Morrison and Repatriation Commission
[2006] AATA 675
•2 August 2006
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2006] AATA 675
ADMINISTRATIVE APPEALS TRIBUNAL )
) No N2005/47
VETERANS' APPEALS DIVISION ) Re VALERIE MORRISON Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mrs Josephine Kelly, Senior Member, and Dr M. Thorpe, Member Date2 August 2006
PlaceSydney
Decision The decision under review is affirmed. [sgd] Senior Member, Mrs Josephine Kelly
Presiding Member
CATCHWORDS
VETERANS’ APPEALS – war widow’s pension – kinds of death argued linked to heavy smoking – hypothesis that Applicant’s operational service caused him to start smoking and that smoking resulted in damaged lungs leading to MRSA lung abscess was unreasonable, obviously fanciful etc.– two kinds of death found acute myeloid leukaemia and lung abscess caused by MRSA – satisfied beyond reasonable doubt that smoking did not cause Applicant’s death – death not war caused – decision under review affirmed
LEGISLATION
Veterans Entitlement Act 1986 s 8, 120, 120A
CASELAW
Repatriation Commission v Law (1980) 31 ALR 140
Repatriation Commission v Hancock (2003) 37 AAR 383
Repatriation Commission v Cooke (1998) 90 FCR 307
Repatriation Commission v Budworth (2001) 66 ALD 285
Repatriation Commission v Towns (2003) 38 AAR 77
Repatriation Commission v Deledio (1998) 83 FCR 82,
Bull v Repatriation Commission (2001) 188 ALR 756
Bushell v Repatriation Commission (1992) 175 CLR 408
Byrnes v Repatriation Commission (1993) 177 CLR 564
East v Repatriation Commission (1987) 16 FCR 517REASONS FOR DECISION
2 August 2006 Mrs Josephine Kelly, Senior Member, and
Dr M. Thorpe, MemberIntroduction
1. Mr Matthew Morrison was an Australian Mariner during World War II between 4 April and 29 October 1945. He died on 30 July 2003, aged 75 years. His widow, Mrs Morrison, applied for a pension which was refused because it was determined that Mr Morrison’s death was not “war-caused”.
2. The death certificate (T4 p10) records the causes of death as:
“(I)(a) Multi resistant staphylococcus aureus sepsis, days
(b) Multi resistant staphylococcus aureus lung abscess, weeks
(c) Multi resistant staphylococcus aureus wound infection, weeks
(d) Immunosuppression, weeks
(e) Acute myeloid leukaemia, weeks
(II) Gastro-intestinal haemorrhage, days”
The Issue
3. The issue we have to determine is whether Mr Morrison’s death was “war-caused”. The case presented for Mrs Morrison seeks to connect her husband’s death with his smoking, which it was argued was caused by his service.
The Law to be applied to determine whether “death” was war-caused
4. Mr Morrison’s death will be war-caused if it arose out of, or was attributable, to his operational service (s 8 of the Veterans’ Entitlements Act 1986 (“the Act”)). Both parties agreed that Mr Morrison’s service was relevantly operational service as defined in s 6B.
5. The Full Court of the Federal Court addressed the meaning of “war-caused” in Repatriation Commission v Law (1980) 31 ALR 140 at 150. In summary, it need not be the sole or dominant cause, but may be a contributing cause to death, although a fanciful relationship is not sufficient.
6. Mrs Morrison’s claim was made after 1 July 1994. Therefore, s 120A of the Act applies, as well as s 120. In summary, these provisions, as interpreted by case law, require the following analysis to be undertaken:
a)Is the applicant the widow of a veteran? (Repatriation Commission v Hancock (2003) 37 AAR 383. The parties accept that Mrs Morrison is the widow of a veteran.
b)On the balance of probabilities, what was the “kind of death” Mr Morrison suffered? (Hancock, Repatriation Commission v Cooke (1998) 90 FCR 307, Repatriation Commission v Budworth (2001) 66 ALD 285). There may be a number of “kinds of death” in a particular case (Hancock, Repatriation Commission v Towns (2003) 38 AAR 77)
c)Considering all the evidence and without making any findings of fact, does it raise an hypothesis connecting Mr Morrison’s death with his operational service?
d)If there is an hypothesis, is there in force under the Act an applicable Statement of Principles (“SoP”) for the “kind of death”?
e)If there is an applicable SoP, is the hypothesis consistent with it?
f)If the hypothesis is consistent with an SoP, or if there is no applicable SoP, the hypothesis is “reasonable”, are we satisfied beyond reasonable doubt that Mr Morrison’s death was not connected with service?
