [pursuant to the WIM Act from an Arbitrator to a Presidential member] by determining that an appeal is to proceed by way of a full review of the arbitrator’s decision, irrespective of the identification of any error by the arbitrator.” The 2010 Act was intended to reverse the effect of Sapina by restricting appeals under s 352 of the WIM Act to cases in which there is “legal, factual or discretionary error.” [105]

3. [166]

   The power s 352(5) confers, which enlivens the power pursuant to s 352(7) to revoke a decision and make a new decision, or to remit the matter to the Arbitrator, is a narrow one “to correct operative error of fact, law or discretion”. [106] The Commission constituted by a Presidential member does not have a general discretion on appeal to reopen or reconsider the Arbitrator's decision. [107]

4. [167]

   An error for the purposes of s 352(5) could have been identified if the Deputy President found the Arbitrator had overlooked material facts, or given material facts undue or too little weight in deciding the inference to be drawn, or if the available inference in the opposite sense to that the Arbitrator chose was so preponderant in the opinion of the Deputy President that the Arbitrator’s decision was wrong. [108]

5. [168]

   Tudor Capital relied on five grounds of appeal. [109] Ground 1 asserted that the Arbitrator reversed the onus of proof when he stated that “the [employer’s] case needed to demonstrate that medical science denied at least one of the two causal pre-conditions to the [respondent’s] case.” [110] Tudor Capital also asserted that the reasoning of the Arbitrator demonstrated that he had had regard to the incorrect standard of proof concerning the medical question as to probable cause of death. [111]

6. [169]

   Ground 2 contended that the Arbitrator had made a number of erroneous findings of fact, including:

7. [170]

   Ground 3 asserted that the Arbitrator had erred in finding [117] that the ventricular fibrillation that caused Mr Christensen’s death was caused by viral myocarditis. Ground 4 contended that the Arbitrator had failed to apply s 9A of the WCA correctly to the facts. [118] Finally, ground 5 claimed that the Arbitrator had wrongly rejected the evidence of Professor Keogh. [119]

Submissions

1. [171]

   Insofar as ground 1 was concerned, Tudor Capital submitted first, that the onus rested on Mrs Christensen to establish her case on the balance of probabilities rather than it being for it to demonstrate that medical science denied at least one of the two causal preconditions of her case. Secondly, it submitted that paragraph [271] of the Arbitrator’s decision showed that his acceptance of Mrs Christensen’s case was based on an assumption that all she was required to show was that medical science was unable to deny the causal “possibility of a link between emotional stress and the risk of viral illness, and the possibility that the cause of the ventricular fibrillation was a viral myocarditis”. In this respect, Tudor Capital submitted that the Arbitrator misdirected himself as to what was required to be proved and by whom.

2. [172]

   Tudor Capital also submitted that the Arbitrator misunderstood the import of EMI (Aust) Ltd v Bes, Adelaide Stevedoring Co Ltd v Forst, [120] and St George Club Ltd v Hines. [121] In short, Tudor Capital submitted that the Arbitrator had to look at the whole of the evidence in determining causation. [122] Tudor Capital submitted that the reversal of the onus of proof caused a miscarriage of justice in that the Arbitrator had misdirected himself as to the assessment of fact and as to the conclusions to be established by each party.

3. [173]

   Insofar as ground 2 was concerned, Tudor Capital submitted that the Arbitrator’s finding in paragraph [272] in that the “injury consisted of the entry of the T cell lymphocytes into the myocardium as a result of a viral illness [Mr Christensen] had acquired …” was not supported by evidence but, rather, was essentially speculative. It made the same submission in respect of the Arbitrator’s conclusion in paragraph [229] that the “[temporal] events operated to weaken [Mr Christensen’s] immune system so that he contracted his viral illness … [which] caused his eventual cardiac arrest.” It argued that this was a significant finding because of the absence of histological confirmation of the presence of viral myocarditis.

4. [174]

   Tudor Capital submitted that there was no evidence that T cell lymphocytes entered Mr Christensen’s myocardium, that his viral illness was acquired following a breakdown of his health or that his health broke down as distinct from having a viral illness. It contended that the evidence of the relationship between Mr Christensen’s viral illness and the emotional stress or frustration he encountered with his employer was tenuous at best and fell far short of supporting the finding that the viral illness was due to emotional stress.

5. [175]

   Tudor Capital contended that the Arbitrator’s conclusion [123] that employment events operated to weaken Mr Christensen’s immune system so that he contracted his viral illness was unsupported by evidence and that the mechanism by which Mr Christensen acquired his viral illness was not established. It contended that there was nothing to suggest that Mr Christensen would not have acquired his viral illness whether or not he had been exposed to the emotional stress the subject of evidence.

6. [176]

   Tudor Capital referred to Professor Rawlinson’s evidence concerning the unproven relationship between psychological stress and viral illness. It also referred to Associate Professor Hudson’s evidence that viral illness such as that which Mr Christensen suffered was common and affected a large percentage of the population annually. It also referred to Associate Professor Hudson’s evidence that, while there was likely a relationship such as Professor Rawlinson discussed, it was not well characterised, explained or understood and that there were multiple confounding factors making it difficult to characterise such a relationship even in a controlled setting of a research trial. Tudor Capital emphasised that the tenuous connection Professor Rawlinson and Associate Professor Hudson contemplated between stress and the risk of viral illness was “unproven” and argued that this was far from establishing on the balance of probabilities that Mr Christensen’s viral illness was acquired from a breakdown of his health due to emotional stress and frustration. Tudor Capital also submitted that the Arbitrator had ignored Associate Professor Hudson’s conclusion that the viral infection was merely “intercurrent”, that is to say, unconnected to the coronary artery disease Mr Christensen suffered and therefore merely coincidental and unrelated to his death. [124] Tudor Capital argued that the “unproven” suggestion did not satisfy Mrs Christensen’s burden of establishing on the balance of probabilities that there was a connection of a causative nature between the events in the course of employment and the viral illness. Accordingly it submitted that the consequence of these factual errors was that the nexus between the alleged stress at work and ventricular fibrillation was not established.

7. [177]

   Insofar as ground 3 was concerned, Tudor Capital complained about the Arbitrator’s findings in the first sentence of paragraph [254] and paragraphs [267] – [268]. It noted the conflicting opinions as between Associate Professor Richards’ opinion that Mr Christensen’s condition was caused by viral myocarditis and Professor Keogh’s that it was brought on by hypertrophic cardiomyopathy. It contended that Mrs Christensen bore the burden of establishing facts which positively suggested that Associate Professor Richards’ opinion was to be preferred.

8. [178]

   Tudor Capital referred to Associate Professor Richards’ report of 2 September 2013 and his oral evidence to the effect that viral myocarditis could be diagnosed in Mr Christensen’s case absent histological findings on autopsy on a clinical basis. Tudor Capital submitted that even assuming some cases of viral myocarditis may be missed, Mrs Christensen had not adduced evidence which explained why on the balance of probabilities Mr Christensen’s alleged viral myocarditis was not detected. It submitted on the basis of Dr Rainer’s evidence that the samples of tissue taken from Mr Christensen on autopsy were sufficient to conclude that there was no real prospect of the presence of myocarditis being missed if it was in fact present. It submitted, in effect, that Dr Rainer’s evidence, he being a cardiac pathologist, concerning the manner in which myocarditis leads to ventricular fibrillation should be accepted and that evidence established that in order for there to be a diagnosis of viral myocarditis, there must have been inflammation and myocyte damage. Tudor Capital criticised Associate Professor Richards’ contention that while the presence of histological changes of viral myocarditis may confirm its presence, the converse did not apply, as a speculative basis to explain the absence of histological changes insofar as it relied on the proposition that the area where the necessary inflammation occurred was not sampled.

9. [179]

   Tudor Capital’s submissions then analysed the evidence concerning the extent of tissue, including Dr Rainer’s evidence that the autopsy comprehensively examined Mr Christensen’s whole heart and that nothing would be missed. Tudor Capital submitted that while Dr Rainer’s evidence appeared to have been accepted by the Arbitrator, [125] acceptance of his evidence meant that Associate Professor Richards’ sampling error theory should have been rejected. It contended that the Arbitrator’s preference for Associate Professor Richards’ opinion concerning sampling error meant that he accepted an hypothesis based on speculation and an unsubstantiated assumption that the autopsy slides failed to sample a focal area of inflammation. Tudor Capital submitted that Associate Professor Richards’ assumption could not be substantiated and, accordingly, was on the probabilities wrong such that the conclusion that Mr Christensen had viral myocarditis was not proven.

10. [180]

    Insofar as ground 4 dealing with s 9A of the WCA was concerned, Tudor Capital submitted that the Arbitrator’s conclusion at paragraph [273] that the pre-existing condition of Mr Christensen’s heart did not play any part in his death and that there was insufficient evidence to “raise that proposition” was wrong and was contradicted not merely by its experts but also by Associate Professor Richards’ opinion in his report of 2 September 2013 that it was “possible that ventricular fibrillation would not have occurred in this case in the absence of underlying myocardial pathology.”

11. [181]

    In this respect, Tudor Capital repeated a number of the submissions it made in relation to the earlier grounds concerning the absence of evidence capable of proving on the balance of probabilities any connection between Mr Christensen’s employment, and his contraction of a viral illness and the fact that at the time of his death Mr Christensen was not at work and was not performing any work duties at all.

12. [182]

    In addressing s 9A(2)(d) concerning the probability that the injury would have happened anyway, at about the same time or at the same stage of the worker’s life, if he or she had not been at work or had not worked in the particular employment, Tudor Capital drew attention to Professor Keogh’s evidence that Mr Christensen was suffering from hypertrophic cardiomyopathy, a condition prone to ventricular fibrillation which could occur at any time. It also referred to the fact that evidence of the hypertrophic cardiomyopathy was the disorder and disarray showing fibrosis and scar tissue, and to Professor Keogh’s evidence that the fibre disarray was specific for hypertrophic cardiomyopathy. Tudor Capital submitted that, accordingly, Mr Christensen suffered from a pre-existing condition which rendered it likely that at some point of time he would suffer sudden death. On this basis, Tudor Capital submitted that on no view could Mr Christensen’s employment be regarded as a substantial contributing factor to the ventricular fibrillation which resulted in his death.

13. [183]

    In respect of ground 5, Tudor Capital submitted that Professor Keogh’s evidence could not be “dispose[d] of” by the Arbitrator on the basis that he was unconvinced by her explanation of her changed opinion. It noted that the Arbitrator had not made a finding that he disbelieved Professor Keogh, nor that her evidence was tainted by dishonesty, was misleading, was a product of advocacy for Tudor Capital or was inherently unreliable.

14. [184]

    In those circumstances, Tudor Capital submitted the Arbitrator was required to enter into the issues covered by her evidence and explain why Associate Professor Richards’ views were to be preferred to those of Professor Keogh and Dr Rainer. It contended that although the Arbitrator set out the medical evidence at length, he did not deal with the conflicting hypotheses as between the parties’ experts. In particular, Tudor Capital submitted, he did not adequately address Professor Keogh’s central hypothesis that the cause of the ventricular fibrillation was hypertrophic cardiomyopathy. It submitted that he had rejected her evidence on an unacceptable basis, namely that she changed her opinion for what he regarded as unconvincing reasons.

15. [185]

    Tudor Capital submitted that had the Arbitrator analysed Professor Keogh and Dr Rainer’s evidence on a probabilistic basis, he would have preferred their explanation for Mr Christensen’s death to that of Associate Professor Richards. It contended that Dr Rainer’s evidence concerning sample size and the unlikelihood of myocarditis having been missed on autopsy sampling was overwhelming.

16. [186]

    Tudor Capital’s submissions addressed in detail Professor Keogh’s explanation for the alteration of her views concerning the cause of Mr Christensen’s death, her oral evidence concerning the nature of hypertrophic cardiomyopathy, her detailed explanations of her reasoning for the cause of Mr Christensen’s death, including her evidence that ventricular fibrillation could have occurred “at any moment”, all of which evidence Tudor Capital submitted was unchallenged but was not really engaged with by the Arbitrator. Tudor Capital submitted that Dr Rainer and Professor Keogh’s evidence was based on the pathological evidence and the application of their expertise to the contents of the autopsy slides.

17. [187]

    Tudor Capital submitted the Arbitrator erred in preferring Associate Professor Richards to Professor Keogh. It argued that while Associate Professor Richards had agreed both that viral myocarditis was not histologically proven and that Mr Christensen suffered from a pre-existing condition of cardiomyopathy of long standing duration, in contrast to its experts, his hypothesis of the case depended on it being established that the negative result for viral myocarditis on histopathology was wrong.

18. [188]

    Mrs Christensen submitted that in order to disturb the Arbitrator’s findings Tudor Capital had to show that the fact finding process miscarried. She contended that the Arbitrator had not overlooked any material facts and that his reasoning was transparent, logical and reasonable.

19. [189]

    Mrs Christensen submitted that Tudor Capital’s submissions constituted merely a disagreement with the Arbitrator’s findings and decision which were reasonably open to him on the evidence. She contended that the Arbitrator undertook a painstaking analysis of the evidence including the experts’ opinions, drew conclusions as to the facts that were available on the basis of probative material and, when required, drew reasonably available inferences. She contended that the Arbitrator had the benefit of seeing the oral evidence in cross-examination of the expert witnesses, [126] and gave his detailed reasons as to why he preferred some evidence over other and his conclusions should not be disturbed or revoked.

20. [190]

    Insofar as ground 1 was concerned, Mrs Christensen submitted that the Arbitrator had not reversed the onus of proof but, rather, at paragraph [271] of which Tudor Capital complained, simply set out the contest between the parties.

21. [191]

    Insofar as ground 2 was concerned, Mrs Christensen again submitted that the Arbitrator had set out the evidence in support of the temporal issue in detail, and had correctly identified the matters which required determination (to which the submissions then referred in detail). Her submissions also referred to the Arbitrator’s analysis of the medical evidence, observing that it was his task to determine the medical issue by analysing all the evidence and deciding which opinions he preferred by reference to the quality and cogency of the reasoning they exposed to support their opinions.

22. [192]

    Mrs Christensen submitted that it was open to the Arbitrator to find that the “disarray present post mortem was equally consistent with a cardiac arrest caused by a viral myocarditis” as the evidence was that myocyte disarray was a key substrate for ventricular fibrillation. As to Tudor Capital’s complaints concerning the Arbitrator’s finding about T cell lymphocytes entering the myocardium, Mrs Christensen relied on Dr Rainer and Professor Keogh’s evidence that that was the mechanism by which viral myocarditis led to inflammation of the heart muscle which, in due course, led to ventricular fibrillation. Accordingly, she submitted that once the Arbitrator accepted Mr Christensen was suffering from a viral illness, it was open to him to find that T cell lymphocytes entered the myocardium leading to ventricular fibrillation.

23. [193]

    Mrs Christensen submitted that the Arbitrator was entitled to rely on Dr Whalley’s, Professor Rawlinson’s and Associate Professor Hudson’s evidence concerning the relationship between emotional stress and viral illness and contended that his finding that Mr Christensen’s viral illness arose out of his employment was open to him on the basis of the expert and lay evidence.

24. [194]

    Mrs Christensen next submitted that the Arbitrator’s finding that the histological evidence of viral myocarditis was missed was open to the Arbitrator based on Dr Rainer’s evidence that not all of the heart was sampled and secondly, that Mr Christensen’s death occurred so suddenly that there may not have been time for the inflammation to manifest.

25. [195]

    Mrs Christensen also submitted that the Arbitrator was entitled to reject Professor Keogh’s evidence on the basis of her resiling from having entertained the possibility in her first report that viral myocarditis was a possible cause of Mr Christensen’s death as “post mortem sampling does not sample the entire of the right and left ventricles.”

26. [196]

    Finally, insofar as the issue of stress induced health allowing the introduction of a viral illness was concerned, Mrs Christensen said that the Arbitrator was entitled to rely on Professor Rawlinson’s and relevant parts of Associate Professor Hudson’s opinions to draw that inference.

27. [197]

    Insofar as ground 3 was concerned, again, Mrs Christensen rehearsed the expert opinion, contending that Tudor Capital’s submissions focused solely upon the histopathological findings at autopsy, whereas other evidence supported the Arbitrator’s conclusion. This included Dr Whalley’s evidence that the autopsy process could be “patchy”, that the inflammatory infiltrate may not show up because of the timing of the post mortem relative to the onset of viral illness, all of which evidence Mrs Christensen contended cast doubt on the autopsy results and whether they could be relied upon to exclude the possibility of viral myocarditis.

28. [198]

    Insofar as s 9A was concerned, Mrs Christensen submitted that the Arbitrator’s rejection of the proposition that the pre-existing condition of hypertrophic cardiomyopathy caused Mr Christensen’s death was reasonably open to him on the evidence, repeating in this respect her contentions concerning the proposition that viral myocarditis may not turn up on autopsy if death followed shortly after the entry of the virus into the myocardium. She contended that there was no other contributing factor to Mr Christensen’s injury such that the Arbitrator’s reasoning in respect of s 9A was logical and that, in the circumstances, there was no conclusion other than s 9A was satisfied and that the Arbitrator had been entitled to conclude that connection between Mr Christensen’s employment and the injury was “real and of substance”.

