JOANNE A'BECKETT and COMCARE
[2009] AATA 604
•14 August 2009
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2009] AATA 604
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V 200600773
GENERAL ADMINISTRATIVE DIVISION ) Re JOANNE A'BECKETT Applicant
And
COMCARE
Respondent
DECISION
Tribunal Mr Egon Fice, Member Date14 August 2009
PlaceMelbourne
Decision The Tribunal affirms the decision under review. (sgd) Egon Fice
Member
COMPENSATION – compensation for work-related death – deep vein thrombosis – pulmonary embolism – autopsy report – translation difficulties – injury simpliciter – disturbance of the normal physiological state – dramatic physiological change – arising out of or in the course of employment – role of anti coagulation medication – acute myocardial infarction – coronary artery disease – causation – results in death – materially contributed to death – evaluation of causal chain – risk of cardiovascular event – heart enlargement – pulmonary hypertension – use of epidemiological studies
Commonwealth Employees’ Compensation Act 1930
Safety, Rehabilitation and Compensation Act 1988 s 17, s 18, s 38(4), s 62
Workers’ Compensation Act 1987 (NSW)
Accident Compensation Commission v McIntosh [1991] 2 VR 253
Australian Postal Corporation v Burch (1998) 156 ALR 483
Deeble v Nott (1941) 65 CLR 104
Dunham v Clare [1902] 2 KB 292
Ewers v Curtis (1933) 26 BWCC 553
Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190
Kavanagh v The Commonwealth (1959) 103 CLR 547
Kennedy Cleaning Services Pty Limited v Petkoska (2000) 200 CLR 286
Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452
Lyons v Woodilee Coal and Coke Co (1917) S.C.(H.L.) 48
Migge v Wormald Bros. Industries Ltd (1972) 2 NSWLR 29
Seltsam Pty Ltd v McGuiness and Another; James Hardie & Coy Pty Limited v McGuiness [2000] NSWCA 29
Ystradowen Colliery Co Ltd v Griffiths [1909] 2 KB 533
Zickar and MGH Plastic Industries Pty Ltd (1995) 187 CLR 310
C. Becattini et al, ‘A prospective study on cardiovascular events after acute pulmonary embolism’ (2005) 26 European Heart Journal 77
S. Z Goldhaber, L Visani and M De Rosa, 'Acute pulmonary embolism: clinical outcomes in the international co-operative pulmonary embolism registry' (1999) 353(9162) The Lancet 1386
E.F. Hill and J.B Bingeman, 'Death or incapacity which results from injury and results of incapacity and death' in Principles of the Law of Workers’ Compensation Particularly in Victoria (1981) 73-77
Taber’s Cyclopaedic Medical Dictionary
REASONS FOR DECISION
14 August 2009 Mr Egon Fice, Member 1. Ms Joanne A’Beckett is the widow of Mr David Brunt. Mr Brunt died on 1 September 2005. On 20 December 2005 Ms A’Beckett lodged a claim with Comcare seeking compensation for a work related death. Her claim was made under s 17 of the Safety, Rehabilitation and Compensation Act 1988 (the SRC Act) on behalf of her daughter, Alexandra, who was nine and a half years old at the time of her father’s death. Ms A’Beckett also claimed compensation for Mr Brunt’s funeral expenses under s 18 of the SRC Act.
2. On 19 January 2006 a delegate of Comcare rejected Ms A’Beckett’s claims. Ms A’Beckett sought review of the delegate’s decision. On 28 June 2006, a review officer with Comcare affirmed the primary decision. Although stating that the determination should be affirmed, the reviewing officer dealt only with the s 17 claim. I assume that was because a claim under s 18 depends upon injury to an employee resulting in death. Having found that Mr Brunt’s work injury did not result in his death, it appears the reviewing officer thought it unnecessary to deal with the s 18 claim. However, it raises the question whether the s 18 claim has been reviewed. While I appreciate that the s 18 claim must necessarily follow the decision in respect of the s 17 claim, it seems to me that in order for the Tribunal to have jurisdiction to review the s 18 claim, it must be a claim which has been reconsidered in accordance with s 62 of the SRC Act. Section 38(4) of the SRC Act is not applicable in this case. My opinion is that the Tribunal does not have jurisdiction to review the s 18 claim because its jurisdiction is limited by s 64 of the SRC Act to reviewing reviewable decisions only. Of course, this problem will fall away if I affirm the reviewable decision in respect of the s 17 claim.
3. The issues which I have to determine in this matter are whether:
(a)Mr Brunt suffered an injury as that term is defined in the SRC Act;
(b)if Mr Brunt suffered an injury, did it result in his death; and
(c)whether Mr Brunt died leaving a dependant, as that term is defined in the SRC Act.
EVENTS LEADING TO MR BRUNT’S DEATH
4. Mr Brunt was employed by the Australian Bureau of Statistics (ABS) as an Executive Officer – Level 1. On 14 November 2000, in company with two colleagues from the ABS, he flew to Sydney from Melbourne to conduct visits related to his work. The flight arrived in Sydney at about 6.20pm. Mr Brunt and his two colleagues intended to meet another colleague from the Canberra office and waited for him at the taxi rank. After about five minutes, when their Canberra colleague had not arrived, Mr Brunt suggested that he return to the terminal to look for him. Mr Brunt’s colleagues observed him duck under a steel railing and proceed towards the terminal doors. As he approached the doors, he appeared to crouch down for a minute or two after which he arose and headed through the terminal doors. His colleagues waited in the taxi rank queue for a further five minutes. When neither Mr Brunt nor their Canberra colleague appeared, they proceeded to the terminal and found Mr Brunt sitting on a railing looking ashen, sweating and complaining of faintness/dizziness. One of Mr Brunt’s colleagues purchased a bottle of mineral water which Mr Brunt proceeded to drink. After about five minutes, the party went back to the taxi rank and caught a cab which took them to their hotel. Mr Brunt said he would not be going out to dinner as he thought he would rest up for that evening.
5. The following morning one of Mr Brunt’s colleagues called at his room. Mr Brunt told him that he had not slept during the night, had been vomiting and that he finally called a doctor around 4.00am. Mr Brunt said that the doctor’s diagnosis was that he either had an allergic reaction to something or that he was suffering from food poisoning, both of which would resolve within 24 hours. Mr Brunt decided to remain in his room for the remainder of the day, hoping to be well enough to accompany his colleagues on the scheduled visits on the following day. Upon their return to the hotel around 6.00pm, Mr Brunt’s colleagues asked him if he felt up to going to dinner. He said he was but that he was short of breath and did not wish to go too far. Mr Brunt ate a very light dinner and then went back to the hotel around 9.30pm. One of Mr Brunt’s colleagues checked on him at about 11.00pm that evening only to be told the Mr Brunt was not feeling better and had decided to return to Melbourne the following morning.
6. On Thursday, 16 November 2000, Mr Brunt’s colleagues met him in the hotel lobby at 8.30am to be told that he had booked a flight back to Melbourne at 11.00am.
7. Ms A’Beckett, who had been in contact with her husband by telephone on 15 November 2000, arranged for him to see their family doctor, Dr Longworth, upon his return to Melbourne on 16 November. Mr Brunt took a taxi to his home in Vermont and his wife left her place of work to go home when she became aware he had arrived. When she got to their home, Mr Brunt was lying on the couch; he was pale and having trouble breathing and was very distressed. She helped him into the car and drove him to Dr Longworth. Dr Longworth immediately arranged for Mr Brunt to be admitted to the Emergency Department at Knox hospital. Mr Brunt was confirmed to have a pulmonary embolus following a scan.
8. On the following day, 17 November 2000, Mr Brunt suffered a cardiopulmonary arrest. He was given immediate advanced cardiopulmonary life‑support which resulted in the return of his vital signs but he remained in a shocked state due to the mechanical obstruction of the pulmonary embolus. Mr Brunt was transferred to an operating theatre where the cardiothoracic surgeon reported gross right heart dilatation and a large saddle embolus straddling the bifurcation of the pulmonary artery. The surgeon reported large masses of thrombus effectively obstructing both left and right main pulmonary arteries. Despite being able to clear the clot, the cardiothoracic surgeon reported that during the lengthy process, it was not possible to maintain adequate oxygenation. Mr Brunt was resuscitated for over an hour and the lack of oxygen during this period resulted in hypoxic brain injury. As a result of that injury, he suffered significant cognitive impairment. The cognitive abnormalities included very poor short-term memory, lack of insight into the fact that he had cognitive problems, fluctuating attention, reduced speed of information processing, poor initiation, poor planning and limited organisational abilities. Prior to suffering the hypoxic brain injury, Mr Brunt was regarded as having an extremely high intellectual functioning.
9. Because of Mr Brunt’s severe brain injury, it was considered unsafe to have him discharged to home where he would be living alone and unsupported while his wife worked. He was not considered to be capable of managing his own affairs. On about 9 December 2000 he was transferred to the Victorian Rehabilitation Centre. His behaviour became unpredictable. He could be attentive at one moment and then be screaming and abusing people in the next. He would get frustrated, very angry with everyone and demanding. Ms A’Beckett said that at times he could be very frightening. On 20 February 2001 Ms A’Beckett announced that she would be separating from Mr Brunt. Nevertheless, she and her daughter continued to visit Mr Brunt at the Victorian Rehabilitation Centre.
10. In late March 2001 Mr Brunt was discharged from the Victorian Rehabilitation Centre and moved to an independent living unit. The State Trustees were appointed to administer his affairs. Mr Brunt was not capable of resuming his employment and it seems that he decided to travel in Australia and overseas. He often sent postcards to Ms A’Beckett and her daughter while overseas. In 2003 he returned to Perth to live with his father.
11. It appears that Mr Brunt left Perth to fly to Hong Kong on 21 July 2005. Ms A’Beckett did not hear from him again until after his body was discovered in a hotel room in Bangkok on 1 September 2005. A translation of an autopsy report records Mr Brunt’s direct cause of death as:
Mild haemorrhage under the membrane(s) of the brain with Acute Myocardial Infarction caused by Coronary Artery Disease.
Mr Brunt was 41 years old at the time of his death.
DID MR BRUNT SUFFER AN INJURY?
12. The term injury (prior to the 13 April 2007 amendment) was defined in s 4(1) of the SRC Act as follows:
(1)In this Act:
injury means:
(a)a disease suffered by an employee; or
(b)an injury (other than a disease) suffered by an employee, that is a physical or mental injury arising out of, or in the course of, the employee’s employment; or
(c)an aggravation of a physical or mental injury (other than a disease) suffered by an employee (whether or not that injury arose out of, or in the course of, the employee’s employment), that is an aggravation that arose out of, or in the course of, that employment;
but does not include a disease, injury or aggravation suffered as a result of reasonable administrative action taken in a reasonable manner in respect of the employee’s employment.
13. Ms A’Beckett claimed that the onset of Mr Brunt’s pulmonary embolus amounted to an injury (injury simpliciter), not being a disease, in that it constituted a sudden or ascertainable or dramatic physiological change or disturbance of his normal physiological state.
