Hadfield and Repatriation Commission
[2007] AATA 1559
•18 July 2007
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2007] AATA 1559
ADMINISTRATIVE APPEALS TRIBUNAL ) N° V 200600236
)
VETERANS' APPEALS DIVISION ) Re: MARY CATHERINE HADFIELD Applicant
And:
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal:The Hon Howard Olney AM QC, Deputy President,
Regina Perton, Member, and Dr K. Breen, Member
Date:18 July 2007
Place:Melbourne
Decision:The Tribunal affirms the decision under review.
(sgd) Howard Olney
Member
VETERANS' AFFAIRS – Federal Court remittal – widows' pension – operational service – hypothesis that service caused smoking habit which caused lung cancer which metastasised into cerebral tumour causing death – analysis of medical evidence – cause of death cerebral haemorrhage related to amyloid angiopathy – material did not raise reasonable hypothesis connecting veteran’s death with service – decision affirmed
Veterans' Entitlements Act 1986
Statement of Principles Instrument № 51 of 2006
Statement of Principles Instrument № 52 of 1999
REASONS FOR DECISION
18 July 2007 The Hon Howard Olney AM QC, Deputy President
Regina Perton, Member, and Dr K. Breen, Member
1. Mrs Mary Catherine Hadfield (the applicant) seeks review of a decision of the Veterans’ Review Board (VRB) made on 16 June 2004 affirming a determination of the respondent (the Commission) to refuse the applicant’s application for a war widow’s pension.
2. The applicant is the widow of the late Frederick Selby Hadfield (the veteran) who died on 17 February 2005, aged 83 years. The veteran had rendered operational service during World War II as a member of the Australian Army.
3. The application to the Tribunal asserts that the VRB erred in fact and/or law in failing to find that the (veteran’s) death was war caused within the meaning of the Veterans’ Entitlement Act 1986.
4. The application initially came before the Tribunal in June 2005 and on 1 August 2005, after a full hearing, the Tribunal affirmed the decision of the VRB. The applicant sought to challenge the Tribunal’s decision by way of appeal to the Federal Court; however, the parties agreed that the matter should be remitted to the Tribunal for rehearing. On 7 March 2006 the Federal Court made an order by consent that the Tribunal’s decision of 1 August 2005 be set aside and that the Tribunal, differently constituted, hear and decide the matter the subject of that decision according to law.
5. The Tribunal as presently constituted commenced hearing the application on 21 November 2006. Unfortunately, the matter was not concluded until 30 April 2007 due to the unavailability of some witnesses when the application was first listed for hearing.
6.Evidence was heard from the following witnesses on the dates indicated:
(a)21 November 2006:
·Dr Richard Byron Collins, a Consultant Forensic Pathologist; and
·Dr Roger Woodruff, a medical oncologist and haematologist.
(b)16 April 2007:
· Professor Richard Mark Fox, Honorary Consultant in the Department of Clinical Haematology and Medical Oncology, Royal Melbourne Hospital;
· Professor John Francis Cade, Director of Intensive Care, Royal Melbourne Hospital; and
· Associate Professor Peter John Mitchell, Director of Neuroradiology and Neurointervention, Royal Melbourne Hospital.
(c)30 April 2006:
· Professor Stephen Misha Davis, Director of Division of Neurosciences, Royal Melbourne Hospital.
7. Drs Collins and Woodruff and Professor Cade had given evidence at the previous Tribunal hearing as had the applicant. The transcript of the previous hearing as well as the exhibits tendered at it were available to the Tribunal and accepted as part of the record. At the earlier hearing evidence had also been given by Dr Bernard Gilligan who had since died.
THE VETERANS’ ENTITLEMENTS ACT 1986)
8. Section 13(1) of the Veterans’ Entitlement Act 1986 (VEA) provides that where the death of a veteran was war‑caused the Commonwealth is, subject to the Act, liable to pay pensions by way of compensation to the dependants of the veteran. Section 14 of the VEA makes provision for the making of a claim for a pension, (s 13 and s 14 are in Part II of the Act).