29. [199]

    Insofar as ground 5 was concerned, Mrs Christensen submitted that the Arbitrator properly analysed Professor Keogh’s evidence, was entitled to reject aspects of it based on her refusal to make concessions and her failure to sufficiently explain her retraction of her initial opinion that viral myocarditis was a possible cause of Mr Christensen’s death. She contended that a fair reading of the Arbitrator’s reasons was that he did not find Professor Keogh’s opinion helpful because her refusal to make concessions resulted in her becoming an advocate for Tudor Capital’s position rather than an unbiased expert. Mrs Christensen submitted that “the Arbitrator had observed that Professor Keogh became defensive and dogmatic in her responses under cross-examination, and appeared to adopt an adversarial approach, thus diminishing the weight of her opinion.” [127]

30. [200]

    Tudor Capital made lengthy submissions in reply. Without intending any criticism, those submissions to a large extent rehearsed those made in chief concerning the fact that there was histopathological evidence, that Mr Christensen had hypertrophic cardiomyopathy and that Mrs Christensen’s case depended upon two steps accepted by the Arbitrator only to the extent of possibility which was insufficient to establish the common law test of balance of probabilities. They also emphasised the adequacy of the sample of tissues taken on autopsy to identify viral myocarditis if present.

31. [201]

    Tudor Capital submitted there was no evidence to support the Arbitrator’s finding that the presence of post mortem myocyte disarray was equally consistent with a cardiac arrest caused by viral myocarditis. It drew attention to Professor Keogh’s evidence that myocyte disarray is a “hallmark” of hypertrophic cardiomyopathy both in her report of 8 August 2013 and in her oral evidence at Black 169, Black 171 and 172, evidence which was supported by that of Dr Rainer at Black 157. Tudor Capital also referred to Dr Rainer’s evidence that the point about myocyte disarray was that it represented evidence of a disease process which had been operative for a period of months to years and had resulted in eventual fibrosis, hypertrophy and myocyte disarray. [128]

32. [202]

    Insofar as the Arbitrator concluded that he was not satisfied that the extent of sampling of Mr Christensen’s tissues was able to negate the fundamental problem of patchiness in the post mortem process, Tudor Capital submitted that that conclusion was not logical. It pointed out that the Arbitrator had accepted that Associate Professor Richards’ assumption as to the sample size was incorrect at paragraph [261]. Further, it drew attention to the fact that the two pathologists who had viewed the autopsy material and concluded that there was no evidence of viral myocarditis did not regard the sample size as inadequate to form that opinion. It emphasised Dr Rainer’s opinion that the sample size was adequate. It also relied upon Professor Keogh’s conclusion having viewed the autopsy slides, that Mr Christensen’s heart had been adequately sampled. Tudor Capital contended that cross-examination intended to persuade Dr Rainer and Professor Keogh to concede that there was a possibility of sampling error could not prove that it had occurred. It contended that it was not open to the Arbitrator to reject the histopathological findings on the basis of sampling error.

33. [203]

    Tudor Capital submitted that the rejection of Professor Keogh’s evidence was erroneous and led inevitably to a preference for Associate Professor Richards’ opinion. It also submitted that the rejection of Professor Keogh’s evidence was inconsistent with the apparent acceptance of Dr Rainer’s evidence concerning the conclusions to be drawn from the autopsy slides.

Deputy President’s decision

1. [204]

   The Deputy President determined the application on the papers pursuant to s 354(6) of the WIM Act. [129] He first identified the errors of fact and law Tudor Capital relied upon. [130] He then canvassed the course of the hearing, the factual background and the medical dispute. [131] Next, he summarised the parties’ submissions before the Arbitrator. [132] Finally, the Deputy President set out the Arbitrator’s reasons. [133]

2. [205]

   In the course of setting out the Arbitrator’s reasons, the Deputy President referred to the passage where the Arbitrator recorded Professor Rawlinson’s qualification to his conclusion that it was “likely that stressful events in Mr Christensen’s life partly contributed to his susceptibility to viral illness in early September 2008”, that qualification being “there was no other cause found for Mr Christensen’s death at autopsy”. [134] He also noted Associate Professor Richards’ evidence that “[i]n the absence of previous evidence of cardiomyopathy or atherosclerosis and in the presence of a viral illness seen before death and in the presence of ... (not transcribable) ... associated with a viral illness seen before death I think the inescapable conclusion is that he had viral myocarditis as the cause of death.” [135]

3. [206]

   The Deputy President rejected the first ground of appeal. He accepted Tudor Capital’s submission that the Arbitrator was required to consider the whole of the evidence. [136] He also accepted that “the manner in which the Arbitrator structured his reasons causes difficulty when attempting to determine, with precision, the process of reasoning which he adopted.” [137]

4. [207]

   Nevertheless, the Deputy President was not persuaded that, read in the context of the Arbitrator’s reasons as a whole, the Arbitrator’s statement that Tudor Capital’s case “needed to demonstrate that medical science denied at least one of the two causal pre-conditions to [Mrs Christensen’s] case” constituted a reversal of the onus of proof. [138] The Deputy President accepted that the Arbitrator’s words were “apt to mislead”, [139] nevertheless, he held:

5. [208]

   The Deputy President then considered Tudor Capital’s contention that the standard of proof adopted by the Arbitrator “was less than the balance of probabilities”. [140] That contention was based on the Arbitrator’s statement that “[t]he possibility of a link between emotional stress and the risk of viral illness, and the possibility that the cause of the ventricular fibrillation was a viral myocarditis have both been accepted”. [141]

6. [209]

   The Deputy President held that while Tudor Capital’s submissions had considerable force, [142] when regard was had to the Arbitrator’s reasons as a whole, it was clear that the Arbitrator “had regard to correct principle concerning [the] standard of proof.” [143]

7. [210]

   In respect of ground 2, which asserted factual error on the part of the Arbitrator, the Deputy President dealt with each of the five factual findings challenged by Tudor Capital individually. He concluded in each case that Tudor Capital had failed to demonstrate any relevant error on the part of the Arbitrator. [144]

8. [211]

   As to Tudor Capital’s complaint that the Arbitrator held that the disarray present post mortem, found on histological examination, was caused by viral myocarditis, [145] the Deputy President accepted Mrs Christensen’s submission “that the evidence established the presence of myocite [sic, myocyte] disarray as found on post mortem and that such disarray was a key substrate for ventricular fibrillation [and] [t]he Arbitrator had not found that the myocite [sic, myocyte] disarray was caused by viral myocarditis.” He observed that no specific submission was put (presumably by Tudor Capital) in relation to this suggested factual error, and that it had not been made out. [146]

9. [212]

   As to Tudor Capital’s complaint that the Arbitrator’s conclusion that T cell lymphocytes entered the myocardium, was based upon speculation, the Deputy President referred to Dr Rainer and Professor Keogh’s evidence that damage was caused to the heart in a case of myocarditis by T cell infiltration or T lymphocytes. He noted that Mr Christensen had a virus. He held that it was open to the Arbitrator to infer that the more probable cause of the ventricular fibrillation was Mr Christensen’s contraction of myocarditis which, on the evidence, involved entry into the myocardium of T cell lymphocytes and that his preference for the hypothesis advanced by Mrs Christensen’s expert medical witnesses was founded upon the clinical history. Accordingly, no error was made out. [147]

10. [213]

    As to Tudor Capital’s complaint that the Arbitrator held that emotional stress was the cause of the viral illness, the Deputy President observed that Tudor Capital appeared “to accept that there was evidence, albeit ‘tenuous’, of such a relationship” and, noting that the appeal was not by way of review, rejected the challenge on the basis that Tudor Capital appeared to be seeking to reiterate argument advanced before the Arbitrator. Accordingly, no error was made out. [148]

11. [214]

    As to Tudor Capital’s complaint that the Arbitrator held that histological evidence of viral myocarditis was missed, [149] the Deputy President accepted Mrs Christensen’s submission that there was evidence before the Arbitrator which permitted that conclusion. That evidence included that of Professor Keogh “as to the possibility of a viral myocarditis, notwithstanding the absence of histological evidence.” The Deputy President noted that Professor Keogh had sought to retract her statements as to the possibility of myocarditis, but accepted that the Arbitrator had not been persuaded by that retraction. He held that the inference the Arbitrator drew was available on the evidence and there was, accordingly, no relevant error. [150]

12. [215]

    As to Tudor Capital’s complaint that the Arbitrator held that stress induced ill health “allowed the introduction of a viral illness” into Mr Christensen’s body, the Deputy President accepted Mrs Christensen’s submission that the expert medical evidence of Professor Rawlinson and, to an extent, Associate Professor Hudson’s, permitted the inference drawn by the Arbitrator concerning a causal link between the work related stress and development of the viral illness, such that error was not established. [151]

13. [216]

    Ground 3 asserted that the Arbitrator had erred in accepting Mrs Christensen’s expert evidence that the ventricular fibrillation was caused by viral myocarditis. The Deputy President noted that Tudor Capital’s submissions sought to emphasise that no evidence of myocarditis was found on post mortem. However, he considered the difficulty with that argument was the “abundant evidence as to myocarditis being the likely cause of the ventricular fibrillation leading to death.” [152]

14. [217]

    That evidence included Dr Whalley’s evidence that, notwithstanding the absence of histological evidence, myocarditis was the “most likely cause of [Mr Christensen’s] death”. The Deputy President regarded it as significant that Dr Whalley had expressed the view that the post mortem findings did not suggest changes indicating “arrhythmogenic right ventricular dysplasia” or “hypertrophic cardiomyopathy”. [153]

15. [218]

    The Deputy President noted that Professor Keogh had ultimately preferred hypertrophic cardiomyopathy as the likely cause of the fatal ventricular fibrillation, a view expressed following abandonment of her earlier preferred view that “the most likely cause [was] acute myocardial ischemia with primary arrhythmia”, referring to Professor Keogh’s first report of 15 June 2012 (at [19]). The Deputy President noted that in that report, Professor Keogh had “clearly misstated the view of Dr Whalley where it was asserted that a similar view to that of Professor Keogh was held by Dr Whalley.” [154] The Deputy President also noted Professor Keogh’s earlier acceptance that, albeit less likely, viral myocarditis may have been an “underlying conditio[n] leading to [Mr Christensen’s] death.” [155]

16. [219]

    The Deputy President next referred to Associate Professor Richards’ evidence:

17. [220]

    The Deputy President ultimately held that the weight to be attached to Associate Professor Richards’ evidence was a matter for the Arbitrator. In the Deputy President’s view, on the evidence, the Arbitrator’s finding as to probable cause of death was open to him. The finding did not, as Tudor Capital argued, constitute “conjecture”, [156] but, rather, the facts proved formed a reasonable basis for the Arbitrator’s conclusion. [157]

18. [221]

    By ground 4, Tudor Capital claimed that at paragraph [273] of his reasons, the Arbitrator failed to apply s 9A(1) of the WCA correctly. In particular, Tudor Capital attacked the Arbitrator’s statement that he was not satisfied that “the pre-existing condition of [Mr Christensen’s] heart played any part in his death.” The Deputy President considered that, although not expressly stated in Tudor Capital’s submissions, Ground 4 appeared to assert that the Arbitrator had “committed factual error concerning the relevance” of Mr Christensen’s pre-existing heart condition. [158]

19. [222]

    Tudor Capital contended that the Arbitrator’s conclusion was contradicted both by its experts’ and Associate Professor Richards’ evidence. The latter was a reference to the following passage in Associate Professor Richards’ report of 2 September 2013.

20. [223]

    The Deputy President accepted that the Arbitrator disregarded Mr Christensen’s pre-existing cardiac condition as being a factor that “played any part in his death” and, too, that he failed to consider Associate Professor Richards’ report of 2 September 2013. The Deputy President noted, however, that the Arbitrator’s adoption of the term “pre-existing condition” appeared to be a reference to Professor Keogh’s preferred hypothesis that the ventricular fibrillation was caused by the underlying hypertrophic cardiomyopathy. The Deputy President expressed the view that at paragraph [273], the Arbitrator “was addressing the nature of the two distinct and conflicting hypotheses, being the presence of relevant myocarditis or relevant hypertrophic cardiomyopathy.” [159]

21. [224]

    Although the Deputy President accepted that the Arbitrator erred in disregarding the evidence of Associate Professor Richards to which Tudor Capital referred, the Deputy President was nevertheless of the opinion that such error did not affect the Arbitrator’s decision. He observed that the Arbitrator’s conclusion was that employment “was the main substantial reason for the breakdown of [Mr Christensen’s] health and subsequent death”. He reasoned that s 9A(1) employed the indefinite article and, as found in Department of Education & Training v Sinclair, [160] “these words, particularly the use of the indefinite article, admit the possibility of other, possibly non-employment related, substantial contributing factors…”. [161]

22. [225]

    In the Deputy President’s view, the Arbitrator’s finding concerning the requirements of s 9A was not vitiated by his apparent disregard of Associate Professor Richards’ suggested concession. The Deputy President noted that Associate Professor Richards’ acceptance of the possibility that ventricular fibrillation would not have occurred in the absence of an underlying myocardial pathology was qualified in the second sentence in the passage from his 2 September 2013 report, being that which I have emphasised at paragraph [222] of these reasons. The Deputy President noted that the Arbitrator had earlier stated his reasons for accepting that the ventricular fibrillation was caused by myocarditis and, accordingly, held that it was open for him to conclude that employment, given the causal nexus discussed in the course of his reasons, was a substantial contributing factor to the injury leading to Mr Christensen’s death. [162]

23. [226]

    After noting that he had rejected Tudor Capital’s challenges to various factual conclusions the Arbitrator had made, the Deputy President identified the question arising under ground 4 as being whether, upon the assumption those factual conclusions were correct, the terms of s 9A had been made out. [163] He continued:

24. [227]

    By ground 5, Tudor Capital asserted that the Arbitrator wrongly rejected the evidence of Professor Keogh in circumstances where he had not disbelieved her, nor found that her evidence had been tainted by dishonesty, was misleading, the product of advocacy for a party or was inherently unreliable. It relied upon Wiki v Atlantis Relocations (NSW) Pty Ltd [164] where it was relevantly held that a fact finder is obliged to engage with differences between expert evidence capable of being resolved rationally by examination and analysis and that failure to do so gives rise to justifiable grievance as to the way in which justice is administered. In the Deputy President’s opinion, the thrust of this submission was that the Arbitrator did not have regard to Professor Keogh’s demeanour (a submission Mrs Christensen disputed) and, accordingly, failed to engage with her evidence. [165]

25. [228]

    The Deputy President held that the Arbitrator’s hesitance in accepting Professor Keogh’s delayed explanation for her change of view was understandable in circumstances where she only retracted in cross-examination her view in her first report that viral myocarditis was one explanation for Mr Christensen’s death, although less likely than acute myocardial ischemia with primary arrhythmia. [166] The Deputy President observed that the failure to inform the Commission of Professor Keogh’s changed opinion was contrary to cl 5(4) of the Expert’s witness code of conduct. [167]

26. [229]

    The Deputy President held that observations the Arbitrator made concerning Professor Keogh’s evidence, confirmed that the Arbitrator had taken Professor Keogh’s demeanour into account when evaluating her evidence. He also considered that it was “beyond dispute” that the Arbitrator had engaged with the evidence in accordance with his obligation to do so as stated in Wiki. [168]

27. [230]

    Accordingly, the Deputy President confirmed the Arbitrator’s findings and orders and remitted the matter to the Arbitrator for further directions and hearing concerning the question of apportionment.

Issues on appeal

1. [231]

   Tudor Capital’s notice of appeal advanced eight grounds of appeal, however in oral submissions Tudor Capital confined its grounds of appeal to the following issues. First, that the Arbitrator and the Presidential Member failed to identify an “injury” for the purposes of s 9 within the meaning of that term in s 4 of the WCA, leading to confusion in the application of s 9A. [169] Secondly, that there was no, or no sufficient, evidence of myocarditis because the only evidence in support of myocarditis was conditional on the premise that there was no sufficiently severe pre-existing condition capable of triggering ventricular fibrillation and, therefore, Mr Christensen died due to myocarditis. This premise was said to underpin the reasoning of Associate Professor Richards, forming the basis of Mrs Christensen’s case. Tudor Capital submitted its evidence demonstrated that condition was inapplicable. Thirdly, that there was strong evidence of severe hypertrophic cardiomyopathy, removing the condition on which Mrs Christensen’s case was built. [170] Fourthly, that the Deputy President’s reasoning processes were inadequate, in particular, there was no sufficient analysis of the medical evidence. It was acknowledged that this last point was really supportive of the second and third points in that the conclusions about myocarditis and cardiomyopathy should have been reached if a proper analysis had been made.