(Repatriation Commission v Deledio (1998) 83 FCR 82, as qualified by Hancock and Bull v Repatriation Commission (2001) 188 ALR 756; Bushell v Repatriation Commission (1992) 175 CLR 408, Byrnes v Repatriation Commission (1993) 177 CLR 564, East v Repatriation Commission (1987) 16 FCR 517).
The “kind of death”
7. The first matter in dispute that we have to determine is what was the kind or kinds of death suffered by Mr Morrison. The medical evidence was complicated and confusing. It is necessary to set it out in some detail.
8. Dr Garvey is a general and diagnostic surgeon who gave evidence in support of Mrs Morrison’s case. He provided two written reports and gave evidence by telephone after concurrent oral evidence had been given by three doctors called by the Repatriation Commission. They were Professor Levi, a consultant physician specialising in medical oncology, Professor O’Rourke, cardiologist, and Associate Professor Breslin, consultant thoracic physician.
9. At the end of two days’ hearing, the Tribunal found it necessary to have a response to Dr Garvey’s evidence from Associate Professor Breslin. A further hearing was held when Associate Professor Breslin and Dr Garvey gave concurrent evidence in person. Professor Levi also provided a further report commenting on Dr Garvey’s evidence.
10. In his first report, Dr Garvey’s conclusion, relevantly, was that:
“... Mr Matthew Morrison’s death from multi-resistant Staphylococcus aureas (MRSA) sepsis (the principal cause of death) developed from a lung abscess on a background of chronic bronchitis and emphysema.”
11. In coming to this opinion, Dr Garvey referred to a smoking questionnaire dated 14 October 2003 signed by Mrs Morrison which stated that Mr Morrison had a heavy service-related smoking habit (at least 20 to 30 cigarettes per day). It also stated that Mr Morrison had at least 43 pack year history of cigarette smoking, commencing smoking when he joined the Merchant Navy and stopping in 1988 because of bronchial problems. Dr Garvey also said that Mr Morrison was forced to take up smoking because of war service as he was encouraged by his peers. The smoking questionnaire stated that Mr Morrison smoked “to relieve the stress he felt from leaving home and parental guidance for the first time”.
12. Dr Garvey quoted from the report prepared by Mr O’Keefe, historian, to the effect that Merchant Mariners would probably have smoked because of the stress of enemy naval activity.
13. Dr Garvey referred to a diagnosis of chronic obstructive airways disease by Dr Vickers when Mr Morrison presented with chronic bronchitis in 1989, the symptoms of which had been present for years. He also referred to a letter from Mr Morrison’s family doctor which indicated that heart and lung disease had been present in the order of 20 to 30 years.
14. In this first report Dr Garvey provided no basis for the inclusion of emphysema in his opinion.
15. In a further report, Dr Garvey provided a critique of the opinions of Professor Levi, Professor O’Rourke, and Associate Professor Breslin. Dr Garvey said that he agreed with Professor Levi’s conclusion that staphylococcal pneumonia was the major cause of death, and affirmed “that this was on a background of his immune-suppressed state due to acute myeloid leukaemia, and damaged lungs due to chronic bronchitis and emphysema caused by a war service-related smoking habit” (emphasis added).
16. In this report Dr Garvey referred to a chest X-ray of 5 June 2002 which he said ‘showed “hyper-inflated lungs” consistent with early emphysematous change, a smoking-related condition’.
17. At the beginning of the concurrent evidence session with Associate Professor Breslin, Dr Garvey emphasised that he was only saying that the hyper-inflated lungs were consistent (our emphasis) with emphysema, “I’m not saying they prove it”.
18. When he gave evidence by telephone, he began by stating that cigarette smoking caused chronic bronchitis which made the lung vulnerable to infection from organisms. The damaged lung then served as a site for MRSA (methicillin resistant staphylococcus aureas ) to lodge and set up an abscess which caused Mr Morrison’s death. He was asked to comment on Associate Professor Breslin’s opinion that Mr Morrison had no demonstrable evidence of lung damage due to smoking, Dr Garvey said that it was “very subtle and very hard to find. It’s at a very, very microscopic level that may have been overlooked”. He said smoking damages the tissue of the lungs because it interferes with the ciliary epithelium, “that is the very fine coating of the lung” (emphasis added). He relied on a 1979 textbook, Pathologic Basis of Disease by Robbins and Cotran, p 836, (“Robbins”) which linked cigarette smoking to Chronic Bronchitis (it is four to 10 times more common in heavy smokers), and the following paragraph of a 1999 journal article:
”As cigarette smoking is associated with an increased permeability of the airway epithelium, micro-organisms are provided a portal of entry into the pulmonary interstitium and parenchyma. In addition, smoking has been implicated in alterations of macrophage and T-lymphocyte populations in the lung, thereby further contributing to the increased susceptibility to bacterial infections.”