9. So far as presently relevant s 120(1) of the VEA provides that where a claim under Part II for a pension in respect of the death of a veteran relates to the operational service rendered by the veteran the Commission shall determine that the death of the veteran was war‑caused unless it is satisfied, beyond reasonable doubt, that there is no sufficient grounds for making that determination.
10. In applying s 120(1) in respect of the death of a person related to service rendered by the person the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining that the death was war‑caused if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the death with the circumstances of the particular service rendered by the person (VEA s 120(3)).
11. Section 120(4) further provides that except in making a determination to which, inter alia, s 120A(1) applies, the Commission shall in making any determination or decision in respect of a matter arising under the Act, decide the matter to its reasonable satisfaction.
12. Section 120A applies to the applicant’s claim. Subsection 120A(3) provides (so far as relevant) that for the purposes of s 120(3), a hypothesis connecting the death of a person with the circumstances of any particular service rendered by the person is reasonable only if there is in force a Statement of Principles (SoP) determined under s 196B(2) that upholds the hypothesis.
THE APPLICANT’S HYPOTHESIS
13. When the matter was before the Tribunal on the previous occasion two hypotheses were advanced to link the veteran’s death to his operational service. However, in opening the applicant’s case at the remitted hearing her counsel indicated that only one hypothesis would be propounded (Transcript p 3) namely:
The veteran’s service caused the commencement of a smoking habit which subsequently continued after discharge, and which was responsible for a lung cancer which metastasised into Mr Hadfield’s brain; the cerebral tumour then bled and caused his death.
The remitted hearing proceeded on the basis that the applicant relied on this single hypothesis. The Tribunal has taken no account of evidence given at the previous hearing relating to an alternative hypothesis which was then propounded.
14. On 30 October 2006 the Repatriation Medical Authority, under s 196B(2) and S 196B(8) of the VEA, revoked a then existing instrument concerning cerebrovascular accident and determined in its place an SoP concerning cerebrovascular accident - No 51 of 2006 (hereafter referred to as SoP 51/2006). If the requirements of the current SoP are not met, the Tribunal must consider any other SoPs that were current at or after the time of claim. In this case, it is Instrument No 52 of 1999 as amended by Nos 32 of 2002 and 57 of 2003.
For the purposes of SoP 51/2006 cerebrovascular accident means inter alia, intracerebral haemorrhage presenting as a stroke (para 3(b)). In SoP 52/1999, cerebrovascular accident includes intracerebral haemorrhage which is defined as bleeding within the cerebrum, brain stem or cerebellum.
Clause 5 provides that at least one of the factors set out in clause 6 must be related to the relevant service rendered by the veteran.
For present purposes the relevant factor in clause 6 is sub-paragraph 6(p)(vi) which applies in relation to the bleeding of an intracerebral space occupying lesion at the time of the clinical onset of cerebrovascular accident.
The term intracerebral space occupying lesion is defined in clause 9 to mean one of the following entities occupying a delimited area within the brain:
a.abscess;
b.cyst;
c.neoplasm; or
d.tubereculoma
15. In terms of SoP 51/2006 the applicant’s hypothesis asserts that the cerebral haemorrhage suffered by the veteran resulted from the bleeding of the neoplasm which had metastasised from a lung cancer which had been caused by the veteran’s smoking habit acquired during his operational service. There is no suggestion that abscess, cyst or tuberculoma were involved.
16. It is common cause that the veteran’s operational service gave rise to the commencement of a smoking habit which continued after discharge. The other elements of the hypothesis are matters upon which there is no direct evidence apart from the opinions of the expert medical witnesses.