14. Dr Michael Leyden, a consultant physician, first examined Mr Brunt when he was in the Intensive Care Unit at the Knox Private Hospital, not long after his cardiac arrest and embolectomy. Dr Leyden said that Mr Brunt had been diagnosed with Protein C and Protein S deficiency, which is a clotting disorder, predisposing him to developing blood clots. According to Dr Richard Clements, a rehabilitation physician involved with Mr Brunt’s care, the undetected clotting disorder predisposed Mr Brunt to developing blood clots. However, he said the precipitating factor of the pulmonary embolus was almost certainly the flight to Sydney, a short period during which Mr Brunt’s lower limbs would have been relatively immobile; a circumstance which is associated with the formation of deep venous thrombosis (DVT).
15. In the course of his examination-in-chief, Dr Leyden was read the account given by Mr Brunt’s work colleague (Mr Hutchinson) about the flight from Melbourne to Sydney. In response, Dr Leyden said that it sounded like a very classic story of a clot on the lung, a pulmonary embolus. When asked if that event could be described as a sudden and ascertainable or dramatic physiological change or disturbance of the normal physiological state, Dr Leyden replied: It certainly is.
16. Professor Hatem Salem, Professor of Medicine, clinical haematologist and haemato-oncologist, provided a report dated 14 August 2008. The first question he was asked to address was whether Mr Brunt suffered a sudden physiological change or disturbance of the normal physiological state on 14 November 2000. His answer was an emphatic yes. He said that Mr Brunt left home feeling well and following his flight to Sydney, became quite unwell. Something went wrong and it happened very quickly.
17. As to the nature of the physiological change or disturbance, Professor Salem explained that Mr Brunt developed a major clot in the veins of his leg which subsequently separated and lodged in his lungs. He had several clots in his lungs that were tolerated until a very large one caused his cardiac arrest three days later.
18. In the course of his examination-in-chief, Professor Salem was read Mr Hutchinson’s uncontroverted evidence about what happened on arrival at Sydney airport. He said that this was a wonderful history and a very typical history of someone who has had a pulmonary embolism or clot on the lung. He said the fact that Mr Brunt suddenly felt faint would imply that there was a sudden reduction in the flow of blood going to the lungs and therefore the return of blood to the heart would be diminished, causing an acute drop in blood pressure. That would result in the person feeling very faint. He said a clot can disperse and allow more blood flow which would result in the person regaining a little more life until the clot began to regrow or another clot came along and caused further damage.
19. Under cross-examination, Professor Salem explained that the breathlessness which Mr Brunt experienced at Sydney airport would suggest he had a proximal clot. This meant Mr Brunt did not have a clot in the periphery of his lungs, but rather centrally, causing an obstruction to the blood flow on the right hand side of the heart. This resulted in the left side not getting sufficient blood so that when the left ventricle contracted, there was insufficient blood going out causing the pressure to drop. That, in turn, caused Mr Brunt to feel faint and unwell.
20. Professor Salem also explained that in general, clots of the nature suffered by Mr Brunt were not just simple small-sized clots. In fact, they are quite lengthy like:
…the size of a snake, and they start off from, usually, from the lower leg and will propagate towards the heart. At the tip of the clot a small piece will break off and may cause the symptoms…
that Mr Brunt experienced in Sydney. Then, another piece may break off and cause the symptoms he experienced in Melbourne.
21. Mr J Lenczner of counsel, who appeared on behalf of Comcare, submitted that the surgeon who conducted surgery on Mr Brunt following his cardiac arrest, Mr Rosalion, said that he found a number of clots but the one that seemed to have done the damage was called a saddle clot. He asked Professor Salem which of the clots actually caused the cardiac arrest. Professor Salem said he did not know but he suspected that small bits of the proximal clot dislodged permitting greater blood flow which allowed Mr Brunt to come back to Melbourne. The proximal clot then reformed and hence Mr Brunt’s massive cardiac arrest following his hospitalisation in Melbourne. He said it would be unusual for someone to get two saddle clots in a row. It was common that when scans were done on patients, they disclosed the person to have multiple clots. He explained the nature of the disease is that the thrombus breaks off and then distributes widely. That might cause the patient to tolerate the situation at a certain level, but if the patient attempted to go up a flight of stairs or to run, he would probably be in trouble. In his experience, it was unusual for big clots to dissolve spontaneously.
22. Mr Lenczner referred to a report prepared by Dr Ross Baker, a clinical haematologist and consultant physician, dated 8 April 2008. In that report Dr Baker said it was likely that when Mr Brunt arrived in Sydney, a significant pulmonary embolism had already occurred. Therefore, it was more likely that Mr Brunt had already developed a venous thromboembolism prior to his flight. Professor Salem was asked whether that was a reasonable proposition. He responded that it was very difficult to know when DVT started. Professor Salem said there could be no doubt that Mr Brunt’s episode of pulmonary embolism on arrival in Sydney was acute. The fact that Mr Brunt got off the aircraft at Sydney, walked out into the terminal and suddenly became very faint and unwell, looking ashen grey in colour, indicated an acute event. That, he said, was typical of pulmonary embolus. Mr Brunt may have had small clots going to his lung for weeks or months, but they never caused him a problem. The acuteness of the event described by Mr Hutchinson would suggest Mr Brunt had a big clot at that time.
23. Professor Salem was taken to a second report prepared by Dr Baker, dated 24 October 2008. In that report, Dr Baker said it was very difficult to be certain exactly when the pathological process of venous thrombosis develops. Professor Salem agreed with that proposition. Professor Salem was then asked if he agreed with Dr Baker’s opinion that the rate of DVT progressing to pulmonary embolism is one of clinical uncertainty; and that in some people, there is a slow process of accumulation of blood clots which break off from the leg veins and travel to the lungs. At a certain point the blood clots cause symptoms suggestive of pulmonary embolism. Sometimes this can take weeks to months to develop. Professor Salem agreed with that proposition. When Mr Lenczner suggested to Professor Salem that not much more could be said about the size of the blood clot experienced by Mr Brunt on landing at Sydney, other than it was obstructing the blood flow in some fashion, Professor Salem said it must have been a substantive clot because of the symptoms reported. When Mr Lenczner suggested to Professor Salem that the clot was not substantive enough to cause him a cardiac arrest or any other injury at that time, Professor Salem responded that it did not totally occlude the artery, but rather it partially occluded the artery and the blood flow had dropped by probably 50 per cent plus.
24. Mr Lenczner then referred Professor Salem to Dr Baker’s statement where he said, in Mr Brunt’s case, it was likely that what happened was a slow process of embolisation of small blood clots from his asymptomatic DVT taken into his lung. The final event causing the cardiac arrest was a large piece of blood clot that occluded the blood flow to the pulmonary vessels of the heart. Mr Lenczner suggested to Professor Salem that Dr Baker’s view was that emboli were going more to the periphery of the lungs and the clot which ultimately caused the obstruction resulting in a cardiac arrest was a new clot which had broken off. Professor Salem disagreed with that proposition. He said:
No, of course not and I think the facts speak for that. The guy was well, suddenly he’s different; ash grey, sweaty and faint. Now that can not be caused by small clots. That must have been caused by a big clot. It’s impossible. This is A, B, C, of medicine …
25. Professor Salem also explained that if a person had small emboli in the lungs, they would suffer shortness of breath because of the reduced gas exchange within the lungs. The difference between a small and large embolus is that with a large embolus, the person would feel faint and unwell, appear ash grey and experience all the symptoms that Mr Brunt had; whereas if he had small emboli, he would just suffer a shortness of breath when exerting himself.
26. In his report dated 24 October 2008, Dr Baker said it was very difficult to be certain exactly when the pathological process of venous thrombosis develops. Once a patient develops possible symptoms of venous thromboembolism, objective confirmation is required through further testing such as leg ultrasounds, lung scans, CT pulmonary angiograms or other tests. Dr Baker said in Mr Brunt’s case, it was likely there was a slow process of embolism of small blood clots from his asymptomatic left DVT into his lung. The final event causing the cardiac arrest was a large piece of blood clot which occluded the blood flow through the pulmonary vessels of the heart.
27. In his examination-in-chief, Dr Baker accepted there was no doubt that Mr Brunt had symptoms when he arrived in Sydney. He reiterated that a diagnosis of pulmonary embolism is difficult and it was only appreciated when Mr Brunt returned to Melbourne, and the diagnosis was made. It was not uncommon for people to have quite significant thrombosis in their legs or lungs and have surprisingly few symptoms. However, where people have only small clots, they may have very significant symptoms and so the direct relationship between the pathology and the symptoms may vary significantly. It was not until after Mr Brunt had received treatment at Knox Hospital on his return to Melbourne that he sustained a cardiac arrest. That was caused by a large piece of clot travelling from the leg into Mr Brunt’s lungs, occluding the main pulmonary blood vessels.
28. Under cross-examination Dr Baker was taken to the transcript of Professor Salem’s evidence where he referred to Mr Brunt suffering an acute event in Sydney, that being a typical pulmonary embolus. He was asked whether he accepted the description by Professor Salem and he answered yes. He was also asked whether that scenario could be identified as a pathological change and Dr Baker said yes, he has a disease. A little later in the cross-examination, Dr Baker said that DVT and pulmonary embolism are in the same continuum of disease. When it was put to him again that Mr Brunt fell ill after he got off the aircraft at Sydney because a pulmonary embolus had occurred, Dr Baker said he agreed.
29. In re-examination, Mr Lenczner asked Dr Baker what he understood by the expression sudden pathological change. Dr Baker said pathology is what you can observe as really what’s causing the symptoms. Therefore:
… the occlusion of blood vessels would be pathology. The symptoms may be pain or shortness of breath, or other symptoms of pulmonary embolism, but the pathology is the actual what you can observe.
When asked to describe what pathology was taking place when Mr Brunt arrived in Sydney, Dr Baker said what was causing Mr Brunt’s symptoms was that he had DVT of which he was unaware. Small amounts of blood clots were coming off, going into his lung and causing his symptoms. He distinguished this condition from the pulmonary embolism, described as a saddle embolism, which Mr Brunt suffered at Knox Hospital.
30. The question which this evidence raises is whether what Mr Brunt experienced on arrival at Sydney airport could be described as an injury simpliciter. There are many cases in the Federal Court of Australia and the High Court of Australia which have examined the meaning of the word injury, as used in various Workers’ Compensation Acts. The High Court’s decision in Kavanagh v The Commonwealth (1959) 103 CLR 547 is a good example. In that case, Mr Kavanagh, who worked for the Commonwealth, left the floor where he was performing his duties to go to the convenience. When he returned he said he felt ill and had diarrhoea. He suddenly vomited and was later found to have suffered a ruptured oesophagus as a result of the vomiting. The cause of the vomiting could not be explained. He died in hospital some six days later from broncho-pneumonia and heart failure. The question for the court to answer was whether the rupture of Mr Kavanagh’s oesophagus was a personal injury by accident arising in the course of his employment. Dixon CJ said, at 553:
The first question is whether the rupture of the gullet in these circumstances is to be considered an injury by accident. In my opinion it must be so considered. It is a sudden destruction of tissue by force or pressure. It is true that the force or pressure was not exerted from without the body, but that I think makes no difference nor does it make any difference if it occurred, as it may have done, as a consequence of another organ of the body, namely the stomach, responding to a virus infection: …
Taylor J said, at 569:
There is no doubt that the rupture was personal injury by accident; …
Windeyer J also said he had no doubt that what Mr Kavanagh suffered was an injury by accident in the sense which the expression has in this branch of the law. He said it was quite unlike an episode that is an ordinary consequence of the progress of a disease.