19. In another explanation, Dr Garvey said that the ciliary epithelium “is, the very fine lining of the alveoli of the lung” (emphasis added) which he described as “where the interchange between the gas and the bloodstream takes place in the lungs”. He also said that smoking and/or chronic bronchitis destroys the barrier between the lung and blood vessels, “so there is a portal of entry through which blood-borne spread of organisms can lodge in the lung tissue” and “the barrier between the bloodstream and the pulmonary alveoli is damaged so there is a portal of entry”. He said that when he referred to the epithelium he was talking about the alveoli.
20. When asked whether it was the case that chronic bronchitis was “not necessary for this exercise”, his response was “I prefer not to answer that question because it’s speculative. I only want to stick to the factual matters.” He went on to say that “we know that smoking causes damage to the lungs and chronic bronchitis causes damage to the lungs. The interplay between those two factors is speculation because it’s not known exactly how that occurs”.
21. Dr Garvey agreed that he would defer to the opinion of Associate Professor Breslin that chronic bronchitis was not a diagnosis, but really just a description of cough and sputum production. He also would defer to Professor Breslin in relation to asthma and conditions of the lung related to respiratory matters.
22. Contrary to his stated agreement with Professor’s Levi’s opinion, set out above, Dr Garvey said that “immune suppressions (sic) did not exist”. He relied on a white cell count on 5 June 2003, about six weeks before Mr Morrison’s death. He said that “This is not the picture of an individual who is immuno-compromised. This is a picture of an individual who has an elevated white cell count in response to infection”. He did agree that he would defer to Professor Levi in relation to oncology. He said that immuno-compromised individuals do not suffer from MRSA lung abscesses but from very strange lung abscesses. He said that prior to the hearing he had done a search on the role of immuno-compromised individuals and lung abscesses, and there is no case reported in the scientific literature of an immune-compromised individual suffering from MRSA lung abscess. “It doesn’t exist in the immune-compromised individual”.
23. Later, he denied saying that Mr Morrison was not immuno-compromised: “I’m saying that I would like to see some evidence of that immuno-compromised situation in that individual”.
24. When questioned about his expertise in relation to abscesses, Dr Garvey said that he did a full-time research degree in the Department of Medical Microbiology at the University of New South Wales from 1971 in which he obtained first class honours. “I consider myself well-versed in medical microbiology”. He has not practised in micro-biology but has an interest in the subject. He does not treat asthma, chronic bronchitis, pneumonia, emphysema, or leukaemia. He also agreed that medical practitioners make clinical judgments in the absence of facts frequently and that just because those facts are not known does not mean the clinical judgement is incorrect. He agreed that Professor Levi’s opinion about immuno-suppression may be correct.
25. He agreed that what he was talking about was really in the nature of hypotheses, but went on to say that every person who smokes gets lung disease. He later said: “people who smoke have damage to their lungs. Whether it’s overt and measurable … or whether it’s at a very microscopic level, it affects everyone.” In answer to a later question, Dr Garvey said:
“I said people who smoke get lung damage. I didn’t say – at least I hope I didn’t say lung disease, because smoking-related lung disease is not an area of my expertise. I hope I would have said smoking-related lung damage, because that is common knowledge”.
26. In response to a question whether the pathological changes caused by smoking in Mr Morrison would persist or be repaired if he had stopped smoking, five, 10, 15 or 20 years ago, Dr Garvey said that he could not assist because he had no information on which to give an answer.
27. Further, Dr Garvey said that any lung damage, even if it is not discernible or measurable, contributed to Mr Morrison’s death. This opinion was based on the pathological appearance of the lung in patients who suffer from chronic bronchitis due to smoking as evidenced in the Robbins extract.
28. When Dr Garvey was asked to clarify his position in relation to smoking and chronic bronchitis, he said that smoking of itself damages the lung, and “chronic bronchitis follows on from smoking and it is a matter of destruction of the ciliary epithelium … in the most inner lining of the alveolus of the lung, meaning that the lung is not able to withstand inhaled micro-organisms.” That’s the connection between smoking and chronic bronchitis. He relied on the extract from Robbins in relation to chronic bronchitis.
29. He described Mr Morrison’s situation as “the infected organisms come from the wrist into the heart and then from the heart are pumped into the lung and then at that interface between the very fine epithelia of the lung and the bloodstream the damage occurs”.
