Shillingsworth v Murray

[2004] NSWCA 465

CITATION:	SHILLINGSWORTH v MURRAY [2004] NSWCA 465
HEARING DATE(S):	22 November 2004
JUDGMENT DATE:	1 April 2005
JUDGMENT OF:	Mason P at 1; Sheller JA at 72; Beazley JA at 1
DECISION:	Appeal allowed.
CATCHWORDS:	Workers' Compensation Act 1987, s9A - whether employment a substantial contributing factor to injury - pre-existing congenital weakness - conflict between evidence of medical experts - whether error of law in process whereby judge came to prefer one expert over the other - absence of reasons for conclusion. (ND)
PARTIES :	Ronald SHILLINGSWORTH Graham MURRAY
FILE NUMBER(S):	CA 40276/04
COUNSEL:	Appellant: M Daley Respondent: M Elkaim SC/ D R Moore
SOLICITORS:	Appellant: Brydens Law Office (Liverpool) Respondent: Hunt & Hunt

LOWER COURTJURISDICTION:	Compensation Court
LOWER COURT FILE NUMBER(S):	CC 4094/02
LOWER COURT JUDICIAL OFFICER :	Ashford J

CA 40276/04
CC 4094/02

MASON P
SHELLER JA
BEAZLEY JA

Friday 1 April 2005

Ronald SHILLINGSWORTH v Graham MURRAY

JUDGMENT

1 MASON P and BEAZLEY JA: For the appellant to succeed in this appeal against an award for the respondent he must establish that he is aggrieved by the Compensation Commission’s award “in point of law”.

2 The appellant suffered catastrophic injury in the form of a left pontine cerebral haemorrhage that happened in the course of his employment working for the respondent as a cotton chipper on 13 January 1997. It was conceded that he was rendered totally incapacitated and entitled to maximum lump sum benefits should he establish his entitlement to an award.

3 Unfortunately for the appellant, the law had been amended one day previously, by the insertion of s9A of the Workers’ Compensation Act 1987 (the Act). That section provides:

9A No compensation payable unless employment substantial contributing factor to injury
(1) No compensation is payable under this Act in respect of an injury unless the employment concerned was a substantial contributing factor to the injury.
(2) The following are examples of matters to be taken into account for the purposes of determining whether a worker’s employment was a substantial contributing factor to an injury (but this subsection does not limit the kinds of matters that can be taken into account for the purposes of such a determination):
(a) the time and place of the injury,
(b) the nature of the work performed and the particular tasks of that work,
(c) the duration of the employment,
(d) the probability that the injury or a similar 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 that employment,
(e) the worker’s state of health before the injury and the existence of any hereditary risks,
(f) the worker’s lifestyle and his or her activities outside the workplace.
(3) A worker’s employment is not to be regarded as a substantial contributing factor to a worker’s injury merely because of either or both of the following:
(a) the injury arose out of or in the course of, or arose both out of and in the course of, the worker’s employment,
(b) the worker’s incapacity for work, loss as referred to in Division 4 of Part 3, need for medical or related treatment, hospital treatment, ambulance service or occupational rehabilitation service as referred to in Division 3 of Part 3, or the worker’s death, resulted from the injury.
(4) This section does not apply in respect of an injury to which section 10, 11 or 12 applies.

4 Section 9A added the requirement that “the employment concerned” be shown to have been “a substantial contributing factor to the injury” (see subsection (1)). The manner in which that requirement is to be determined is explicated positively and negatively in subsections (2) and (3). The scope of the section is discussed in Mercer v ANZ Banking Group Limited (2000) 20 NSWCCR 70 and subsequent cases in this Court and in the Commission. This appeal proceeded on the basis that the principles were sufficiently expounded in Mercer.

5 The case advanced for the appellant in the Commission was that his employment on the day in question had contributed to the injury. It was contended that his work as a cotton chipper on 13 January 1997 required him to repetitively bend, lift and twist and to perform strenuous physical work involving prolonged exposure to hot and hard working conditions.