31. In Zickar v MGH Plastic Industries Pty Ltd (1995) 187 CLR 310 the High Court was required to deal with the situation where Mr Zickar claimed that his suffering a cerebral aneurism satisfied the meaning of injury as defined in s 4 of the Workers’ Compensation Act 1987 (NSW).Mr Zickar experienced a rupture of an aneurism. Toohey, McHugh and Gummow JJ said, at 334:
… that the aneurism was an autogenous disease but the appellant's claim to personal injury within par (a) is based on the rupture which occurred. … If there was no rupture there would be no event answering the description of personal injury and the appellant would be driven to rely upon par (b) of the definition. But there was such an event and the presence of a disease does not preclude reliance upon that event as personal injury.
Their Honours also referred to Accident Compensation Commission v McIntosh [1991] 2 VR 253 where Murphy J, with whom Crockett and Cummins JJ agreed, said:
… If the rupture is due to blood pressure, arteriosclerosis, arteriovenous malformation, or any other congenital or diagnostic aetiology, it is nonetheless a rupture - something quite distinct from the defect, disorder or morbid condition, which enables it to occur.
32. Kirby J in Zickar’s case took a slightly different approach. In his view, following changes to the New South Wales Workers’ Compensation Act which in effect split the definition of injury from the definition of disease, he said, at 351:
… No longer is there a dichotomy between "personal injury" in its full sense and “disease injury" within the additional part of the definition. A worker is entitled to succeed if he or she can bring a claim within either head of recovery. …
and, further, at 352:
The approach to the definition of “injury" which I favour does not necessarily mean that every catastrophe connected with a progressive disease will fall within the definition of “personal injury", primarily so defined. Whether, in the case of a progressive disease, leading inevitably to a sudden or identifiable pathological change, it can be said that such change constitutes a “personal injury” can be left to determination on a case by case basis. …
… The sudden tear which caused the haemorrhage and the clot constituted a “personal injury". It was no less so because it was internal …
33. In Australian Postal Corporation v Burch (1998) 156 ALR 483, the Full Court of the Federal Court of Australia was required to determine whether a stroke suffered by Mr Burch was a disease or injury as those terms were defined in the SRC Act. In a joint decision, Heerey, Sundberg and North JJ referred to the decision of Dixon CJ in Kavanagh’s case. The court said that although cases such as Kavanagh accepted that an incident involving an internal rupture or breaking was an injury, it did not mean that as matter of law, rupture or breaking was an essential prerequisite defining an injury (in the ordinary sense) of an internal nature (at 487). The Court held that Mr Burch’s stroke was an injury as it was a disturbance of the normal physiological state or an ascertainable lesion or dramatic physiological change (at 488).
34. A more recent decision is that of the High Court in Kennedy Cleaning Services Pty Limited v Petkoska (2000) 200 CLR 286. Mrs Petkoska collapsed at work on the occurrence of a brain lesion which caused a stroke. She had suffered from rheumatic mitral valve disease for some years. Gleeson CJ and Kirby J referred to Zickar’s case. While they accepted there were differences in the approaches taken by the Justices comprising the court in that case, they said the points in common which all members of the majority recognised and emphasised were more important. Their Honours said, at 298:
These included the reminder that a long line of decisions in Australia had recognised that an "injury", being a sudden or identifiable physiological change, could nonetheless qualify within the ordinary application of that expression appearing in workers' compensation legislation, although the change was internal to the body of the worker. It did not have to be external or necessarily produced by external causes.
and further, at 299:
Secondly, the mere fact that a sudden physiological change is in some way connected with an underlying “disease" process does not, of itself, prevent the classification of such a change as an "injury" within the primary statutory provisions that apply to such a case.
35. Gleeson CJ and Kirby J referred to the way this question was approached in Zickar and in McIntosh and Burch. They said, at 300:
All of those cases require that consideration be given to the precise evidence, on a fact by fact basis, concerning the nature and incidents of the physiological change accepted at trial. If this evidence amounts, relevantly, to something that can be described as a sudden and ascertainable or dramatic physiological change or disturbance of the normal physiological state, it may qualify for characterisation as an "injury" in the primary sense of that word.
36. In Petkoska’s case McHugh, Gummow and Hayne JJ, with whom Gaudron J agreed, referred to the Full Court of the Federal Court’s decision in Petkoska where Finn and Merkel JJ said:
… that it was not a prerequisite to the finding of an “injury” which is of an internal nature, that the physical event or incident involve a “rupture or breaking”, and that an occlusion, causing a disturbance of the normal physiological state will suffice.
McHugh, Gummow and Hayne JJ said, at 308:
The circumstance that a sudden physiological change has been caused or provoked by disease does not prevent it from constituting a "physical injury" for the purposes of s7(1).
Their Honours’ concluded, at 309:
The respondent was stricken by reason of a disease, but she also sustained an injury "in the course of" her employment.
37. The first question which I must address is whether it can be said that Mr Brunt suffered an injury shortly after his arrival at Sydney airport on 14 November 2000. The evidence given by Mr Hutchinson that he found Mr Brunt sitting on a railing looking ashen, sweating and complaining of faintness/dizziness, all the medical practitioners agree was consistent with the symptoms of pulmonary embolism. Although Dr Baker described this as a disease process, he nevertheless agreed Mr Brunt suffered a sudden and identifiable pathological change at that point in time. Although the degree of occlusion suffered by Mr Brunt was not precisely identified, and Dr Baker and Professor Salem disagreed about that, the inescapable fact is that at that time, Mr Brunt suffered a sudden and ascertainable or dramatic physiological change or disturbance of his normal physiological state. That is despite the fact that it was a consequence of the disease venous thromboembolism suffered by Mr Brunt.
38. It was not disputed that the cause of Mr Brunt’s pulmonary embolism was the breaking off of emboli from a thrombus in his lower limb. Whatever the size of the emboli that travelled to Mr Brunt’s lungs, their arrival there caused a dramatic change in his physiological state. In fact, he felt so unwell that he did not go out with his colleagues to dinner that night but stayed in his room where he said he did not sleep, was vomiting and finally called the doctor about 4.00am. On the doctor’s advice, Mr Brunt decided to rest in his room for the remainder of the following day, 15 November 2000. That evening he went to dinner with his colleagues but he could not walk very far as he was short of breath. When Mr Hutchinson checked with him around 11.00pm that night, Mr Brunt said he was not feeling any better and had decided to return to Melbourne the following morning. He did this and took a taxi home from Melbourne airport. When his wife met him at home, she described his state in the following way:
I went inside and found David lying on the couch. He looked terrible. He was pale and having trouble breathing, and really very distressed. And I had to help him. He couldn’t stand up by himself. And so I helped him to the car, put him in the car, and drove him to Dr Longworth’s.
Her husband was then admitted to the Emergency Department at Knox Hospital.
39. Mr Lenczner submitted that, in accordance with what Gleeson CJ and Kirby J said in Petkoska’s case, to satisfy the definition of injury (other than a disease) in the SRC Act, it was necessary that Mr Brunt’s claimed injury was distinct from the underlying pathology which constitutes the disease. He said that in order to qualify as an injury in the context of a disease process, the event relied upon must be distinct from the underlying disease and cause the injury to occur. That submission is undoubtedly correct in the context of determining whether an event can be properly described as an injury simpliciter. However, Mr Lenczner further submitted that prior to 17 November 2000, what Mr Brunt experienced was a progression of the disease thromboembolism. Thromboembolism is defined in Taber’s Cyclopaedic Medical Dictionary as:
An embolism; the blocking of a blood vessel by a thrombus that has become detached from its site of formation.
40. Mr Lenczner submitted that the disease process included the production of an embolus or emboli and was progressive rather than a sudden, ascertainable or dramatic physiological change or disturbance of the normal physiological state. He further submitted that the events which occurred on 14 November 2000 preceding his cardiac arrest on 17 November 2000 were part of the disease process and therefore could not be described as an injury simpliciter.
41. With respect, I cannot agree with Mr Lenczner’s analysis of the events on 14 November 2000. It is not consistent with the definition set out in Taber’s Cyclopaedic Medical Dictionary and is also contrary to the evidence given by Dr Baker and Professor Salem. As I understood the evidence of those two medical practitioners, Mr Brunt developed a deep vein thrombus probably well before his flight to Sydney on 14 November 2000. That does not necessarily mean he had any symptoms. Dr Baker said people can have quite significant thrombosis in their legs or lungs and have surprisingly few symptoms. DVT is the primary cause of pulmonary embolism. Pulmonary embolism is the occlusion of one or more of the pulmonary arteries by thrombi that originate elsewhere.
42. In Mr Brunt’s case, it appears that the thrombus originated in his leg. According to Professor Salem, as the deep vein thrombus develops, pieces may break off at the tip and travel through the heart to the pulmonary arteries. The clots can be quite lengthy and have a jellylike texture. Although there was some dispute between the medical practitioners about the extent of the occlusion which resulted in Mr Brunt suffering pulmonary embolism, Dr Baker and Professor Salem agreed that Mr Brunt suffered an acute event of pulmonary embolus when he got off the aeroplane at Sydney airport.
43. In my opinion, it matters not, for the purposes of determining whether Mr Brunt suffered an injury simpliciter when he disembarked from the flight at Sydney on 14 November 2000, whether the occlusion of his pulmonary arteries resulted from a number of small emboli or whether a larger embolus was present. Whatever the mechanics were at that time, the occlusion or occlusions suffered by Mr Brunt on arrival in Sydney were sudden and resulted in identifiable physiological changes as described by Ms A’Beckett and by Mr Hutchinson who witnessed the event. The evidence indicates that the occlusion of Mr Brunt’s pulmonary artery or arteries was an event distinct from the DVT or the underlying disease. It satisfies what Gleeson CJ and Kirby J said in Petkoska’s case at 300:
If the propounded "injury" is distinct from the underlying pathology that constitutes a "disease" that directly or indirectly caused the sudden event to occur, it is unnecessary to proceed to the alternative and additional basis whereby, in such cases, compensation may also be recovered for the disease process if the statutory preconditions are met.
44. It is analogous with what Toohey, McHugh and Gummow JJ said in Zickar’s case at 334:
It may be accepted that the aneurism was an autogenous disease but the appellant's claim to personal injury within para (a) is based on the rupture which occurred.