30. Dr Garvey gave the following evidence during the concurrent evidence session with Associate Professor Breslin on 5 May 2006. He began by correcting “two points” in the transcript of his evidence. He said “fine coating of the lungs”, quoted earlier in this decision was a mistake, “probably a slip of the tongue” and the word “lungs” should read airways. Similarly, he said that there was an error where he referred to ciliary epithelium being on the very fine alveoli (quoted earlier). In his report dated 18 April 2006, Associate Professor Breslin had said that Dr Garvey’s evidence is actually littered with factual errors, and had pointed out these and other errors.
31. Dr Garvey went on to comment about Associate Professor Breslin’s response to his earlier evidence. Dr Garvey said that the point he was making was that smoking deranges the cilia, that is the very fine processes that occur on the lining of the epithelium of the bronchial airways, either anatomically or physiologically.
32. He also said that the last paragraph in the transcript of his earlier evidence said “Smoking increases lung damage both to the alveoli and to the bronchi”. In fact the transcript does not contain such evidence.
33. On this occasion, Dr Garvey said that there were two aspects of smoking causing damage to the lungs – chronic bronchitis, and the alveoli. He described smoking damage to the ciliary mechanism in the airways as in chronic bronchitis and on the other hand smoking damage to the “spongy stuff”, the alveoli. at the end of the airways. In support of the damage to the alveoli, he relied on the 1999 journal article referred to earlier and said: “The paper itself wasn’t actually about damage to the alveoli, it was about chronic bronchitis. … and made reference to other references that explain how cigarette smoking damages the alveoli”.
34. He explained the proposition he put during his earlier evidence this way. Damage to the alveoli occurs as a direct toxic effect from cigarette smoking, and that impairs the immune cells that are in the alveoli themselves. The damage allows passage of micro-organisms either way from the bloodstream to the air and from the air to the bloodstream. Normally there is movement in both directions. A blood-borne infection would tend to lodge in the lung at an area of pre-existing damage. This would happen without immune suppression.
“According to current wisdom organisms can pass from the blood stream into the lung tissue and then are expelled from the alveoli and are coughed up. They are grabbed by phagocytes which are white cells that eat up organisms and then carried by this ciliary mechanism into the bronchi and are coughed up in sputum.”
35. In support of this proposition Dr Garvey relied on a 1980s textbook called Leeson and Leeson on Histology¸ which was not tendered into evidence, and “common knowledge”. This was in the context of an hypothesis.
36. Dr Garvey restated his hypothesis in relation to chronic bronchitis as follows. “The ciliary mechanism is impaired by cigarette smoking and so organisms that might normally traverse this barrier and be expelled in the sputum by coughing are not transported along the bronchial airways.”
37. When questioned about the mechanism that gets organisms from the alveoli to the ciliary epithelium, Dr Garvey responded: “This is something that I’m not terribly sure about. By my reading of that particular issue is that where there was lung damage an abnormal communication exists from the alveoli to the respiratory bronchiolus and if there is damage in that region which allows an abnormal communication would occur between the torn alveoli and those torn bronchiolus.”
38. Dr Garvey said that the reading he had done was “Just general reading that I’ve read in a textbook of medicine for this case”. He conceded that he was not an expert in this area, which was “a very, very technical area”, and that Associate Professor Breslin was more eminently qualified to express an opinion, but relied on his experience in thoracic surgery in 1976 when he saw “the damage that can occur to the lung from cigarette smoking” , and in 1981.
39. Dr Garvey criticised Professor Levi’s clinical assessment that Mr Morrison was immune suppressed. Dr Garvey said that it was poorly documented if that was so, and that there are no cases in the literature concerning MRSA and lung abscess and acute myeloid leukaemia.
Professor Levi
40. Professor Levi’s explanation of what happened, which was initially accepted by Dr Garvey, was that Mr Morrison’s acute myeloid leukaemia resulted in rapid loss of immune function with a consequent susceptibility to infection. There was an initially localised cellulitis at the site of the catheter in his right wrist, and subsequent blood borne spread of the staph aureus infection to the lungs which resulted in multiple staph abscesses which was the immediate cause of his death. He described it as a classical textbook case.
41. Professor Levi did not consider that there was evidence to indicate that adult onset asthma was of any consequence in Mr Morrison’s final illness, and did not contribute to his death. In his opinion, any possible damage to the lung associated with smoking influences the airways and not the potential for blood borne spread to the lungs. “This is indeed an embolic phenomenon and has no influence as to whether or not any pre-existing structural abnormality exists within the lungs. This is irrespective of whether the abnormality can be seen at post-mortem or is microscopic.”
42. He referred to the textbook and literature references, which we understand to be those relied on by Dr Garvey. He said that as an oncologist he was not particularly familiar with them, but they confirm Professor Breslin’s evidence. “The comments made regarding potential for subsequent infection all revolve around disturbances and damage of the airways epithelium increasing the risk of airways infection.” He concluded that Mr Morrison’s lung infection was blood borne from his wrist and “there is no relationship to any potential pre-existing damage to the lung.”