2. [232]

   In support of these issues, Tudor Capital submitted that the Deputy President erred in point of law by:

   1. (1)

      finding that stress and emotional upset, being the “stress as found” by the Arbitrator, satisfied the statutory definition of “injury” within s 4 WCA;

   2. (2)

      having identified error in the Arbitrator’s conclusion that Mr Christensen’s pre-injury condition played no part in his death, making his own findings with respect to causal contribution in reliance upon an inference favourable to Mrs Christensen that the opinion of Associate Professor Richards would have remained unchanged despite new evidence as to the severity of the pre-existing hypertrophic cardiomyopathy. Tudor Capital submitted that such an inference was not available because Mrs Christensen bore the onus and had either chosen, or neglected, to call evidence from Associate Professor Richards to satisfy that onus;

   3. (3)

      failing to correct the Arbitrator’s finding with respect to “injury”, that is, that the “injury” was constituted by T cell infiltration, when there was no evidence that this had occurred;

   4. (4)

      failing to consider and/or misdirecting himself as to the need to consider Tudor Capital’s defence pursuant to s 11A WCA, that is, whether Mr Christensen had suffered a psychological or psychiatric disorder (s 11A(3)) and whether such a disorder was the result of reasonable action taken by way of performance appraisal (s 11A(1));

   5. (5)

      making a finding of ultimate fact, that is, that Mr Christensen’s employment caused injury which led to his death, when there was insufficient evidence properly to base such a finding upon;

   6. (6)

      exceeding or avoiding his statutory task; and

   7. (7)

      failing to provide sufficient reasons dealing with all of the matters in dispute.

Tudor Capital’s submissions

1. [233]

   Tudor Capital contended the Deputy President’s errors in determining the appeal from the Arbitrator’s decision were jurisdictional errors amounting to a constructive failure to exercise jurisdiction. It also argued that the Deputy President’s findings with respect to injury, the limited nature of those findings and his failure to deal properly with s 9A of the WCA constituted errors of law. It further argued that the nature of its appeal was effectively extended to questions of fact because questions of fact were in issue on the appeal against the Arbitrator’s decision. Accordingly, it contended that the manner in which the Deputy President dealt with those questions of fact, if erroneous, would constitute jurisdictional error.

2. [234]

   Tudor Capital submitted that Mrs Christensen’s case was built upon what were said to be medical possibilities made probable by temporal events, that being the fact of some work stress, a probable concurrent viral illness and a probable death by ventricular fibrillation.

3. [235]

   Its fundamental submission was that the evidence was insufficient to prove that work stress caused Mr Christensen to acquire a virus, or that that virus resulted in myocarditis. It submitted, however, that the Arbitrator lost sight of the necessity to determine whether Mrs Christensen’s evidence was sufficient to establish Mr Christensen’s death was caused by viral myocarditis, by in effect merging his consideration of that issue with the coincidence that at the time he died, Mr Christensen had a virus or, prioritising the temporal events at the expense of consideration of the “injury” issue. Thus, it complained, the Arbitrator concluded [171] that the temporal events he described in his reasons caused emotional stress to Mr Christensen, leading to him suffering a viral illness which most likely caused T cell infiltration into the myocardium, before he considered the “medical question”.

4. [236]

   Tudor Capital contended that both the Arbitrator’s and the Deputy President’s reasons revealed a general confusion in the identification of the “injury” the subject of the claim. It claimed that confusion resulted in error in the establishment of “injury” for the purposes of s 4, error in the application of s 9A and confusion as to what was required for the purposes of establishing, with sufficient evidence, facts in issue at various stages along the chain of causation.

5. [237]

   Tudor Capital also submitted that the Deputy President’s consideration of ground 4 of its appeal from the Arbitrator was affected by the uncertainty as to his decision with respect to “injury”. If the injury was, as the Deputy President found, “stress as found” and the manifestation of that injury was that Mr Christensen was “more susceptible to contraction of the virus” then, Tudor Capital submitted, consideration would have to be given, and a finding made, as to the “nature and incidence of the physiological change” which constituted an increased susceptibility. Next, for the purposes of assessing this s 9A issue, it would be necessary to assess how much “more susceptible” Mr Christensen was made, an assessment which would necessarily have to take into account his pre-existing susceptibility to flu like illness and the extent to which such illnesses were experienced in the general community entitling a conclusion that the increase in Mr Christensen’s susceptibility by reason of work related stress was substantial. Tudor Capital complained that this exercise was not done. Finally, Tudor Capital submitted, that the “stress as found” was a psychological injury, perhaps being contended to have some kind of physiological effect which, in turn, gave rise to a possible issue under s 11A, a matter which was not addressed by the Deputy President, such omission constituting an error of law.

6. [238]

   Tudor Capital submitted that because of the limitations on the Deputy President’s powers pursuant to s 352(5) of the WIM Act, he did not have power to substitute his own opinion for that of the Arbitrator without first identifying error and expressing his own conclusion as to the correction of that error.

7. [239]

   In support of its submission that the Arbitrator and the Presidential Member failed to identify an “injury”, Tudor Capital submitted that in order to determine whether there was an “injury” for the purposes of s 4 of the WCA, the Deputy President should have identified “a physiological change or disturbance of [Mr Christensen’s] normal physiological state”. [172] It contended that to define the “injury” as “the experience of stress” as the Deputy President had done, [173] could not satisfy the legal requirements of an “injury” for the purposes of s 4 of the WCA as explained in May.

8. [240]

   Nor, Tudor Capital contended, could a speculated increased susceptibility to viral illness as the Arbitrator found be considered to constitute “precise evidence, on a fact by fact basis, concerning the nature and incidence of the physiological change”.

9. [241]

   Further, Tudor Capital contended that viral myocarditis could not constitute a physiological change as it was a diagnosis of multiple pathological changes, being inflammation in the heart caused by the body’s immune defence system (the entry of T cells), causing the heart to go out of rhythm. Tudor Capital gave the example of the bursting of an aneurism as a clear physiological change.

10. [242]

    In oral submissions, Tudor Capital acknowledged that the acquisition of the viral illness (i.e. the entry of a virus into the body) could be an “injury” as recognised in Favelle Mort Ltd v Murray, [174] as, too, could be the entry of T cell lymphocytes into the myocardium in the sense that each constituted a physiological change. However, it contended that Mrs Christensen’s case was that the “injury” was the continuum or process identified in the ARD, rather than one of its several parts.

11. [243]

    Tudor Capital submitted that the Deputy President reinterpreted Associate Professor Richards’ evidence concerning the absence of previous evidence of cardiomyopathy when he dealt with what he recognised was an error by the Arbitrator in failing to acknowledge and deal with the pre-existing cardiomyopathy. [175] It also complained that the Deputy President mistakenly undertook that exercise in the context of s 9A rather than in terms of sufficiency of evidence and, too, by inferring that Associate Professor Richards would maintain this view despite the evidence from Professor Keogh and Dr Rainer.

12. [244]

    Tudor Capital also submitted that the Deputy President could not reach his conclusion in paragraph [107] that the Arbitrator’s error in disregarding Mr Christensen’s pre-existing cardiac condition as a factor that “played any part in his death” had not affected the Arbitrator’s decision, without analysing the evidence given by Dr Rainer and Professor Keogh. It contended that both the Arbitrator and the Presidential Member failed to engage in, and analyse, the competing medical opinions. Instead, the Arbitrator had said he was not satisfied with Professor Keogh saying that she no longer conceded myocarditis as a possible cause, then determined the case on the basis of possibilities for which there was no evidence.

13. [245]

    Tudor Capital submitted that had the Arbitrator had regard to the objective evidence, he should have recognised that the autopsy slides excluded a diagnosis of myocarditis. It contended that the Arbitrator gave no reasons which could explain his rejection of Dr Rainer’s evidence that Mr Christensen’s heart had been extensively sampled and that the size of the sample was sufficient to overcome any potential sample defect, nor Professor Keogh’s evidence to the effect that Mr Christensen’s whole heart had been sampled. It argued that had the Deputy President properly analysed the expert evidence, he would have recognised the Arbitrator erred as a matter of fact in accepting the sampling error theory. It argued that the Deputy President had erred in point of law in failing to recognise that there was no rational connection between particular evidence and a finding of fact in order to say that there was some evidence capable of supporting the finding.

14. [246]

    Tudor Capital submitted that the identification of “injury” was a necessary precondition to the proper evaluative judgment as to whether a worker’s employment had been a substantial contributing factor to that injury (s 9A, WCA). It contended that Mrs Christensen bore the onus of establishing the requisites of s 9A and, that, in determining whether Mr Christensen’s employment was a substantial contributing factor to the injury, the Deputy President was required to take into account the matters specified in s 9A(2) of the WCA.

15. [247]

    Tudor Capital contended that the manner in which Mrs Christensen alleged the relevant “injury,” by identifying along a continuum from the virus (or stress on the Deputy President’s finding) to the end point, being death, separate instances said to constitute an “injury” within the meaning of s 4, created confusion regarding the application of s 9A and the sufficiency of evidence. It submitted that the identification of “injury” with precision was a necessary precondition to the proper evaluative judgment as to whether a worker’s employment had been a substantial contributing factor to the injury.

16. [248]

    For example, if the injury identified was the infiltration of the T cells, answering the question asked of s 9A, namely whether employment substantially contributed to the injury to the cells, became an almost impossible task as there was no evidence as to factors which made this more or less likely.

17. [249]

    Tudor Capital contended that if Mr Christensen’s injury was associated with the contraction of a viral illness, then s 9A(2) mandated that consideration be given to when and where the virus was contracted, to the probability that the virus would have been contracted anyway and to Mr Christensen’s state of health before the injury, including the fact that he was prone to contracting the flu. Tudor Capital submitted that an error in the identification of injury, and a failure to consider relevant s 9A matters, necessarily led to an error of law.

18. [250]

    Tudor Capital submitted that the Deputy President rejected the Arbitrator’s conclusion (in dealing with the time and place of the injury pursuant to s 9A(2)) that the “injury” occurred at 11:30pm at Mr Christensen’s home when the T cells entered the myocardium, concluding, instead, that the “injury” was the “stress”. [176] Tudor Capital contended that, in so finding, the Deputy President did not appear to recognise that this was the Arbitrator’s formal finding as to “injury”. Instead, the Deputy President identified Mr Christensen’s “experience of stress” as the relevant “injury”. Tudor Capital submitted that this was in error as, if the Arbitrator’s finding concerning “injury” was incorrect, the Deputy President was required to state that fact, state what the injury was (in the sense of explaining the physiological changes) and give his reasons for so concluding. It would also then have been necessary for the Deputy President to consider ss 9A and 11A in the light of the “injury” he had identified.

19. [251]

    Some of Tudor Capital’s submissions on these grounds of appeal overlapped to an extent with those made in relation to the “injury” ground, but are repeated to the extent necessary to contextualise Tudor Capital’s argument.

20. [252]

    Tudor Capital’s submission that there was no sufficient evidence of myocarditis is related to its contention that there was strong evidence of severe hypertrophic cardiomyopathy. Tudor Capital contended that the evidence of severe hypertrophic cardiomyopathy disclosed by the autopsy slides and the expert evidence about their significance, removed the condition or assumption on which Mrs Christensen’s case was built. That condition/assumption found in Associate Professor Richards’ evidence, was that there needed to be a trigger for the ventricular fibrillation however, there was no evidence of another pre-existing condition, therefore, notwithstanding the minimal evidence of myocarditis, it must have been the trigger. Since the condition was taken away by the strong evidence of severe hypertrophic cardiomyopathy, Tudor Capital contended that Mrs Christensen’s case was not based on sufficient evidence.

21. [253]

    Tudor Capital contended that the Deputy President ignored relevant material and relied on irrelevant material such as to affect his exercise of power. It submitted that in dealing with ground 1 of the appeal below, the Deputy President misdirected himself as to the evidence concerning medical possibility. In particular, he overlooked the fact that the evidence given in support of Mrs Christensen’s case was qualified, to the effect that a conclusion that a virus caused myocarditis and that myocarditis caused ventricular fibrillation was open, providing that pre-existing cardiomyopathy was mild. This was because mild pre-existing cardiomyopathy was not itself likely to trigger ventricular fibrillation. However, the evidence revealed by the autopsy slides was that the pre-existing cardiomyopathy was more severe than had been assumed and could have operated independently as a trigger for ventricular fibrillation. Tudor Capital further contended that Mrs Christensen’s medical evidence rested on the assumption that there may have been sampling error at autopsy such that histological evidence of myocarditis was missed. Following analysis of the autopsy slides, however, the possibility of sampling error became highly unlikely and the absence of histological evidence of myocarditis became more significant.

22. [254]

    Tudor Capital submitted that it was incumbent on the Deputy President when responding to ground 1 of the appeal from the Arbitrator to refer to this evidence and explain why it was capable of elevating mere speculation or conjecture concerning the possibility that evidence of myocarditis was missed, either due to sampling error or its focal to diffuse manifestation, to a conclusion on the balance of probabilities.

23. [255]

    Tudor Capital repeated the submissions it had made to the Deputy President that the Arbitrator erred in applying EMI (Aust) Ltd v Bes for the proposition that the histology evidence could be ignored, or at least overcome, because “medical science [did] not say in this individual case that there [was] no possible connection between the events and the death” [177] and that EMI (Aust) Ltd v Bes, Forst and Hines required the whole of the evidence to be considered in determining causation.

24. [256]

    Tudor Capital relied upon Tubemakers of Australia Limited v Fernandez [178] where Mason J explained that in considering medical evidence that a disability was caused by certain matters, it was open to the decision maker to infer that on the probabilities the matter identified caused or materially contributed to the occurrence of the condition and, in doing so, have regard, in addition to the medical evidence, to other significant circumstances which might include surrounding circumstances such as a disability prior to the causative event, a temporal relationship between the alleged causative event and the disability and the fact that no alternative cause was established or suggested in the evidence. Tudor Capital emphasised that part Mason J’s reasons where his Honour explained that a “plaintiff will fail if all that he can show is that his disability might have been so caused … mere proof of default followed by injury does not show that the default caused the injury”.

25. [257]

    Tudor Capital submitted that in referring to Murray v Shillingsworth, [179] the Deputy President led himself into error by failing to understand fully the qualifications upon the medical evidence given in support of Mrs Christensen’s case. Tudor Capital submitted that the legal issue before the Deputy President was “whether the evidence on the point [was] sufficient, in the sense that it [was] evidence which if fully accepted could properly base the finding of fact.” [180]

26. [258]

    Tudor Capital also submitted that by overlooking or giving too little weight to the evidence based on the autopsy slides, the Deputy President led himself into legal error in his consideration of the remaining four appeal grounds before him. In particular, with respect to ground 5 of the appeal from the Arbitrator, it submitted that the Deputy President’s criticism of Professor Keogh was ill-founded and reflected his failure to appreciate the significance of the evidence in the autopsy slides. It contended that had the Deputy President approached the assessment of the differences in the evidence between Associate Professor Richards and Professor Keogh in the way mandated in Wiki, he would have realised that the differences between the expert witnesses could be resolved rationally by examination and analysis.

27. [259]

    Such an analysis would have revealed that Professor Keogh’s changed opinion was caused by the evidence in the autopsy slides. It also would have revealed that the evidence as to the severity of the pre-existing cardiomyopathy following inspection of the slides was not brought to Associate Professor Richards’ attention, or, if it was, he was not asked to respond even though Mrs Christensen had the opportunity to obtain his further opinion.

28. [260]

    Tudor Capital contended that the evidence before the Arbitrator, and the Deputy President, was insufficient to prove:

29. [261]

    Tudor Capital argued that the facts surrounding Mr Christensen’s death, taken in isolation, could not “make it more likely than not” that the stress caused him to suffer a viral illness that he would not otherwise have suffered. Further, assuming that Mr Christensen was suffering from a virus, and that he experienced ventricular fibrillation at a time when he was suffering the effects of a viral illness, the viral illness would have only had relevance to the ventricular fibrillation if myocarditis was caused by the viral illness. However, Tudor Capital repeated its submission that there was no histological evidence of myocarditis. The conclusion that myocarditis had occurred was based on the unlikely event that there was a sampling error or that death followed the initiation of myocarditis so quickly that no histological trace was left.

30. [262]

    Ultimately, Tudor Capital submitted, Mrs Christensen’s case that myocarditis caused Mr Christensen’s death rested on Associate Professor Richards’ assumption that as pre-existing cardiomyopathy was mild, and Mr Christensen had an intercurrent viral illness, [181] he could see no other available trigger for ventricular fibrillation other than hypertrophic myocarditis. However, once the evidence established that the extent of pre-existing hypertrophic cardiomyopathy was severe, so as to be a “time bomb” requiring no additional trigger to cause arrhythmia, the only basis for elevating the likelihood of myocarditis from possibility to probability was lost.

31. [263]

    Tudor Capital submitted that the Deputy President’s reasoning processes were inadequate, in particular, that he failed to sufficiently analyse the medical evidence.

