Granrud v Ararat Rural City Council
[2009] VCC 286
•8 April 2009
| IN THE COUNTY COURT OF VICTORIA | Revised |
| AT WARRNAMBOOL CIVIL DIVISION WORKERS COMPENSATION |
Case No. CI-08-00467
| THOR GRANRUD | Plaintiff |
| v | |
| ARARAT RURAL CITY COUNCIL | Firstnamed Defendant |
| and | |
| QBE WORKERS COMPENSATION | Secondnamed Defendant |
---
| JUDGE: | HIS HONOUR JUDGE HICKS |
| WHERE HELD: | Warrnambool |
| DATE OF HEARING: | |
| DATE OF JUDGMENT: | 8 April 2009 |
| CASE MAY BE CITED AS: | Granrud v Ararat Rural City Council |
| MEDIUM NEUTRAL CITATION: | [2009] VCC 286 |
REASONS FOR JUDGMENT
---
Catchwords:
---
| APPEARANCES: | Counsel | Solicitors |
| For the Plaintiff | Mr. I. R. Fehring | Stringer Clark Solicitors |
| For the Defendant | Mr. I. S. Gourlay | Lander & Rogers Lawyers |
| HIS HONOUR: |
1 By Further Amended Statement of Claim dated 3 February 2009 the plaintiff seeks a declaration pursuant to s.98C of the Accident Compensation Act 1985 (the Act) that he is entitled to compensation for non-economic loss in accordance with that section.
2 In order to do so, the plaintiff must prove, on the balance of probabilities, that he has suffered a compensable injury between 12 November 1997 and 20 November 2000, being the date the plaintiff ceased employment (“The relevant period”).
3 The plaintiff was employed by the Ararat Rural City Council between 13 August 1984 and 20 November 2000. The nature of his work involved working in road gangs, and building and maintaining bridges in the Ararat Shire.
4 In August 1991 the plaintiff suffered a myocardial infarction. On 14 October 1991 an angiogram was performed.
5 A claim for compensation in respect of the myocardial infarction was made by the plaintiff on 16 October 1991. Liability was admitted, and compensation was paid pursuant to that claim.
6 In March 1992 the plaintiff returned to work for the defendant. In October 1994 he was again admitted to hospital with further chest pains. He was off work for some three months. An angiogram was performed in November 1994.
7 The plaintiff subsequently returned to work approximately three months later in February/March 1995. In April 1999 he was again admitted to hospital with further chest pains.
8 Subsequently, the plaintiff returned to work, but in March 2000 he was admitted to hospital with prolonged episodes of angina.
9 In approximately May 2000 the plaintiff returned to work. However, in November 2000, he was again admitted to hospital with prolonged episodes of angina.
10 On 22 November 2000, the plaintiff ceased working for the Ararat Rural City Council.
11 As liability had been accepted, compensation was paid to the plaintiff in the form of weekly payments until he reached the age of 65. The plaintiff is currently 67 years of age, being born in Norway on 22 January 1942.
12 In July 2001, an angiogram was performed. On 16 July 2001 a stent was inserted, and on 25 October 2001 the plaintiff underwent coronary angioplasty with insertion of a coronary stent.
13 On or about 9 May 2003 the plaintiff lodged a claim for impairment benefits pursuant to s.98C of the Act.
14 On 22 July 2003 the secondnamed defendant rejected the plaintiff’s claim for impairment benefits.
15 Paragraph 7 of the Further Amended Statement of Claim states:
“From 12 November 1997 until 20 November 2000 the plaintiff was required in the course of his employment to perform heavy work including lifting, driving, and carrying equipment. His employment duties included the operation of a water tanker. Such work required repeated lifting of a large, heavy and awkward hose which is attached to the water tanker. His duties included on repeated occasions the lifting of bags of lime and/or cement. He was required to lift heavy equipment into and out of trucks. He repeatedly performed the work duties described above whilst he experienced chest pain.”
16 In Paragraph 8, Particulars of Injury are listed as follows: “disturbance of cardiac function, myocardial degeneration, myocardial infarction, myocardial ischaemia and the aggravation thereof, breathlessness, dizziness, chest pain, depression and anxiety.” The defendants deny that the plaintiff suffered injury as alleged in paragraphs 7 and 8 of the further amended statement of claim.
17 Prior to the commencement of the case, I asked both counsel to (1) specify the injury or injuries; (2) state the date of the injury or injuries; (3) state which reprint of the Act applies to the proceeding; and (4) state the order which should be made if their respective client is successful.
18 The plaintiff’s counsel responded in writing as follows. As to the injury, he stated:
(a) Ischaemic heart disease; (b) Myocardial ischaemia; (c) Aggravation of coronary artery disease.
19 As to the date of injury, the plaintiff responded: “From the period of 12 November 1997 to the date the plaintiff ceased work, 20 November 2000.”
20 As to the relevant Reprint of the Act, both counsel agree it was Reprint No 11.
21 As to the order sought, the plaintiff stated as follows:
“The plaintiff has suffered injury arising out of or in the course of his employment over the period of 12 November 1997 to 22 November 2000 by way of:
(a) Ischaemic heart disease; (b) Myocardial ischaemia; (c) Aggravation of coronary artery disease.”
22 It was submitted on behalf of the defendants that the proceeding ought be dismissed.
23 Section 5 of Reprint No 11 of the Act states:
“injury means any physical or mental injury and, without limiting
the generality of the foregoing, includes—
...
(b)
a disease contracted by a worker in the course of the worker’s employment (whether at, or away from, the place of employment) and to which the employment was a significant contributing factor;
(c)
a recurrence, aggravation, acceleration, exacerbation or deterioration of any pre-existing injury or disease where the worker’s employment was a significant contributing factor to that recurrence, aggravation, acceleration, exacerbation or deterioration.”
24 The plaintiff alleges that injury (b), myocardial ischaemia, resulted in injury to the heart muscle which was an injury in the primary sense or, as it is sometimes described, “injury simpliciter”, whereas (a), ischaemic heart disease, and (c), aggravation of coronary artery disease, are injuries in the extended sense. In respect of injuries (a) and (c), the plaintiff has to prove that employment was a significant contributing factor to such injury.
25 The defendants deny that the plaintiff suffered compensable injury during the relevant period from 12 November 1997 to 20 November 2000.
26 The issue in dispute is therefore whether the plaintiff suffered compensable injury during the relevant period. Whilst it was submitted on behalf of the plaintiff he had suffered “injury simpliciter”, most of the attention in this proceeding was directed to considering whether the recurrent angina attacks experienced by the plaintiff as a result of the physical work he performed during the relevant period caused further heart muscle damage, (the plaintiff having previously suffered myocardial infarction in 1991) or aggravation of the plaintiff’s pre-existing coronary artery disease.
The Evidence
27 Counsel for the plaintiff called the plaintiff and two medical practitioners, whilst the defendants’ counsel called one medical practitioner. A joint Court Book was tendered in evidence together with several additional exhibits.
The Plaintiff’s Evidence
28 It should be stated at the outset that no real challenge was made to the plaintiff’s evidence.
29 The plaintiff gave evidence that he commenced working for the firstnamed defendant in approximately 1984. He was part of a road gang doing work in and around the Shire of Ararat. He initially started off as part of a bridge gang. This involved heavy work relating to the construction of bridges.