Associate Professor Breslin
43. Associate Professor Breslin’s opinion was that Mr Morrison’s pre-terminal illness respiratory condition was late onset bronchial asthma, and chronic bronchitis by definition, which is cough and sputum for most days for three months of the year for two or more consecutive years. He said that that is not a diagnosis but can occur in a variety of conditions. Clinical onset of the asthma and chronic cough and sputum were around the same time, in the early 1990s.
44. He said that there was no evidence of lung damage in the post mortem. There was no evidence of emphysema or bronchiectasis on CT scans. Mr Morrison’s airways disease was asthma, because his lung function returned to normal on occasions. Because his lung function did return to normal on occasions, Mr Morrison did not have chronic obstructive airways disease. He did not have emphysema.
45. Associate Professor Breslin did not consider that the late onset asthma was related to Mr Morrison’s cigarette smoking. Rather he considered that Mr Morrison was constitutionally predisposed to it from the point of view of the nasal polyps, which are commonly seen with late onset bronchial asthma and can occur in both smokers and non-smokers. Smoking induced airways disease is characteristically non reversible, and once airways disease develops with air flow limitation, it is characteristically resistant to reversing and sufferers tend not to get back to normal lung function.
46. In Associate Professor Breslin's opinion, Mr Morrison developed a completely unrelated condition of chronic myeloid leukaemia in 2003. He died of an acute leukaemic blast transformation with subsequent complicating staphyloccocos abscesses, including in his lungs. Professor Breslin agreed with the death certificate. The leukaemia predisposed Mr Morrison to the infections from which he died. His chronic bronchitis and asthma played no part in his death. The asthma did not predispose him to the staphylococcus abscesses. There is no evidence of any predisposition to staphylococcus lung abscesses in patients with asthma with chronic bronchitis.
47. Associate Professor Breslin commented on Dr Garvey’s reports. Dr Garvey stated in his report of July 2005 that “chronic obstructive airways disease was diagnosed in 1989” when Mr Morrison presented with chronic bronchitis. Professor Breslin said that condition was not present. He also disagreed with Dr Garvey’s conclusion that Mr Morrison died of chronic bronchitis because there was no link between that and a lung abscess. In relation to Dr Garvey’s 2006 report, Associate Professor stated that there was no damage to the lung post mortem.
48. In his report of 18 April 2006, Associate Professor Breslin addressed Dr Garvey’s earlier telephone evidence. In addition to the error about the alveoli having ciliated epithelium, Associate Professor Breslin noted the following errors and explained why they were errors:
.the connection between smoking and destruction of the ciliary epithelium is not chronic bronchitis and went onto explain why in detail;
.the usual acute exacerbations of chronic bronchitis referred to in Dr Garvey’s journal reference occurs in the airways, not the alveoli, and occurs with the three organisms mentioned in that article;
.that Mr Morrison’s white cell count was high is not an indication that immune suppression was not present; in leukaemia the while (white) cell count is almost always high but the white cells are not functioning correctly because they are malignant. To suggest that somebody with leukaemia is not immune suppressed because the white cell count is high displays a fundamental misunderstanding of the leukaemic and myeloproliferative disorder diseases. It is my opinion that the reason this case is causing the Tribunal such difficulty is because a great amount of inaccurate facts has been given to the Tribunal;
.the organisms that travelled from the catheter site lodged not in the bronchi, but in the lung tissue containing blood vessels; they multiply in the blood of those vessels. Any supposed microscopic damage that smoking may have done to the lungs has no effect on the multiplication of those organisms, rather it is the immune suppression that prevented the normal defences clearing them up; the organisms multiply and spread not by invading the alveoli by spreading indiscriminately in all the surrounding tissue , just like a boil does in the skin;
.the quotation from the journal article is irrelevant because the organisms came from the blood not the airway;
. there is no evidence that the MRSA organisms that lodged in the perialveolar blood vessels had an assisted portal of entry into the lungs because of very microscopic damage not seen at post-mortem. They do not need such a portal as they just multiply, and their toxic secretions and those of macrophages that engulf them. damage the lung as they go and make their own portal of entry;
.smoking did not facilitate the lodgement of bacteria in the lungs. The organisms are held up in the lungs because of the size of the capillaries and the number of organisms clumped together which physically get trapped in the capillaries.