45. It is not a prerequisite to finding an injury was sustained that the event or incident involves a rupture or breaking. As Finn and Merkel JJ of the Federal Court of Australia said in Petkoska’s case (and this was not the subject of argument before the High Court), an occlusion, causing a disturbance of the normal physiological state, will suffice.
46. The occlusion which occurred in Mr Brunt’s pulmonary artery or arteries clearly caused a disturbance of his normal physiological state. That event was distinct from the underlying disease, DVT. Therefore, I do not accept Mr Lenczner’s submissions on this point. Furthermore, I find although Mr Brunt may have suffered from a further or new massive pulmonary embolism on 17 November 2000 which resulted in his cardiac arrest that does not alter the fact that he suffered an injury on 14 November 2000. This is despite the fact that Dr Baker said in cross-examination that DVT and pulmonary embolism are one and the same disease, collectively known as venous thromboembolism. While I have no doubt that many medical practitioners would disagree with the distinctions which have been drawn by the courts between injury and disease, I am bound by those decisions. Discrete events involving rupture, breaking or occlusion which cause a disturbance of the normal physiological state, although arising out of an autogenous disease, are properly described, for the purposes of the SRC Act, as an injury simpliciter. Accordingly, I find that Mr Brunt suffered an injury simpliciter shortly after his arrival at Sydney airport at about 6.20pm on 14 November 2000. In order to satisfy the definition of injury in s4 (1) of the SRC Act, Mr Brunt’s injury must have arisen out of or in the course of his employment.
ARISING OUT OF OR IN THE COURSE OF EMPLOYMENT
47. Much has been said, in many cases, about the two expressions, arising out of, and arising in the course of, employment. Many of these cases were discussed in detail in Kavanagh, Zickar and Petkoska’s case.
48. In Kavanagh’s case, Dixon CJ referred to the expression arising out of and in the course of employment being replaced in the Commonwealth Employees’ Compensation Act 1930 by changing the expression so that it became disjunctive. He said, at 556:
Whatever language was chosen to institute the contrast the first expression was treated as requiring a causal connexion between the employment or its incidents and the second as requiring that the pursuit of the employment should be an accompanying condition.
49. Dixon CJ formed the view that the words arising in the course of employment did not connote or imply even a slender causal connection with employment. This was supported by Fullagar J who said at 558:
… The conclusion seems inevitable that the main object of the changing of the conjunction was to eliminate the necessity of finding such a causal connexion. If there was such a causal connexion, the injury was to be compensable even though it did not occur while the worker was engaged in his employment or anything incidental to his employment. If, on the other hand, the injury occurred in the course of the employment, it was to be compensable even though no causal connexion could be found between it and the employment. And it necessarily follows, I think, that the words "arising in the course of his employment" ought not to be regarded as meaning anything more or less than "arising while the worker is engaged in his employment".
50. Taylor J canvassed the authorities in detail and said that (at 564):
…by no means all of those who have attempted to explain the expression “in the course of the employment” have assigned a merely temporal denotation to it.
He also noted that the general tendency had been to identify the course of the employment with the performance of the duties of the employment or other activities incidental to it. Taylor J concluded that in order to fall within the expression in the course of, it would have to be shown that an applicant sustained his injury in the course of performing the work which he was employed to do or in the course of doing something incidental to that work (at 568-569).
51. Menzies J was of the view that a review of the cases led to the conclusion that if a worker was injured while doing something incidental to what he was employed to do, that would be sufficient and no other association between the injury and the work was necessary (at 572).
52. Although the statute which the Kavanagh Court had to interpret referred to injury by accident, which expression does not appear in the SRC Act, I am of the view that the analysis of the expressions arising out of, and in the course of is applicable to this case.
53. Mr Brunt’s pulmonary embolism occurred during his travel from Melbourne to Sydney to attend work-related meetings with colleagues. Although I accept it could not properly be said that his injury occurred while he was engaged in his employment, and therefore it could not be said to have arisen out of employment, the travel to Sydney was clearly an activity incidental to his employment. There was no contradictory evidence regarding the purpose of the travel. Therefore, I find that the injury sustained by Mr Brunt as a result of pulmonary embolism on 14 November 2000 was an injury for the purposes of the SRC Act.
DID MR BRUNT’S PULMONARY EMBOLISM RESULT IN HIS DEATH
54. In order for Ms A’Beckett to succeed in her claim, she must satisfy s 17(1) of the SRC Act. It states that s 17 applies where an injury to an employee results in death.
55. The courts have said much about the meaning of the expression results from or causes. It matters not, in my opinion, that the expression in s 17 uses the stylistically different expression: ie results in. There can be no doubt that the expression imports a notion of causation as was explained by the New South Wales Court of Appeal in Migge v Wormald Bros. Industries Ltd (1972) 2 NSWLR 29. Asprey JA said that the expression takes up the concept of causation as it is known to the law, without seeking to modify it. He then said, at 44:
The legal concept of causation when applied to the field of personal injury takes the person injured as it finds him, with all his pre-dispositions and susceptibilities, whatever they may be.
56. It has also long been accepted that the cause of a work injury or death resulting from an injury sustained in the course of employment need not be direct. In Comery v New Hucknall Colliery Co (1919) 12 BWCC 1, Scrutton LJ said, at 9:
Now, the claimant under the Workman’s Compensation Act must prove an accident arising out of and in the course of his employment, and that injury or death resulted from it. The result need not be a direct or natural or even probable consequence of the accident if in fact it is a result of the accident. It is enough that the accident caused or contributed to or accelerated death, and it appears from the authorities that the accident may contribute to the death if it causes such a state of things in the man’s body that he is physically more susceptible to the cause which ultimately kills him.
This passage by Scrutton LJ was cited with approval in Ewers v Curtis (1933) 26 BWCC 553, at 557. Romer LJ said, at 558:
If the dependants show that the accident has caused the body of the workman to be more susceptible to the disease which kills him, it is enough; and it is not necessary to prove, what is impossible to prove, that if he had not been injured he would not have caught the disease.
57. The High Court of Australia (Williams J), in Deeble v Nott (1941) 65 CLR 104, referred with approval to the House of Lords decision in Lyons v Woodilee Coal and Coke Co (1917) S.C.(H.L.) 48 where Lord Buckmaster said:
… that as there are many causes of most events, it (ie the connection between the work and the disease) must be a connection which is not, as a matter of common sense, too remote.
58. When dealing with the case where incapacity resulted from a compensable injury, Bray CJ, of the Supreme Court of South Australia, said in Bratovich v Rheem (Aust) Pty Ltd (1971) 2 SASR 33, at 40:
It is clear law that it is not necessary for an incapacity to result solely from a compensable injury before compensation is payable as a consequence of that injury: Harwood v Wyken Colliery Co. …
It has long been accepted that if a man suffers from a condition such as a heart disease which will in any event totally incapacitate him at some time and an employment injury precipitates the development of the disease and incapacitates him then and there, he is entitled to compensation in respect of that injury.
59. My attention was also drawn to the text Principles of the Law of Workers’ Compensation Particularly in Victoria by E F Hill and J B Bingeman, 1981, where the authors deal with the chain of events leading to incapacity or death. They state, at 75:
It is unnecessary that the death or incapacity was the natural or probable consequence of the injury; it is sufficient that the death or incapacity results from the injury (or was materially contributed to by the injury) by a chain of causation unbroken by any novus actus interveniens (Morris v George; Bushby v Morris). Where, for example a man died of myocardial infarction (death of part of the heart muscle due to depravation of oxygenated blood) which was the last of series of infarctions and of itself not work related, it was sufficient that death from that infarction was more probable because the first of the series caused such damage that it was probable that death would ensue from infarctions subsequent to the first from which there had been no complete recovery (Conkey & Sons v Miller).
60. The Court of Appeal in Kooragang Cement Pty Ltd v Bates (1994) 35 NSWLR 452 examined the application of the phrase results from in the context of the 1926 and 1987 New South Wales Compensation Acts. Kirby P explained that the expression is not a term of art but rather an ordinary English phrase. He also explained that it was appropriate to take into account the fact that the phrase appeared in a compensation statute. He then said, at 461:
Such a statute should not be construed narrowly, for it provides benefits which are extremely important to those affected. By the same token, the statute may not be construed unrealistically so as to stretch unreasonably the burdens imposed upon employers and their insurers. Those burdens require a relevant employment connection, as defined in the statues, before compensation will be held payable.
From the earliest days of compensation legislation, it has been recognised that causation is not always direct and immediate.
61. Kirby P referred to the old decisions in Dunham v Clare [1902] 2 KB 292 and the Ystradowen Colliery Co Ltd v Griffiths [1909] 2 KB 533, a decision of the English Court of Appeal. He then said, at 462:
Since that time, it has been well recognised in this jurisdiction that an injury can set in train a series of events. If the chain is unbroken and provides the relevant causative explanation of the incapacity or death from which the claim comes, it will be open to the Compensation Court to award compensation under the Act.
62. After considering a number of other cases, Kirby P said, at 463 – 464:
The result of the cases is that each case where causation is in issue in a workers’ compensation claim, must be determined on its own facts. Whether death or incapacity results from a relevant work injury is a question of fact. The importation of notions of proximate cause by use of the phrase “results from”, is not now accepted. By the same token, the mere proof that certain events occurred which predisposed a worker to subsequent injury or death, will not, of itself, be sufficient to establish that such incapacity or death “result from” a work injury. What is required is a commonsense evaluation of the causal chain. As the early cases demonstrate, the mere passage of time between a work incident and subsequent incapacity or death, is not determinative of the entitlement to compensation. In each case, the question whether the incapacity or death “results from” the impugned work injury (or in the event of a disease, the relevant aggravation of the disease), is a question of fact to be determined on the basis of the evidence, including, where applicable, expert opinions.
63. When I began hearing this case on 28 October 2008 the only evidence available to both parties regarding the cause of Mr Brunt’s death was a translation of a death certificate. In that certificate the cause of death was said to be:
Bleeding under the membrane(s) of the brain’s right hemisphere.
The translator’s note on the death certificate stated that the translation was a literal translation of the Thai text. According to the translator, the lack of contextual information made it impossible to identify where exactly in the brain the bleeding occurred. Understandably, because Mr Brunt had been prescribed the anticoagulant drug Warfarin as a result of his blood clotting problems, the initial medical reports focused on the possible relationship between Mr Brunt’s use of Warfarin and the bleeding referred to in the death certificate.
64. However, by the time the hearing of this matter resumed in May 2009, Comcare’s solicitors where able to obtain a translated autopsy report and a Royal Thai Police case report. The Thai police report set out the circumstances in which MrBrunt’s body was discovered in a hotel room in Bangkok on 1 September 2005 at about 1.00pm. It stated there was no evidence of any fighting or attack. Mr Brunt’s body was discovered on his bed, kneeling at the left hand edge of the bed with his arm crossed over his chest, face down and feet pointing towards the end of the bed. The police report also said that Mr Brunt’s body was sent to the Forensic Institute, Chulalongkorn Hospital, for autopsy in order to determine the cause of death. It also said that three types of medication were identified amongst his belongings; although the exact nature of that medication was not identified.