6 The parties relied particularly upon the evidence of Dr Kendall, a consultant physician (for the appellant) and Dr Matheson, a consultant neurosurgeon (for the respondent). The two specialists adopted diametrically opposed positions. Oral evidence was given by the appellant, Dr Kendall and Dr Matheson. Each witness was cross-examined.

7 The primary judge, Ashford J, held that there were differences of significance between the patient’s history relied upon by Dr Kendall and the true facts. She rejected the evidence as being unsound and unhelpful in determining the medical issue (J21). Applying s9A, she concluded that the requisite degree of causal link was not established, effectively because she preferred the evidence of Dr Matheson which satisfied her that “there was no part of the applicant’s employment with the respondent which constituted a substantial contributing factor to injury” (J42).

8 The appellant was born on 13 June 1963. In October 1996 he commenced employment with the respondent as a cotton chipper. The work involves walking along rows of cotton using a long handled hoe chipping out weeds on either side of the line of cotton. It requires bending and picking out weeds by hand after cutting them out with the hoe.

9 The cerebral haemorrhage was an injury suffered in the course of employment within the meaning of s4 of the Act (Zickar v MGH Plastics Industries Pty Ltd (1996) 187 CLR 310).

10 The trial judge concluded that the appellant had a pre-existing cavernoma.

11 In these circumstances, the question was whether the appellant could persuade the Commission that the nature and conditions of his employment was a substantial contributory factor to his injury.

The critical medical evidence

12 Dr Kendall was not an easy witness. He had been in practice for 50 years. At times he was argumentative, unwilling to accept factual assumptions put to him, and unable to provide immediate chapter and verse for particular scientific opinions. His written report addressed the cause of the stroke in the following terms (Blue 21):

Whilst some pre-existing pre-disposition to cerebral haemorrhage is reasonable to postulate, there is no doubt that his injury occurred during work and must be attributed to the heavy physical exertion on that hot day. In my experience where such an intimate nexus exists, such nexus is accepted and I would say rightly so.
He was not in the habit of exerting himself heavily outside the work sphere and it is reasonable to assume that had he not been exposed to heavy work on that day his stroke would not have happened.

13 Dr. Kendall’s position was that there was no evidence of a congenital malformation [Black 27]. He considered that it was unlikely that a cavernous haemangioma would be present in the pons, the location of the appellant’s cerebral haemorrhage, and that it was more likely that the appellant’s stroke occurred because “he was exerting himself heavily”. He considered it was against the probabilities that the stroke would have been caused by a pre-existing abnormality and that it was only remotely possible that the appellant could have had a stroke resting at home. Dr. Kendall also said that “irrespective of what one postulates to have been the weakness in that particular blood vessel, whether it was a cavernous haemangioma or another weakness, it would still have been provoked by the exertion”. He further commented [at Black 30] that it was usually “a combination of circumstances” that caused a stroke.

14 In cross-examination he resiled from attributing any relevance to the temperature, and he accepted that it was not a particularly hot day (Black 21H). If anything, a hot day would reduce blood pressure (19). See also Dr Matheson at 41).

15 Dr Kendall also accepted the possibility that the stroke was spontaneous (27H) and that it may have been caused by factors not involving hypertension (26). He accepted that there was no evidence of a history of the appellant’s blood pressure being grossly elevated (26).

16 As regards the impact of a substantial ingestion of alcohol shortly before work on the day in question, he stated that this would reduce blood pressure (19, 21), a proposition on which he was not challenged.

17 He accepted that heavy alcoholism could be a risk factor for stroke, but only if it led to hypertension (29V). There was, however, no evidence that the appellant had hypertension due to alcoholism or any cerebral vascular disease due to alcoholism (26K, 24G).

18 Dr Kendall agreed that people with cavernomas may run into trouble in their second and third decades, and that usually by the fourth decade (ie the appellant’s age bracket) they have a problem (28S).

19 The core proposition that this witness adhered to steadfastly was the opinion that a rise in blood pressure due to exertion made it more probable that he would have a stroke. This was more likely if he had a congenital cavernoma (27K, 30N, 31J, 26N-P). Unable to produce a textbook or journal article in support, he nevertheless remained adamant that his proposition was “found in all textbooks … including Harrison, [Technical Medicine] (23N). It was “an everyday observation. It’s almost medically a res ipsa” (23M).