49. During concurrent evidence, in response to the further oral evidence of Dr Garvey, Associate Professor Breslin said he was “very confused because a lot of what I heard this morning was news to me and it doesn’t fit this case at all”. In summary, he said that cilia are not structurally damaged by smoking, although they may be functionally damaged. He said that damage in the alveoli is emphysema which means structurally, the disappearance of the alveloli cells and the capillary. Mr Morrison had no evidence of emphysema on x-ray, high resolution CT scan, in lung function tests or microscopically on post mortem. The hyper-inflation of the lungs referred to by Dr Garvey may have many causes. It may occur in people who are fit or in asthmatics, which Mr Morrison was. It was not diagnostic of emphysema.
50. He disagreed with Dr Garvey’s remark that normally organisms pass from the capillary to the alveoli. He said that normal blood is organism free “otherwise we’re sick. So that there aren’t normally organisms passing through the capillary to the alveolus in a normal lung…. It happens when you’ve got organisms in the blood which is called septicaemia, or bacteria if there are not a lot of them.” He described how in the case of an infection in the wrist, the organisms travel through the blood and lodge in the capillary in the alveolus. “They don’t lodge there because that lung is damaged, because if that lung had emphysema there would be no capillary at that particular spot. There would only be capillaries where there was no emphysema.” The organisms then multiply in the blood because that is where the nutrition is. That results in an embolic pulmonary abscess. The usual way to get pneumonia is from bugs that come down the airway and then into the alveoli where they multiply. It is quite unusual to get pneumonia from bugs coming through the capillary.
51. During the evidence of Associate Professor Breslin, Dr Garvey said that emphysema was not an essential element of his hypothesis in relation to the alveoli (p 52 Transcript). Associate Professor Breslin’s response was that “Then any damage that was present is not anywhere except, with great respect, in Dr Garvey’s mind.” There was no evidence that cigarette smoking had caused structural abnormality to Mr Morrison’s alveoli capillary membrane.
52. Associate Professor Breslin did not accept Dr Garvey’s evidence that there is no literature on leukaemia, lung abscesses and immune suppression, and undertook to provide the Tribunal with references to such articles, which he did after the hearing. They were also provided to the parties. Counsel for Mrs Morrison advised the Tribunal that he did not wish to make submissions on that material.
Dr Garvey’s response to Associate Professor Breslin’s evidence in concurrent evidence and the latter’s response
53. Having heard Associate Professor Breslin’s response to his oral evidence, Dr Garvey’s position may be summarised as follows. He said that there was no evidence that Mr Morrison had alveoli damage. He was putting forward an hypothesis, relying on common knowledge that smoking causes lung damage, and Mr Morrison had a history of smoking. Later he said that emphysema was not the only form of lung damage through cigarette smoking and that when he got the post mortem report it did not confirm emphysema. He no longer relied on emphysema.
54. He linked the chronic bronchitis with the hypothesised microscopic damage to the alveoli as follows. The phagocytes (white blood cells) engulf the organisms so that they become part of the phagocytes which “convey the organism to the exterior by coughing it up”. Associate Professor Breslin said that macrophages, scavenger cells, would attempt to engulf and deal with the bacteria “which I contend in this man would be an impaired response because of his immune suppression, (that is) the response of getting rid of infection is impaired, suppressed, improvident. If that’s true but I’m still waiting for the chronic bronchitis bit.”
55. Dr Garvey’s response was that the organisms are transported from the alveoli in the air space and then carried outside. “Now these blood cells, these phagocytic cells are, I think, I’m not a hundred per cent sure about this, but I think that there is some movement, ability to move themselves … and if there is damage present …normal communication exists between the alveoli and the internal bronchi. And it’s through that communication that the cilia transport the phagoctyes and carry the organisms to the outside.”
56. Dr Garvey said that chronic bronchitis was relevant because it impaired the ciliary transport mechanism in the airways, which contributed to the retention of the organisms in the lung, multiplying, causing abscess. Therefore, both the alveoli damage and the chronic bronchitis contributed to the lung abscesses.
57. Associate Professor Breslin responded that only 20 per cent of people who smoke heavily all their lives actually get airways disease or emphysema: “… everybody who smokes doesn’t have some mythical, undocumentable damage to their alveoli.” He repeated his earlier evidence that there was no evidence that Mr Morrison’s alveoli were damaged, that is that he had emphysema, radiologically, from his lung function, or at post mortem, and such damage was looked for. There was no evidence of any structural or functional abnormality of the alveoli and a lot of evidence against it.
58. In relation to the “abnormal communication”, referred to by Dr Garvey, Associate Professor Breslin said there was no evidence to support that. He confirmed his opinion that Mr Morrison had chronic bronchitis because he had asthma, not because of his smoking. By definition, about 50% of people with asthma have chronic bronchitis.