65. The autopsy report described the cause of death as:
Mild haemorrhage under the membrane(s) of the brain with Acute Myocardial Infarction caused by Coronary Artery Disease.
The autopsy report records that 20 millilitres of subdural haemorrhage was found on the right hemisphere of the brain. As far as Mr Brunt’s heart was concerned, the autopsy report stated:
700 grams in weight, significantly enlarged, with a large number of adhesions between the epicardium and pericardial sac, left and right ventricles were 1.9 centimetre and 0.9 centimetre in width respectively, left and right coronary arteries were about 90-95% constricted, dead cardiac muscles – both old and new – were found in large area of wall of ventricles, atherosclerosis found in the aorta.
The histopathology results with respect to the heart were described as:
Cardiac muscle nucleus generally enlarged and congested, a large number of fibrus found accumulated in cardiac muscle cells, accumulation of fats and thickening of coronary arteries found.
Of the kidneys, the autopsy report stated:
Acute tubular necrosis found in ureteral cells, renal artery wall thickened.
66. Laboratory results following the autopsy recorded no alcohol or Digoxin in the blood sample and no amphetamines/methamphetamines, opiates, benzodiazepines, or antidepressant groups in the urine sample.
67. After Comcare’s solicitors obtained the autopsy report, a number of further medical opinions were sought regarding the cause of death. The focus shifted away from bleeding on the brain to acute myocardial infarction caused by coronary artery disease. Professor Anthony J Landgren, a specialist in anatomical and forensic pathology, prepared three written reports for this hearing. In his first report dated 25 August 2007, Professor Landgren opined that Mr Brunt died from an intracranial haemorrhage as a complication of Warfarin anticoagulation therapy which had been prescribed following a pulmonary embolus. However, having subsequently been given a copy of the translated autopsy report, Professor Landgren agreed with Professor David Ranson, a specialist in forensic medicine and pathology, that the subdural haemorrhage described in the translated death certificate and the autopsy report was of low-level significance and it was unlikely to have caused Mr Brunt’s death. Dr Baker also agreed that the small subdural haematoma was not likely to be a significant factor in the cause of death.
68. In essence, Ms A’Beckett submitted that from the day in November 2000 that Mr Brunt suffered a pulmonary embolism at Sydney airport after the flight from Melbourne, he experienced a continuous process of going down hill. Mr Spittle QC, on behalf of Ms A’Beckett, said there was a series of events which occurred culminating in Mr Brunt’s death at a significantly early point in his life, at the age of 41.
69. Mr Spittle submitted that the pulmonary embolism suffered by Mr Brunt led to significant physiological changes including cardiomegally (enlargement of the heart) and scarring (adhesions) on the surface of the heart. Each of those conditions by themselves would be significant in a context of establishing the cause of death. However, they acted jointly to give rise to the terminating event. He submitted that it would be wrong to artificially single out one or more of those events to establish a cause of death. Although Mr Spittle agreed that the aetiology of coronary artery disease was distinct from development of a pulmonary embolus, he submitted the diseases nevertheless had factors in common. In any event, Mr Spittle submitted that coronary artery disease was merely one of the aspects of the entire picture which led to Mr Brunt’s death. According to Mr Spittle, the test as far as s 17 of the SRC Act is concerned, only requires that Mr Brunt’s pulmonary embolism materially contributed to his death. However, as Kirby P said in the Kooragang Cement case, mere proof that certain events occurred which predisposed a worker to subsequent injury or death will not, of itself, be sufficient to establish that such incapacity or death resulted from a work injury. What is required is a common sense evaluation of the causal chain.
70. According to Professor Landgren, survivors of massive pulmonary embolism are known to be at increased risk of cardiovascular events. Cardiovascular events include acute myocardial infarction, right and left heart failure due to increased pulmonary blood pressure, recurrent pulmonary embolism and the complications of anticoagulation therapy. Professor Landgren said that in the Australian context, Mr Brunt’s autopsy report could describe the cause of death as:
… acute myocardial infarction in a man with severe coronary artery disease, severe heart enlargement and a significant past history of massive pulmonary embolism treated by surgical embolectomy and ongoing anticoagulation.
71. Professor Landgren said the cause of Mr Brunt’s death should recognise his significant past history of massive pulmonary embolism and the strong association this has with subsequent fatal cardiovascular events. It should also recognise other significant autopsy findings including heart enlargement.
72. Professor Landgren explained that the relationship between heart enlargement and pulmonary embolism was complex and not well understood. There were a number of possible explanations why the heart can enlarge after a person has suffered pulmonary embolus, including ongoing obstruction to the pulmonary arteries causing raised blood pressure within the heart, and the heart muscle having to work harder. He said that Mr Brunt’s cardiac arrest was most likely due to the fact that he had previously experienced a large pulmonary embolus. In fact, Professor Landgren described Mr Brunt as having had a massive pulmonary embolism; having to have his chest opened to remove the clot; and having ongoing medical treatment.
73. Professor Landgren’s description seems to me to refer to the event which took place when Mr Brunt was in Knox Hospital on 17 November 2000 which resulted in his cardiac arrest. What Professor Landgren was referring to, it seems, was the large occlusion referred to as a saddle clot which was removed by surgery. If, for the purposes of the SRC Act, an occlusion constitutes an injury, then it may be that the event which took place at Knox Hospital on 17 November 2000 could be properly described as a second injury. Both Dr Salem and Dr Baker described a small piece of the thrombus breaking off and causing the symptoms Mr Brunt experienced in Sydney, but then a larger piece breaking off while he was in Melbourne which in fact occluded the main pulmonary blood vessels. While it might be arguable that, for the purposes of s 17 of the SRC Act, Mr Brunt’s death must be causally related to the occlusion he suffered shortly after disembarking on the flight from Melbourne to Sydney, rather than the event which took place at Knox Hospital two days later, I am not prepared to distinguish between the two events. That is because the evidence does not permit me to be more precise about whether the saddle clot which caused Mr Brunt’s cardiac arrest on 17 November 2000 was a discrete event. As Dr Salem said, it is common when scans are conducted on people who have had a clot in the lung to find multiple clots. In fact, essentially, they have multiple clots. Although Dr Baker said that a saddle clot or embolus means a large free-forming clot that goes to the lungs rather than smaller clots that go to the periphery of the lungs, in his view, this was all part of the dynamic process. He described it as the continuum of the disease of DVT and pulmonary embolism.
74. Mr Lenczner put to Professor Landgren that Mr Brunt’s pulmonary embolism did not play any part in the creation of his heart enlargement. Professor Landgren disagreed and said that massive pulmonary embolism has a strong association with subsequent heart enlargement due to problems with pulmonary hypertension, which is an increase in the blood pressure on the right side of the heart. He agreed there was no evidence in any medical records that Mr Brunt suffered from pulmonary hypertension. However, Professor Landgren said that where a major blood clot lodged at the origin of the pulmonary artery, there were also very likely to be smaller blood clots going further into Mr Brunt’s lungs, obstructing small vessels in positions where they could not be removed surgically. Because of those obstructions, Mr Brunt’s blood pressure would have increased; and to overcome that increase in pressure, his heart had to work harder. As a consequence, his heart muscle would have thickened and there may also have been secondary affects going to the other side of the circulation producing generalised heart enlargement. He said that the right side of the heart begins to enlarge first and then subsequently, there is whole heart enlargement.
75. Professor Landgren explained that in his experience (from autopsy examinations and having seen hundreds of persons who have died from massive pulmonary embolism), when persons died acutely, that is soon after they have had the pulmonary embolism, almost invariably they had smaller blood clots scattered throughout their lungs blocking the small pulmonary vessels. However, as Professor Landgren conceded, in those cases there was no evidence of an enlarged heart because the persons he was referring to had died straight away. He agreed that it took months or possibly years before heart enlargement might become evident. Professor Landgren was also asked about the effect of the Warfarin dissolving any emboli which might develop. He agreed that was part of the role played by Warfarin and it was also designed to prevent the development of clots. However, Professor Landgren said the medication is not perfect and that anticoagulation did not solve all of the problems. He explained that surgery would not have been effective in removing ongoing smaller clots in his lungs and those clots went through a process called organisation and scarring which, effectively, permanently blocked off small blood vessels. He said a second cause might be systemic hypertension. He also explained that coronary artery disease heart enlargement is most commonly due to dilation of the heart. The heart expands because the muscles are so badly damaged that they no longer function properly.
76. Professor Landgren was asked whether in every case after pulmonary embolism with accompanying treatment of anticoagulation medication, the patient would end up with scarring on the smaller arteries as a consequence of emboli remaining there. He said he didn’t know. He said there was some reserve capacity in the pulmonary vessels and there must be a significant effect on the smaller vessels to get to the point where a patient develops pulmonary hypertension. He agreed there was no evidence to suggest that Mr Brunt’s pulmonary embolism was in any way related to his coronary artery disease. Professor Landgren was firmly of the view that Mr Brunt’s enlarged heart was a contributing factor to his death. He said that an enlarged poorly functioning heart, if subsequently affected by problems with blood supply to the muscle (resulting from coronary artery disease) is more prone to suddenly stopping or going into an abnormal rhythm. It is an additional reason why the heart might stop working. Professor Landgren considered it incorrect to attempt to separate out the cause of death resulting from coronary artery disease from heart enlargement. Although not referred to in the autopsy report, in his opinion, to ignore a heart that was twice normal size in circumstances where a person has died suddenly with a significant history of massive pulmonary thromboembolism would be incorrect. He insisted that Mr Brunt’s death was multifactorial and to single out one component would be misleading.
77. Professor Landgren also said that the medical literature as it currently stands shows a strong association between early death and the events of a clinically significant pulmonary thromboembolus. He referred to two research studies: The first entitled ‘A Prospective Study On Cardiovascular Events After Acute Pulmonary Embolism’, published in the European Heart Journal in January 2005 (the Becattini Study); and the second entitled ‘Acute Pulmonary Embolism: Clinical outcomes in the International Co-operative Pulmonary Embolism Registry’ (ICOPR), published in The Lancet in April 1999 (the Goldhaber Study). Referring to the Becattini Study, Professor Landgren said it was the largest prospective study of medium to long term survivors of pulmonary embolism. According to Professor Landgren, it demonstrated that cardiovascular events are the major cause of death in patients who have survived a clinically significant acute pulmonary embolism and that they were subject to at least a tenfold increase in risk compared to an aged matched population. The Goldhaber Study disclosed a similar increased risk.