32. [264]

    Tudor Capital contended that there was uncertainty as to what the Deputy President concluded in respect of:

33. [265]

    Tudor Capital also argued that uncertainty existed as to whether the Deputy President understood that Associate Professor Richards’ evidence was based on an assumption that Mr Christensen’s pre-existing cardiomyopathy was mild, an assumption which, in the absence of any challenge to Tudor Capital’s later expert evidence, was untenable.

Mrs Christensen’s submissions

1. [266]

   Mrs Christensen submitted that underlying the appeal was Tudor Capital’s contention that the Arbitrator was in error in accepting her case on the causal connection, and that the Deputy President failed to correct that error on appeal. She argued that when the Arbitrator’s reasons were examined, it was apparent that he understood the competing cases and did not err in accepting her case, and reject Tudor Capital’s case, as part of an evaluative probabilities-based fact finding task. She submitted that the Arbitrator’s reasons could not be found to be in error on a “no evidence” basis as there was evidence which, if fully accepted, could properly base the findings of fact.

2. [267]

   Mrs Christensen explained her case as being based on work stress, a viral illness, breathlessness and myocarditis set in the temporal context. That is to say, in essence, Mr Christensen had been under stress at work, such stress could, and did, adversely affect his immune system, leading to him contracting a viral illness from which he was still suffering when he died, leading to the inference that he died from viral myocarditis. She accepted that if the only evidence in support of viral myocarditis was conditional, and the condition was shown to be inapplicable, Tudor Capital would have established an error of law in the Deputy President’s decision.

3. [268]

   Mrs Christensen submitted that Tudor Capital’s case on the autopsy slides was that they were definitive and that if something was not shown on the slides in the histopathology, it could not have occurred. Mrs Christensen accepted that the real evidence about the sampling and the effectiveness of it was Dr Rainer’s evidence, but argued that his evidence demonstrated that the autopsy slides could not be either definitive or conclusive in the way Tudor Capital suggested. She submitted that Professor Keogh’s views about the extent of the sampling of Mr Christensen’s heart did not reflect Dr Rainer’s understanding of how the heart had been sampled and, moreover, did not reflect, and was undermined by, her lack of understanding of the focal to diffuse phenomenon. Mrs Christensen submitted that Dr Rainer’s evidence removed the conclusiveness of the autopsy slides and opened the gateway to the temporal analysis the Arbitrator undertook.

4. [269]

   Mrs Christensen submitted that both the Arbitrator and the Deputy President recognised that her claim concerned a physical matter which had sufficient associated physiological change or disturbance in a manner which satisfied the High Court’s decision in May. In this respect she referred to the Arbitrator’s finding that the “injury” was entry of the T cell lymphocytes into Mr Christensen’s myocardium, [182] which the Deputy President identified as the Arbitrator’s conclusion on the medical dispute before him. [183]

5. [270]

   Thus, Mrs Christensen submitted the Arbitrator found that the virus infiltrated Mr Christensen’s heart at the time he suffered breathlessness a few hours before his death. She explained that, on her case, when the virus infiltrates the heart muscle (myocardium) the physiological process involves the alteration of the cells which attracts an inflammatory response, which is basically the virus “boring a hole in the membrane of the muscle cell”. Next, the viral illness affecting Mr Christensen’s heart then resulted in him suffering ventricular fibrillation (itself a physiological change). Finally, the ventricular fibrillation caused cardiac arrest which then caused Mr Christensen’s death (itself, she contended, a sufficient physiological change).

6. [271]

   Mrs Christensen disputed Tudor Capital’s submission that her case was based on a psychiatric or psychological injury. She submitted that she had made it clear that that was not her case below, referring to the Deputy President’s extraction of a passage of her evidence before the Arbitrator, [184] and the Arbitrator’s reasons. [185]

7. [272]

   Mrs Christensen denied that no relevant “injury” was identified. She submitted that Mr Christensen suffered an “injury” within the meaning of s 4 of the WCA when his work conditions led to his health deteriorating which, in turn, resulted in a viral illness which itself resulted in viral myocarditis, causing the ventricular fibrillation. She contended that the onset of viral myocarditis was the primary “injury” claim for the purposes of s 4(a). In her submission, the viral illness, viral myocarditis and the ventricular fibrillation all constituted distinct “physiological changes” for the purposes of s 4(a).

8. [273]

   Mrs Christensen contended that May did not require that the most immediate cause of Mr Christensen’s death be directly from the work conditions, but, rather, the less direct pathway of the work conditions causing a viral illness having that impact was legally sufficient. [186]

9. [274]

   Mrs Christensen contended that the absence of any discussion in the Deputy President’s reasons about viral illness not being a sufficient physiological change or disturbance to constitute “injury” before the Arbitrator was explained by the fact that there was no ground of appeal or any written submissions addressing that issue. She argued that as this issue was not part of the appeal to the Deputy President, and was one which could have been addressed by medical and scientific evidence, Tudor Capital should not be permitted to raise it now.

10. [275]

    Mrs Christensen disputed Tudor Capital’s submission that her case about the causal relationship between work conditions of stress and viral illness was conjectural or speculative. She contended that the Arbitrator recognised that this was not a case where medical science dictated there was no possible connection between the temporal events and Mr Christensen’s death. She submitted that the Arbitrator based his conclusion on causation by connecting the deterioration of Mr Christensen’s health with the entry of the viral illness into his body on the accepted evidence of Professor Rawlinson and Associate Professor Hudson that there was a “connection, as yet not fully understood” between stress and viral illness. By recognising that Mrs Christensen’s case was a possibility, the door was open to considering the temporal analysis and its impact on the whole causation question, including the s 9A inquiry.

11. [276]

    Mrs Christensen submitted that Tudor Capital’s factual case defending her claim depended upon two matters, neither of which was accepted by the Arbitrator. They were first, that the post mortem sampling of Mr Christensen’s heart did not show the inflammatory response to infection which was essential for a diagnosis of viral myocarditis and so, factually, the Arbitrator should have concluded that Mr Christensen had not suffered from that condition. Secondly, that hypertrophic cardiomyopathy was an alternative explanation for Mr Christensen’s death.

12. [277]

    Mrs Christensen submitted that the first case was properly rejected by the Arbitrator on the basis that the histopathological markers for the presence of viral myocarditis may not be present, or may not be detected, in circumstances where it is recognised that the presence of the virus in the heart does not immediately affect all of the muscle tissue, but, rather, it progresses from a focal to a diffuse development. Thus, Mrs Christensen contended, Dr Rainer’s answer in cross-examination acknowledging that it was “possible” the sampling process had not included parts of the heart affected by viral myocarditis was a matter the Arbitrator was entitled to rely upon. Mrs Christensen also submitted that the Arbitrator was correct to conclude that the autopsy slides were not “forensically determinative”. She argued that the weight to be given to the evidence was an evaluative matter for the Arbitrator.

13. [278]

    As to the second aspect of Tudor Capital’s case, Mrs Christensen submitted that the hypertrophic cardiomyopathy case was weakened by a number of matters. First, was Dr Rainer’s evidence in cross-examination to the effect that the fibrosis identified in the slides was not so severe that it was highly probable that arrhythmia would occur at that point in time but, rather, that it could have occurred at any point in time. [187] While Mrs Christensen accepted this aspect of the cross-examination of Dr Rainer was directed to s 9A(2)(d) and (e) of the WCA, she contended that the effect of Dr Rainer’s evidence was to weaken the case that, on the probabilities, the cause of the ventricular fibrillation at the time that it, in fact, occurred was a pre-existing hypertrophic cardiomyopathy.

14. [279]

    Secondly, Mrs Christensen submitted that the hypertrophic cardiomyopathy case was weakened by the absence of what Professor Keogh contended were symptoms of hypertrophic cardiomyopathy: breathlessness, palpitations and tiring easily. Mrs Christensen accepted that Mr Christensen suffered breathlessness prior to his death and, as that was also a symptom of viral myocarditis, its occurrence did not advance or diminish either party’s case, but relied on the absence of the other two symptoms.

15. [280]

    Thirdly, Mrs Christensen submitted that the hypertrophic cardiomyopathy case was weakened by the evidence of other consulting medical practitioners who considered the question of hypertrophic cardiomyopathy but dismissed it. [188] Mrs Christensen submitted the Arbitrator considered the evidence to which I have referred and accepted her medical case and made his findings of fact accordingly. Mrs Christensen submitted that in those circumstances, there could be no “no evidence” error nor a “sufficiency of evidence” error in the Arbitrator’s causal connection findings.

16. [281]

    Mrs Christensen further submitted that, as a result of the matters to which I have referred, the temporal sequence of events and her accepted medical case became the more persuasive and satisfactory answer to the probabilities-based causation inquiry. She submitted that, to the extent that inferences were drawn, the evidence permitted affirmative satisfaction, notwithstanding other possible explanations could not be excluded.

17. [282]

    Mrs Christensen also submitted that as Tudor Capital had sought to prove its factual case in defence of her claim, it was appropriate for the Arbitrator to consider whether it succeeded. That, Mrs Christensen contended, involved no reversal of the onus of proof, but, rather, an orthodox and correct process of fact finding where an employer, in responding to the claim made, sets outs to prove its own factual case on the medical dispute and temporal sequence dispute.

18. [283]

    Mrs Christensen took issue with Tudor Capital’s assertion that the Deputy President “effectively rejected” the Arbitrator’s finding that the injury occurred at 11:30pm at Mr Christensen’s home when the T cells entered his myocardium. She asserted that the Deputy President instead rejected Tudor Capital’s submission that “the injury occurred at 11:30 pm at [Mr Christensen’s] home when he was having a cup of tea.”

19. [284]

    Mrs Christensen submitted that the Deputy President made no error in determining that the “stress as found” by the Arbitrator satisfied the statutory definition of “injury” in s 4(a) of the WCA and that his reasons aligned with those of the Arbitrator.

20. [285]

    Mrs Christensen submitted that consideration was given to the factors in s 9A, as reflected in the Arbitrator’s findings that employment was “the main substantial reason for the breakdown of [Mr Christensen’s] health and subsequent death” reflecting s 9A(1) and that he was not satisfied that “the pre-existing condition of [Mr Christensen’s] heart played any part in his death” reflecting s 9A(2). [189] She also argued that on the identified injury, s 9A(2)(d) and (e) did not operate. [190]

21. [286]

    Mrs Christensen contended there was sufficient evidence to justify the Arbitrator’s decision in respect of the causal connection between Mr Christensen’s work stress, the virus, the myocarditis and the ventricular fibrillation resulting in death, and that that evidence afforded a proper basis for the Arbitrator’s findings of fact.

22. [287]

    In response to Tudor Capital’s contention that there was no, or no sufficient, evidence of myocarditis, Mrs Christensen contended that the concession by Dr Rainer that there was a possibility myocarditis was missed notwithstanding the extensive sampling process, combined with the body of probative evidence given by Associate Professor Richards that myocarditis caused Mr Christensen’s death, dispelled any suggestion of error of law on the part of the Arbitrator or the Deputy President.

23. [288]

    Mrs Christensen relied, again, on her argument that any inflammation of Mr Christensen’s heart tissue may have been so limited that it was not detected on the autopsy slides.

24. [289]

    Mrs Christensen accepted that hypertrophic cardiomyopathy was an alternative theory to explain Mr Christensen’s death, but said that it was a possibility that ceased to be the probable explanation for Mr Christensen’s death. Mrs Christensen relied on the evidence of Dr Rainer to the effect that it would be possible for hypertrophic cardiomyopathy to be present, as identified by the fibrosis, and for there to be a subsequent attack by a virus producing a viral myocarditis.

25. [290]

    Mrs Christensen took issue with Tudor Capital’s submission that Associate Professor Richards’ evidence, that viral myocarditis was the cause of Mr Christensen’s death, was subject to a premise that there was no sufficiently severe pre-existing condition capable of triggering Mr Christensen’s ventricular fibrillation, which was undermined by the evidence of “severe cardiomyopathy”. She submitted this case was never put to Associate Professor Richards, the Arbitrator or the Deputy President. She argued that Associate Professor Richards had throughout his reports used the terms mild and severe in conjunction with cardiomyopathy and on numerous occasions expressed an opinion that Mr Christensen’s cardiomyopathy was mild.

26. [291]

    Mrs Christensen submitted that it was incumbent upon Tudor Capital clearly to identify the distinction between mild and severe cardiomyopathy as the case it was going to run before she could decide whether Associate Professor Richards should be recalled, particularly in a setting where he had not been cross-examined as to this issue. Accordingly, Mrs Christensen submitted that Tudor Capital should not be permitted to run the mild-severe argument on appeal.

27. [292]

    Mrs Christensen submitted the Arbitrator had properly analysed the experts’ evidence. She contended he had rejected Professor Keogh’s opinion on the basis of its logic and rationale on the “co-incidental pre-existing condition” question and the post mortem sampling question. She also argued that the Arbitrator had not rejected Professor Keogh’s opinion on the extent of the sampling on a demeanour basis as was apparent, but, rather, because the autopsy slides were “no more than the post-mortem sampling” which had been the basis for her original opinion which entertained viral myocarditis as a possible cause of death. [191] She also relied on the fact that the Deputy President was of the view that the Arbitrator had engaged with the evidence as required by Wiki. [192]

28. [293]

    Finally, Mrs Christensen submitted the Deputy President’s reasons were not uncertain as Tudor Capital contended. She argued that the nature of the “injury” suffered by Mr Christensen, and the extent to which his employment contributed to it, were clearly identified by both the Arbitrator and the Deputy President. [193] She also contended that the Arbitrator did deal with the fact that the evidence of Associate Professor Richards was based upon an assumption that any pre-existing cardiomyopathy was mild. [194] She also submitted that the Deputy President appreciated the issue of the presence of mild cardiomyopathy and Professor Keogh’s view. [195]

29. [294]

    Mrs Christensen further submitted that the proposition implicit in Tudor Capital’s submissions was that Mr Christensen’s cardiomyopathy was not mild because later expert evidence demonstrated as much. However, she argued that the evidence did not establish that all the fibrosis was severe.

Tudor Capital’s reply submissions

1. [295]

   Tudor Capital disputed Mrs Christensen’s submission that its case was not raised in the Commission. It contended that its case had been consistently put as being the inadequacy of the evidence to make good Mrs Christensen’s claim. In addition, it said it had put that that submission had to be considered in the context where Associate Professor Richards’ evidence about viral myocarditis was conjectural, whereas that of Dr Rainer and Professor Keogh was based on objective histological evidence which Mrs Christensen had not sought to rebut.

Consideration

1. [296]

   A party to proceedings before the Commission constituted by a Presidential member aggrieved by a decision of the Presidential member in point of law may appeal to the Court of Appeal. [196]

2. [297]

   In such an appeal, Tudor Capital must identify an award or decision of the Presidential Member in point of law, as the subject matter of the appeal which aggrieves it. [197] Decisions in point of law refer to the substance of the decision-making process and not merely its presentation. [198] It is the existence of a point of law which “is ... not merely a qualifying condition to ground the appeal, but also the subject matter of the appeal itself.” [199] There is an error in point of law if the Presidential member considers a question other than the one mandated by s 352(5) of the WIM Act, [200] or if the primary facts as found are necessarily within or outside a statutory description and a contrary decision has been made. [201]

3. [298]

   There will be a constructive failure to exercise jurisdiction, as Tudor Capital contended occurred in this case, where a decision-maker “has purported to resolve the parties’ dispute but has not in fact done so”, [202] or where the decision-maker has erred “in understanding the facts, applying the law and reasoning to a conclusion … if [that] revealed ‘a basic misunderstanding of the case brought by an applicant, [so that] the resulting flaw is so serious as to undermine the lawfulness of the decision in question in a fundamental way’”. [203]

4. [299]

   On an appeal limited to error in point of law, the party not bearing the burden of proof may establish such an error by demonstrating that there was no sufficient evidence capable of supporting an ultimate fact. [204] In that situation, the party not bearing the onus of proof puts an argument, which assumes against that party that the other party’s evidence has been accepted, but submits that it was not capable, in the sense of not being sufficient, to establish the relevant fact. [205] What amounts to material that could support a factual finding is ultimately a question for judicial decision. Thus, if the Deputy President erred in determining that the Arbitrator did not err in a factual or legal conclusion, his conclusion can be reviewed in this Court as long as the error was operative in the ultimate decision dismissing the appeal. [206]

5. [300]

   In order to say that there was some evidence capable of supporting a finding, it is necessary that there be a rational connection between particular evidence and a finding of fact. [207]

6. [301]

   Failure to consider the factors referred to in s 9A(2) by reference to the relevant underlying facts, involves a misconstruction of the provision and as such involves error in point of law. [208]

7. [302]

   Insofar as Mrs Christensen complains that Tudor Capital is seeking to raise a new ground of appeal not raised before the Deputy President, on an appeal confined to a grievance in point of law, there are circumstances in which a new issue may be raised. As was explained in Davis v NSW Land and Housing Corporation, [209] in considering whether to permit that course in the exercise of the court’s discretion, the court will take into account Coulton v Holcombe [210] considerations and, too, considerations specific to the limited nature of an appeal confined, in that case to a question of law, in this case to being in point of law.