30 The plaintiff stated that in approximately August or September of 1991 he had chest pain and suffered a heart attack. He was informed by his doctors that he had suffered a heart attack, and he was admitted to hospital. On 14 October 1991 an angiogram was performed. He gave evidence that as a result of his heart attack he was off work from approximately September 1991 to March 1992. He went back to work and performed some road maintenance work, including the maintaining of trees alongside highways. He gave evidence that in 1994 he had about three months off work due to difficulties with chest pain, and when he returned to work he was performing much the same duties.
31 In approximately 1998 he changed from performing duties involving tree cutting and working on roads to work in a new section called “Road Construction and Building Work”. He believed that in approximately February 1989 he joined the road-building department. He stayed in that department for the remainder of his employment with the firstnamed defendant.
32 The plaintiff gave evidence that the nature of the work, as far as the road- building section was concerned, was ripping up bitumen, ripping up all the dirt, and then making a new road.
33 The plaintiff gave evidence that his main function was as the operator of the water tanker, which was an old, converted milk tanker.
34 He stated that he would go to the nearest creek or dam near the area where they were working to get water. Sometimes it would be 10 kilometres away, sometimes only half a kilometre away. His water tanker had a big hose which had a diameter of approximately 8 to 10 inches, which he had to take off the truck by himself, drag it to the waterhole, and then place the end of the hose, which contained a metal cage as a filter, into the water. The water would then be sucked into the tanker, and afterwards the plaintiff was required to again lift the heavy cage and heavy hose out of the water and then take it and place it upon the top of his truck. Whilst the plaintiff gave evidence that he had other duties which included from time to time carrying heavy bags of lime and/or cement, his main work was on the water tanker. He operated the water tanker alone.
35 The plaintiff gave evidence that he was regularly required to be on top of the truck dragging the large hose off, and then on top of the truck putting the hose back on. He performed this work by himself, often in isolated areas. The length of the hose was approximately 30 metres.
36 He gave evidence that on a normal day he would have to fill his tanker at least half a dozen times. The plaintiff stated that he would regularly get chest pains over this period of time whilst doing this work and used to take Anginine by way of medication.
37 The plaintiff stated that often when he began to have chest pains he would sit for a quarter of an hour just chewing Anginine and hoping that it would become better, because he was of the belief that, if he did not do this, he would drop dead.
38 He complained about the work that he was required to do. After a period of time his employers changed the position of the hose on the truck. He stated that that occurred about 12 months before he finished work. He stated that he had complained for years, but nothing had been done.
39 He stated that he had a very positive attitude to work, and even after regularly getting chest pains and visits to the hospital, he still desired to keep working, and did in fact return to work as soon as possible.
40 The plaintiff gave evidence that from time to time he would also have to put traffic signs out. This involved getting traffic signs in and out of his truck.
41 He stated he had experienced chest pains regularly over the years. Over the last four or five years of working for the Council he experienced chest pains approximately three times a week. He said that he regularly took Anginine as a result of such chest pains.
42 He gave evidence that he would take his medication sometimes three or four times a day, and other times it might be once a week, depending on how strenuous the work was, how stressed he got, and what he was lifting.
43 Over the last 12 months of his employment the plaintiff stated that he noticed his chest pains getting more frequent. He remembered being taken to hospital on occasions as a result of his chest pains over the last period of his employment with the Ararat Council. He gave evidence that the pain could be quite severe.
44 He gave evidence of the factors leading up to his ceasing employment in November 2000. He was working at a place called Langi Logan and was doing a construction job when he experienced bad chest pains. He radioed for the grader driver to get him, and he was taken to hospital.
45 Cross-examined by counsel for the defendant, Mr Gourlay, the plaintiff gave evidence that he had given up several of his hobbies since experiencing chest pains at work, and that since November 2000, he has driven a lot less. Under cross-examination he stated that he suffered his heart attack in approximately August 1991 and that he received compensation for his time off work. He stated that he had gone several times over the years to hospitals and had angiograms. He had learnt a reasonable amount about his heart over the relevant time after speaking to so many doctors. He had ongoing testing, being performed in respect of his heart, during the 1990s.
46 Further, he gave evidence that in October 1994 he had an irregular heartbeat and was taken to hospital. He had three months off work, and subsequently made a claim for compensation. He could not remember the nature of the duties he performed after returning to work following the episode in 1994. He was of the view that for approximately two days he performed light duties only, such as poisoning work, and cutting trees. He soon though returned to road construction work. It was approximately February 1998 that he went back to road construction work.
47 He agreed that after his 1991 heart attack he was on medication which included nitro patches, anti-cholesterol drugs and Sotalol, and that he continues with much the same dosage now as he did then.
48 The plaintiff was cross examined as to what would he do if he experienced chest pains given his knowledge of the heart and his own condition. He stated that, if they were very severe, he would take his medication, or otherwise he would just stop and have a rest. He agreed that that was basically his regular pattern. He agreed that strain and other things would trigger the pains. He stated that once he experienced chest pains he would sit down and stop what he was doing, and then take his tablets. He stated that sometimes he just could not stop his work, and he would take his medication and keep going, as the road gang depended on him. His pattern was sometimes to sit down, and, once the symptoms ceased, he went straight back into work.
49 From 1997 until November 2000 he consulted his doctor a lot of times about chest pains. He stated that he would not go every time he had pains, but did go a lot of times. In the last couple of years he damaged his right shoulder and saw a doctor about that for a little while.
50 The plaintiff said that, since he ceased work with the firstnamed defendant, he has continued to see cardiologists and had further heart trouble in July 2001. He stated that he used to smoke a pipe regularly prior to his heart attack in 1991.
51 In re-examination he was asked what was his general pattern when he experienced chest pains at work. He stated that he would take Anginine if it got too bad. If it was just slight, he would sit down. He was asked what he would do if the pain continued, and he said that he would keep taking Anginine and Sotalol. He was told by his doctor to only take three or four, but sometimes he would take up to six. He said, “You either drop dead or you get help, but what can you do when you’re out in the middle of the bush?”
Medical Evidence
The Plaintiff’s Medical Evidence52 Dr Rene Andre Dupuche gave evidence that he is a general physician with a specific interest in cardiology.
53 He stated that ischaemic heart disease is a general term applied to diseases of the heart that arise from a lack of blood flow to the heart muscle and which is almost always, but not necessarily always, the consequence of a coronary artery disease, namely the deposition of cholesterol and other material in the artery so as to narrow its lumen or size.
54 He gave evidence that coronary artery disease is normally in two stages, and the first stage is the artery slowly becoming involved with the imposition of cholesterol in the artery wall. This stage may go on for some period of time before anything symptomatically happens to the patient.
55 The second stage involves changes that occur in the coronary arteries that will lead to symptoms. The symptoms will be things like chest pain, perhaps arrhythmias, and sometimes death. The second stage occurs when something has happened to the arteries which brings the problem to the surface, which is then manifested by chest pains, shortness of breath, collapse, arrhythmia or sudden death.
56 He gave evidence that plaque builds up in the artery walls like rust in a pipe, which will cause the artery to crack or fissure or bleed into it, and this will suddenly cause plaque to crack, and that crack leads to a thrombosis or clot developing on the crack that causes some reduction of blood flow and blocks the artery, which brings on the symptoms.
57 He was asked what triggers the second phase, and he stated that sometimes the plaque may simply crack for no apparent reason, but that forces may be applied to the fragile plaque such as heightened blood pressure, heightened pulse rates, or circulatory excitation that might occur during anxiety. He stated that an additional factor was an increased demand for oxygen. When you work harder you make your heart beat harder, and it needs more oxygen, and that is why it results often in an anginal situation, which is a stage earlier than an infarction.