THE PRIMARY FACTS
17. Before entering upon a consideration of the expert evidence it will be convenient to set out certain relevant facts which are not in contention, namely:
(a)The veteran rendered operational service (as defined by the VEA) during the Second World War;
(b)The veteran died on 17 February 2003 aged 83 years;
(c)The veteran’s death certificate shows the cause of death as Cerebral haemorrhage – days;
(d)The applicant is the widow of the veteran;
(e)The veteran commenced a smoking habit during his operational service which he continued after discharge;
(f)In May 2001 the veteran underwent an x-ray examination of his chest and a CT scan of his chest at Northcote Radiological Clinic. Those procedures were reported as follows:
CHEST 11 May 2001
The heart size is borderline. No lymphadenopathy is noted. The lungs are mildly hyperinflated consistent with chronic obstructive airways disease. There is a 6mm rounded opacity in the right midzone at the level of the right hilum. The lungs elsewhere are clear. The pleural spaces and pulmonary vasculature appear normal.
CONCLUSION – Small nodule in the right midzone, ? primary carcinoma. Chronic obstructive airways disease. Borderline uncomplicated cardiomegaly. A CT scan of the chest is advised.
DR. A. VELLIOS
Ct Scan Of The Chest 17 May 2001
Post contrast helical scans from the lung apices to the upper abdomen were performed including a dynamic run through the mediastinum and hilar region. The examination was performed with the patient breathing gently throughout the procedure.
There is no mass lesion noted. The previously suspected mass on the plain film is probably due to composite vascular shadowing. Mild interstitial opacity is noted in the paravertebral gutters towards both bases with the right side slightly more affected. The pleural spaces are normal.
No hilar or mediastinal lymphadenopathy is noted. The trachea and major bronchial branches appear normal. Other than several simple cysts in the left kidney, the upper abdominal viscera included in this examination is normal.
CONCLUSION – There is no lung mass lesion or other evidence of malignancy noted. Mild interstitial pulmonary fibrosis in the paravertebral gutters towards both bases.
DR. A. VELLIOS
(g)On 8 February 2003, the veteran was admitted to St Vincent’s Hospital, Melbourne. The contemporary hospital records indicate the key diagnosis as stroke.
(h)On the day of his admission to hospital the veteran underwent a chest X-ray and a CT brain scan. These procedures were reported as follows:
CHEST X-RAY –(vi)
Previous chest X-rays are not present for comparison.
There is a small ovoid 2.5cm well circumscribed opacity in the right lower zone medially. The remainder of the lungs are clear. The cardiac and mediastinal contours are normal.
CONCLUSION --
2.5cm ovoid opacity in the right lower zone. Previous films are needed to exclude a neoplastic process. If previous films are not available, then this could e further assessed with CT.
Reported by: Dr K Chauah
CT BRAIN -- (MG)
CLINICAL NOTES:
Post ictal with continuing confusion. ? Intracecerebral haemorrhage. Previous history of epilepsy.
REPORT
Non contrast axial scans were performed from skull base to vertex.
Several images at the skull base are degraded by motion artefact. There is a hyperdense intracerebral haemorrhage which measures 4x1.5cm in diameter centred in the dee[ white watter [sic] of the high right parietal lobe. There is a thin surrounding rim of hypodense oedema. There is mild mass affect with no midline shift and no hydrocephalus.
Generalised age-related atrophy is present. Encephalomalacia in the frontal lobes bilaterally is consistent with old bilateral anterior cerebral artery territory infarcts. Periventricular hypoattenuation is compatible with chronic small vessel deep white matter ischaemic changes.
CONCLUSION
4x1.5cm acute intracerebral haemorrhage in the high right parietal lobe. The most common cause for an acute haemorrhage in this location in a patient of this age is amyloid anglopathy.
Reported by: Dr K Chuah
(i)a further chest X-ray was performed on 10 February 2003 and reported thus:
CHEST X-RAY -- (LP)
Frontal PA film performed and comparison is made with series 1 done on the 8th February 2003. No focal lung collapse or consolidation seen. The ovoid soft tissue opacity seen within the right lower lung zone is less well defined on today’s examination. The left pleural space has not been captured on this film.
Loss of joint space affects the right shoulder joint with erosion of the lateral end of the right clavicle.
Reported by: Dr E Pun
(j)On 14 February 2003 a second brain scan was performed. The report was as follows:
CT BRAIN - sf
CLINICAL NOTES
Myoclonic status post intracerebral bleed. ? Extension of haemorrhage.