20 Dr Matheson disputed Dr Kendall’s opinion that the most probable explanation for the appellant’s stroke was a transient increase in blood pressure brought about by physical exertion working as a cotton clipper. His reason was that physical exertion only produces “a small rise in blood pressure. It can produce high rises in its veinous pressure while you’re exerting yourself and there is no known correlation between physical exertion and developing strokes” (35K).

21 Dr Matheson initially said that he knew of no learned paper or study that would suggest there was any connection between physical exertion and developing strokes (35). Later, in cross-examination, he gave the following significantly different evidence (38K-O):

Q. Is not one of the treatments of choice for a person that has had a stroke, or suspected of having an aneurism or some other defect in the brain, in part to advise them to avoid heavy or rigorous activity.
A. Yes it’s written in all the books and I’ve never seen the sense in it.
Q. You would disagree with every text writer that has ever written a book on the subject in neurology. Is that right.
A. Yes and to the extent that I never make that restriction on my own patients.
Q. Can I ask you this. The reason why every other doctor, or at least those writing these text books and papers, would advise that restriction is for fear that the vigorous exercise will give rise to increase in cranial blood pressure which may act on an area of weakness to cause another stroke. That is the reason behind it, is it not.
A. That’s the reason behind it but the absurdity of the reason is that we now treat subarachnoid haemorrhage by raising their blood pressure not by lowering it. So now that information is just wrong.

22 Later he accepted as correct, with reference to ordinary strokes, that it was:

the view of all those clinicians, doctors, that strokes can be multi-factorial, that there can be a weakness which can be acted upon by an increase in blood pressure to give rise to a stroke that may never have happened but [due to] increase in the blood pressure (38R-T).

23 He further explained a distinction between veinous and arterial blood pressure. Because of the auto-regulation of the brain it is only arterial blood pressure that is relevant for strokes, at least unless the systolic blood pressure (ie the high reading) exceeds 180 (35, 37P, 38, 39M). He accepted the possibility that the auto regulation mechanism might break down for various reasons (39). The appellant’s activity would not have produced such a situation (35, 38). It requires “huge stress” to produce that situation (40C).

24 Dr Matheson considered the appellant’s history of alcohol consumption satisfied any reasonable medical test of alcoholism and increased the incidence of this type of stroke for a variety of reasons (36).

25 This diametrically opposed evidence presented the judge with a very difficult situation. What was self-evident to Dr Kendall was impossible for Dr Matheson. Dr Kendall cited one textbook that he did not produce, but on which he was not challenged. Dr Matheson said in effect that the textbooks were all wrong. Each expert was dogmatic in the correctness of his view about the capacity or incapacity of strenuous but not excessive exercise to increase the risk of stroke.

26 Different views were also asserted about the impact of alcohol in the short and long term. Dr Kendall reluctantly conceded a statistical correlation in some circumstances, but asserted that they were absent in the present case.

27 The appellant accepts that it was open to the judge to accept Dr Matheson, at least in the sense that the doctor was qualified to express the opinion that he did and that, if accepted, it showed that the appellant’s claim failed.

28 Nevertheless, there were on the appellant’s submission errors of law that vitiated the ultimate decision (see Miller v Commissioner of Police [2004] NSWCA 356 at [26]). In the appellant’s submission these errors justify the setting aside of the award and the remitter to the District Court for a new trial of the s9A issue. The suggested errors focus upon the process whereby the trial judge came to reject Dr Kendall and accept Dr Matheson and/or the absence of reasons disclosed in the judgment for such conclusion.

The judge’s core reasoning

29 Her Honour summarised the evidence of Dr Lorentz (J22-24), noting his view that, if the diagnosis of cavernoma was correct, employment was not a cause or contributory cause of the condition and employment was not a substantial contributing factor. In Dr Lorentz’s view, it was unlikely that physical exertion played a significant role in the causation of the haemorrhage which was probably a congenital malformation.