58 He gave evidence that when there is a degree of obstruction in the artery, increased work of the heart will increase the demand for blood flow, which may not be provided because of the narrow vessel. When a person suffers angina, which is chest pain, there may on occasions not be actual damage to a heart muscle. He stated however that repeated onsets of angina are an indication that the heart is not being supplied with sufficient blood.
59 He was asked what effect such repeated episodes would have on the heart muscles. Dr Dupuche replied:
“Well if it goes on long enough, what you will often find is that you’ll have small areas of damage sort of scattered throughout the heart muscle without any sort of major single area which is what you would get with an infarct (but) there will be some patients who will sustain very very minor heart damage by repeated numerous episodes of angina.”
60 Dr Dupuche was of the opinion that cumulatively, over a long period of time, there may become significant and sufficient scarring of the heart to cause heart failure due to a lack of pumping capacity, but that it would be a slow process, and it would require many episodes of angina.
61 Specifically, the question was put to Dr Dupuche that, if the plaintiff had suffered continuous chest pains once or twice a week over the last three years of employment, what would be the consequence of that upon the man’s heart? Dr Dupuche stated:
“What I would say is that if this had occurred hundreds of times over this period of time, working away and having hundred of these episodes, this would I think inevitably have an effect upon his heart muscle, but you see it’s question of the number of occasions, I suppose. If you keep chipping away, sooner or later you’ll do some damage.”
62 Dr Dupuche was asked what would be the result of the one or two chest pains per week occurring over a three–year period. He stated:
“I would say there would be more likely to be muscle damage than not, because that’s 150 episodes a year. If its three times a week, that’s 150 episodes per year over four or five years. That’s an awful lot of episodes of deprivation of blood flow to the heart muscle….that’s got to be an effect on the heart muscle. ”
63 Dr Dupuche stated subsequently:
“My view is that since this man suffered hundreds of episodes, as I think we calculated last time, hundreds of episodes of quite severe pain when working, which he often tended to ignore, or at most he took some Anginine and then went back to work, I am contending that in these many hundreds of cases he cannot have escaped without damaging his heart muscle fibres to a significant degree.”
64 Dr Dupuche stated that there was no test that would necessarily pick up such damage to the heart muscle. It may be clinically undetectable. He was also of the view that continuing to work with advanced coronary disease would add to the coronary narrowing.
65 Dr Dupuche was of the opinion that continuing to work in the manner described by the plaintiff not only affects the demand upon the heart muscle and the ischaemia which may result in damage to the myocardium, but in addition it may also affect a coronary artery, and affect the plaque in that coronary artery. The artery, and the plaque within the artery in particular,
would be made worse by numerous episodes of overwork. In particular─
“If you keep bashing that plaque by raising your blood pressure, increasing the circulation the banging away within the artery because you’re working hard, I’m saying that would have an effect upon the plaque and make it worse, make it less stable, so you are preparing it in a sense for “the ultimate explosion” and later working hard in the context explained would aggravate the coronary artery disease.”
66 Under cross-examination, Dr Dupuche stated that myocardial ischaemia can occur by scarring which may be due to small episodes of lack of blood flow. Dr Dupuche said that in a particular individual you may not be able to say if such scarring of the heart muscle occurred, but cumulatively, over time, it most probably will.
67 He stated that, as far as his qualifications were concerned, he has spent considerable time in the cardiology department of St Vincent’s Hospital, and was a coronary care physician for two years until he decided he did not want to specialise in cardiology alone. He stated that he continually treats patients with cardiac problems.
68 He was specifically asked by Mr Gourlay:
“If the plaintiff did not continue to work on in the face of his symptoms such as chest pain, you would not expect there to be any damage done to the man’s heart, would you?”
Dr Dupuche responded:
“He may have had many episodes where perhaps there wasn’t any heart muscle damage, but, with a story like that, some quite severe episodes and numerous Anginine tablets being taken, I’m stating that cumulatively over a long period of time he’s likely to have had some damage to the heart muscle, even if it’s only microscopic, one drip at a time, but cumulatively I wouldn’t accept that there couldn’t be any damage.”
69 He stated further that following the plaintiff’s myocardial infarct in 1991, he would have had some muscle of the heart which was dead. However, in relation to that that was not dead, the cumulative effect of repeated chest pains is likely to have had an effect.
70 Mr Gourlay took Dr Dupuche through the plaintiff’s medical history, including his history of angiograms and other tests.
71 Dr Dupuche was asked this question:
“Could one infer that there has been an initial quite rapid increase in blockage or stenosis up until 1994, and then up until 2001 there’s been a continual progression but perhaps not as rapid?”
Answer:
“Yes, that’s what the figures and the numbers would suggest, that
the plaintiff is suffering a progressive underlying heart condition.”
72 In considering a person with such an underlying condition, Dr Dupuche was of the view that it was inappropriate for a person in that situation to indulge in activities that would be provocative of episodes of angina and cardiac ischaemia “because in the long run you’re going to hurt yourself.” He stated that to carry on doing heavy work may cause incremental heart muscle damage during that time, although not sufficient to cause a major heart attack, to cause arrhythmia, or to cause the plaintiff to drop dead, but nonetheless injurious to the heart muscle, and cumulatively becoming quite significant. It would be the cumulative nature of such episodes which would cause additional damage.
73 It was put to Dr Dupuche that the plaintiff had an underlying progressive heart disease which had occurred since 1991 and was likely to be causing some progressive disease and anginal response. Additionally it was put, the plaintiff worked between 1991 and November 1997, and this may have caused some anginal responses. As the law stands the plaintiff has to prove that between November 1997 and 2000 there was a sufficient number of these anginal responses to cause damage to the muscle. Dr Dupuche said in response:
“It is almost certain that that is the case, that the plaintiff had severe coronary disease which is well established, and that he thereafter participated in activities that would have increased the effect of these blockages,”
He later stated that the plaintiff was doing things that would tend to aggravate the effects of the disease between November 1997 and November 2000. He stated:
“What I am saying is that during this period of time (November 1997 to November 2000) that this man was participating in activities which must inevitably have caused subtle heart muscle damage in an incrementally additive way over time, so each single episode of inappropriate activity might not have done much to him, but over time, over years, I am sure it would, and I maintained it would.”
Earlier he was asked this question:
“As you’re aware, doctor, this man during that period, had at least three – perhaps four but certainly three admissions to hospital because of chest pain and what is described in the records as prolonged chest pain. Does that assist you in ---?---That would suggest that the episodes of ischaemia were more sever and more prolonged and with that would come more heart muscle damage.”
74 Under further cross-examination, Dr Dupuche responded that, whilst it was preferable that once the plaintiff had angina pain, he rest and be protective of his heart muscle rather than to continue to work, nevertheless continuous and cumulative episodes of anginal pain still may have been significant and caused some damage, albeit very tiny, for each event. It would be like a dripping tap. This is so even if he had stopped work immediately on suffering angina.
75 Dr Dupuche stated that he disagreed with the views of Dr Hammond who was to be called by the defendant. Dr Dupuche accepted that he has diametrically opposed views on this matter compared with that of Dr Hammond.
76 He was asked this question by Mr Gourlay in cross-examination:
“In arriving at the conclusion which you offer to the Court, as you said a few moments ago, you say there were hundreds of episodes and some of those must have done some damage. Does that mean you’re relying to a large extent on the duration of the episodes of pain?”
Answer:
“No, I’m not relying. Obviously, the longer the episode of pain, the more likely it is that the episode will be injurious to the heart muscle. But I said earlier that you don’t even have to have pain, so the fact that the pain was short does not, in my opinion, automatically mean that it was an insignificant episode and caused no damage.”