8. [303]

   However, in my view, Tudor Capital is not seeking to raise a new argument on appeal. As it submitted, its case has always been that there was no, or no sufficient, evidence to support the conclusion that viral myocarditis was the cause of Mr Christensen’s death. Its argument in this Court essentially relied on the proposition that its experts’ opinions established a probable cause based on objective evidence, whereas Mrs Christensen’s case was based on possibility in the absence of objective evidence.

9. [304]

   Even if I had been of the view that Tudor Capital was raising a new argument, I am not persuaded that Coulton v Holcombe considerations would exclude Tudor Capital from advancing arguments based on the view Dr Rainer and Professor Keogh formed after seeing the autopsy slides.

10. [305]

    Counsel for Tudor Capital in this Court frankly accepted that Dr Rainer’s report did not undermine what the evidence ultimately was before the Arbitrator, in the sense that it did not say that the slides revealed severe hypertrophic cardiomyopathy, nor that they revealed that a precipitating cause (for ventricular fibrillation) was not needed. However, the slides did compare a heart showing myocarditis with a slide of Mr Christensen’s heart from which it was evident that the latter manifested no signs of myocarditis and, too, that Mr Christensen had been suffering from significant hypertrophic cardiomyopathy. [211] Despite being aware from Associate Professor Richards’ report of 30 April 2015 that he was not qualified to interpret the autopsy slides, Mrs Christensen did not seek to tender a report from a person so qualified.

11. [306]

    Moreover it was evident from Professor Keogh’s report of 13 March 2015 in which she commented on the autopsy slides, that she was of the view that the chronic cardiomyopathy they depicted was the cause of death. Associate Professor Richards commented on that report in his report of 30 April 2015.

12. [307]

    Furthermore, Mrs Christensen had the opportunity after Dr Rainer and Professor Keogh gave evidence on 19 May 2015 to adduce further evidence. She was aware from Associate Professor Richards’ reports, that his viral myocarditis theory was based on the absence of an alternative theory and the absence of evidence of hypertrophic cardiomyopathy. She availed herself of that opportunity, asking Associate Professor Richards to comment on an aspect of Professor Keogh’s evidence as he did in his report of 11 June 2015. That report also addressed an aspect of the focal to diffuse progression theory. [212]

Issue 1: injury

1. [308]

   Wrapped up in Tudor Capital’s challenge to the manner in which the Deputy President dealt with the issue of injury is its complaint that his failure to identify an “injury” for the purposes of s 9 within the meaning of that term in s 4 of the WCA lead to confusion in the application of s 9A.

2. [309]

   Section 4 of the WCA defines injury as “personal injury arising out of or in the course of employment”. Its application depends upon at least three considerations. What constitutes a “personal injury” and in what circumstances does such an injury arise out of the course of employment, or occur in the course of employment.

3. [310]

   As Gleeson CJ and Kirby J explained in Kennedy Cleaning Services Pty Ltd v Petkoska, [213] by the time Zickar v MGH Plastic Industries Pty Ltd [214] was decided, “a long line of decisions in Australia had recognised that an ‘injury’, being a sudden or identifiable physiological change, could nonetheless qualify within the ordinary application of that expression appearing in workers’ compensation legislation, although the change was internal to the body of the worker … or necessarily produced by external causes.”

4. [311]

   Gleeson CJ and Kirby J’s observations in Kennedy Cleaning were applied by the plurality in May [215] in upholding an appeal from the Full Court of the Federal Court which had held that Mr May had established that he had suffered a compensable injury within the meaning of that term in s 14(1) of the Safety, Rehabilitation and Compensation Act 1988 (Cth) (SRC Act), having regard to the definition of that term in s 4(1)(b) of the SRC Act. [216]

5. [312]

   Mr May had served in the Royal Australian Air Force (RAAF). He became “significantly disabled” by dizziness, cutting short “what might have been a very promising career as a pilot in the RAAF”. [217] He applied for compensation under s 14(1) of the SRC Act. He asserted his dizziness was an “injury (other than a disease)” within the definition of that term in s 4(1)(b) of the SRC Act, [218] being a consequence of vaccinations he received while he was employed with the RAAF. The Administrative Appeals Tribunal (Tribunal) which considered his application did not doubt that Mr May suffered from dizziness, but concluded there was no medical evidence to establish a connection between his vertigo and the vaccinations he received while in the RAAF. [219] It held that it was “not satisfied on the balance of probabilities that Mr May suffered a physical injury – an injury simpliciter – amounting to a sudden or identifiable physiological change in the normal functioning of the body or its organs that can be attributed to the vaccinations he received while serving in the RAAF.” [220] Buchanan J dismissed Mr May’s appeal from the Tribunal’s decision. [221]

6. [313]

   The Full Court of the Federal Court allowed Mr May’s appeal from Buchanan J’s decision. Its critical findings, as summarised by the plurality in the High Court, were:

7. [314]

   The question on the appeal in the High Court was whether Mr May’s dizziness was an “injury” for the purposes of the SRC Act and therefore compensable under s 14 of that Act. “Injury” was defined in s 4(1)(b) of the SRC Act relevantly to mean “an injury (other than a disease) suffered by an employee, being a physical or mental injury arising out of, or in the course of, the employee’s employment”.

8. [315]

   The definition in s 4 of the WCA, uses the expression “personal injury”, rather than “a physical or mental injury”. However, otherwise there is no relevant distinction between the definitions and, as Tudor Capital submitted, and Mrs Christensen did not gainsay, the reasoning in May is equally applicable to s 4.

9. [316]

   The plurality held:

10. [317]

    The plurality explained that, against this background, the SRC Act required the tribunal of fact to give consideration to “the precise evidence, on a fact by fact basis, ... accepted at trial” [223] and then to ask certain questions in order to determine whether an employee is suffering an “injury (other than a disease)”. [224] Those questions, insofar as here relevant, are:

11. [318]

    The plurality was critical of the Full Court’s conclusion “that the inquiry demanded by the statutory definition of ‘injury’ was ‘whether the person has experienced a physiological change or disturbance of the normal physiological state (physical or mental) that can be said to be an alteration from the functioning of a healthy body or mind.’” [225] The plurality held that “[t]o the extent that conclusion suggested that subjectively experienced symptoms, without an accompanying physiological or psychiatric change, are sufficient to provide a positive answer to the first or third questions set out above, that conclusion should be rejected.” [226] This was because, relevantly, it overlooked “that the Act provided that the appellant was liable to compensate in respect of ‘an injury’ and that the focus of the Act is on ‘an injury’” and that “the word ‘injury’ in ‘injury (other than a disease)’ … means ‘injury’ in its primary sense [which] …necessarily requires consideration of the ‘precise evidence, on a fact by fact basis, concerning the nature and incidents of the physiological change’”. [227]

12. [319]

    The plurality expanded this discussion by observing that “the proper construction of the Act recognises that an employee may genuinely complain of being unwell, but, in the context of the ‘injury (other than a disease)’ limb of the definition of ‘injury’, unless that employee can satisfy the tribunal of fact that he or she has suffered an ‘injury’ (in the primary sense of the word), s 14 of the Act will not be engaged.” [228]

13. [320]

    The plurality held that the “nature and incidents of the physiological [or psychiatric] change” would determine whether there was an “injury (other than a disease)”. Their Honours accepted that the evidence may take into account common sense inferences drawn from a sequence of events, referring to Forst, [229] but “there must be more than an assertion by an employee that he or she feels unwell.” [230]

14. [321]

    The plurality emphasised the absence of any “medical explanation for Mr May’s ‘illness’, which had been described as a ‘subjective description of a collection of symptoms’”. [231] There was no objective evidence of Mr May suffering “vertigo” in the period following his vaccinations, nor was there any substantial pathology to explain Mr May’s symptoms. The lack of any pathology consistent with Mr May’s symptoms, meant that no diagnosis could be made. [232] As the “nature and incidents of the physiological [or psychiatric] change” suffered by Mr May were not established, he had not proved that he had suffered an “‘injury’ in the primary sense of that word.” [233]

15. [322]

    In a separate judgment, Gageler J agreed with the orders proposed by the majority. His Honour first observed:

16. [323]

    Gageler J observed that if the Full Court’s formulation of “injury” as “a physiological change or disturbance of the normal physiological state (physical or mental) that can be said to be an alteration from the functioning of a healthy body or mind” was to be “read as equating a physiological change or disturbance sufficient to constitute an injury with any alteration from the functioning of a healthy mind or body”, that construction of “injury” would involve a significant departure from the particular sense in which repeated explanations of injury in terms of a definite or distinct physiological change or disturbance had sought to convey. [234] His Honour continued:

17. [324]

    Gageler J held that the Full Court was correct in holding that “an injury [could be] established on the basis of an account by a claimant of the disturbances to her or his body or mind, without the necessity for a diagnosis of a recognised medical condition, or corroborating pathology or medical opinion” and also in its observation that “[w]hether or not the evidence of a claimant will be sufficient, if it is not supported, corroborated or confirmed by independent medical opinion or pathology, will be a matter for the Tribunal’s satisfaction on the evidence in each particular case”. However the Full Court had erred in inferring that the Tribunal proceeded on a different basis. [235]

18. [325]

    Gageler J concluded that the Tribunal had not erred in law in finding that it was “not satisfied on the balance of probabilities that Mr May suffered a physical injury — an injury simpliciter — amounting to a sudden or identifiable physiological change in the normal functioning of the body or its organs”. The mere fact that the Tribunal accepted that Mr May had experienced debilitating dizziness, which could “loosely” be described as “vertigo”, did not compel the conclusion in addressing the sufficiency of the evidence that Mr May suffered an “injury” in the ordinary sense. In his Honour’s view, it was a case where “[c]ommon experience provided no guidance, and the medical evidence was inconclusive.” [236]

19. [326]

    The use of the disjunctive in s 4 means that “two quite different tests are involved, one or other of which is sufficient to be satisfied for the purposes of s 9.” [237] The first limb, “arising out of”, requires there to be a causal element between the employment and the injury. [238] The second limb, “in the course of employment”, involves a “temporal element and does not of itself contain a causative element.” [239] It refers to “an injury sustained while the worker is engaged in the work which he is employed to do or in something incidental to that work”. [240] As soon as the employee “ceases to be so engaged the time span ends and with it the course of employment.” [241]

20. [327]

    As I have said, Mrs Christensen put her case on both bases in s 4, that is to say, contending that Mr Christensen’s “injury” was one “arising out of or in the course of employment”. This is not surprising, having regard to the sequential nature of the matters set out in the Amended ARD as constituting the “injury”: “stress caused by employment (including by rendering Mr Christensen susceptible to a viral illness) which caused or aggravated ventricular fibrillation, cardiac arrest and death”.

21. [328]

    Professor Rawlinson addressed the stress issue in terms of Mr Christensen suffering psychological stress and there being a connection between that and him contracting a viral illness. [242] In that context, at least, I understand the “injury” was one identified as “arising out of” his employment, although depending on what was said to constitute the “injury”, that would not detract from a conclusion that it might also have occurred in the course of that employment. Otherwise the claim has to have been put as “arising out of” Mr Christensen’s employment as there was, of course, no evidence as to precisely when he first exhibited symptoms of the viral illness while the ventricular fibrillation and cardiac arrest occurred at the family home shortly before his death.

22. [329]

    Whichever way the claim was put, identification of an “injury” for the purposes of ss 9 and 25 was insufficient. Mrs Christensen also had to establish that Mr Christensen’s employment with Tudor Capital “was a substantial contributing factor to the injury” within the meaning of s 9A of the WCA.

23. [330]

    “[T]he concept and purpose of the introduction of s 9A was to remove the possibility of compensation for injury with only a ‘remote or tenuous connection with work’”. [243] When s 9A(1) speaks of “the employment concerned” being a substantial contributing factor to the injury, the legislation is not referring to the fact of being employed, but to what the worker in fact does in the employment. [244]

24. [331]

    Like the test for whether an injury is one “arising out of” employment, s 9A involves a causative element. However, as Basten JA said in Badawi, “[t]he test imposed by s 9A is intended to be more stringent: s 9A(3)” than the test for “arising out of” the employment in s 4. [245]

25. [332]

    Insofar as a finding that the temporal element in the second limb of the definition of “injury” (course of employment) is satisfied does not require a causative test, a person claiming compensation must establish for the purposes of s 9A that there was a causal connection which is “real and of substance” between the “injury” and the “employment concerned” in order to establish an entitlement to compensation under the WCA. [246]

26. [333]

    The question under s 9 is differently expressed to that which arises under s 9A. The question under each provision must be considered separately. It is not sufficient to find that injury arose out of “employment” and to thereby be able to conclude that the employment concerned was a “substantial contributing factor”. Such a reasoning process is expressly proscribed by s 9A(3). [247]

27. [334]

    Whether in the s 9 or s 9A context, causation is “a fact-laden conclusion which the courts have been told must be based on common sense”. [248]

28. [335]

    The Deputy President, in determining whether Mrs Christensen was entitled to compensation under s 9A(1), was required to determine whether “the employment concerned was a substantial contributing factor to the injury”, and, in undertaking that task, to take into account the matters specified in s 9A(2) to the extent that they are relevant. [249] The s 9A requirement that employment be “‘a substantial contributing factor’ to the injury … particularly the use of the indefinite article, admit[s] the possibility of other, possibly non-employment-related, substantial contributing factors”. [250] A finding as to relative contributing factors is a finding of fact and a question of impression and degree. [251]

29. [336]

    Determining whether the Deputy President erred in the exercise of the s 352 appellate function turns on a consideration of his reasons taken as a whole, and is not limited to the use of particular words or phrases. [252]

30. [337]

    In my view, applying that test, it is apparent that the Deputy President erred when he found that the “injury” was Mr Christensen’s “experience of stress … [making] him susceptible to the contraction of an infective virus.” [253] It is manifest that, in so finding, the Deputy President made a finding of “injury” which differed from the “injury” the Arbitrator identified. As Tudor Capital submitted, the Deputy President’s finding did not align with the Arbitrator’s findings and reasons, nor, in particular, with the injury the Arbitrator had identified, being the “entry into the myocardium of the virus” [254] or the “entry of the T cell lymphocytes into the myocardium.” [255] Rather, the focus of the Deputy President’s finding contrasted starkly with the Arbitrator’s. Whereas the “injury” the Arbitrator identified focused on the penultimate point of the process Mrs Christensen relied upon as constituting “injury” in the Amended ARD, the Deputy President’s finding looked to an earlier and vaguer concatenation of work-related events purely subjective to Mr Christensen.

31. [338]

    In addition, in so holding, in my view, the Deputy President implicitly identified an error of fact on the Arbitrator’s part. Such an error was an operative one as, not least, identification of “injury” was the threshold question for the purposes of s 9.

32. [339]

    Further, in making his finding of “injury” the Deputy President failed to undertake the precise consideration on a fact by fact basis of the evidence as explained in Kennedy Cleaning and May to determine whether Mr Christensen’s “experience of stress” or susceptibility to the contraction of an infective virus, could constitute an “injury” within the meaning of that term in s 4 of the WCA. [256] Thus the Deputy President failed to identify any “physiological change or disturbance of [Mr Christensen’s] normal physiological state” [257] which caused the “experience of stress” he identified as “the relevant injury”. Such an inquiry would have been necessary whether or not the stress was said to constitute a “psychological injury” within the meaning of s 11A(3), as the definition of the latter requires identification of an “injury (as defined in section 4) that is a psychological or psychiatric disorder”.

33. [340]

    No doubt the Deputy President’s omission in this respect was because neither party, in particular Mrs Christensen, pointed to any evidence that the psychological stress Mr Christensen was found to have experienced was a function of any physiological change. Indeed, tellingly, in her written submissions in this Court, Mrs Christensen appeared to reframe the case of psychological stress presented before the Commission, to contend her factual case that Mr Christensen’s “work conditions led to his health deteriorating resulting in a viral illness and viral myocarditis.” [258] She only contended the last two conditions involved a physiological change.

34. [341]

    In this respect, too, the Deputy President erred in point of law in reasoning to his conclusion without engaging with the statutory test in s 4 of the WCA. This was, in my view, a constructive failure to exercise jurisdiction.

35. [342]

    Further, once the Deputy President identified “the relevant injury” as Mr Christensen’s “experience of stress”, it was incumbent upon the Deputy President to determine whether, as Tudor Capital submitted, the “experience of stress” was a “psychological injury” within the meaning of s 11A(3).

36. [343]

    As I have pointed out, Professor Rawlinson discussed the “relationship between psychological stress and viral illness”, as that upon which he was being asked to provide an opinion, in terms of whether the stress to which Mr Christensen was exposed made him more susceptible to contracting an infection. [259] The Deputy President did not directly refer to this evidence. Associate Professor Hudson also addressed this issue in the same terms in responding to Professor Rawlinson’s view “as to the link between psychological stress and infection”, [260] as did Professor Keogh. [261] Although the Deputy President referred to their evidence, [262] he appears to have failed to appreciate its significance when he came to identifying the “injury” in terms of Mr Christensen’s “experience of stress”.