30 The judge summarised the evidence of Dr Matheson in the following terms:

25. Dr J Matheson prepared reporting (sic) relating to his examination of the applicant and he was called to give evidence. He obtained a history of a collapse on 13 January 1997 whilst cotton picking and that the application had no memory of events. He noted that initially the diagnosis of cavernoma and pontine haemorrhage had been made but subsequent MRI scan did not show a surgically treatable lesion. By way of past history he noted the applicant had smoked a lot in the past but did not smoke now and that he was not hypertensive.
26. He diagnosed a left pontine haemorrhage possibly from a cavernoma with residual left lower motor neurone 7th and 8th nerve palsy and right hemiparesis. He thought his condition static. He did not believe this to be a work related condition noting him to have had a stroke at work but not because of work. He thought that if this had been a cavernoma this was a benign inherited tumour which would bleed from time to time and has nothing to do with work and even if that lesion was not present, there was a stroke of the brain stem not associated with work. He thought alcohol could be a factor in these types of strokes but they could be spontaneous as well, not traumatic and not related to straining.
27. He disagreed with the opinion of Dr Kendall that performing physical exertion would produce a transient rise in blood pressure sufficient to cause a cerebral haemorrhage, saying this would not overcome the autonomous regulation of the brain in respect of arterial pressure such regulation not being affected unless there was an extreme rise in pressure and not from physical exertion.
28. He agreed there to be an increased risk of stroke in heavy drinkers noting there to be an increased bleeding tendency but thought the most likely cause to have been a cavernoma.

31 There were also findings about the weather conditions on the day in question and the time by which the appellant’s symptoms had manifested themselves. Ashford J held:

31. The respondent has tendered a printout of the Daily Meteorological Observations for Collarenebri for January 1997. On 13 January 1997 it is noted the maximum temperature was 24.9C with a minimum of 20.4C at 9.00am and 21.8C min and 23.7 max at 3.00pm.
32. This gives some difficulty in accepting the weather conditions at Collarenebri on 13 January 1997 to be excessively hot. Indeed it appears to have been a relatively mind summer day. From the evidence it appears the applicant started work at about 6.00am and it is also clear he had been drinking heavily the night before to the extent he agreed that at the time he commenced work he still smelled of alcohol. Whilst the applicant said his difficulties began about 11.00am it appears from other evidence that it was not long after he commenced work that he began to experience right sided limb numbness and he was at the Collarenebri hospital around 9.00am that day.

32 Ashford J cited Mercer. She referred to her own decision in Dominguez v Sanchez Constructions Pty Ltd (2000) 20 NSWCCR 295 where she found the applicant to have suffered injury in the course of employment by way of rupture of an intercranial vessel following an angry altercation with a fellow worker about work performance, finding this to be a substantial contributing factor to injury.

33 Her Honour’s conclusions adverse to the appellant’s case were:

38. However in the present case I do not think such a link is established. The applicant is a relatively young man. He apparently considered himself physically fit and engaged in clearly heavy work as a cotton chipper during the season for about 10 years. He played football previously. There was nothing unusual about 13 January 1997. The applicant had been drinking heavily the night before on his own admission. Nevertheless he was able to attend work at about 6am and began work. He alleges his symptoms began about 11am after performing that work.
39. From the hospital notes he was seen there at 9am and symptoms came on prior to that time. He alleges it was very hot – between 30-40°. Yet the meteorological studies show the temperature to be very mild and around 20.4° at 9am.
40. I do not think the applicant tried to mislead the Court. He is obviously suffering a grave disability. This was obvious from his presentation in court. In all there does not appear to be anything different about that morning from any other when the applicant attended work.
41. The medical evidence is such that on balance of probabilities it appears the applicant suffered a left pontine haemorrhage more likely than not a rupture of a cavernoma which occurred spontaneously and I accept the opinion of Dr Stening in that regard.
42. I accept and prefer the evidence of Dr Matheson to that of Dr Kendall for the reasons already given and I am satisfied there was no part of the applicant’s employment with the respondent which constituted a substantial contributing factor to injury.
43. I have the greatest sympathy for this applicant and it gives me no pleasure in making an award for the respondent.
Grounds of appeal

34 The grounds of appeal pressed by the appellant interlocked and overlapped to a degree. They were addressed by the appellant’s counsel Mr Daley in an order that opened up the issues helpfully.