78. The authors’ of the Becattini Study admitted that a potential limitation of that study was that it did not include a control group. Professor Landgren did not see this as significant, stating this was a prospective study of cardiovascular events and he could not imagine a control group for a prospective study of thromboembolism other than people who hadn’t experienced that condition. He said it was not a form of research where one would have a control group. The research was phenomenological in nature looking at a group of people with a specific problem rather than comparing one treatment against another. Mr Lenczner also pointed out to Professor Landgren that there was no control group in the Goldhaber Study. Again, Professor Landgren said it was phenomenological research, looking specifically at people suffering from a diagnosed problem and their outcomes. Mr Lenczner suggested to Professor Landgren that he did not have any particular speciality. Professor Landgren disagreed and said that one of his diagnostic specialties was cardiac pathology. He said that in over 7,000 autopsies, he had seen hundreds of cases of acute pulmonary embolism and probably hundreds and hundreds of cases of people who have died as a result of cardiac enlargement, and thousands who have died from coronary heart disease. However, he conceded that he could not recall one case which is a precise match to this case.
79. As far as the adhesions were concerned, Professor Landgren indicated that there are multiple causes including damage to the heart muscle. He did not believe that the adhesions found on autopsy played a significant part in Mr Brunt’s death. He agreed that the possibility of the acute myocardial infarction having been the cause of the adhesions should be excluded. However, the adhesions may have resulted from some previous damage to the heart muscle. In summary, Professor Landgren was careful to state he was not claiming there was necessarily a causal relationship between pulmonary embolism, an enlarged heart and myocardial infarction. He repeated that the mechanisms were not well understood and the research demonstrated strong associations which he had observed in the course of his work as a pathologist. He agreed that the two studies to which he referred were not designed to establish cause. Rather, they were designed to identify risks which patients face after they have had an acute pulmonary embolism. Professor Landgren agreed that Mr Brunt’s death, at age 41 years, was significantly earlier than would have been expected.
80. In his report of 19 March 2009, Professor Ranson said the discovery of the autopsy report regarding Mr Brunt was critical to understanding how and why he had died. However, he cautioned it did not mean the conclusions in the report were necessarily true and correct and, in this particular case, there were issues of translation which may arise to complicate the scenario or the death investigation. Professor Ranson was of the same view as Professor Landgren regarding the subdural haemorrhage found following Mr Brunt’s death. In his opinion, that bleeding would not, on its own, have had any significant impact on the cause of Mr Brunt’s death. Relying on the autopsy findings, Professor Ranson said Mr Brunt died of his heart disease. In his opinion, Mr Brunt’s heart disease was ischaemic heart disease and it was due to narrowing of the coronary arteries supplying the heart muscle with blood. He said this pathology developed in conjunction with enlargement of the heart which may have originated from high blood pressure as disclosed by the thickening of renal arties on microscopy of the kidneys. He suggested, in the context of an Australian death certificate, the cause of death could be given as:
1(a) acute myocardial infarction; and
2(b) coronary artery disease.
81. Professor Ranson was asked why he did not include the enlargement of Mr Brunt’s heart as part of the cause of death. While accepting that enlargement of the heart can be a cause of death in its own right, Professor Ranson said in this particular case there was evidence from the autopsy report of scarring of the heart, and in fact new damage – ischaemic change of the heart in keeping with the coronary artery disease, occlusion, and as the most direct and immediate cause of death, acute myocardial infarction of the heart muscle associated with the narrowing of the coronary arteries.
82. Professor Ranson said the significance of the enlargement of the heart was far more difficult to ascertain. He explained there were a number of possible ways in which a person might get enlargement of the heart and they relate to systemic diseases where the heart muscle is put under great strain; and also to anatomical problems such as valvular disease and so on. He said essential or natural hypertension will also cause enlargement of the heart because it places it under greater working strain. Where a person has a pulmonary thromboembolism there was a period of time when the person may well have had a greater strain placed on the right side of their heart. This was because the right ventricle, which is responsible for pumping blood to the lungs, is attempting to force blood through a blockage thus placing the right side of the heart under greater strain, and that may cause the right side of the heart to enlarge. However, the blockage would need to be there for some significant time for the enlargement to occur. If that were the case, it might have become clinically apparent if there had been regular medical attendances, which he believed was the case with Mr Brunt.
83. Because Mr Brunt’s heart was enlarged on both the left and right sides, and the left side was not usually associated with pulmonary obstruction issues, it was Professor Ranson’s view that the overall enlargement was generally related to issues surrounding essential hypertension or other factors which could cause left side enlargement. He explained that the measurements of 1.9 centimetres and 0.9 centimetres in width of the left and right ventricles respectively were a reference to thickness rather than width (a translation problem) and they indicated that both of those chambers were enlarged or thickened. Professor Ranson also explained that there was a wide variety of disease processes that can be associated with enlargement of the wall of the left ventricle including ischaemic heart disease and other conditions such as hypertension which may be associated with arteriosclerotic disease of the arteries. The fact that the autopsy disclosed a thickening of arteries in respect of the kidneys (renal disease) was a feature associated with hypertension.
84. As far as enlargement of the right side of the heart is concerned, Professor Ranson said there was no evidence to suggest that Mr Brunt had a significant load on the small vessels from the embolism to suggest that his right heart was put under significant strain. While he agreed it can happen in some situations where pulmonary embolism occurs, he said there was no direct evidence of that in Mr Brunt’s case.
85. Professor Ranson was also referred to the Becattini and Goldhaber Studies. He said there was much ongoing research on the connection between arteriosclerotic diseases and diseases associated with DVT and its complications upon the embolism. Although Professor Ranson agreed there was a cluster of information indicating that people who develop a pulmonary embolism have a possible increased risk or relative risk of another disease, the studies did not postulate exactly how that occurs. He said an association is not necessarily indicative of causation and that is an important distinction. He explained that some of the features of an association with DVT and an association with cardiovascular disease may have their origins in a common risk factor. That does not mean to say that one is itself causative of the other.
86. When asked whether his experience of some 30 years as a pathologist had caused him to make an association between pulmonary embolism and enlarged heart disease, he said because he had not carried out a formal study, he could not say that was the case. Although he was certain there were occasions when a person with pulmonary embolism subsequently had ischaemic heart disease, he had no evidence as a result of this experience to indicate that this was a pattern or trend. On the other hand, he said that coronary artery arteriosclerosis is something which in his experience was very commonly associated with damage to the heart muscle and his observation was confirmed by the clinical literature linking angina and ischaemic heart disease and myocardial infarction with the narrowing of coronary vessels.
87. Under cross-examination Professor Ranson accepted the proposition that the tests applied by science to the question of causation are very different from the tests applied by the law. Nevertheless, he said he was trying to give his opinion as a pathologist on what he considered to be his view and interpretation of the material. He was not attempting to apply a legal test, which he correctly said was for the Tribunal.
88. Professor Ranson agreed he could not discount the possibility that as a result of Mr Brunt’s pulmonary embolism, he suffered some damage to the heart muscle. He also agreed that because of the degree of coronary occlusion identified, Mr Brunt was at risk of sudden death at any time, but particularly when he may have been physiologically stressed. While he agreed that sudden death of an individual in their early forties was rare, he nevertheless said that such deaths did occur and even occurred at a younger age. But it was not a regular occurrence.
89. Professor Ranson was taken to the reference in the autopsy report to old and new death of the heart muscle. He said there was some difficulty with the exact meaning of the terms used in the report and in particular the word fibrous which he presumed was intended to be fibrosis which was found accumulated in cardiac muscle cells. He explained you do not get fibrosis in the cells but rather around them. He said where one has a dense scar indicating a critical event causing damage and death of the heart muscle, that would normally be referred to as an old myocardial infarction. However, individuals who have a narrowing of their coronary arteries may suffer from wide spread areas of patchy fibrosis in the myocardium which is often referred to as the broader anatomical appearance of ischaemic heart disease. He was unable to say whether the autopsy report was referring to one or the other and therefore could not be positive that Mr Brunt suffered a major myocardial infarction. He agreed that the availability of a clinical medical background was of great importance in ascertaining the cause of death.
90. Under cross-examination regarding the Becattini and Goldhaber Studies, Professor Ranson again said that while those studies might provide useful information regarding association, they do not normally provide good information regarding causation. He said although association data provides useful research data when one is looking for how patients might be managed and to prevent certain cardiovascular events occurring in the future, they did not provide a pathological proof of causation. In fact, he explained that associations may simply disclose there are common factors involved. They are good for assisting clinicians in deciding the best way to manage potential risk and provide supportive treatment of preventative measures looking at lifestyle changes. By controlling a range of associations, it might be possible to influence the occurrence of the event but it does not mean to say the cause is known.
91. Mr Spittle suggested to Professor Ranson that if Mr Brunt had not had a pulmonary embolism he would have lived on beyond the age of 41. Professor Ranson said he was not sure that he could answer that question because it depended on the particular weight which was given to various pieces of the evidence. He said Mr Brunt had very severe coronary artery disease and he had a myocardial infarction, fresh death of heart muscle, which he believed occurred in association with the blockage of those arteries. Mr Brunt could have died at a range of times depending on the level of occlusion of his coronary arteries and depending on the level of physiological stress which his body might have been under. He said he had seen sudden death in people in their forties and in their thirties and twenties with the type of coronary artery occlusion disease suffered by Mr Brunt, and although it was rare in the younger age groups, it certainly happened.
92. Professor Ranson also explained that the lack of the use of a control group in the Becattini Study did impose some limitations. He said there was a need to be able to compare the study group which had the problem being followed up, with a study group that didn’t have the problem, and then to observe the relative difference between them. He said that was an important part of a study and, although not an associated study, it is an area which tends to help show the significance or reality of the increased risk. As far as reference to new death of the heart muscle was concerned, particularly in the context of the blockage of the coronary arteries, Professor Ranson said it appeared to him that there was a newer event, although occurring in a setting of established coronary artery disease, which appeared to be the main problem and in fact the cause of death.
93. Dr Baker provided a report dated 13 May 2009. In that report Dr Baker said the most likely cause of Mr Brunt’s death on 1 September 2005, based on the information from the autopsy report, was significant coronary artery disease. This had caused an acute myocardial infarction and probably led to arrhythmia resulting in sudden death. Dr Baker also referred to Mr Brunt’s general practitioner’s records indicating he had multiple risk factors for premature coronary artery disease, including treated high cholesterol, treated high blood pressure and that he was overweight with a calculated body mass index of 29.2. He said it was likely Mr Brunt’s premature coronary artery disease produced the acute myocardial infarction causing his death. It was his view that those events were unrelated to any of the events which occurred in 2000 relating to Mr Brunt’s pulmonary embolism.
94. The enlargement of Mr Brunt’s heart, according to Dr Baker, was more likely to be the result of his coronary artery disease because of evidence of previous myocardial infarction. That indicated Mr Brunt had previous events which contributed; and it was well known that in persons who have a tendency for ongoing myocardial infarction, the heart slowly dies. It copes with that by dilating and that is what was disclosed by the post-mortem. It was not just one side of the heart that was dilated which may be seen as the result of a massive pulmonary embolism, but the whole heart, left and right side; and that was very consistent with coronary artery disease. Dr Baker was of the opinion that the pericardial adhesions were insignificant and were unlikely to be the cause of Mr Brunt’s death.