77 Dr Dupuche was also of the opinion that, whilst there was no pathology or evidence for his view and that of Professor Nestel in relation to Mr Granrud’s situation, he was still of the view that the processes he outlined and the consequences did in fact occur. Dr Dupuche was of the view that the tests that were performed on Mr Granrud over the time of his working life with the defendant were not of a kind to pick up microscopic injury to the heart muscle. Dr Dupuche stated:
“Well….how I like to respond to that is there is an assumption in the point being made that amongst these hundreds of episodes of pain they were all angina and I am disputing that, I am saying that it seems improbable, highly improbable to me that you could have hundreds and hundreds of episodes of quite severe chest pain in a situation where it is known you have got coronary disease and you’re going to escape scot free, no cardiac damage at all over this period of time. I think that’s a proposition that is highly improbable and so my contention is that in amongst all of these hundreds of episodes there are those in which heart muscle damage occurred.
I do not believe that because Dr Hammond and the echo cardiologist can’t see it on their imperfect technology. I don’t think that means it’s not there. I think it simply means they can’t see it.”
78 Professor Paul John Nestel is a fellow of the Cardiac Society of Australia and New Zealand, and practises as a consultant physician at the heart centre of the Alfred Hospital. Professor Nestel gave evidence that atherosclerosis is the build-up of plaque which may lead to obstruction within the artery; these plaques are made up of different fats, blood clot, thrombosis tissue, and inflammatory material; and that myocardial ischaemia is an area of the heart muscle that has had an inadequate supply of blood in relation to its work requirements.
79 With respect to the relevant period of time from November of 1997 to 2000, Professor Nestel was asked what would be the effect of repeated angina episodes? He stated:
“Well, such attacks, while representing the reduction in blood flow to parts of the heart muscle, need not cause any damage, but in a general way they will lead to focal – that is small areas – of death of heart muscle, or necrosis of heart muscle, that generally heals partly with scar tissue, fibrous tissue….which can weaken the overall function of the heart and may give rise to areas of abnormal heart rhythm.”
80 Professor Nestel stated under cross-examination, that─
“Angina is a symptom of myocardial ischaemia. That is, it occurs when the blood supply is inadequate at the time. Now if the blood supply is inadequate for a very short period of time, that it is very unlikely to cause damage to heart muscle. But if the period of ischaemia or insufficient blood supply lasts for a longer period of time, and I’m not going to specify whether I’m talking about one minute or five minutes, then there’s a likelihood of some necrosis of the heart muscle.”
81 Professor Nestel was asked this question:
“With respect to this man and the work, if that’s accepted, Doctor, what would you say is, on balance, likely to be the effect upon his heart?”
Answer:
“I think it is - given that the attacks of angina were sufficiently intense and of sufficient concern to his general practitioner that he was admitted to hospital I would conclude it is likely that at least some of those episodes of myocardial ischaemia would have led to some myocardial necrosis with healing through scar tissue.”
Professor Nestel stated:
“I believe from the evidence that I’ve read the extent of his physical exertions that occurred during his work were sufficient to cause angina while he was working and given the two pathological examples that we’ve just discussed, I would conclude that his employment was a substantial contributing factor.”
82 With respect to the coronary atherosclerosis, Professor Nestel said the following:
“Well, as I’ve said in my report, in general that would not be expected to worsen or aggravate the degree of atherosclerosis, with one important exception, and that is if the build-up of atherosclerosis inside the coronary artery is a gradual process, which generally involves repeated small ruptures of that plaque that build up and produce an obstruction, then it’s well established that physical activity, if sufficiently severe, will lead to increased likelihood of ruptures within those plaques.”
83 Later, Professor Nestel stated:
“The natural process of atherosclerosis is through repeated small plaque ruptures, and it is well established that plaque rupture not only to a minor extent but to a major extent causes occlusions and death and can relate to episodes of heavy physical exertion, and that is why there is a possibility that his work may have aggravated the natural progression of the disease.”
84 Professor Nestel also said:
“The proposition I put forward at the very beginning is that this is a disease that progresses naturally unless very substantial interventions are made, but that knowing the pathology of the atherosclerosis, knowing that episodes of physical exertion can lead to plaque rupture, it is possible that the natural condition was aggravated by episodes of physical labour which we know were sufficient to produce angina or myocardial ischaemia in this man. So they were not insubstantial.”
85 Professor Nestel stated further:
“If we’re talking about underlying coronary atherosclerosis, my opinion, as stated last time, is that the growth or expansion of the atherosclerotic lesion takes place through repeated minor ruptures of the plaque – of the atherosclerotic plaque until such time as it is large enough to cause obstruction and there is adequate – more than adequate, overwhelming evidence that physical activity of a certain degree of intensity may lead to a plaque rupture and indeed does leave the plaque rupture in the case, for instance, of a major myocardial infarction, but a similar stress will lead to minor plaque ruptures that could lead to the expansion growth of atherosclerotic plaque.”
The defendant’s medical evidence
86 Dr Jeremy John Hammond, cardiologist, gave evidence that he has practised as a cardiologist for some 25 years. He holds a Fellowship of the American College of Cardiology and a Fellowship of the Cardiac Society of Australia and New Zealand, together with other qualifications.
87 On behalf of the defendant, he was asked to examine the plaintiff on 8 April 2002, 1 December 2004, 5 July 2007, 6 May 2008 and 13 January 2009.
88 Dr Hammond gave evidence concerning the underlying coronary disease that the plaintiff had suffered from at least 1991. He was then taken through the various angiograms that were taken of the plaintiff on 14 October 1991, 25 November 1994 and 13 July 2001.
89 Dr Hammond stated:
“The reports describe the occlusion of the right coronary artery persist on each of the three angiograms. However, the disease involved in the left anterior descending coronary artery, the coronary atherosclerosis, was described as relatively mild in 1991. In 1994 the disease had progressed to be described as causing a 50% to 60% stenosis or narrowing of that vessel, the left anterior descending coronary artery, and in 2001, disease of the left anterior descending coronary artery is described as being in the range of 60% to 70% stenosis. So there has been progression or worsening of the coronary atherosclerosis or coronary artery disease in that site of that period of time.”
90 He was asked this further question:
“Can you say anything about the rate of progression or the speed
of the progression?”
Answer:
“The disease appears to have progressed relatively rapidly between 1991 and 1994, changing from what is described as mild atheroma only to 50% to 60% stenosis, so I would call that relatively rapid progression. Thereafter the disease appears to have changed relatively slowly in that between 1994 and 2001 the description is of stenosis 50% to 60% in ’94 and then 60% to 70% in 2001. So the disease had a more rapid progression between ’91 and ’94 and a much slower course between ’94 and 2001.”
91 Dr Hammond was asked this question by Mr Gourlay:
“Doctor, this man engaged in physical work throughout the period 1991 until November 2000 and as a result of that physical exertion experienced attacks of angina, would those attacks of angina necessarily have any effect on the underlying atherosclerotic process?
Answer:
“No.”
Question:
“Could you elaborate?”
Answer:
“The presence of angina, as I mentioned before, is really a symptom of the state of the heart at that time, the heart muscle. The heart muscle is distinct from the arteries supplying the muscle and the heart muscle is complaining, if you like, that it wants to stop that particular activity at the time is not going to impact directly on the condition of the atherosclerosis which is distinct anatomically and pathologically, if you like, from the heart muscle itself.”