35 Some of the particular grounds of appeal, like some of the particular responses, really led up blind alleys, in our view. These will be mentioned at appropriate places in our reasons. But we wish to go to the heart of the issues as they emerged in the submissions of counsel for both sides in this Court.

36 The dispositive finding was acceptance of the evidence of Dr Matheson, which led her Honour to be “satisfied there was no part of the applicant’s employment with the respondent which constituted a substantial contributing factor to injury” (J42). If this conclusory finding stands, there could be no question but that the “substantial contributing factor” required by s9A was not demonstrated by the applicant upon whom the onus rested.

37 A starting point for the appellant’s challenge is the recent decision of this Court in Wiki v Atlantis Relocations (NSW) Pty Ltd (2004) 60 NSWLR 127. Ipp JA (with whom Bryson JA and Stein AJA agreed) discussed the judicial obligation to give reasons in the context of a conflict between experts that are properly qualified, none of whom have been found to be dishonest, or misleading, or unduly partisan, or otherwise unreliable. He cited the earlier judgment of this Court in Moylan v Nutrasweet Co [2000] NSWCA 337 where Sheller JA (with whom Beazley JA and Giles JA agreed) adopted much of the reasoning of Henry LJ in Flannery v Hallifax Estate Agencies Ltd [2000] 1 WLR 377. In particular, the Court stated the following principles (Wiki at 136[62]):

… save where an expert is guilty of a deliberate attempt to mislead (as happens only very rarely), a coherent reasoned opinion expressed by a suitably qualified expert should be the subject of a coherent reasoned rebuttal, unless it can be discounted for other good reasons….
… [W]here the dispute involves something in the nature of an intellectual exchange, with reasons and analysis advanced on either side, the judge must enter into the issues canvassed before him and explain why he prefers one case over the other.

38 These principles reveal the relationship between the grounds of appeal contending that her Honour came to the critical conclusion by a flawed process and the grounds complaining of absence of disclosed reasons.

39 We shall explain below why these principles have application to the present case. But we note at the outset the riposte from the respondent to the effect that Ashford J was unimpressed with the testimony of Dr Kendall. This is true, but that view was informed (in part) by a preference for Dr Matheson. Furthermore, the reasons for discounting and rejecting Dr Kendall failed to address what we have described above as the core proposition to which he adhered. That proposition was that a rise in blood pressure due to exertion of the type experienced by the appellant, made it more probable that he would have had a stroke. Dr Kendall’s evidence at Black 21 shows that this conclusion did not stand upon the false support of the history recorded in Dr Kendall’s written report (as Ashford J effectively concludes at J21). There was, in truth, a contestable scientific proposition on which the two experts joined issue (in a manner of speaking) where (on a likely reading of Dr Matheson’s evidence) it was ultimately common ground between them that the Kendall view was supported by the medical literature. There was some support for Dr Kendall’s views in the unchallenged evidence of Dr Milder (Blue 27N) and Dr Seymour (Blue 104H), neither of which is referred to in the judgment.

40 A difficult medical issue presented itself to the trial judge. She had the dubious “assistance” of two experts who expounded diametrically opposed propositions on points that, from this perspective, appear quite critical. It may be extremely difficult for a trial judge in an adversary system when placed in this position. If ever there were a situation calling for the judicious use of any power in the court to appoint a third expert this was such a case. The difficulty in which her Honour was placed heightened the obligation to give careful reasons addressing the essentials of the testimonial conflict. In our opinion, the judge failed to do so to a degree constituting error of law.

41 The appellant submitted that her Honour failed to demonstrate in her reasons that she had addressed the gravamen of the issues joined between the two experts and/or that she had in truth failed to do so.