Non contrast axial scans have been performed from skull to base to vertex.
[REPORT]
Hyperdense right parietal lesion, consistent with haematoma, is unchanged in dimensions. There is an associated surrounding oedema, without significant subfalcine/uncal/tonsillar herniation (although rotation of patient’s head makes assessment difficult). Maximal axial dimensions of this elliptical lesion are 4 x 2cm and it is visible over 4x 10mm slices. The degree of surrounding oedema is essentially unchanged, although is difficult to compare due to head tilt.
No increase in ventricular size (symmetrical and within normal limits). Bilateral anterior encephalomalacia persist, consistent with previous insult.
No extra-axial collection.
OPINION
Haermatoma size unchanged. No significant increase in surrounding oedema. No definite subfalcine/tonsillar/uncal herniation. No increase in ventricular size. No evidence of re-bleed.
Reported by: Dr C Holden
(k)No post-mortem examination of the veteran was carried out.
18. The contents of the foregoing paragraph are described as the primary facts as they represent events which are readily capable of positive proof. To the extent that they include the expression of opinions, those opinions were arrived at, and recorded by, the relevant medical practitioners who had direct involvement with the veteran at the time. None of the expert witnesses who gave evidence before the Tribunal had any direct contact with the veteran. Their opinions as expressed in their evidence are based upon the material set out above and contemporary clinical notes and records.The following paragraphs contain analysis of the testimony of each of the expert witnesses.
Dr Collins
19. Dr Byron Collins is a legally qualified medical practitioner who specialises in the fields of forensic pathology and anatomical pathology. He has been a Fellow of the Royal College of Pathologist of Australasia since 1979 and practices as a consultant forensic pathologist in Melbourne. For the purposes of these proceedings Dr Collins has provided three written reports (dated respectively 17 August 2004, 26 May 2005 and 13 September 2006). He also has given oral evidence at both the initial Tribunal hearing and at the remitted hearing. Each of the written reports was provided at the request of the applicant’s solicitors.
20. The report of 12 August 2004 indicates that the materials forwarded to Dr Collins with the solicitors’ letter of instruction included the veteran’s death certificate, documents from St. Vincent’s Hospital and radiological reports from Northcote Radiological Clinic. Upon his initial review of the available material Dr Collins expressed some reservations as to the accuracy of the death certificate. He said:
In my view, the origin of the ‘hyperdense’ area in the deep white matter of the parietal lobe of the right cerebral hemisphere, identified on the CT scans of the brain performed on the 8th and 14th February 2003 during the veteran’s terminal admission to St. Vincent’s Hospital, has not been definitively ascertained. Such an area could be produced by the following mechanisms:
(i)bleeding into the brain tissue (intra-cerebral haemorrhage),
(ii)bleeding into a pre-existing lesion, such as either a primary of secondary tumour.
…
In relation to (ii), having regard to the deceased’s smoking history and the identification of an ovoid, soft tissue opacity in the right lower lung zone following chest -Xrays on 8th and 10th February, 2003, it is entirely reasonable to hypothersize that this was a primary malignant lung tumour which has metastasized to the brain, with this secondary tumour deposit suddenly undergoing bleeding, thereby causing the clinical signs and symptoms which necessitated his terminal hospital admission.
…
In essence therefore, the late veteran died following complications of a “space occupying lesion in the right cerebral hemisphere,” which may have been a pure intracerebral haemorrhage or a metastatic tumour which had undergone haemorrhagic degeneration.
The report makes reference to the then current SoPs for cerebrovascular accident and in particular (for present purposes) to factor 5m(v) which it is said
“is relevant to intracerebral haemorrhage depending upon, of course, the acceptance of the real possibility of a pre-existing lesion within the brain.”
21. Prior to preparing his report of 26 May 2005 Dr Collins was supplied with additional documentation consisting of;
a.reports of Professor Cade dated 30 December 2004 and 15 April 2005;
b.reports of Dr Woodruff dated 16 September 2004 and 9 December 2004; and
c.reports of Dr Gilligan dated 15 September 2004, 12 January 2005 and 13 May 2005.