37. [344]

    An “injury” which is a finding of “psychological stress”, prima facie raises the question, in my view, as to whether Mr Christensen’s “injury” was a “psychological injury” within the meaning of s 11A(3). The Arbitrator said that he regarded the “issue of psychological injury as being something of a red herring”, but, despite his assertion that he would explain this view, did not do so. [263] Similarly the Deputy President failed to consider this issue, even in terms of concluding that the consequence of his decision as to “injury” was that the Arbitrator had erred in failing to discharge his statutory function. The Deputy President’s failure in this respect was a constructive failure to exercise his jurisdiction to correct errors on the Arbitrator’s part.

38. [345]

    Alternatively, if, as Mrs Christensen contended, it should be concluded that the Deputy President had not re-defined the Arbitrator’s finding of injury, I would nevertheless be of the view that the Deputy President should have held the Arbitrator erred in law in failing to consider on a step by step basis as required by Kennedy Cleaning (noting May had not been decided when the proceedings were before the Commission), which aspect of the process to which he referred in his dispositive paragraph [271] was the relevant injury for the purposes of s 4 and in what respect it was the consequence of a physiological change.

39. [346]

    Absent isolation of the relevant “injury”, as Tudor Capital submitted, the Arbitrator could not properly undertake the evaluative process s 9A required of determining whether the employment concerned was a substantial contributing factor to the injury. Thus I would accept Tudor Capital’s submission that the “injury” Mrs Christensen identified in the Amended ARD, and which appears to have formed the basis of the Arbitrator’s compendious findings of “injury”, [264] led to confusion in the application of both ss 4 and 9A. The Deputy President should have recognised that was an operative error of law on the Arbitrator’s part and corrected it. Once again, the Deputy President’s failure in this respect was a constructive failure to exercise his jurisdiction.

40. [347]

    In dealing with ground 4 of Tudor Capital’s appeal concerning s 9A of the WCA, the Deputy President appeared uncertain as to whether Tudor Capital was asserting that the Arbitrator had committed a factual error concerning the relevance of the “pre-existing condition” of Mr Christensen’s heart. With respect, this uncertainty was misplaced. Tudor Capital’s submissions unequivocally asserted that the Arbitrator’s conclusion that he was “not satisfied that the pre-existing condition of his heart played any part in his death” [265] was wrong and was contradicted both by its experts’ evidence, as well as by that of Associate Professor Richards.

41. [348]

    The Deputy President accepted that “the Arbitrator at [273] … disregarded [Mr Christensen’s] pre-existing cardiac condition as being a factor that ‘played any part in his death’” and did so without considering the evidence of Tudor Capital’s experts and Associate Professor Richards as to the relevance of the underlying cardiac pathology. [266] The Deputy President rationalised that omission on the part of the Arbitrator by saying:

42. [349]

    It is difficult to understand this rationalisation. At paragraph [273], the Arbitrator had rejected the proposition that “the pre-existing condition of his heart played any part in [Mr Christensen’s] death”. As the Deputy President had found, he did so without referring to critical evidence. Insofar as Tudor Capital’s experts were concerned, that evidence was that the pre-existing condition of hypertrophic cardiomyopathy was the cause of Mr Christensen’s death.

43. [350]

    Although the Deputy President appeared to recognise “the Arbitrator at [273] was addressing the nature of the two distinct and conflicting hypotheses, being the presence of relevant myocarditis or relevant hypertrophic cardiomyopathy,” [268] his analysis of Tudor Capital’s complaint by reference to Department of Education & Training v Sinclair, proceeded on the premise that those conditions were concurrent contributing factors to Mr Christensen’s death. That, as I have said was contrary to the case both Tudor Capital and Mrs Christensen put to the Arbitrator. There are a number of problems with this conclusion.

44. [351]

    First, the Deputy President’s rationalisation of the Arbitrator’s error did not address Tudor Capital’s complaint which was that the Arbitrator had erred in concluding that Mr Christensen’s hypertrophic cardiomyopathy did not play any part in his death. That complaint, in turn, required consideration of the Arbitrator’s statement that there was insufficient evidence for that proposition. [269] Determining this issue required the Deputy President to analyse the expert evidence before the Arbitrator which Tudor Capital submitted was inconsistent with the Arbitrator’s conclusion. That included the evidence adduced from Dr Rainer and Professor Keogh concerning the significance of Mr Christensen’s severe and long standing hypertrophic cardiomyopathy, the significance of what the autopsy slides revealed and their opinions that, absent histological evidence of myocarditis, ventricular fibrillation consequent upon hypertrophic cardiomyopathy was the more probable explanation for Mr Christensen’s death.

45. [352]

    The Deputy President’s failure to undertake that analysis revealed he misunderstood Tudor Capital’s case in such a way as to undermine the lawfulness of his decision in a fundamental way, such as to constitute an error in point of law.

46. [353]

    Secondly, it was not open to the Deputy President to palliate the Arbitrator’s failure to have regard to Mr Christensen’s pre-existing cardiac condition as being a factor that “played any part in his death”, [270] by reliance on Department of Education & Training v Sinclair which, when properly understood, did not excuse what was plainly an error on the Arbitrator’s part in failing to have regard to material evidence.

47. [354]

    In Department of Education & Training v Sinclair, Mr Sinclair claimed an ongoing partial incapacity for work with the Department of Education and Training (Department) as a result of a psychological injury (an Adjustment Disorder) he claimed arose out of, and in the course of, that employment. The connection with his employment was that the Adjustment Disorder was said to have flowed from the investigation of allegations, and the making of charges, by the Department that Mr Sinclair’s personal association with one of his students at a school at which he worked was close and improper, and may have been sexual in nature. [271]

48. [355]

    There was evidence before the Commission from Dr Synnott, a consultant psychiatrist, retained on the Department’s behalf that Mr Sinclair’s employment with the Department was a substantial contributing factor to Mr Sinclair developing an Adjustment Disorder, but that other causes were matters personal to him. [272]

49. [356]

    In the passage of Department of Education & Training v Sinclair to which the Deputy President referred, Spigelman CJ was considering what, in his view, were the absurd consequences in such a case of a literal reading of the combined operation of ss 9A and 11A. It is unnecessary to set out his Honour’s analysis. It is sufficient to note that it took place in the context of evidence that Mr Sinclair’s depression was causally related both to his employment and to personal matters which were, accordingly, concurrent contributing factors. [273]

50. [357]

    The Deputy President rationalised the Arbitrator’s failure to have regard to the pre-existing cardiac condition which Mr Christensen suffered by reference only to an extract of Associate Professor Richards’ report to which he referred. [274] However Tudor Capital’s case was that the Arbitrator’s conclusion was contradicted not only by Associate Professor Richards’ evidence, but also by its experts’ evidence. [275] That was, of course, a reference to Dr Rainer and Professor Keogh’s evidence concerning the severe hypertrophic cardiomyopathy.

51. [358]

    On Tudor Capital’s case, severe hypertrophic cardiomyopathy and viral myocarditis were not probable concurrent contributing factors to Mr Christensen’s death but, rather, alternative explanations for his fate. That is to say, on Tudor Capital’s expert evidence, the ventricular fibrillation which uncontroversially caused his death was explained by him suffering from severe hypertrophic cardiomyopathy, while on Mrs Christensen’s case, his death was explained by him having suffered from viral myocarditis.

52. [359]

    The Deputy President’s reliance upon Department of Education & Training v Sinclair in this context, in my view, demonstrates again that he misapprehended Tudor Capital’s case in a manner which meant that he failed properly to determine whether the Arbitrator had erred in law in failing to apply correctly s 9A of the WCA.

Issues 2 and 3: evidence of myocarditis/evidence of severe cardiomyopathy

1. [360]

   Tudor Capital challenges the Deputy President’s failure to correct what it contended were the Arbitrator’s errors of fact: that work (emotional) stress caused Mr Christensen’s viral illness, that the virus resulted in myocarditis and that the myocarditis caused ventricular fibrillation which caused Mr Christensen’s death. Tudor Capital contended that the evidence was insufficient to support those conclusions.

2. [361]

   The proceedings before the Commission were not governed by the rules of evidence. [276] The Workers Compensation Commission Rules 2011 (NSW), r 15.2, required that when informing itself on any matter, the Commission was to bear in mind the principles that evidence should be logical and probative and that evidence based on speculation or unsubstantiated assumptions was unacceptable.

3. [362]

   In South Western Sydney Area Health Service v Edmonds, [277] I observed that r 70 of the Workers Compensation Commission Rules 2003 (NSW), the precursor of r 15.2, “broadly reflects fundamental principles of the common law concerning admissibility of evidence.” However, it does not reintroduce the rules of evidence as, if it did, it would be inconsistent with the WIM Act, s 354. [278] As French CJ observed in Kostas “the rules of evidence, excluded by statute, [should not be allowed] to ‘creep back through a domestic procedural rule’”. [279]

4. [363]

   Nevertheless, “[a]lthough not bound by the rules of evidence, there can be no doubt that the [Workers Compensation] Commission is required to be satisfied that expert evidence provides a satisfactory basis upon which the Commission can make its findings” and “the question of the acceptability of expert evidence will not be one of admissibility but of weight.” [280]

5. [364]

   The Commission is required to draw its conclusions from material that is satisfactory, in the probative sense, in order that it act lawfully and in order that conclusions reached by it are not seen to be capricious, arbitrary or without foundational material. [281] In cases where the experts differ, the lay tribunal must apply logic and common sense to the best of its ability in deciding which view is to be preferred or which parts of the evidence are to be accepted, an exercise which cannot be carried out without knowing the essential integers of the expert opinion. [282]

6. [365]

   The Arbitrator directed himself that he could find a causal connection between “stress and the breakdown of [Mr Christensen’s] health allowing the entry into his system of a viral illness, or the subsequent entry of the virus by virtue of the T cell lymphocytes into [Mr Christensen’s] myocardium causing ventricular fibrillation and cardiac arrest” on the basis that “medical science does not say in this individual case that there is no possible connection between the events and the death” and a “commonsense evaluation of the causal chain”. [283]

7. [366]

   As I have said, in May, the plurality accepted that in determining whether there was an “injury”, the evidence may, “where appropriate … take into account common-sense inferences drawn from a sequence of events”. [284] Gageler J in his separate reasons, also accepted that, as the Full Court of the Federal Court held, there were cases where a conclusion of “injury” could be reached “on the basis of an account by a claimant of the disturbances to her or his body or mind, without the necessity for a diagnosis of a recognised medical condition, or corroborating pathology or medical opinion" and that "[w]hether or not the evidence of a claimant will be sufficient, if it is not supported, corroborated or confirmed by independent medical opinion or pathology, will be a matter for the Tribunal’s satisfaction on the evidence in each particular case”. [285]

8. [367]

   However, as I have said, that did not avail the claimant in May, where “[c]ommon experience provided no guidance, and the medical evidence was inconclusive.” [286] The temporal coincidence between the onset of Mr May’s dizziness/vertigo and the vaccinations he had received was not sufficient, absent medical evidence, to establish that he had suffered “an injury” in the sense required by the definition.

9. [368]

   In support of their acceptance that, in determining causation, resort can be had to common sense inferences, the plurality in May cited two passages from the judgments of Rich ACJ and Dixon J in Forst.

10. [369]

    Forst concerned a compensation claim brought under the Workmen’s Compensation Act 1932-1935 (SA) by the widow of a deceased waterside worker who, after performing two tasks at work which involved muscular exertion, collapsed and died. There was extensive medical evidence to the effect that the cause of death was coronary thrombosis, however opinions were divided as to whether death from coronary thrombosis could be related to exertion. The employer’s case was that it was “equally probable or more probable that the artery leading to the heart became occluded without any extraneous causation but merely by the progress of the disease from which Mr Christensen was suffering.” [287]

11. [370]

    At first instance, a special magistrate acting as an arbitrator found that the workman’s death was due to coronary thrombosis, but that death from coronary thrombosis could not generally be related to exertion and, therefore, that the workman's death could not satisfactorily be said to have been caused by his exertion. Accordingly, he refused to award the widow compensation. The widow was successful in an appeal to the Supreme Court of South Australia. An appeal to the High Court was dismissed by Rich ACJ, Starke and McTiernan JJ, with Dixon J dissenting.

12. [371]

    In the passage to which the plurality in May referred, Dixon J first accepted that “upon a question of fact of a medical or scientific description a court can only say that the burden of proof has not been discharged where, upon the evidence, it appears that the present state of knowledge does not admit of an affirmative answer and that competent and trustworthy expert opinion regards an affirmative answer as lacking justification, either as a probable inference or as an accepted hypothesis.” [288] It is this passage which has become the important and guiding principle. [289]

13. [372]

    Secondly, Dixon J disagreed, in particular, with Rich ACJ’s view that one could first reason from common sense without reference to medical evidence. [290] In his view, “whether an inference [could] or should be drawn from the fact that … the collapse of [Mr Christensen] occurred after unusual exertion seems … to depend on the answer first given to the pathological question whether there is any natural connection between exertion and the formation of a thrombus.” Although his Honour accepted it was “[t]empting … particularly in matters of bodily health, to argue from a sequence of external events”, in his Honour’s view “such reasoning is justified only when positive knowledge or common experience supplies some adequate ground for believing that the events are naturally associated.” [Emphasis added.] His Honour accepted that the evidence upon which the special magistrate acted was to the effect that there was no such ground. [291]

14. [373]

    Forst was considered in EMI (Aust) Ltd v Bes. In that case, another widow’s compensation claim, the deceased worker died from injuries received when his car struck a telegraph pole. His widow asserted his death was consequent upon a blow he received to his head at work, 12 or so days earlier. Following that incident, there was evidence that the deceased had persistent headaches of which he constantly complained and took analgesics to treat them. On the day of the accident, he was driving to see a doctor. His daughter gave evidence that on that day he seemed “vague and slow in his reactions” and had earlier (but presumably after the blow to his head) driven his car in a manner which nearly caused an accident. [292]

15. [374]

    In the Workers Compensation Commission, Gibson J accepted that the cause of the deceased’s car hitting the power pole was the fact that while at the wheel, he suffered from syncope (temporary loss of consciousness caused by a fall in blood pressure) due to the intake of “analgesics in association with post-concussional headaches and severe emotional disturbance.” [293] In so finding, his Honour considered competing medical evidence as to the cause of the syncope. There was no objective evidence of a post-concussional state, but one medical practitioner was prepared to accept it was a possible cause of the syncope. [294]

16. [375]

    On appeal, the question was whether it was open to Gibson J to act on this opinion “if he thought that it was in keeping with the probabilities of the case …using the temporal experiences as a background leading up to an examination of the medical scientific evidence.” [295]

17. [376]

    As I have said, Herron CJ referred to Dixon J’s first proposition in Forst as establishing an important and guiding principle. His Honour also recognised the force of Dixon J’s second warning about reasoning from a sequence of external events absent “positive knowledge or common experience [supplying] some adequate ground for believing that the events are naturally associated.” [296]

18. [377]

    Herron CJ also referred to St George Club Ltd v Hines [297] and Ramsay v Watson, [298] in which the Full Court of the Supreme Court of New South Wales and the High Court respectively had expressed the view that the fact that there may be medical evidence as to the nature and cause, or probable cause of an ailment, was not conclusive. Rather, it was for the tribunal of fact “to weigh and determine the probabilities … [in which respect the decision-maker] may be assisted by the medical evidence … [but] must ask themselves ‘[a]re we on the whole of the evidence satisfied on a balance of probabilities of fact?’” [299]

19. [378]

    On the basis of these cases, Herron CJ expressed the principle upon which Mrs Christensen relies that:

20. [379]

    Applying that approach, Herron CJ concluded it was open to Gibson J to draw “the inference that there was a causal connexion between the work incident and the syncope which caused the death.” He emphasised that in drawing inferences in this context, it was necessary to determine whether an inference could be found to have “some greater degree of likelihood”. [301]

21. [380]

    The principles enunciated in Forst, Ramsay v Watson and EMI (Aust) Ltd v Bes were applied by Spigelman CJ in Seltsam [302] in the context of his Honour considering the existence of a causal relationship on the balance of probabilities. [303] In these passages, to some of which the Arbitrator referred, and speaking of proof of the causation of diseases where the primary facts consisted, in large measure, of epidemiological studies, [304] Spigelman CJ said:

22. [381]

    The evidence was that any connection between psychological stress and an increased susceptibility to viral illness was “unproven”, [305] and “not well characterised, explained or understood.” [306] In addition, from the outset it was dependent, in part, upon there being “no other cause found for Mr Christensen’s death at autopsy” [307] and/or the absence of “any cardiac pathology likely to predispose him to sudden death”, or the absence of severe ventricular hypertrophy which might be associated with increased risk of sudden death, as opposed to the presence of mild ventricular hypertrophy. [308]

23. [382]

    An “unproven” connection between psychological stress and an increased susceptibility to viral illness does not, in my view, amount to “positive knowledge”, supplying “some adequate ground for believing that the events are naturally associated.” [309] It was not suggested in the Commission that “common experience” could provide that answer.