95. Dr Baker was referred to Professor Landgren’s evidence that small emboli remained permanently in Mr Brunt’s lungs resulting in pulmonary hypertension which then led to the enlargement of his heart. Dr Baker said that such an explanation was problematic because the lungs often, unlike the heart, have a duel blood supply and there is quite a degree of room for repair, after a pulmonary embolism, to enable the lungs to go back to completely normal. He said it often surprised him seeing people come in acutely unwell, having had a cardiac arrest, and with appropriate treatment with anticoagulation, within a week they would be back to normal. He said without anticoagulation medication, if a person had a predisposition for the development of thrombosis, and further thrombosis occurs, further pulmonary emboli may well occur. That would cause pressure to build up in the heart because the lungs become clogged with the clot. He said often these people are not on anticoagulants or they have further thromboembolism of which they may not be aware; although what brings them to the attention of doctors is that they may become very symptomatic, for example, shortness of breath on exertion. That would indicate further thromboembolism and pulmonary hypertension which predominately affects the right side of the heart rather than both sides of the heart.
96. The fact is that the post-mortem showed heart damage and coronary artery disease and this is a very common cause of dilated cardiomyopathy. If Mr Brunt had significant pulmonary hypertension, he would have been very unwell. According to Dr Baker, because Mr Brunt was using Warfarin, that would have been protecting him from further thromboembolism. He said it was very uncommon for people to develop pulmonary hypertension while on anticoagulants.
97. Dr Baker also referred to the Becattini and Goldhaber Studies relied on by Professor Landgren. In his view, the association between pulmonary embolism and DVT with premature cardiovascular events such as acute myocardial infarction is likely to be due to the common risk factors for the two diseases rather than a cause and effect relationship. He also pointed out that in the Becattini Study, the association was only apparent after anticoagulation therapy had ceased. He understood Mr Brunt to be on anticoagulation medication. He described the distinction between association and causation in the following way:
… association means things that are found in common and the causation is actually a pathology resulting in a disease.
98. Dr Baker also said the circumstances referred to in both studies were different from those experienced by Mr Brunt. He noted that the Becattini Study group were people who developed DVT or pulmonary embolism, had a period of anticoagulation and then after their anticoagulation stopped there was an observation not only of having recurrent thrombosis but also coronary artery disease. The most important difference in this study was that the group observed had stopped Warfarin therapy. As for the Goldhaber Study, he said it did not provide much assistance because it looked at people presenting with thromboembolism and looking three months after the event. He said it was not surprising that the major cause of death, which was cardiovascular, resulted from the recurrence of thrombosis in the three month period on anticoagulants. Only around one per cent of people in that study suffered from coronary artery disease and the population was more elderly. The average age was in the sixties. This was very different to Mr Brunt’s situation.
99. In cross-examination Mr Spittle suggested to Dr Baker that as a result of the massive pulmonary embolism Mr Brunt suffered while at Knox Hospital, there was damage to the heart muscle. Dr Baker disagreed and explained there was a difference in damage to the heart muscle as opposed to cardiac arrest. He explained that a saddle embolus which occludes the heart muscle may cause a cardiac arrest due to the blockage of blood flow. However, that does not result in heart muscle dying, as the heart muscle is very resilient to hypoxia. He gave the example that in heart surgery, where the heart is stopped for a period of time, the blood flow may cease for up to an hour while bypass surgery is performed. Nevertheless, the heart does not suffer any damage. He said it is very uncommon to have heart damage after a massive pulmonary embolism. There may be some mild inflammation but that is only a transient factor once the blood flow has returned. He said that there are heart changes, which are acute events, simply because of the increased pressure due to the occlusion. That does not equate to damage to the heart muscle.
100. When Mr Spittle suggested to Dr Baker that Mr Brunt’s coronary arteries were normal at the time of the events in November 2000, Dr Baker responded that a normal ECG does not necessarily mean normal coronary arteries but rather, in the absence of evidence, it means the patient does not have significant coronary artery disease. With the type of stress Mr Brunt experienced you would expect to see that. When asked to explain why it was that some five years after the events of November 2000, Mr Brunt was found to have advanced coronary artery disease with 90 to 95 per cent occlusion in the left and right main coronary arteries, Dr Baker said Mr Brunt appeared to have developed premature coronary artery disease and this condition does occur in young people in their thirties and forties. He said those events are uncommon or unusual but they are not rare. He also explained that Mr Brunt’s general practitioner’s records indicated he had a number of risk factors. He was being treated for high cholesterol and hypertension, and he was in the overweight category, bordering on obesity. He said these were well-known risk factors for premature coronary artery disease.
101. Mr Spittle also explained to Dr Baker that prior to the events of November 2000, Mr Brunt had been quite active physically and, after experiencing a pulmonary embolism, there was some immobility. Following the events of November 2000, Dr Clements reported that Mr Brunt would not be able to do any physical activity such as running, and air travel would not be advised. Mr Spittle suggested to Dr Baker that Mr Brunt’s state of immobility would have a bearing on the advancement of the coronary artery disease. Dr Baker agreed that exercise has an impact on all the risk factors associated with coronary artery disease. He said persons who suffer from pulmonary embolism and have surgery resume perfectly normal lives with perfectly normal cardiovascular status. He has seen people with pulmonary embolism at Mr Brunt’s age return to normal activities provided they are on anticoagulants and provided their heart function is back to normal, within six weeks of a massive pulmonary embolism.
102. In Dr Baker’s opinion, Mr Brunt’s cause of death was very clear. He said it resulted from coronary artery disease which, although it may have common risk factors with pulmonary embolism, is a completely separate disease. Therefore, although the two diseases may be related from the perspective of risk factors, they are unrelated in many other aspects. He also said it could be argued that being treated with Warfarin since 2000 would reduce the risk of myocardial infarction due to coronary artery disease.
103. In cross-examination Dr Baker was directed to Professor Landgren’s report regarding the Becattini Study and the increased risk of cardiovascular events. Dr Baker again pointed out that the study examined a group of people who were not on anticoagulation therapy. He said that when referring to cardiovascular risk, the majority of people who presented with pulmonary emboli re-presented with further pulmonary emboli rather than acute myocardial infarction. He said the studies referred to by Professor Landgren were concerned with recurrent pulmonary emboli, in patients who were off anticoagulation medication, and that was the association shown by the studies. He said the Becattini Study shows that the majority of cardiovascular events were recurrent pulmonary emboli. Only one per cent of the deaths in that study were from acute myocardial infarction resulting from coronary artery disease.
104. Although Mr Spittle suggested that the cardiovascular events referred to also included people who were on anticoagulation therapy, Dr Baker pointed out that in the Goldhaber Study, which was only a three month study, the majority of the events referred to were recurrent pulmonary emboli rather than acute myocardial infarctions. He also pointed to the difference in age of the subjects in the two studies and that the second study involved an elderly age group population. When it was put to Dr Baker that it was not possible to say there was no connection whatsoever between cardiovascular events and pulmonary embolism, Dr Baker responded that the common risk factors are the connection between those events. However, the acute myocardial infarction, the actual mechanism which caused Mr Brunt’s death, was probably unrelated.
105. The cases to which I have referred above make it clear that the connection between Mr Brunt’s pulmonary embolism and his death need not be direct or immediate. However, the connection must not, as a matter of common sense, be too remote; and mere proof that certain events occurred which predisposed Mr Brunt to myocardial infarction will not be sufficient to establish the causal connection. I am required to evaluate the causal chain, from a common sense perspective. In doing so, I am mindful of the fact that medical science relies on a significantly higher standard before a causal connection will be found.
106. The expert medical opinions which were drafted prior to the discovery of the autopsy report are not of any assistance to me in establishing causation. That is because they focused on the death certificate statement indicating the cause of death was bleeding under the membrane of the brain’s right hemisphere. Following the production of the autopsy report, all three medical experts who provided opinions as to the cause of Mr Brunt’s death agreed that the small subdural haematoma was not likely to be a significant factor in the cause of death. The dispute lies in whether Mr Brunt’s pulmonary embolism set in train a chain of events which ultimately resulted in him suffering a myocardial infarction in Thailand on 1 September 2005.
107. I find, on the balance of probability, Mr Brunt’s pulmonary embolism which occurred in November 2000 did not result in his death on 1 September 2005. The problem of establishing the causal connection became acute following the location of the Thai autopsy report. Of the three medical practitioners who gave evidence following the production of the autopsy report, only Professor Landgren was of the opinion that a connection existed.
108. Professor Landgren was persuaded by the fact that the autopsy indicated significant heart enlargement and the presence of scarring on the surface of the heart. In essence, Professor Landgren’s opinion was that a causative link existed between Mr Brunt’s pulmonary embolism in November 2000 and his enlarged heart because of smaller clots lodging in his pulmonary arteries, causing pulmonary hypertension. He found support for his opinion in the Becattini and the Goldhaber Studies published in reputable journals. He also relied on his extensive experience as a pathologist.
109. In my opinion, the explanations given by Professor Ranson and Dr Baker for the heart enlargement are more likely to be correct. That is because, as a preliminary point, there was no evidence at all that Mr Brunt suffered pulmonary hypertension at any time in the five years following his pulmonary embolism in November 2000. There is evidence that during that five year period he received regular medical attention but there is no evidence of any symptoms of pulmonary hypertension having developed. I accept Dr Baker’s opinion that if Mr Brunt had developed a significant clinical problem as a result of increased pulmonary artery pressure, some symptoms would have been evident during the regular medical attention he received, particularly shortness of breath on exertion. Furthermore, if Mr Brunt did suffer from pulmonary hypertension, that would have affected the right side of his heart rather than both sides. There was no disagreement between the three medical practitioners about the fact that coronary artery disease causes an increase in blood pressure, which results in dysfunction of the heart muscle causing the entire heart to become enlarged.
110. In addition, as Professor Ranson said in his evidence, although enlargement of the heart can be a cause of death in its own right, in Mr Brunt’s case there was evidence from the autopsy report of ischaemic damage to the heart muscle consistent with coronary artery disease. That appeared to be the immediate cause of death rather than enlargement of the heart. He also said if Mr Brunt’s heart enlargement was due to some form of pulmonary arterial occlusion, it would need to have been there for a significant time for the enlargement to occur. If the heart were to have problems failing as a result of enlargement, it might become clinically apparent, particularly if Mr Brunt was receiving regular medical attention. He also said the fact that Mr Brunt’s heart was enlarged on both sides was not usually associated primarily with pulmonary obstruction issues but more generally related to issues surrounding essential hypertension or other facts which would cause left side enlargement.
111. All of the medical practitioners agreed that the obstruction of Mr Brunt’s coronary arteries was very significant. Although Professor Landgren agreed that it was a significant pathological finding, he nevertheless said there are people walking around in our community who have coronary arteries with that degree of obstruction and who are not having heart attacks. While I accept that to be the case, the autopsy report also referred to old and new heart muscle death. Professor Ranson interpreted that as meaning there was evidence of scarring or fibrosis of the heart muscle and features of more recent ischaemic damage were infarction. According to Professor Ranson, the reference to new death of heart muscle in the context of the blockage of his coronary arteries indicated a very new event and the most likely cause of death. According to Dr Baker, the degree of heart damage found on post‑mortem would indicate that, if the damage could be attributed to his pulmonary embolism in 2000, he would have been unwell from that time with persisting shortness of breath, requiring cardiac medication and further therapy. However, that was not the evidence.