Having observed that there appeared to be a consensus of opinion as to the possibility of the existence of a haemorrhagic lesion in the veteran’s parietal lobe of the right cerebral hemisphere which resulted in his death, Dr Collins took issue with Professor Cade’s rejection of the hypothesis that the legion in the brain was a metastatic tumour arising from a primary malignancy involving the right lung. Professor Cade said in his report of 15 April 2005 that;
…this lesion was shown on CT scan of the chest in 2001 not to be a mass but probably to be a composite vascular shadow. There is therefore no evidence of potential lung cancer in this patient.
In Dr Collins’ view, Professor Cade was not necessarily correct in his assumption that there was apparently no lesion within the right lung which could give rise to a cerebral metastasis. He supports this view by reference to the following extracts from the radiological reports of May 2001 and February 2003:
(i)“There is a 6mm rounded opacity in the right mid zone…”Dr. A. Vellios, 11/5/2001;
(ii)“There is no mass lesion noted…suspected mass probably due to composite vascular shadowing.” Dr. A. Vellios 17/5/2001;
(iii)“There is a small ovoid 2.5cm well circumscribed opacity in the right lower zone medially.” Dr K. Chuah 8/2/2003;
(iv)“The ovoid soft tissue opacity seen within the right lower lung zone is less well defined on today’s examination.”(? Radiologist).
(NOTE: This is quoted from the chest x-ray report of Dr. E. Pun of 10 February 2003)
The report continues:
In summary, it appears that, in the 2001 films, there was an “opacity” in the right mid zone, whilst in the 2003 films an “opacity” was identified in the right lower zone and it could therefore be reasonably argued that there is a real possibility that the “opacities” were two entirely different entities. …
If this hypothesis as to “duality of lesions” is accepted, then there is still evidence for the existence of a primary lesion in the right lung, which could have metastasized to the brain.
In support of the reasonableness of the hypothesis Dr Collins added the following references;
(i)Extract from Robbins Pathologic Basis of Disease, 6th Edition, 1999. “More distant spread of bronchogenic carcinoma occurs through both lymphatic and haematogenous pathways….The liver (30% - 50%), brain (20%) and bone (20%) are additional favoured sites of metastases,
(ii)Advisory from Disability Compensation Branch, No.13 of 2000 prepared by Medical Officers of the Department of Veterans’ Affairs concerning metastatic neoplasms primary site “unknown,”
site of metastases: common primary site: approximate likelihood
Brain lung 70%
(iii)Right parietal lobe of the brain is an uncommon site for a cerebral haemorrhage consequent upon hypertension.
22. Dr Collins’ report of 13 September 2006 was prepared after he had been provided with copies of the reports of Professor Fox dated 16 July 2006 and 25 August 2006 and that of Professor Davis dated 24 July 2006. Having read the further reports in association with the previously supplied material Dr Collins wrote:
1. On the information presently available, the existence of a primary lung tumour cannot be reasonably excluded.
2. I am prepared to accept that the late Mr Hadfield suffered from amyloid angiopathy. However, its mere existence does not automatically elevate it to then being the most likely underlying pathological process in relation to the causation of the fatal intracerebral haemorrhage.
It is likely that a considerable proportion of individuals of the late veteran’s age would suffer from amyloid angiopathy, simply as a manifestation of the ageing process.
3. In my view, there are facts in this case which point towards the intracerebral haemorrhage as being the result of a bleed within a necrotic tumour mass in the right parietal lobe, although its definitive existence cannot be proven in the unfortunate absence of the ultimate diagnostic procedure – the autopsy.
In summary, my opinions expressed at the Administrative Appeals Tribunal Hearing basically remain unchanged.
23. Dr Collins gave oral evidence on 21 November 2006. In the course of both evidence-in-chief and cross-examination (which was both extensive and searching) the opinions expressed in his written reports were tested. He was also questioned in some detail on the views expressed in the written reports of Professors Mitchell, Davis and Fox as well as some aspects of the evidence of Dr Woodruff, Professor Cade and the late Dr Gilligan given at the previous hearing. It is fair to say that the opinions expressed by Dr Collins before the Tribunal are consistent with those expressed in his written reports.