”There is no evidence that I’m aware of that smoking causes such abnormal pathways between alveoli and terminal bronchioles. There is no evidence that the major way we get rid of an infection in the lungs is to cough up the organisms. That is not the way you cure pneumonia. The organisms, sure you cough them up, that’s why they’re in the sputum, but the major defence against pneumonia is not coughing the bugs, it’s the body dealing with them inside you where they are, not that they all to get on to this escalator and get coughed away.”
59. During cross-examination counsel for Mrs Morrison questioned Associate Professor Breslin about damage before emphysema that cannot be seen “making it more likely that bacteria in the blood would lodge where that damage is”. The Professor’s response was:
“No, not at all. There’s simply no evidence for that. It’s fatuous. It’s just fantasy. There is no evidence that people in the pre-emphysemative stage have some damage that allows bacteria to get trapped in the capillaries.”
60. Dr Garvey then specified another kind of damage to alveoli caused by smoking, other than emphysema. Smoking in pregnant women causes decreased surfactant which is another form of damage to the alveolus of the lung in the unborn child. When the Tribunal pressed Dr Garvey, because we were talking about a man and not an unborn child, he said:
“It’s causing some anatomical derangement, microscopically and it is affecting the inflammatory cells that would normally reside in that space between the endothelium … that is, the tissue on the alveoli side of the lung.”
61. Associate Professor Breslin disagreed. He said that the cells that provide information, which we understand to be a typographical error and should read prevent inflammation, do not have a very long life span. It is a dynamic process, they are there today but not tomorrow, “… indeed, the cells that I came into this room with in my alveoli capillary membrane are not there now. Other ones have replaced them.” He explained that there is a cell type that forms the alveolus and other specialised types of cells that secrete surfactant, which is a surface tension agent that stops the alveoli from collapsing.
“Now, the reason that babies get into trouble is because they don’t produce surfactant. No evidence that people that have smoked but haven’t got emphysema collapse their alveoli because of reduction in surfactant. That doesn’t happen. …”
“And finally, Dr Garvey keeps saying that these are at microscopic level. He had a microscopic examination at post-mortem. It’s not something that we can never get to the bottom of in this man because he didn’t have it. He had it.”
62. Dr Garvey’s response was that the microscopy examination of the lung post-mortem showed sections of lung “…. Show a picture of acute pulmonary injury with diffuse … exudate and haemorrhage seen from the alveoli”. To which Associate Professor Breslin responded:
“… That’s what you get in pneumonia. You get fibra and you get alveoli haemorrhage, you get alveoli damage. That’s were pneumonia was. … If you looked at areas that were not the seat of pneumonia and some of his lung was, thee’s (sic) no evidence from the post mortem report that those areas were abnormal … there is no evidence that before the pneumonia those areas were abnormal because the area where there was no pneumonia at the time that he died was not abnormal.”
63. Dr Garvey said that he had no response, it does not need a response and he had made his point. He did not disagree that the damage was consistent with pneumonia but returned to his argument that there was no documentation, no evidence, that this bacteria causes lung abscess on immune compromised individuals. This was “absolutely and totally” disputed by Associate Professor Breslan orally, and he provided a list of references after the hearing as outlined earlier. We note that Dr Garvey said at this point of the evidence in relation to his assertion that there was no evidence:
“Well, I’ve done the search Dr Thorpe, and I’ve done it twice. I did it before the previous hearing and I did it last night before this hearing”.
64. Dr Garvey said that smoking caused structural damage of the alveoli involving the separation of cells and increased permeability. Associate Professor Breslin disagreed. He said if smokers had increased permeability of their alveoli capillary membrane they would have pulmonary oedema, and they do not. Dr Garvey said that the support for his view came from articles he had read and studied for the hearing and not from his own practice and experience. There was structural and functional damage to the alveoli.
Professor O’Rourke
65. Professor O’Rourke’s evidence was concerned principally with the question of any contribution to Mr Morrison’s death by ischaemic heart disease. He considered that there was no such contribution. That was not an issue in these proceedings and accordingly we do not need to consider it further. However, Professor O’Rourke did comment in his report that “chronic bronchitis may have facilitated the development of pulmonary sepsis which was a major factor in his death”. During his oral evidence, he deferred to the opinions of Professor Breslin and Professor Levi, who he acknowledged were more appropriately qualified to address that issue.
Consideration
66. We prefer the evidence of Dr Levi and Associate Professor Breslin to that given by Dr Garvey. They gave evidence within their areas of expertise and experience. We found them to be impressive witnesses. While we accept that Dr Garvey was raising hypotheses which is relevant to a later step in the Deledio analysis, in our opinion his evidence was not based on any expertise in the areas addressed. He conceded that he would defer to Associate Professor Breslin and Professor Levi in their respective fields. Dr Garvey also said that his evidence was based on what he had read for this hearing and his general knowledge. He also referred to an interest in medical microbiology arising from his studies in the early 1970s, and experience in thoracic surgery in 1976 and 1981. We not consider that study and that experience qualify him as an expert in those fields.