92 Dr Hammond was of the view that repeated attacks of angina consequent upon physical work are not likely to result in any physical damage. With respect to the proposition put forward by Dr Dupuche and Professor Nestel concerning microscopic heart damage occurring, he stated as follows:
“In reference to this, the proposition that microscopic or tiny areas of heart damage may occur, as I’ve alluded to in my report, this is a theory, hypothesis, that is discussed frequently at medical meetings. But in the reports one sees of autopsies and the microscopic examination of the heart involving people who have died suddenly or died of heart disease, one really does not see that to any great degree. One might see occasionally these areas of small damage alluded but, in general, that’s extremely rare. One would more commonly not see those findings.”
93 Dr Hammond was of the view that in this medical area there have been competing and differing opinions. He described it as an active area of uncertainty. He stated that, in his opinion, repeated attacks of angina consequent upon physical activity at work are unlikely to cause damage to the heart.
94 Dr Hammond was referred to a report of Dr King dated 10 November 1994, wherein Dr King stated:
“No permanent heart muscle damage occurs during an ordinary episode of angina which merely brings the presence of underlying heart disease to a person’s notice.”
Dr Hammond was of the opinion that this remains the mainstream view of the situation.
95 Dr Hammond was of the view that attacks of pain of less than 20 minutes are usually considered to be purely angina in nature with no likelihood of cardiac damage or cell death.
96 Dr Hammond stated that he approached his task by looking at the available evidence. He stated:
“Well, the way that I sort of approached the issue was to see what was the evidence available, if you like, from a medical standpoint, that progressive myocardial damage had occurred during this particular period of time. In terms, if you like, easily identifiable or large areas of damage where it was clear from the information I received that the left ventricular function between 1994 and 2000 remained stable, remained the same. So there was no decline in the left ventricular function which might have occurred, for example, if Mr Granrud had a further major attack or substantial heart attack. And, similarly, there was no decline of function looking at the theory that small attacks might have cumulated to cause significant damage or medically significant damage, if you like. So that was my starting point, was there actually evidence that there had been a change in this period of time. And I was drawn to the conclusion there was no evidence that such a change had occurred.”
97 Under cross-examination, Dr Hammond was asked this question:
“I might put my original question this way. Is your disagreement, and you’ve outlined the disagreement with Professor Nestel and Dr Dupuche, one of science or is it one of clinical judgment?”
Answer:
“I think it is both. I mean I think that these theories, as put forward by Professor Nestel and Dr Dupuche, have got some scientific basis in terms of experimental observations.”
98 Mr Fehring put to Dr Hammond the following questions:
“I am suggesting to you that Professor Nestel, as well as Dr Dupuche, both come, in the end, to a judgment as a medical practitioner that work did contribute to both processes?”
Answer:
“That they saw that on the balance of probabilities in this man with his work history as being a contributing factor, a significant contributing factor to the increase in the narrowing or the expansion, if you like, of the cholesterol…which would narrow the artery. I understand that is their view.”
Question:
“Yes?”
Answer:
“I would have to say I disagree strongly with that view. I think that’s
indulging in speculation.”
99 Dr Hammond said he respected the theory of Professor Nestel and Dr Dupuche. He stated that whilst he accepted the theory as being a possibility, its likelihood was debatable.
100 Dr Hammond agreed that, over the relevant period of time, no echo cardiogram had been performed, and that an echo cardiogram would show an area of infarct in the heart if such area was large enough. He stated that now there are enzyme tests which are regarded as being highly sensitive, the so- called troponin levels, and that these are regarded as being the “gold standard” in terms of evidence of damage or death of heart muscle. However, the test would have to be performed fairly shortly after an onset of the problem.
101 Dr Hammond stated in re-examination:
“But in terms of concrete evidence that myocardial damage had occurred, the two things that I looked at were the reports of the angiograms looking at the left ventricle function which would reflect, if you like, more substantial areas of muscle damage or potential muscle damage and, secondly, the report from the treating local doctor, Dr Jeffries, who indicated Mr Granrud had been to hospital on several occasions with episodes of prolonged chest pain.”
Submissions
102 Both Mr Gourlay and Mr Fehring provided written outlines of their submissions and spoke to them. These could be summarised as follows.
(i) The submissions on behalf of the defendant 103 The submissions of Mr Gourlay on behalf of the defendant could be summarised as follows.
104 Essentially, the plaintiff bears the burden of establishing that he has suffered an injury which entitles him to compensation. The relevant period upon which the claim is based and during which the occurrence of the compensable injury must be established is from 12 November 1997 to 20 November 2000.
105 The definition of “injury” is to be found in s.5 of the Act, as is the definition of “disease.” The plaintiff’s principal submission that what had occurred is the aggravation by work of a disease process. However, some attention was also paid to the proposition that what occurred was injury simpliciter. That is, an attempt by the plaintiff to avoid having to demonstrate that employment had been a significant contributing factor. Rather, the plaintiff is attempting to demonstrate that what occurred was a sudden physiological change and thus an injury simpliciter. The disease provisions remain as an alternative means of the plaintiff proving his claim.
106 It is the defendant’s submission that the plaintiff comes before the Court with a progressive disease, and the pathology of that disease has to be established. That pathology is, in fact, the underlying atherosclerotic process which pre- dated the plaintiff’s heart attack in 1991 and which has progressed thereafter. Reference is made to the decision of the High Court of Australia in Federal Broom Company Pty Ltd v Semlitch (1964) 110 CLR 626. Whilst the words “aggravation, acceleration, exacerbation or deterioration” may have different meanings, it was said in Semlitch that the question posed by each is whether the disease has been made worse in the sense of more grave, more grievous or more serious in its effect upon the person suffering from it. That is the approach which should be adopted in the present case. Pursuant to the provisions of the Act, the next step is employment must be a significant contributing factor to that recurrence or the like.
107 Returning to the concept of injury simpliciter, reference is made to the decision of the High Court in Kennedy Cleaning Services Pty Limited v Petkoska [2000] HCA 45. A sudden physiological change in some way connected with an underlying disease process may be an injury in the primary sense. However, in the present case, there is no evidence of adverse functioning of the plaintiff’s heart muscle. At best, from the point of view of the plaintiff’s case, what has occurred here is an aggravation of a disease occurring over a period of time rather than a sudden physiological change occurring on a particular day. This is so even if it were accepted that microscopic injury to the heart muscle has in fact occurred over such period of time. Similarly, if as a result of the microscopic deterioration of the heart muscle there is a build-up of plaque which creates deterioration, that is again a disease situation rather than an injury simpliciter.
108 Thus, no matter how it is viewed, the burden upon the plaintiff is to establish that the statutory requirements in relation to a compensable recurrence of the like of a disease have been satisfied.
109 Thus, the plaintiff must demonstrate that, between November 1997 and November 2000, employment was a significant contributing factor and events which occurred during a wider time frame, including the heart attack in 1991, are not to be taken into account.
110 The plaintiff’s underlying condition is one of coronary arterial sclerosis. On the bulk of the evidence, it is progressive. However, there is a paucity of material before the Court by the plaintiff in relation to his medical treatment and investigations of his condition. Evidence was not called from treating general practitioners or cardiologists, but only from two medico-legal consultants who espouse a particular theory which could not be described as mainstream. The three coronary angiograms, which have been obtained and which have been commented upon by Dr Hammond, reveal the process of continuing deterioration of the coronary artery disease. Dr Dupuche and Professor Nestel are not as qualified or as eminent as Dr Hammond and offer a theory which is experimental and speculative.