42 The submissions involved, without necessarily being dependent on, the proposition that the dispute at trial turned essentially upon whether the trial judge accepted Dr Kendall or Dr Matheson. The respondent disputed this, but we think that this proposition must be accepted.

43 The respondent pointed to her Honour’s statement (at J41):

The medical evidence is such that on balance of probabilities it appears the applicant suffered a left pontine haemorrhage more likely than not a rupture of a cavernoma which occurred spontaneously and I accept the opinion of Dr Stenning in that regard.

44 It was put that this was a conclusion directed at the ultimate (s9A) issue. We do not agree. Had the parties perceived that Dr Stening’s evidence was critical to the causation dispute one might have expected that the doctor would have been cross-examined at trial. The fact that he was not cross-examined stemmed, in our opinion, from the fact that the respondent correctly perceived that the doctor had refrained from expressing an opinion as to the aetiology of the haemorrhage. Dr Stening was the appellant’s treating doctor after he had had the stroke. His report relevantly stated :

Opinion:
Diagnosis:
This man had a spontaneous bleed into his brain stem which has damaged the neurological pathways at a point where the cranial nerve fibres had already crossed the mid-line to the other side, but the fibres to the lower part of the body crossed lower down. This explains his loss of sensation and movement of the left side of his face and loss of sensation and movement of the right side of his body below his head.
…
Attributability:
There does not appear to be any demonstrable pre-existing condition which might have led to the bleed occurring. However, there is no doubt that tissue damage occurred whilst he was at work. There is no component of his work either chemical or physical or emotional which had necessarily led to the damage of the tissue. In the case, Zickar v MGH Plastics P/L , however, it was found that if tissue damage occurs at work, regardless of antecedent causes, then the injury is compensable. I gather that the law may have been changed in 1998 however.

45 In light of the first and third headings in this section of the report, the reference to “spontaneous” in the first passage should be read as meaning “sudden”, without addressing the causation issue (see also Dr Matheson’s definition at Black 37C). We understand that this was really common ground in the appeal. In any event, our reading of the report is as indicated. The upshot is that Dr Stening was not called to express an opinion on the ultimate issue. More to the point he did not do so, considering the final sentence of the passage quoted above; and the evidentiary pre-requisites so clearly established in Makita Australia Pty Ltd v Sprowles (2001) 52 NSWLR 705.

46 The oral evidence and submissions at trial show that the parties joined issue in reliance solely upon the evidence of their respective (medical) champions, Dr Kendall and Dr Matheson. If there was any appealable error in the reasons supporting the award for the respondent, it must be found in the way that the trial judge addressed that conflict, to which we return.

47 Stripped of reliance upon Dr Stening, the respondent still pressed (faintly) the submission that any appealable errors touching the rejection of Dr Kendall’s testimony and the reasons for rejecting that testimony can be quarantined from the question as to the correctness in law of the judge’s decision to accept Dr Matheson. In our view, this is an unrealistic view of the trial and its outcome. The two doctors were the only expert witnesses. Each was cross-examined, being confronted in effect with the other’s views among several matters. Final addresses grappled with the either/or scenario. And the reasons of her Honour spoke directly in those terms (see J42). The reality of the testimonial conflict was such that her Honour was bound to do so.

48 In suggesting an either/or battle, we have not overlooked the possibility that the “truth” might lie somewhere in between the extreme positions of the two doctors. It is possible that Dr Matheson was wrong in concluding that work played no part, but that the requirements of s9A as to “a substantial contributing factor” were still not satisfied notwithstanding acceptance of Dr Kendall’s view. This third possibility must be acknowledged, but it was not the reasoning of the trial judge, apart from the unsatisfactory conclusory statement in J42.

49 With the principles summarised in Wiki in mind, we can indicate briefly why there must in our view be a new trial of the s9A issue. We have a number of concerns with the exposed reasoning. Some involve discrete matters, others overlap. Not all are of equal materiality.