67. Dr Garvey made fundamental mistakes such as that the alveoli had a ciliated epithelium, and that a high white blood count showed that there was no immuno-suppression. As his evidence was shown to have no factual basis, he retreated from his previous position. For example, he explained his repeated error about cilia in the alveoli as “a slip of the tongue”; he ceased to rely on emphysema; and his explanation for the role of chronic bronchitis, as best we could understand it, altered. By the end of his evidence, his position had fundamentally altered to reliance on damage to the alveoli by smoking and some lesser reliance on chronic bronchitis. Further, we do not accept that the references he provided support the propositions he was putting forward. Finally, his assertion that there was nothing in the literature concerning MRSA and lung abscess and acute myeoloid leukaemia was patently wrong.
68. Evidence from a medical practitioner which extends beyond his or her area of expertise is not of assistance to the Tribunal in the task it has to undertake, and as in this case may result in an unnecessarily lengthy hearing and additional time having to be taken for consideration to unravel the evidence.
69. Counsel for Mrs Morrison argued that the Tribunal had to find that one kind of death suffered by Mr Morrison was from lung abscess, for which there is no SOP. He accepted that we could also find that a kind of death was leukaemia but did not seek to link that with Mr Morrison’s service.
70. The advocate who appeared for the Commission argued that the kind of death was leukaemia, which was the real or operative kind of death. He relied on Fitzgerald v Penn (1954) 91 CLR 268 to support this proposition. With respect, we do not find that case of assistance. It dealt with directions to a jury in a common law negligence case, not the legislation the subject of this decision. We also do not consider that it supported the proposition put to us. We rely on cases that have addressed “kind of death” in s 120A: Hancock and Towns.
71. On the evidence, we find that there were two kinds of death in this case:
(a) acute myeloid leukaemia
(b) lung abscess caused by MRSA.
Is there an hypothesis connecting Mr Morrison’s death with his operational service?
72. By the end of the evidence, we understood the following hypothesis to be relied upon in Mrs Morrison’s case
I.Mr Morrison’s operational service caused him to start smoking;
II.His smoking damaged his lungs as described by Dr Garvey;
III.The resultant damage to his lungs contributed to or caused the lung abscess from which he died..
73. For the purpose of this analysis, we assume that the lay evidence established the necessary causal and temporal link between Mr Morrison’s service and his smoking. We find that an hypothesis was raised on the material before us.
Is the hypothesis reasonable?
74. In Bushell, Mason CJ, Deane and McHugh JJ said that it was not decisive that a medical opinion that supports a hypothesis has little support in the medical profession or among scientists, and later:
… the case must be rare where it can be said that a hypothesis, based on the raised facts, is unreasonable when it is put forward by a medical practitioner who is eminent in the relevant field of knowledge. Conflict with other medical opinions is not sufficient to reject a hypothesis as unreasonable.
75. We find that this is a case where the hypothesis proposed by a doctor is unreasonable. We do not consider Dr Garvey to be knowledgeable in the fields about which he gave evidence for the reasons we have set out earlier. He is certainly not eminent in those fields. Further, we consider the hypothesis proposed by Dr Garvey to be obviously fanciful, impossible, incredible or not tenable or too remote or too tenuous (Bushell p 416). There was no evidence to suggest that smoking had caused damage to Mr Morrison’s lung as Dr Garvey proposed. Lung function test, radiology including a CT scan, and histopathology at post mortem indicated no lung damage as a consequence of smoking. There was no evidence that Mr Morrison was not immuno-supressed. Dr Garvey was speculating with no factual or scientific basis for his hypotheses.
76. We need go no further, however, for completeness we find that assuming that there was a reasonable hypothesis, we would find beyond reasonable doubt that Mr Morrison’s smoking did not cause his death, on the basis of the evidence of Associate Professor Breslin and Professor Levi.
77. For the above reasons we find that that Mr Morrison’s death was not war-caused.
Decision
78. The decision under review is affirmed.
I certify that the 78 preceding paragraphs are a true copy of the reasons for the decision herein of Senior Member,
Mrs Josephine Kelly and Member, Dr Max ThorpeSigned: Ms Preethi Nimmagadda
AssociateDate/s of Hearing 27 and 28 February and 15 May 2006
Date of Decision 2 August 2006
Counsel for the Applicant Mr C. Colborne
Solicitor for the Applicant Dibbs Abbott Stillman
Advocate for the Respondent Department of Veterans' Affairs
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