SHILLINGSWORTH v MURRAY [2004] NSWCA 465

New South Wales Court of Appeal

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

IN THE SUPREME COURT OF NEW SOUTH WALES COURT OF APPEAL

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).