112. Therefore, according to Dr Baker, it is more likely that Mr Brunt developed coronary artery disease after the events of November 2000. This led to minor heart attacks which produced the old heart muscle death and he subsequently had an acute myocardial infarction, being the new muscle death described in the autopsy report, which led to his death. There is considerable logic in this analysis. Furthermore, if that analysis is accepted, it follows that Mr Brunt’s death was associated with coronary artery disease which was not related in any way to his pulmonary embolism.
113. Professor Landgren supported his views about Mr Brunt’s death with the Becattini and Goldhaber Studies. The use to which courts may put epidemiological studies was canvassed in detail by Spigelman CJ in Seltsam Pty Ltd v McGuiness and Another; James Hardie & Coy Pty Limited v McGuiness [2000] NSWCA 29. As Spigelman CJ explained, at [60]:
…epidemiological evidence identifies associations between specific forms of exposure and risk of disease in groups of individuals.
Although epidemiologists do make judgements about whether a statistical association represents a cause and effect relationship, those judgements focus on what is frequently referred to general causation. That is whether or not a particular factor is capable of causing the disease. They do not focus on specific causation; that is, did the particular factor cause the disease in an individual case. He said, at [67]:
Most epidemiological studies identified the strength of an association by a measure called relative risk (RR). RR is defined as a ratio of the incidents of disease in exposed individuals compared with the incidents in unexposed individuals. Therefore a RR of 1.0 means that the exposed individuals have the same risk as unexposed individuals. A RR ratio greater than 1.0 means the risk in exposed individuals is greater than unexposed individuals.
As to the use of epidemiological evidence in legal proceedings, Spigelman CJ said, at [78]:
Epidemiology is, as I have noted above, concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.
and at [79]:
Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn.
114. Spigelman CJ said that the law in Australia is as was stated by Glass JA in Fernandez v Tubemakers of Australia Ltd (1975) 2 NSWLR 190 at 197. In that case, Glass JA said that the finding of a causal connection may be open, without any medical evidence at all to support it or where the expert evidence does not rise above the opinion that a causal connection is possible, only if the evidence offered justifies an inference of probable connection. Whether that standard is met depends on an evaluation of the evidence. Spigelman CJ concluded, at [89]:
In my opinion, evidence of possibility, including epidemiological studies, should be regarded as circumstantial evidence which may, alone or in combination with other evidence, establish causation in a specific case.
115. According to Professor Landgren, the Becattini Study indicated that cardiovascular events are the major cause of death in patients who have survived a clinically significant acute pulmonary embolism. In fact, they have at least a tenfold risk in having a cardiovascular event compared to an age-matched population. The conclusions drawn in the Becattini Study are stated as:
Cardiovascular events are more common in patients with idiopathic pulmonary embolism than in patients with pulmonary embolism associated with transient risk factors. Cardiovascular events are the major cause of death in patients with idiopathic pulmonary embolism.
116. The Becattini Study was conducted over a median follow-up period of 38 months. Three hundred and sixty patients with a first episode of pulmonary embolism were included. The patients’ ages ranged between 18 and 85 years. Patients were included only if they had completed three months of oral anticoagulant therapy without having a recurrence or bleeding. Patients were categorised as patients with idiopathic pulmonary embolism if this occurred in the absence of any transient risk factor for venous thromboembolism. The most significant aspect of the study was that all patients, after receiving an initial three month period of oral anticoagulation, were then randomised to either discontinue anticoagulant treatment, to continue it for an additional three months, or to continue it for an additional nine months. The anticoagulants, Warfarin or Acenocumarol doses were adjusted to achieve a target international normalised ratio (INR) of between 2.0 and 3.0. Patients were instructed to return for follow-up visits at three, six and twelve months from randomisation and every six months thereafter. The study outcomes were cardiovascular events, which were described as recurrent venous thromboembolism, acute myocardial infarction (AMI), stroke and sudden otherwise unexplained death. Cardiovascular death and death due to any cause were also evaluated. Cardiovascular death was defined as any death from pulmonary embolism, AMI, stroke or sudden otherwise unexplained death.
117. During the follow-up period of 38 months, 64 patients experienced at least one cardiovascular event. Of those, one recurrent venous thromboembolitic event and one ischaemic stroke occurred while patients were on anticoagulation treatment, while all the other cardiovascular events occurred after withdrawal of anticoagulant treatment. Of the 64 patients who experienced at least one cardiovascular event, 45 of those presented with recurrent venous thromboembolism, 12 patients with an AMI, 6 patients with stroke and 4 patients with sudden otherwise explained death. Twenty‑three of the recurrences of venous thromboembolism were pulmonary embolism.
118. It should be apparent that there are a number of significant differences between Mr Brunt’s case and the patients involved in the Becattini Study. The first is that those patients who experienced at least one cardiovascular event following a pulmonary embolism had ceased anticoagulant therapy save for two events, one which resulted in a recurrent venous thromboembolitic event and one ischaemic stroke. Although there was some doubt about whether Mr Brunt adhered strictly to his Warfarin regime, ensuring his INR remained between 2.0 and 3.0, the only evidence of failure to comply with his medication regime was at a time when Mr Brunt visited New Zealand when he apparently was tested for Warfarin and the test indicated non-compliance. However, there are numerous pathology reports indicating Mr Brunt generally was compliant. Dr Leyden specifically referred to the pathology reports which, in his 15 June 2007 report, he said he had examined. The pathology reports in evidence between 2001 and 2005 all indicate Mr Brunt’s INR between 1.0 and 3.0. They also indicate that he was regularly attending his general practitioner to have his INR checked.
119. The police report following Mr Brunt’s death in Thailand also indicated that amongst his possessions were three forms of medication. While the medication was not identified, it would seem to indicate Mr Brunt was nevertheless aware of the need to take his medication and that he had it with him on his trip to Thailand in August 2005. Of course I accept there was no evidence that he was in fact taking Warfarin immediately prior to his death. However, on balance, it appears that Mr Brunt was reasonably compliant with his anticoagulation therapy between 2001 and 2005, and his INR was mostly maintained within the recommended limits. I accept that compliance with a long-term medication regime is always a problem. However, the records from Mr Brunt’s general practitioner indicate he was taking Warfarin and that he was attending for follow-up checks. Therefore, it seems to me there is a fundamental distinction between the outcomes described in Becattini Study and Mr Brunt’s case.
120. There is another important factor which has influenced my decision. The predominant cardiovascular event which occurred in 45 of the 64 patients in the Becattini Study was recurrent venous thromboembolism. Only 12 patients out of the study group of 360 (1.07 per cent patients per year – calculated by taking into account the median follow-up period of 38 months) experienced an acute myocardial infarction. As well, the authors of the study admit that the absence of a control group made it difficult to define whether the incidence of arterial events observed in patients with idiopathic (ie disease without recognisable cause) pulmonary embolism was higher than that expected in an age-matched population without pulmonary embolism. This point was raised by Professor Ranson.
121. The Goldhaber Study involved 2,454 eligible patients with acute pulmonary embolism. The primary outcome measure was all-cause mortality at three months. The mean age of the participants was 62.3 years. The median age was 66 years and 63 per cent of patients were aged 60 years or older. Three months after diagnosis with pulmonary embolism, the all-cause mortality rate was 11.4 per cent (280) deaths during the first two weeks after diagnosis and 17.4 per cent (426) at three months. Of the 426 deaths, only five (1.3 per cent) were due to acute myocardial infarction. In fact, 75 per cent of the recorded deaths occurred during the initial hospital admission for pulmonary embolism. Those deaths were most probably due to recurrent pulmonary embolism and the study noted that the frequency might be lowered if more intensive anticoagulation medication was used.
122. One of the basic problems when attempting to compare the results of this study with Mr Brunt’s case is the fact that the study involved an elderly age group population which, according to Dr Baker, results in risk factors for both myocardial infarction and pulmonary embolism being present. In my opinion, neither the Becattini Study nor the Goldhaber Study raises the likelihood of a connection between Mr Brunt’s death and the pulmonary embolism he suffered in November 2000 beyond a mere possibility. While there may be common risk factors involved in pulmonary embolism and coronary artery disease, that does not necessarily mean that pulmonary embolism plays a part in coronary artery disease. In fact, the evidence was that it does not.
123. The problem is that even if the epidemiological studies are regarded as circumstantial evidence, there is no clear link, even on a commonsense basis, between Mr Brunt’s pulmonary embolism and his death in September 2005. The autopsy report, which is clearly the best evidence in this case, describes the direct cause of death as mild haemorrhage under the membrane of the brain with acute myocardial infarction caused by coronary artery disease. All medical practitioners have discounted the brain haemorrhage as being significant and therefore we are left simply with the coronary artery disease causing an acute myocardial infarction. Although Mr Brunt’s heart was significantly enlarged, that can be explained by his coronary artery disease. The fact that his left and right coronary arteries were about 90/95 per cent occluded and there was evidence of both old and new death in his heart muscle, strongly links the cause of death with coronary artery disease. There was no evidence drawing any form of link between pulmonary embolism and coronary artery disease. It is therefore not possible for me to find, on the evidence, that any such link existed. Despite the fact that the link between Mr Brunt’s pulmonary embolism and his subsequent death need not be a direct or natural or even probable consequence, I am unable to find that it caused, contributed to or accelerated Mr Brunt’s death.
DEPENDENCY
124. If I had found that Mr Brunt’s pulmonary embolism resulted in his death, I would have needed to determine whether Mr Brunt’s daughter was wholly dependent on her father at the date of his death. However, although I am mindful of and appreciate the extensive submissions made by the applicant’s representatives regarding dependency, there seems to be no purpose in my making a decision on this issue given my findings above. I have therefore decided not to do so.
CONCLUSION
125. In my opinion, Mr Brunt suffered an injury in the course of his employment on 14 November 2000. However, I have found that the pulmonary embolism suffered by Mr Brunt did not result in his death some five years after that event. His death most likely resulted from an acute myocardial infarction brought on by coronary artery disease. The coronary artery disease was not causally connected to his pulmonary embolism. Accordingly, I find that the decision made by Comcare’s review officer on 28 June 2006 was correct and I affirm that decision.
I certify that the one hundred and twenty‑five [125] preceding paragraphs are a true copy of the reasons for the decision herein of
Mr Egon Fice, Member
(sgd) Olympia Sarrinikolaou
Clerk
Dates of Hearing: 28 ‑ 30 October 2008 and 13‑15 May 2009
Date of Decision: 14 August 2009Counsel for the applicant: Mr S. Spittle (QC)
Mr M. Carey
Solicitors for the applicant: Septimus Jones & Lee Solicitors
Counsel for the respondent: Mr J. Lenczner
Solicitors for the respondent: Sparke Helmore Lawyers
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