111 Returning to the sequence of events following the 1991 episode, the plaintiff had ongoing angina and arrhythmia which led to hospitalisation in 1994 and a further angiogram. The plaintiff was examined by Dr Donald King in November 1994 who, at that time, commented that angina of effort does not result in permanent heart muscle damage but merely brings the presence of underlying heart disease to a person’s notice.
112 Turning to the period 12 November 1994 to 20 November 2000, certainly the plaintiff gave evidence that he performed heavy work and suffered the onset of chest pains whilst working about twice a week over the period, this mathematically adding up to some 300 occasions. It has not been established that he in fact worked on in the face of such symptoms on any specific number of occasions. The accuracy of what the plaintiff said concerning his work duties and concerning suffering chest pain on occasions is not challenged. However, he had an imperfect memory for dates and the like, and this underlines the difficulties created by the failure to call witnesses such as the general practitioner. It is also clear that he had a process for dealing with the onset of chest pain which he had learned over the years. This involved the taking of medication in the case of severe chest pain or the stopping of work and resting. There were times when, according to his evidence, he would take the medication and continue working because he could not stop as a result of a particular situation that he was in. However, he did not take the extra step of saying how often this occurred, which, particularly given Dr Hammond’s evidence, is essential. It is vital to know not just that the plaintiff worked on in the face of pain, but for how long when there were symptoms occurring. Dr Hammond referred to what was described as the gold standard of 20 minutes. However, the plaintiff has not identified the number of occasions that he worked on in the face of symptoms or the length of time for which he so worked.
113 There are three documented occasions on which the plaintiff was admitted to hospital with relevant symptoms, these admissions occurring in April 1999, March 2000 and November 2000. On each occasion he was released after evaluation. There is little other information available. As stated by Dr Hammond, the inference could be drawn that there was the absence of concerns which “rang alarm bells”.
114 The plaintiff has also given evidence of the decline in his condition after the relevant period and in mid 2001. He has had angioplasty and a stent was inserted. However, he has had ongoing symptoms and this makes it all the more difficult for him to identify pathological change, whether by way of injury simpliciter or aggravation of disease process, during the relevant period. Further, another angiogram was performed in 2001 which demonstrated a slower deterioration than that revealed between 1991 and 1994.
115 In relation to the medical evidence called to support the plaintiff, Dr Dupuche is a general physician with an interest in cardiology. He only examined the plaintiff on one occasion. This is in contrast to Dr Hammond who has given a number of reports. Dr Dupuche has formed his opinion on the basis of speculation in relation to matters which are the subject of ongoing research and disagreement in the medical profession. Effectively, Dr Dupuche moved from saying that angina might cause very minor heart damage if there are repeated episodes to saying that there had to be something more than angina. Reference is made to a cross-examination found at pages 175 to 177 of the transcript. This in a way fits in with the evidence of Dr Hammond concerning the gold standard 20 minutes, under which time there would be no damage. Dr Dupuche’s views were given in a generalised way and also conceded that, if there was small, incremental injury to the heart muscle due to many episodes of ischaemia, this could not be quantified or measured. He also seemed to change his mind in relation to the proposition that the disturbance of plaque was the means by which the coronary artery disease progressed. Reference is again made to p.175 of the transcript, at which point Dr Dupuche conceded that, in relation to these matters, everyone was speculating. This reinforces the conclusion of Dr Hammond that, whilst these two doctors may genuinely hold these opinions, they are not mainstream and not generally accepted.
116 Professor Nestel was more ready to concede that matters such as these are in the realm of possibility and speculation, the proposition to which Dr Dupuche ultimately agreed. Professor Nestel’s earlier opinion, as contained in his report, was to the effect that continued work would not in itself have further aggravated underlying coronary atherosclerosis. However, in his oral evidence, for the first time he put forward the exception that manual work was having some effect on the underlying condition.
117 Professor Nestel did say that angina need not cause heart muscle damage, but in general focal necrosis can occur. However, he expressed some uncertainty about the duration of an angina attack which is required in order to do damage. He also agreed that the task of reaching a conclusion or expressing an opinion in the present case was made harder by the absence of any clinical data. As he said at T 121, “… we are in the realm of not knowing in an individual without very specific investigations at the time whether this has caused muscle damage or not”. In addition, by the time Professor Nestel saw the plaintiff in 2006, the post-2001 deterioration had occurred and, without the clinical data, it was very difficult for him to determine what happened in the relevant period.
118 The medical evidence on behalf of the defendant includes the report of Dr King in 1994, to which reference has been made. Dr Hammond is extremely well qualified and also has an association with post mortem reports which gives him an additional advantage in a case such as this and when compared with the plaintiff’s medical witnesses. He has provided multiple reports over the years, has examined the angiograms, and has put forward a sensible opinion which takes account of the alternatives. Essentially, his view is that the plaintiff has progressive coronary artery disease. The plaintiff has myocardial ischaemia and angina. His view is that the plaintiff has not been adversely affected by the relevant work which he has performed. The angina has not affected the underlying coronary artery disease, and there is no definitive evidence that the plaintiff suffered progressive myocardial damage during the relevant period. He has expressed the view that the observations of Dr Dupuche and Professor Nestel are experimental and speculative, and that he strongly disagrees with their opinions. His view is not only disposed of the issue of aggravation of the underlying disease but also of the proposition of injury simpliciter. The required duration of anginal pain must also be remembered. In summary, the appropriate inference should be drawn in relation to the failure to call appropriate witnesses such as the general practitioner and the treating cardiologists. The plaintiff has not discharged the onus which he bears. The proceedings should be dismissed.
(ii) The submissions on behalf of the plaintiff 119 The submissions of Mr Fehring on behalf of the plaintiff could be summarised as follows.
120 If the plaintiff has suffered damage to the myocardium or heart muscle arising out of the course of his employment, that is injury simpliciter. That employment was a significant contributing factor does not have to be demonstrated – see Hegedis v Carlton United Breweries Ltd (2000) 4 VR 296. In the present case, the evidence of Dr Dupuche and Professor Nestel, if accepted, would lead to the unarguable conclusion that the plaintiff suffered an injury sufficient to establish that it was an injury simpliciter. The evidence of those medical experts, when combined with the basically uncontested evidence concerning the plaintiff’s heavy work and his approximately 300 episodes of angina, would establish that he suffered damage to the myocardial muscle arising out of or in the course of his employment with the defendant.
121 There are three avenues by which the plaintiff can succeed and they are not mutually exclusive. One of these is by means of establishing injury simpliciter. The second is by way of ischaemic heart disease being aggravation of the plaintiff’s heart disease. The third is injury by way of aggravation of pre- existing coronary artery disease. Injury simpliciter has been discussed. There is a marked resemblance between the first and second of these avenues, each involving damage to the myocardium, but if the Court is of the opinion that the proper characterisation of this damage is ischaemic heart disease, the plaintiff would have to show that work was a significant contributing factor to that disease. Both Dr Dupuche and Professor Nestel were of the opinion that work was a significant contributing factor to the damage. Further and alternatively, if the injury is properly characterised as the aggravation of coronary artery disease, again the evidence of Dr Dupuche and Professor Nestel establishes that employment had aggravated and/or accelerated that disease by causing repeated ruptures to the coronary plaques when the plaintiff was performing heavy work during the course of his employment. It would be the aggravation of a condition from which the plaintiff suffered well before 1997, and it is not an issue but that the plaintiff did have coronary artery disease.