24. [383]

    However, I accept that in EMI (Aust) Ltd v Bes, Herron CJ was of the view that “if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable”. This case proceeded as I understand it on the basis that the fact medical science said the connection between psychological stress and an increased susceptibility to viral illness was “unproven”, meant it was “possible”. This opened the door to the temporal inquiry. Nevertheless, that inquiry could not be undertaken in isolation from the medical evidence.

25. [384]

    It is in that context, in my view, that the Arbitrator overlooked material facts, or gave material facts undue or too little weight in deciding the inference to be drawn from the evidence as to the cause of Mr Christensen’s death. [310] The Arbitrator’s failure adequately to consider the evidence exposed error of law on his part in determining the issue whether Mr Christensen suffered “an injury” within the meaning of s 4 of the WCA, which the Deputy President did not identify. The Deputy President’s omission in this respect was a constructive failure to exercise his jurisdiction.

26. [385]

    As Tudor Capital accepted, the point about inadequate analysis of the medical evidence, a matter of which it complains in respect to both the Arbitrator’s reasons and also the Deputy President’s reasons, is supportive of its no sufficient evidence ground.

27. [386]

    It is convenient, accordingly, before explaining the reasons for my conclusion to identify the principles concerning both adequacy of reasons and the analysis of competing expert opinion.

28. [387]

    The principles concerning adequacy of reasons are well known. [311] It is apposite, however, to consider how those principles apply in an appeal confined to a grievance in point of law. In that situation, as Macfarlan JA explained in Wilkinson, [312] Soulemezis v Dudley (Holdings) Pty Ltd, [313] “is authority for the proposition that where a right of appeal is given only in respect of a question of law … reasons for a finding of fact ‘can be treated less elaborately than [those on] an issue involving a question of law or mixed fact and law’. Nevertheless the principle that justice must not only be done but must be seen to be done remains applicable”.

29. [388]

    Thus, in Soulemezis, [314] McHugh JA held that “the failure to explain the basis of the crucial finding of fact involves a breach of the principle that justice must not only be done but must be seen to be done” and is an error of law because the decision-maker “has not properly fulfilled the function which the law calls upon a judicial person to exercise”. There will be a failure to give adequate reasons where a decision-maker ignores evidence critical to an issue in a case and contrary to an assertion of fact made by one party and accepted by the decision-maker. [315]

30. [389]

    There being starkly contrasting medical evidence, as Ipp JA held in Wiki, [316] both the Arbitrator and the Deputy President were obliged to consider the evidence in a manner which entailed a rational analysis of the issues. Where the experts are properly qualified and none has been found to be dishonest, or misleading, or unduly partisan, or otherwise unreliable, a decision based solely on demeanour will not provide the losing party with a satisfactory explanation for his or her lack of success. [317] At least in the case of experts, resort to the Court’s observations of the demeanour of witnesses should be a last resort as a means of choosing between their evidence. [318]

31. [390]

    Further, even in a case where there is an adverse credibility finding in respect of one witness, the decision-maker is not relieved from considering evidence which is “unchallenged, unanswered, ostensibly reliable and supported by uncontested contemporaneous records”. [319] Nor does such a finding relieve the decision-maker, or an appellate decision-maker when required, of the duties of analysis and the provision of reasons to demonstrate and explain that such analysis has occurred. Failure to carry out an analysis of such evidence will mean there has not yet been a determination of the case of the party adducing it upon a consideration of the real strength of the body of evidence it presented. [320]

32. [391]

    The Deputy President concluded that that the Arbitrator did, and was entitled to, take into account Professor Keogh’s demeanour when evaluating her evidence. [321] That may be so, although, as I have said, it did not entitle the Arbitrator not to engage with uncontested contemporaneous records such as the autopsy slides. As the Deputy President accepted, the Arbitrator was subject to the further obligation to engage with the evidence. Nevertheless, the Deputy President concluded “[t]hat the Arbitrator did so is beyond dispute.” [322] In my view, the Deputy President erred in this respect, an error which appears also to be a function of the Deputy President’s failure sufficiently to analyse the medical evidence.

33. [392]

    When one has regard to the Arbitrator’s reasons it is apparent that although he set out lengthy passages from the experts’ reports, when he came to his dispositive reasons, he found without analysing the competing evidence that “the disarray present post mortem was equally consistent with a cardiac arrest being caused by a viral myocarditis.” [323] He discussed briefly the reasons he said supported that proposition, reasons which, as I explain below, were affected by error. [324] He then rejected Tudor Capital’s case because he did “not accept the evidence of Professor Keogh or Dr Rainer that the cause of death was the hypertrophic cardiomyopathy.” [325] He did so apparently on the basis that he could not discard the temporal events, in particular, the coincidence that Mr Christensen had a viral illness at the time he died. [326]

34. [393]

    In this respect the Deputy President erred, in my view, in concluding that the Arbitrator had had regard to all the evidence in reaching his conclusion as to “injury”. The passages of evidence in the Arbitrator’s reasons to which he referred as demonstrating the Arbitrator had discharged that obligation, [327] were occasional comments in the course of the Arbitrator’s lengthy recounting of the facts. They did not, however, demonstrate an analytical consideration of the competing theories of the cause of Mr Christensen’s death.

35. [394]

    The differences between the expert evidence were capable of being resolved rationally by examination and analysis. In my view, the Arbitrator’s reasons demonstrate that he failed to undertake that exercise. He effectively rejected Professor Keogh’s evidence on a demeanour basis, as the Deputy President found. Further, he failed to have regard to the significant aspects of Dr Rainer’s evidence particularly regarding the possibility of viral myocarditis being missed as a function of sampling error which Dr Rainer said was “highly unlikely”. The Arbitrator’s approach appears to have been that as long as something was a possibility, evidence to the contrary did not have to be considered. The Deputy President should have held that the Arbitrator’s failure to analyse the competing theories of Mr Christensen’s death by reference to all the medical evidence demonstrated a failure to give adequate reasons and constituted an error of law.

36. [395]

    It is also apparent, in my view, that in rejecting Tudor Capital’s case, the Arbitrator was cognisant of the fact that Mrs Christensen’s case depended on the premise expressed in the early expert reports that there was no explanation for Mr Christensen’s death alternative to that of viral myocarditis and that Tudor Capital’s case was that hypertrophic cardiomyopathy was that alternative explanation. Whether that proposition is expressed as depending upon the condition for Associate Professor Richards’ opinion that there was only evidence of mild hypertrophic cardiomyopathy being removed by the identification of severe hypertrophic cardiomyopathy as was argued on appeal, or merely that the severe hypertrophic cardiomyopathy was the alternative explanation for the death, it was a case which was before the Arbitrator and with which he had to deal.

37. [396]

    In my view, in seeking to address that issue, the Arbitrator erred for the reasons I have touched upon [328] and which I now address in greater detail.

38. [397]

    Even though the Arbitrator accepted Mr Christensen’s “cardiomyopathy was a pre-existing factor”, he concluded it was not the cause of his death because “there is no scientific evidence that establishes that [Mr Christensen] must have co-incidentally have [sic, as in original] died at that precise moment.” [329] This is a fallacy Mrs Christensen’s submissions appear to have embraced as reflected in her submission that the hypertrophic cardiomyopathy was weakened by Dr Rainer’s evidence that the fibrosis identified in the slides was not so severe that it was highly probable that arrhythmia would occur at that point in time (i.e. when Mr Christensen died) but, rather, that it could have occurred at any point in time.

39. [398]

    That fallacy, in my view, revealed a fundamental misunderstanding of Professor Keogh’s and Dr Rainer’s evidence that the severity of Mr Christensen’s hypertrophic cardiomyopathy was such that he could have died at any time and, too, that there did not have to be a trigger for the ventricular fibrillation it caused. It also begged the question that the conclusion to the contrary the Arbitrator had just reached (as to viral myocarditis) was one based on an unproven hypothesis concerning a link between stress and susceptibility to viral illness, and the possibility that a sampling error on autopsy had missed evidence of viral myocarditis, a proposition Dr Rainer and Professor Keogh, the only cardiac experts who had analysed the autopsy slides, had in effect rejected having regard to the extent of the tissue samples.

40. [399]

    The autopsy slides fell into the category of “uncontested contemporaneous records” referred to in Earthline, as, too, did their interpretation by Dr Rainer and Professor Keogh. Dr Rainer’s evidence was that Mr Christensen’s heart had been extensively sampled and that the size of the sample was sufficient to overcome any potential sample defect. Professor Keogh gave similar evidence. Although the Arbitrator held that Associate Professor Richards was incorrect in his assumption as to the size of the samples taken, he did not regard that error as significant, observing in part that “the size of the samples is not critical to [Mrs Christensen’s] contention.” [330]

41. [400]

    However, the sampling size was of great significance to Tudor Capital’s case. Its significance in the context of the analysis of the competing contentions could not, as the Arbitrator appears to have thought, be overcome by the extraction of concessions that it was possible inflammation indicating the presence of viral myocarditis could have been missed. Nor could it be supported by reference to Professor Keogh’s report of 15 June 2012, which also allowed a possibility of a viral myocarditis on the basis that post mortem sampling does not sample the entirety of the right and left ventricles, and without proper analysis of her evidence concerning the development of her opinion concerning the cause of Mr Christensen’s death. [331]

42. [401]

    Further, a conclusion that Associate Professor Richards was incorrect in his assumption as to the size of the samples taken was also significant in terms of his opinion that, as Tudor Capital submitted to the Deputy President, the negative result for viral myocarditis on histopathology was wrong on the basis of possible sampling error. If his opinion as to the possibility of sampling error was disproved by the evidence of the extent of tissue taken as revealed in the autopsy slides, his opinion that viral myocarditis was the probable cause of death was, in my view, substantially undermined. The Arbitrator erred in overlooking the significance of Associate Professor Richards’ error in this respect. The Deputy President erred in failing to identify the Arbitrator’s error.

43. [402]

    The Arbitrator said he was “not persuaded” as to the reasons for Professor Keogh’s abandonment of the opinion in her 15 June 2012 report. This was because, in his view, the autopsy slides “were no more than the post mortem sampling, the defect in which (that they did not sample the entirety of the right and left ventricles, nor the septum) had been the basis for her original opinion.” [332]

44. [403]

    The Arbitrator’s conclusion in this respect reveals a fundamental failure to consider the extensive evidence from both Dr Rainer and Professor Keogh concerning the significance of actually seeing the autopsy slides in 2015 as opposed to having to rely upon Dr Elston’s report, and the extent of sampling they revealed which was far greater than usually taken on autopsy. In addition, Professor Keogh’s evidence was that her first report was written in reliance on the autopsy report which was written by a “generalist pathologist” and that was not the same as seeing the autopsy slides and, one might add, have them analysed by two cardiac specialists.

45. [404]

    Next, the Arbitrator’s conclusion that he was “not satisfied that the extent of the sampling taken was able to negate that fundamental problem with the post mortem process, i.e. it sampled only parts of the relevant tissue”, [333] failed to have regard to Dr Rainer’s evidence that Mr Christensen’s heart had been extensively sampled, that the “28 blocks of tissue taken really comprehensively examine that heart” and that the size of the sample was sufficient to overcome any potential sample defect. Professor Keogh, who also had substantial experience reading cardiac biopsies, as that was something she said she had done since 1986 up to 25 times a week when a pathologist was not available, graphically said the “whole heart … was sliced up and sampled.”

46. [405]

    The evidence upon which the Arbitrator relied in this respect was Dr Whalley’s evidence about the “patchy” post mortem process, a view also originally held by Professor Keogh. [334] However, Dr Whalley did not give any evidence about the autopsy slides and, at the risk of repetition, Professor Keogh’s opinion had been changed because of the autopsy slides. Mrs Christensen accepted in the course of the appeal hearing, that the effect of Dr Rainer’s evidence was that the sampling was not patchy. The Arbitrator’s failure to have regard to the evidence of the only cardiac pathologist who said the extent of the tissue sampling eliminated sampling error, was a critical omission on his part.

47. [406]

    Although Tudor Capital made extensive submissions about the adequacy of the sampling to the Deputy President in addressing ground 3 of its appeal, the Deputy President disposed of that ground without referring to this issue at all. [335] Instead, he effectively dismissed the autopsy slides by asserting “there was abundant evidence as to myocarditis being the likely cause of the ventricular fibrillation leading to death.” [336] In this respect he said that evidence included Dr Whalley’s evidence that “notwithstanding the absence of histological evidence, Dr Whalley considered myocarditis the ‘most likely cause of [Mr Christensen’s] death’.” [337] The Deputy President did not otherwise identify the “abundant evidence”, and, as I have said, himself failed to analyse the arguably cogent evidence to the contrary.

48. [407]

    In my opinion, the Deputy President could not resolve ground 3 of Tudor Capital’s appeal without having regard to, and properly analysing, Professor Keogh’s and Dr Rainer’s evidence about the autopsy slides and the significance of the fact they did not identify viral myocarditis. He did not undertake that exercise.

49. [408]

    Critical to the Arbitrator’s finding that viral myocarditis was the cause of Mr Christensen’s death was his finding that “the disarray present post mortem was equally consistent with a cardiac arrest being caused by a viral myocarditis.” [338] In this respect, he failed to have regard to Professor Keogh’s evidence that the “fibre disarray” apparent on the autopsy slides was “very specific for hypertrophic cardiomyopathy” and that “[m]yocyte disarray [was] not a normal finding [and] occur[ed] with primary myocardial disease, most usually hypertrophic cardiomyopathy”. Dr Rainer also attributed the fibrosis and myocyte disarray observed in the slides to hypertrophic cardiomyopathy.

50. [409]

    It might be accepted, as Mrs Christensen submitted, that myocyte disarray was a key substrate for ventricular fibrillation, but, as I read the evidence, there was no evidence that, in a case of viral myocarditis the myocyte disarray would appear as it did in the autopsy slides. Indeed, in my view, the clear evidence of both Dr Rainer and Professor Keogh was to the contrary. Their evidence was that the autopsy slides, which included the slides of Mr Christensen’s myocyte disarray, did not show evidence of viral myocarditis. There was no contrary evidence.

51. [410]

    The Arbitrator’s conclusion in this respect was an error of fact, and was clearly an operative one as it was a critical part of his process of reasoning to his finding of “injury” for the purposes of s 4, and his rejection of Tudor Capital’s case. [339]

52. [411]

    In failing to identify that error, the Deputy President erred in point of law in that his decision revealed a basic misunderstanding of the facts such as to undermine his decision fundamentally. In this respect, the Deputy President said the Arbitrator did not decide that disarray was an indicator of myocarditis. Rather, he said the Arbitrator found that evidence of myocyte disarray does not exclude the possibility of myocarditis. [340]

53. [412]

    The Deputy President also observed that no specific submission was put (presumably by Tudor Capital) in relation to this suggested factual error, and that it had not been made out. [341] This was an error on the Deputy President’s part. Tudor Capital’s submissions in reply had addressed in detail the evidence that myocyte disarray was a hallmark of hypertrophic cardiomyopathy. [342]

54. [413]

    This was an error in understanding the facts, in my view, and a constructive failure to exercise jurisdiction on the Deputy President’s part.

55. [414]

    I would also accept Tudor Capital’s submission that the Deputy President’s criticism of Professor Keogh was ill-founded and reflected his failure to appreciate the significance of the evidence in the autopsy slides. As I have said, the Deputy President found Professor Keogh’s failure to inform the Commission of her changed opinion, that viral myocarditis was one explanation for Mr Christensen’s death, was a breach of cl 5(4) of the Code, referring to the obligation that if an expert witness changed his or her opinion on a material matter after providing an expert’s report to the party engaging him or her (or that party’s legal representative), the expert witness must forthwith provide the engaging party (or that party’s legal representative) with a supplementary report to that effect containing such of the information referred to in cl 5(1) of the Code as appropriate.

56. [415]

    The Deputy President’s criticism was incorrect. He said he made it because this changed opinion was “not to be found expressly stated in the reports of Professor Keogh”. [343] As I read her reports, Professor Keogh had explicitly rejected viral myocarditis as a possible cause of death in her second report of 14 June 2013, where she also expressed the view that “premature coronary artery disease and features of hypertrophic cardiomyopathy” were the cause of death. She made substantially the same points in her third report dated 8 August 2013.

57. [416]

    The Deputy President made this adverse finding even though, as he acknowledged, no submission to this effect had been made to him [344] and even though no such proposition had been put to Professor Keogh. [345] Although Kuhl concerned a party-witness, the fundamental principle of fairness underlying the statements in the decision, that a person the subject of adverse criticism by a decision-maker in a manner of significance to the outcome of the case should be given the opportunity to deal with the potential criticism, should equally apply to non-party witnesses. [346]

58. [417]

    I also note that the Deputy President made another adverse statement about Professor Keogh when he wrote that in her first report she had misstated a view of Dr Whalley. [347] Once again, this proposition was not, as I read the evidence, put to Professor Keogh, nor was it a criticism Mrs Christensen made. Although I accept there appears to be a discrepancy between what Professor Keogh wrote about what Dr Whalley had said, one might have thought if there was any substance in it, Mrs Christensen would have cross-examined her about it.