50 Our concerns include the absence of explanation as to the materiality of the reference to heavy drinking the night before at J38; the absence of any weighing of the s9A integers in the global statement of satisfaction, based on Dr Matheson, that there was no part of the appellant’s employment which constituted a “substantial contributing factor to injury” (J42); the failure to address or explain preference for Dr Matheson’s apparently extreme view of causal irrelevance of raised blood pressure when it was at variance with medical literature, even (or especially) according to Dr Matheson’s own testimony; and the failure to acknowledge that Dr Kendall adhered to his scientific opinion in his oral evidence, despite accepting the falsity of the original history recorded in his written report.

51 Should the new trial be restricted any way? An important medical issue in the case was whether the appellant suffered from a congenital cavernoma. Ashford J held, at [41] that Dr. Stening’s view was that he did. She also preferred Dr. Matheson’s view to the same effect over that of Dr. Kendall to the contrary as we have discussed above. It is necessary to revisit some of the medical evidence to properly consider this question.

52 In his report dated 20 June 1997, Dr. Stening reported that an initial view had been taken that the severe brain stem haemorrhage suffered by the appellant was due to a cavernous haemangioma. However, an MRI had failed to reveal a cause for the haemorrhage and, as we have already noted, Dr. Stening concluded that there did not appear to be any demonstrable pre-existing condition which might have led to the bleed occurring. Dr. Stening did not alter that view in his later report, dated 20 January 1999. The trial judge therefore erred when she held that Dr. Stening’s opinion was that the appellant had a ruptured cavernoma.

53 Dr. Milder, consultant neurologist, provided a medico-legal report to the appellant’s solicitors dated 21 February 2000. Dr. Milder explained that a lesion of the type suffered by Mr. Shillingsworth “maybe idiopathic [cause unknown], secondary to hypertension or a bleeding tendency, or to an underlying vascular malformation [cavernoma]”. Dr. Milder pointed out that the radiological studies undertaken at St. George Hospital did not support “a possible underlying vascular malformation”. He was therefore of the opinion that:

“The cause is therefore idiopathic (unknown) or secondary to transient hypertension. Should the latter be the case, an elevated blood pressure may be related to the physical stresses placed upon him during the cotton picking season.”

54 Dr. Milder suggested that a cardiological opinion should be sought in that regard, but that does not appear to have been done.

55 Dr. Kendall’s evidence has been discussed above, see[12] and following.

56 In addition to Dr. Kendall’s evidence to which we have already referred, Dr. Kendall was also challenged in cross-examination with the radiological report of Dr. Schnier, a radiologist from St. George Hospital, concerning a repeat MRI taken on 8 February 1997. In that radiological report, Dr. Schnier reported:

“It is still not definitely possible to say whether the lesion is an idiopathic haemorrhage or cavernous haemangioma, although the latter is favoured. The typical structure of the cavernous haemangioma would be obliterated by the haemorrhage. If calcification is present within the lesion on CT scan a cavernous haemangioma would be most likely.”

57 Dr. Kendall responded to Dr. Schnier’s report stating:

“As I said before, irrespective of whether one postulates that or not, he would have been more vulnerable but he was not just a stroke waiting to happen to put it more colloquially”.

58 There was no evidence that a CT scan had been done, nor was there any medical explanation of Dr. Schnier’s proffered view or of his expertise to proffer the comment or its inconsistency with Dr. Stening’s opinion.

59 The position therefore, in relation to the appellant’s medical evidence, was that the radiological evidence did not establish the cause of the stroke. There was the evidence of Dr. Kendall, a physician, who was of the opinion that a combination of causes may have caused the appellant’s stroke but that the triggering cause was the appellant’s physical exertion on the day. More significantly, the two doctors with relevant expertise, Dr. Stening, the treating doctor, and Dr. Milder, consultant neurologist, in reports given well after the date of Dr. Schnier’s radiological report, were both of the opinion that there did not appear to be a demonstrable pre-existing condition, or in other words, that the appellant’s stroke was not caused by the cavernous haemangioma.

60 The other medical experts called on behalf of the appellant were called in respect of his disabilities and those experts deferred to the evidence of the neurologists in respect of the question of the cause of the appellant’s stroke.