122 Returning to the concept of injury simpliciter, reference is made to the following extract from the decision of the High Court in Kennedy Cleaning:-
“If this evidence amounts, relevantly, to something that can be described as a sudden ascertainable or dramatic physiological change or disturbance of the normal physiological state, it may qualify for characterisation as ‘injury’ in the primary sense of that word. If such an injury happens within the protected period of employment, it is ordinarily compensatable[sic] without proof of a specific causal connection with the employer’s work.”
123 In the present case, the plaintiff suffered sudden but small and repeated death of heart muscle when he experienced angina at work, and as described by Dr Dupuche and Professor Nestel.
124 If significant contributing factor has to be established, the relevant test is set out in Popovski v Ericsson Australia Pty Ltd (1998) VSC 61. The work contribution must be demonstrated to be more than de minimus and to be a material contribution, but it does not have to be the major cause of the injury. In the present case, the evidence establishes that the plaintiff suffered numerous angina attacks when carrying out heavy or strenuous work. That strenuous work would cause increased heart activity and demand, and the inability of the heart to obtain sufficient blood supply. Hence, the angina attacks are significantly contributed to by employment demanding increased heart activity superimposed on narrow arteries.
125 In answer to an enquiry of mine, Mr Fehring directed me to the evidence of Professor Nestel to the effect that, if the blood supply is inadequate for a very short period of time, that is very unlikely to cause damage to heart muscle. However, if the period of ischemia or insufficient blood supply lasts for a longer period of time – Professor Nestel could not specify whether he was then referring to one minute or five minutes – there is then a likelihood of some necrosis of heart muscle.
126 It was further submitted by Mr Fehring that the opinion of Dr Hammond in relation to the goal standard of 20 minutes was not put in cross examination to either Dr Dupuche or Professor Nestel. Reference was made to the Ruling in Browne v Dunn and what should flow from a breach of that rule.
127 The plaintiff can be accepted as a hardworking person whose evidence should be accepted. It should be accepted in relation to the occasions when he kept working despite chest pain in a situation where he had to finish his work. It is also evident from the medical material that the plaintiff was admitted to hospital on three occasions during the relevant period and when suffering from chest pain, and on the last two occasions in March and November 2000 the chest pain was for a prolonged period and with onset at work. In this regard, it is not correct for Mr Gourlay to ask the court to draw an adverse inference because treating medical practitioners were not called to give evidence. In fact their written material was tendered by consent.
128 In relation to the evidence of Dr Hammond, whilst he has been critical of speculation on the part of the plaintiff’s expert witnesses, he in fact engaged in speculation himself concerning, for example, the results of tests that may have been carried out during the plaintiff’s hospitalisation. His primary view is that angina does not cause or contribute to myocardial damage. However, he did accept that a person could have a silent myocardial infarction where myocardial damage has been done even though the person suffering from it has not been aware of this occurring. Commonsense and medical sense would dictate that a person can have damage to the heart muscle when there is a lack of blood supply to the heart during the performance of heavy work, and angina pains are the symptom of this. Further, it is clear that on some occasions continuing angina does result in myocardial damage. The plaintiff has to establish his case before the court not to a degree of scientific certainty, as seemed to be demanded by Dr Hammond, but on the balance of probabilities. On the balance of probabilities, the evidence of Dr Dupuche and Professor Nestel should be preferred.
129 As stated, Dr Hammond’s position is based upon an irreconcilable inconsistency. Then, because he is of the view that there is no scientific proof of the theories put forward by Dr Dupuche and Professor Nestel, he is not prepared to say that, on the balance of probabilities in this case, that they are correct. However, whether or not a theory has been scientifically established is not the appropriate test. Furthermore, the report of Dr King predates the relevant events and is not of assistance. In addition, to suggest that Dr Hammond’s views are “mainstream” takes the matter no further, and whether or not a theory or opinion could be described as “mainstream” is not to the point and is also not the appropriate test.
130 In conclusion, the court should find that the plaintiff experienced repeated angina attacks which arose out of or in the course of his employment over the relevant period. His employment was a significant contributing factor to the attacks. As a result, the plaintiff’s heart could not be adequately supplied with blood and he suffered myocardial damage. Further, his coronary artery disease was aggravated by repeated plague ruptures which occurred due to the heavy work and the angina attacks.
(iii) The reply on behalf of the defendant 131 The submissions of Mr Gourlay in reply could be summarised as follows.
132 An injury simpliciter is an event and, as discussed in Kennedy Cleaning, distinct from the underlying pathology. A burst aneurism would be an example. What the plaintiff is really saying in relation to injury simpliciter and microscopic damage is that a type of gradual process injury occurred over three years by reason of a large number of injuries simpliciter. This is a concept which is unknown to the law and is illogical. In the present case there is no evidence that, on any particular day (including the three occasions on which the plaintiff attended hospital), the plaintiff worked on for a specified period of time in the face of symptoms, tests were conducted at the hospital, and as a result something, even microscopic damage, could be identified as having happened on that day. Were all those links in place, the occurrence of an injury simpliciter might be established. However, that evidence simply does not exist.
133 The defence of the defendant was put squarely to the plaintiff’s expert witnesses during cross examination. Each was recalled, and Dr Dupuche was further cross examined. Professor Nestel was not cross examined for a second time as his evidence upon recall did not take matters further.
134 It is correct that limited material from treating medical practitioners was tendered by consent, but such material was indeed limited. What is left is an insufficiency of evidence.
Decision
(a) Findings of fact 135 I find the plaintiff to be a witness of truth who gave evidence which I accept as being accurate and reliable, and also bearing in mind that there was no real challenge to his evidence, I make the following findings of fact in relation to the background or context in which this dispute, which is primarily of a medical nature, has arisen:
(i)
Prior to commencing employment with the defendant, the plaintiff had a history of symptoms consistent with the presence of coronary artery disease, and had suffered a myocardial infarction in 1991.
(ii)
During the course of his employment with the defendant, the plaintiff performed demanding, heavy physical work.
(iii)
Whilst performing such work, the plaintiff, on numerous occasions probably totalling something in the order of 300, suffered chest pains which were attacks of angina.
(iv)
On many of these occasions the plaintiff either took medication or rested until the pain abated. However, there was some when the plaintiff continued to perform physical work in the face of symptoms. However, there is no satisfactory evidence as to the number of these occasions or as to the duration of continuing physical work in the face of symptoms.
(v)
On three occasions during the relevant period, the plaintiff attended hospital, and I am satisfied that the attendances related to the symptoms of chest pain which he was experiencing. However, exactly what were the results of examinations and investigations carried out at the hospital on each occasion is far from clear. It may be safe to assume that, as the plaintiff was discharged comparatively quickly on each occasion, another myocardial infarction was not diagnosed. However, otherwise there is no clear or satisfactory evidence concerning the results of tests and investigations.
(vi)
In relation to the hospital admissions, on the last two occasions that he was so admitted the plaintiff had been experiencing chest pain for a prolonged period, and the onset of that pain had commenced whilst the plaintiff was working.
(vii)
After the relevant period and in mid-2001 the plaintiff’s condition declined and surgery was performed.
(b) Ruling 136 As it evident, the case centres to a very considerable extent on competing medical theories or opinions. Against the factual background which I have just outlined, I make the following ruling.