59. [418]

    To the extent that adverse view of Professor Keogh might be seen to have influenced his apparent acceptance of the Arbitrator’s criticism of Professor Keogh and, in turn, the Deputy President’s failure to have regard to her evidence, there was a constructive failure of his jurisdiction.

60. [419]

    The effect of Professor Keogh’s and Dr Rainer’s evidence was that an affirmative answer that viral myocarditis was the cause of Mr Christensen’s death lacked justification either as a probable inference or as an accepted hypothesis. [348] The Arbitrator’s failure adequately to have regard to significant aspects of their evidence in reaching his decision to the contrary, and the errors of fact he made in the course of reaching his conclusion were errors in the course of his fact-finding exercise the Deputy President ought to have identified. In concluding that the Arbitrator adequately analysed the medical evidence, and in failing himself adequately to analyse that evidence, there has been a constructive failure of jurisdiction on the Deputy President’s part.

61. [420]

    Contrary to Mrs Christensen’s submission, the hypertrophic cardiomyopathy case was not weakened, in my view, by the evidence of other consulting medical practitioners who considered the question of hypertrophic cardiomyopathy, but dismissed it. None of the other experts considered the autopsy slides. As I have said, Mrs Christensen had the opportunity, once Associate Professor Richards advised that he was not qualified to comment on them, to retain an expert who could, but did not do so. It was her case in resisting the hypertrophic cardiomyopathy case which was weakened by the absence of such evidence.

62. [421]

    Although I accept that Professor Keogh and Dr Rainer’s evidence cast considerable doubt on the viral myocarditis theory, I do not think it is open to this Court to conclude that Mrs Christensen’s case should have been dismissed. Rather, in my view, having identified the errors to which I have referred, the Deputy President should have remitted the matter back to another Arbitrator for determination in accordance with a decision correctly identifying the errors into which the Arbitrator had fallen. It should have been remitted to another Arbitrator having regard to the views the Arbitrator had expressed about Professor Keogh.

Orders

1. [422]

   In my view, the conclusion that the Arbitrator erred in the respects identified, in particular, in failing properly to analyse Tudor Capital’s expert evidence, and that the Deputy President failed to identify this error means there has been a constructive failure to exercise the jurisdiction s 352 of the WIM Act conferred.

2. [423]

   I propose the following orders:

   1. (1)

      Appeal allowed;

   2. (2)

      Set aside the decision of the Workers Compensation Commission made on 25 February 2016;

   3. (3)

      Remit the matter to the Commission for redetermination;

   4. (4)

      Respondent to pay the appellant’s costs of the appeal and to have a certificate under the Suitors’ Fund Act 1951 (NSW) if so entitled.

3. [424]

   The Court has identified a judgment in the matter, Tudor Capital Australia Pty Ltd v Christensen (No 2), [349] delivered by the President of the Commission, Judge Keating on 8 April 2016 in which he ordered Tudor Capital to pay Mrs Christensen’s costs of the appeal. Neither party, in particular Tudor Capital, referred the Court to this judgment. If following perusal of these reasons, an application is to be made insofar as Judge Keating’s costs order is concerned, it should be made in accordance with Pt 36, UCPR.

4. [425]

   MACFARLAN JA: I agree with the judgment of McColl JA. I add the following observations concerning the question of procedural fairness that Mrs Christensen, the respondent, raised in response to Tudor Capital’s appeal.

5. [426]

   Tudor Capital submitted to this Court that the opinion of Associate Professor Richards (an expert called by Mrs Christensen) that Mr Christensen’s death was caused by viral myocarditis was contradicted by the evidence of Professor Keogh and Dr Rainer (experts called by Tudor Capital). Professor Keogh and Dr Rainer relied upon autopsy slides of Mr Christensen’s heart to conclude that the cause of his death was hypertrophic cardiomyopathy (a pre-existing condition, unrelated to Mr Christensen’s employment). Tudor Capital pointed out that Associate Professor Richards’ evidence that myocarditis caused Mr Christensen’s death was stated to be based upon the absence of evidence of a relevant pre-existing condition, and Associate Professor Richards did not regard himself as qualified to interpret the autopsy slides.

6. [427]

   Mrs Christensen submitted to this Court that no contentions to this effect were put by Tudor Capital to the Arbitrator and that if they had been, Mrs Christensen may have called further evidence to meet them. Mrs Christensen submitted that in these circumstances, Tudor Capital should not be permitted to put the contentions to this Court. However, the following matters indicate that: 1) Mrs Christensen was clearly aware of this evidence; 2) was, or at least should have been, aware of the arguments in Tudor Capital’s favour to which it gave rise; and 3) had ample opportunity to respond to the evidence and arguments.

   1. (1)

      Associate Professor Richards’ evidence that myocarditis was the cause of Mr Christensen’s death was stated to be based upon the absence of evidence of any pre-existing cause of his death ([56], [58], [62] and [67] above).

   2. (2)

      In his report of 12 March 2015 Dr Rainer said that he had reviewed the autopsy slides and concluded that they showed pre-existing cardiomyopathy in Mr Christensen’s heart, leading to his conclusion that Mr Christensen died from cardiomyopathy ([78]-[82] above).

   3. (3)

      Dr Rainer’s oral evidence, given on 19 May 2015, was to similar effect ([83]-[91]).

   4. (4)

      In her report of 13 March 2015, Professor Keogh stated that the same autopsy slides revealed that Mr Christensen had chronic cardiomyopathy which, she was “highly certain”, was the cause of Mr Christensen’s death ([115]-[116] above). Her oral evidence given on 19 May 2015 was to the same effect ([117]-[124] above).

   5. (5)

      At a subsequent hearing on 11 June 2015, Mrs Christensen tendered a further report of Associate Professor Richards in which he responded to an aspect of Professor Keogh’s oral evidence, but not that aspect to which I have referred to in (4) above.

   6. (6)

      Oral addresses to the Arbitrator took place on 16 June 2015 and written submissions were subsequently filed on behalf of the parties, including by Mrs Christensen on 27 November 2015. This was well after Dr Rainer and Professor Keogh had given the evidence referred to above.

   7. (7)

      In address to the Arbitrator, counsel for Tudor Capital referred to Dr Rainer’s and Professor Keogh’s evidence that cardiomyopathy was the cause of Mr Christensen’s death and also referred in that context to the autopsy slides ([129]-[133] above). Further, counsel pointed out that Associate Professor Richards had conceded that he was not a pathologist and accordingly had not looked at the autopsy slides ([134] above).

   8. (8)

      At no time after Tudor Capital’s experts first gave evidence referring to the autopsy slides did Mrs Christensen seek the opportunity to call, or to consider calling, evidence in relation to this aspect of the experts’ evidence. Nor in the proceedings before the Arbitrator did she complain that she had been denied procedural fairness.

7. [428]

   As a result of these matters, Mrs Christensen’s submission to this Court that she was denied procedural fairness should be rejected.

8. [429]

   PAYNE JA: I have had the advantage of reading the reasons of McColl JA in draft. In what follows, familiarity with the facts and issues described by McColl JA is assumed. Although I agree with her Honour’s proposed orders, my reasons for doing so are somewhat different and can be expressed shortly.

The conditional evidence thesis

1. [430]

   I take a different view to other members of the Court about a topic which occupied a good deal of the oral submissions in this appeal. The background to this issue was that the evidence of Associate Professor Richards was that the likely cause of death was myocarditis. Associate Professor Richards described the evidence of hypertrophic cardiomyopathy (HCM) as “mild”. Associate Professor Richards said:

2. [431]

   It will be recalled that the autopsy into Mr Christensen’s death had found evidence of HCM but did not conclude that HCM was the cause of death.

3. [432]

   In this Court, a principal submission advanced by the appellant was that “mild” HCM was a “condition” of Associate Professor Richards’ evidence which was contradicted by the pathology slides which were tendered by the appellant on the last day of evidence. These slides, it was submitted, demonstrated that the deceased suffered from “severe” HCM. It was submitted, therefore, that the Deputy President erred in failing to correct the decision of the Arbitrator who accepted the evidence of Associate Professor Richards. This was because there was “no evidence” of HCM being mild, and thus the Deputy President was compelled to correct the finding of fact made by the Arbitrator that Mr Christensen’s death was likely caused by myocarditis. The failure of the Deputy President to do so was submitted to be an error in point of law.

4. [433]

   The context in which the submission was advanced by the appellant in this Court is important.

5. [434]

   Until the last day of evidence before the Arbitrator, the case advanced by the appellant was that the likely cause of Mr Christensen’s death was coronary artery disease. As McColl JA explains, the pathology slides (which became Exhibit 12) were discussed in evidence by Dr Rainer and Professor Keogh. The evidence of Dr Rainer and Professor Keogh, while concluding that HCM was the likely cause of death, did not squarely address Associate Professor Richards’ evidence. In particular the “mild”, “sufficient” or “severe” nature of HCM revealed by the slides was not the subject of evidence.

6. [435]

   Associate Professor Richards was not cross-examined about the “mild”, “sufficient or “severe” nature of HCM at all. It is not at all clear from his evidence that the characterisation of the severity of HCM demonstrated by the slides would have affected his ultimate conclusion. He was not asked what he meant by “mild”, or indeed anything else about HCM. Associate Professor Richards was cross-examined to try and establish that the likely cause of Mr Christensen’s death was coronary artery disease. It was never put to Associate Professor Richards that HCM was the likely cause of death.

7. [436]

   On this topic, the respondent had also tendered in its case e-mail correspondence from Professor Duflou, who opined that HCM was not a primary cause of Mr Christensen’s death.

8. [437]

   The submissions made by the appellant to the Arbitrator make clear that the suggested “severe” progression of HCM, allegedly shown on the pathology slides, was not advanced as a reason to disregard Associate Professor Richards’ evidence. The appellant did not submit to the Arbitrator that Associate Professor Richards’ evidence could be disregarded because the “mild” HCM condition was contradicted. To the contrary, counsel then appearing for the appellant submitted that:

9. [438]

   That is, the appellant did not submit that this was a case where the only available conclusion was that Mr Christensen’s death was caused by HCM, and not by myocarditis. Although the rules of evidence did not apply before the Arbitrator, as a matter of procedural fairness it was incumbent upon the appellant clearly to identify the case which it made about the “severe” HCM shown by the pathology slides before any conclusion could be drawn that Associate Professor Richards needed to be recalled to address that case.

10. [439]

    This is particularly so in circumstances where the “mild”, “sufficient” or “severe” progression first emerged after Associate Professor Richards had given evidence. In proceedings such as those before the Arbitrator it should be expected that each party would clearly put the other side on notice that a witness should be recalled if it was going to be submitted that the witnesses’ evidence should be rejected in whole for a reason which only emerged after that witness had given evidence. The appellant did not do so.

11. [440]

    I have addressed the appellant’s case before the Arbitrator in this detail only to put in context the appellant’s submissions before the Deputy President. It is equally clear that the “mild”, “sufficient or “severe” thesis as a basis to reject Associate Professor Richards’ evidence was not put to the Deputy President.

12. [441]

    Unsurprisingly, the Deputy President did not address the matter in this way as he was not asked to do so. If the “mild”, “sufficient or “severe” progression thesis had been clearly advanced before the Arbitrator, as it should have been, the respondent would have been on notice that it was obliged to recall Associate Professor Richards to give evidence. Equally importantly, the respondent lost the opportunity to call Professor Duflou, then NSW’s Chief Forensic Pathologist, who had expressed the view based on his analysis of certain pathology slides (it is unclear if he had access to the slides that became Exhibit 12), that a “primary cause” of Mr Christensen’s death was not HCM. No doubt there would have been a forensic challenge posed by the possibility of differences in medical opinion between Professor Duflou and Associate Professor Richards, but in my view the respondent’s loss of opportunity to consider calling Professor Duflou and re-calling Associate Professor Richards was caused by the appellant’s conduct of the case before the Arbitrator.

13. [442]

    The appellant is bound by the conduct of its case. If the argument made for the first time in this Court had been advanced before the Arbitrator, it could have been met by evidence from Associate Professor Richards and Professor Duflou. The appellant in those circumstances should not be permitted to rely on a new submission in this Court: Coulton v Holcombe (1986) 162 CLR 1; [1986] HCA 33; per Gibbs CJ, Wilson, Brennan and Dawson JJ; University of Wollongong v Metwally (No 2) (1985) 59 ALJR 481; [1985] HCA 28; and Whisprun Pty Ltd v Dixon (2003) 77 ALJR 1598; [2003] HCA 48.

14. [443]

    I would not permit the appellant to raise, for the first time in this Court, the “mild”, “sufficient” or “severe” progression thesis. The Deputy President did not err in failing to correct an “error” made by the Arbitrator in circumstances where the appellant did not ask for that correction to be made and in circumstances where, if that correction had been sought, the Deputy President should rightly have declined to make the correction on the basis that the respondent would thereby be denied procedural fairness.

15. [444]

    If this were the only issue to be determined, I would have dismissed the appeal. The appellant’s case, however, was not so limited.

“Injury” and s 9A

1. [445]

   I have concluded that the Deputy President erred in his identification of the “injury” within the meaning of s 4 of the Workers Compensation Act 1987 (NSW) (WCA) and, thus, failed properly to address the requirements of s 9A of the WCA.

2. [446]

   I agree with McColl JA that it is apparent that the Deputy President concluded that the relevant “injury” was Mr Christensen’s “experience of stress…making him susceptible to the contraction of an infective virus”.

3. [447]

   There are two fundamental difficulties with the Deputy President’s finding of “injury”.

4. [448]

   The first is that, although no order was made correcting any part of the Arbitrator’s decision for error of fact, law or discretion, this “injury” was not the “injury” found by the Arbitrator. I agree with McColl JA that the “injury” found by the Deputy President is a psychological injury requiring consideration of s 11A of the WCA.

5. [449]

   The second is that this definition of “injury” does not, at least in the way expressed by the Deputy President, identify a physiological change, let alone permit a “fact by fact” analysis of the nature and incidents of the physiological change. Failure to do so is an error in point of law: Kennedy Cleaning v Petkoska (2000) 200 CLR 286; [2000] HCA 45 at [39]; Military Rehabilitation and Compensation Commission v May (2016) 257 CLR 468; [2016] HCA 19 at [45]-[48].

6. [450]

   Absent a correct identification of the relevant “injury”, the Deputy President was in no position correctly to determine the question posed by s 9A of the WCA. Section 9A of the WCA, provides, relevantly:

7. [451]

   No compensation is payable unless an applicant demonstrates that the “employment” of the worker was a “substantial contributing factor” to the “injury”. In Pioneer Studios Pty Ltd v Hills [2012] NSWCA 324 Allsop P explained at [27]:

8. [452]

   The incorrect identification of the “injury” by the Deputy President had the effect that he could not properly consider whether the test in s 9A of the WCA was met and whether the Arbitrator had erred in law, fact or discretion in the way he separately addressed the issue. The Deputy President’s failure correctly to address the elements of s 9A was a further error in point of law.

9. [453]

   For these reasons I would allow grounds 1 and 2 of the appellant’s notice of appeal.

Remaining grounds of appeal

1. [454]

   Although I have concluded that the Deputy President fell into error, I am not able to conclude that Mrs Christensen’s case should have been dismissed.

2. [455]

   Given the conflict in the expert evidence, it is inevitable that this matter must be remitted to the Workers Compensation Commission to be determined in accordance with the reasons of this Court.

3. [456]

   Consideration of each of the remaining grounds of appeal does not lead to any different conclusion. Grounds 3 to 6 raise in different ways the incorrect identification of an “injury” by the Deputy President and a consequent failure properly to address the requirements of s 9A of the WCA. The problem of the competing expert evidence remains, even assuming that the appellant succeeds on each of these grounds.

4. [457]

   Ground 7 complains that the correct characterisation of the respondent’s case is one alleging a psychological injury requiring consideration of s 11A(3) of the WCA. As I have said, I accept that the “injury” identified by the Deputy President was a psychological injury requiring consideration of s 11A of the WCA. Given that the matter is to be remitted I should briefly address this issue.

5. [458]

   I do not accept that the correct characterisation of the respondent’s case before the Deputy President (or in this Court) was one alleging a psychological injury. It was common ground that a viral illness would be a sufficient psychological change to constitute an “injury”: Favelle Mort Ltd v Murray (1976) 133 CLR 580; [1976] HCA 13.

6. [459]

   Although, perhaps, the respondent’s submissions below were not as clear as they could have been about the precise identification of the “injury” alleged, in my view the “experience of stress” was never suggested by the respondent to constitute an “injury”.

7. [460]

   The only remaining ground of appeal, ground 8, complains about the adequacy of the Deputy President’s reasons. Little attention was paid to this ground by the appellant orally or in written submissions. In effect the complaint was one which sought to agitate factual issues. I would reject ground 8 for this reason.

Orders

1. [461]

   I agree with the orders proposed by McColl JA.