61 The respondent called evidence from Dr. Lorentz, consultant physician neurologist, by way of tender of his medico-legal report, Dr. Matheson, consultant neurosurgeon, and Dr. Schnier, to whom reference has already been made and whose radiological report was tendered.

62 Dr. Lorentz noted that scanning subsequent to the initial investigations at Dubbo and St. George hospitals did not reveal a cavernoma but added “it is possible that the haemorrhage has destroyed the previous cavernoma or malformation”. He said that if the diagnosis of a cavernoma was correct then that was a pre-existing condition. As noted [28] he thought the cause of the haemorrhage “was probably a congenital arteriovenous malformation”. Dr. Lorentz did not proffer any reason for this opinion. However, the appellant did not choose to cross-examine Dr. Lorentz.

63 Dr. Matheson provided a medico-legal report to the respondent’s solicitors on 28 October 2002. In that report he made a diagnosis of “left pontine haemorrhage – query from cavernoma” and expressed the opinion that the appellant “has had a stroke at work but not because of work. If he has a cavernoma present this is a benign inherited tumour which will bleed from time to time and has nothing to do with work”. [Blue 89]

64 In his first report, Dr. Matheson did not proffer a preferred view as to whether a cavernoma was more likely than not to have been present. However, in a later report of 18 August 2003, Dr. Matheson stated that the appellant’s cerebral haemorrhage “was probably produced by a cavernoma in view of his relatively young age but alcohol induced haemorrhage of this nature can occur” [Blue 94]. This was the view to which he adhered in his oral testimony and which was accepted by the trial judge, as discussed above.

65 We should refer to a short report by Dr. Stening to Dr. Sahukar of Dubbo, also dated 20 June 1997 in which Dr. Stening says that “an MRI showed that there was no surgically treatable lesion”. Dr. Matheson commented upon this in his report dated 28 October 2002. He said:

“[Dr. Stening] made the somewhat cryptic comment that in June 1997 he had another MRI scan which did not show a surgically treatable lesion. Cavernoma’s of the pons are of course dangerous to treat and I presume Dr. Stening is referring to the fact that he considered the cavernoma inoperable but he may have alternatively been implying that there was none present. We need to get this clarified by Dr. Stening or else I need to review the MRI scans myself.”

66 It would appear from Dr. Matheson’s comment that he did not, at that time at least, have access to Dr. Stening’s report of 20 January 1999 referred to above, where Dr. Stening stated that an MRI failed to reveal a cause for the haemorrhage. It appears that Dr. Matheson did not review the MRI as he suggested he would need to do if the matter was not “clarified by Dr. Stening”.

67 Dr. Matheson accepted in cross-examination that there was no hard evidence that the appellant had a cavernoma (Black 36-37) and accepted that the cause of strokes can be multifactorial.

68 In summary, then, the respondent’s medical evidence on whether the appellant had a cavernoma was based on an assumption that he did. There was no hard evidence that was the case. None of the respondent’s expert medical witnesses advanced a reason why they endorsed the assumption the appellant probably had a congenital malformation/ cavernoma, other than Dr. Matheson’s opinion about the appellant’s young age.

69 Once it realised that her Honour was wrong in her finding as to Dr. Stening’s evidence, we are of the opinion that the medical evidence taken as a whole, was not sufficiently certain to make it desirable that the trial on the medical issue should be limited.

70 Having so concluded, nothing in these reasons is intended to imply that acceptance of Dr. Stening’s view or that of Dr Kendall would bring the appellant home. If that doctor’s view (or some variant of it) were accepted it would be but the start of a difficult balancing exercise in the application of the facts and expert opinion to the issue presented by s9A.

71 We propose the following orders:

1. Appeal allowed.

2. Set aside the award for the respondent.

3. Remit the matter for re-hearing in the District Court.

4. Respondent to pay appellant’s costs of the appeal and to have, if qualified, a certificate under the Suitors’ Fund Act 1951 .

72 SHELLER JA: I have had the benefit of reading in draft the joint judgment of Mason P and Beazley JA with which I agree.

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Last Modified: 07/16/2007