(i) Injury simpliciter 137 In arriving at a ruling in this regard, I have regard to the principles as enunciated in Kennedy Cleaning. I have also borne in mind the submissions of both counsel and the evidence of the medical experts. Given the facts of the present case, I prefer the submissions of Mr Gourlay in relation to whether or not an injury simpliciter has been established. Even placing the evidence of Dr Dupuche and Professor Nestel at its highest from the point of view of the plaintiff’s case, it cannot be said that any one of the approximately 300 episodes of angina resulted in injury to the heart muscle. There was no sudden ascertainable or dramatic physiological change or disturbance in the normal physiological state. There was no event, such as the example of a burst aneurysm, given by Mr Gourlay. Again, putting the plaintiff’s case at its highest, what occurred was a series of microscopic changes. I agree with Mr Gourlay that it would be novel law, as well as being illogical, to say that these could be in some way bundled together so as to become an injury simpliciter. In short, I am not satisfied that an injury simpliciter has been established.
(ii) Injury in the extended sense – the occurrence, aggravation, acceleration, exacerbation or deterioration of a pre-existing injury or disease
138 In determining this issue it has required a consideration of the principles set out in cases such as Popovski in relation to what constitutes a “significant contributing factor”. Again, I have borne in mind the submissions of counsel and the evidence of the medical experts.
139 I am satisfied that the plaintiff has discharged the burden of proof in relation to this issue. I am satisfied that the work contribution has been shown to be more than –
(a) minimal; and (b)
a material contribution to the aggravation and the like of the plaintiff’s ischaemic heart disease.
140 That the plaintiff did suffer from pre-existing cardiac problems is evident. Much then hinges upon whether further microscopic damage was done to his heart muscle at the time of the numerous angina attacks. The alternative is that such attacks were simply a symptom consistent with the existence of the underlying disease, and that the disease was in no way being progressed and no damage was being done. Of course, these alternate views lie at the heart of the conflicting medical opinions of Dr Dupuche and Professor Nestel on the one hand and Dr Hammond on the other.
141 Whilst all are impressive and well-qualified witnesses, I prefer the evidence of Dr Dupuche and Professor Nestel. I prefer their approach for the following reasons:
(a)
The view which they espouse seems to me to make sense. That continuing to work in the face of chest pain can cause damage to the heart muscle is not really an issue in the case. Rather, the question is one of timing and extent. It seems to me logical that, if there are repeated incidents or episodes where the plaintiff continued to perform heavy physical work in the face of chest pain, some damage, however microscopic, would be done to the heart muscle. The individual incidents of damage, particularly when accumulated, represent aggravation or the like or the underlying disease. This seems to me to be logical, and I do not accept the evidence of Dr Hammond in relation to the “gold standard” of 20 minutes in this regard. As stated, I prefer the evidence of Dr Dupuche and Professor Nestel which refers to no such requirement.
(b)
In any event, there were occasions when the attacks of angina pain persisted for a significant, if not precisely determined, period and commenced at or were associated with work. The latter two attacks that required a trip to hospital were of this nature.
(c)
Continuing with the logic of the situation, it seems to me more probable that a person who suffers chest pains of a cardiac nature whilst performing heavy physical work and particularly when he or she persists with such performance despite chest pains, is suffering some damage to the myocardium, however sub-clinical or microscopic that may be. The alternative, namely that nothing bad or injurious is happening, seems to me to be less probable.
(d)
Whilst Dr Hammond did not accept that the opinions of Dr Dupuche and Professor Nestel applied in the present case, he did accept that there was a scientific basis for such opinions. In other words, whilst their opinions may not have been “mainstream” in his opinion and to use his word, he nevertheless concedes that their thesis has a proper and scientific basis. It is not some ill-founded belief that springs from some form of alternative medicine.
(e)
Of course, the ultimate question when considering competing medical or expert evidence is one for the court.
As was said in Dahl & Anor v Grice (1981) VR 513 by Young CJ at page 514:
“It is not for the expert witness to answer the question which the jury has to answer although modern practice often permits an expert to give his opinion in the form of an answer to that question. The jury must say on all the evidence whether the conclusion contended for was more probable than not.”
Of course, there is no jury in the present case, so that I am the judge of both matters of fact and law. For that reason, the above quotation is apposite. What is being said in essence is that the ultimate decision, based upon the evidence including expert evidence, is one for the court.
As was said by Gobbo J in Dahl at page 522:
“There are a number of reasons why it is undesirable at the opinion as to causal connection be stated in terms of probabilities. In the first place, this is the role of the tribunal of fact and the ultimate task rests with the judge or jury, as the case may be… Though there are many exceptions in practice to the general rule as to not asking questions that by their terms call for an answer to the ultimate issue, it is a rule that is soundly based in its endeavour to reserve to the tribunal of fact the actual responsibility for the resolution of the ultimate issue.”
Gobbo J referred to the observations of Lord Loreburn in Woods v Thomas Wilson Sons & Co Limited (1915) 8 BWCC 288 at page 296 as follows:
“It is quite true that every case must be proved, and something more is needed than a state of facts which is consistent with one view or the other. That something more is supplied if the facts show a probability one way or other. No one can frame a formula by which you can measure probabilities. We must judge in each case as we would in other affairs of life.”
Gobbo J also referred to the Judgment of Mahoney JA in Fernandez v Tube Makers of Australia Limited [1975] NSWLR 190 at page 199 as follows:
“…there must, in my opinion, be afforded to the jury some scope of an inductive conclusion. The state of medical skill may be such that it can be said by the expert that, if the condition occurs after such and such a period, then the possible causes to be excluded as to the actual cause in the particular case. But where, as in the present case, this cannot be done, then, if a possible cause occurs sufficiently closely related to the condition, the jury may draw the inference of causal connection.”
At page 200, Mahoney JA stated that the question was:
“ … whether the evidence showed that the connection between the possible cause and the condition which occurred was sufficiently close to warrant a reasonable mind, faced with the problem of determining the question upon the evidence before it, concluding that the possible was the actual cause.”
As stated, Gobbo J was referring to the above extracts with approval, and was adopting the approach set out therein.
142 In adopting a similar approach to that set out in (e) above, I have reached the conclusion that, in this particular case, the views espoused by Dr Dupuche and Professor Nestel are to be preferred and that, in my role as judge of the facts, the necessary links between the plaintiff’s physical endeavours in the course of his employment and the aggravation or the like of his underlying disease have been established.
143 Thus, my ultimate finding of fact is that the physical stresses and strains of the plaintiff’s employment with the defendant during the relevant period (12 November 1997 to 20 November 2000) caused recurrent and frequent angina attacks, and this significantly contributed to further heart muscle damage.
144 I find that the plaintiff suffered a compensable injury during the relevant period.
145 Whilst it is not essential to my decision, I should say that I am of the view that the submissions of Mr Gourlay in relation to the inference that should be drawn due to the plaintiff’s failure to call certain of the plaintiff’s treating medical practitioners is weakened by the fact that material from such practitioners was allowed into evidence by consent. I appreciate that Mr Gourlay redirected his submission more towards the adequacy of evidence. In any event, in my opinion, any inference to be drawn is not of sufficient weight to overturn the finding at which I would have otherwise arrived, and at which I have so arrived.
146 Given the conclusion I have reached in relation to the plaintiff’s myocardial ischemia and the aggravation or the like of such disease, there is no need for me to move on to a consideration of the arguments concerning coronary artery disease and the disturbance of plaque if that be considered a separate issue. I might say that, were it necessary, I would again have preferred the opinions of Dr Dupuche and Professor Nestel and the submissions made by Mr Fehring. At least some of the factors set out above would again be applicable.
Conclusion
147 In summary, I am of the view that the plaintiff has discharged the burden of proof and has established that he suffered an injury which entitles him to compensation pursuant to s.98C of the Act.
148 I shall hear the parties as to the appropriate formal orders that are sought.
- - -
0
3
0