24. In the context of a discussion concerning the radiological reports dated 8 and 14 February 2003 the following exchange took place between the applicant’s counsel and Dr Collins:
Dr Collins, the reports identify a haemorrhage and the size of the haemorrhage, what is the effect, if any, of the identification of a haemorrhage in a scan of that type on interpretation?--- Well, it may have a masking effect on underlying substances or structures which have different density from the actual haemorrhage itself and so it's a function of the ability of the CT scan or whatever other sort of x-ray modality you are going to use as to try and identify every little - different piece of tissue, that is, that goes to make up, in this case, the haemorrhage or a lesion that is within the brain.
Yes?---So the difficulty in this situation is that if the haemorrhage were of significant or large proportions, as it is here, then it would have the very real propensity to mask any underlying, more subtle pathology which could well have been seen if the haemorrhage hadn't been there. And, as I alluded to earlier, I spoke about the oedema surrounding this haemorrhage; this may also compound the problem. So just because one might have a picture on a CT scan that says to anybody who reads it, this is a haemorrhage - it may well be a haemorrhage and I don't think there's any doubt really in this case that there is blood in this region, but what we don't know with any degree of certainty is what's in that structure that's been possibly destroyed by the blood. (Transcript p 18)
And later, after counsel had referred the witness to Associate Professor Mitchell’s report of 25 October 2006, there was the following exchange:
Professor Mitchell concludes that the haemorrhage was secondary to amyloid angiopathy?---Yes.
Could you comment on that conclusion?---Yes, I think that's a reasonable conclusion to come to because there are other features in the CT scan of the brain identified that show that in all probability this man did have small vessel disease relating to age which had caused some problems within the cerebral substance itself. So yes, it is a possibility that the haemorrhage was related to a rupture from one of these ageing blood vessels.
Dr Collins, does that exclude another hypothesis or conclusion?---In my view, it doesn't. If that were the only finding on a CT scan then it would be a reasonable working diagnosis as to the cause of the haemorrhage. However, in this case there are findings on the chest x-ray which are at least consistent with a mass in the lower zone of the right lung. (Transcript p19)
25. Counsel for the Commission cross-examined Dr Collins on a wide range of issues particularly in relation to the opinions of the other expert witnesses as expressed in their written reports and in some cases the evidence they gave at the previous hearing. For the most part Dr Collins did not disagree with the other opinions except as to the degree of certainty with which they were expressed. By way of example, there was an exchange between counsel and witness concerning Professor Davis’ report of 24 July 2006. At page three of the report Professor Davis set out his opinion in a series of eight numbered paragraphs. In paragraph 3 the Professor said;
I would conclude that this haemorrhage was almost certainly due to amyloid angiopathy …
and at paragraph 7 he said
the overwhelming likely cause of the haemorrhage was amyloid angiopathy …
After these matters were referred to, the transcript records the following exchange of questions and answers;
Now, do you disagree with that statement?---Well, obviously I do. I think the - the difficulty in these reports, having regard to my experience as a pathologist which is different from a clinician, is that I am more reluctant to be as dogmatic as they are, from my experience. Now, they're quite reasonable statements to make, but I just don't believe that one can be that dogmatic and, in fact, at point 3 it's obvious that Professor Davis is not totally convinced because he says it's almost certain. And then he says - he changes that almost certainly to an overwhelmingly likely cause, but I have a reservation in being that dogmatic, that's all.
So really you are not disagreeing, you just say you were relying upon the space, as it were, occupied - by the fact that nobody could say that something is 100 per cent certain?---It's not quite as simple as that, it boils down to nothing is certain in medicine and one has to have a degree of reticence in accepting any clinical diagnosis as being necessarily sanctioned by a post-mortem examination. I can just - that's what happens in medical practice, as we all know, that we can be entirely certain about something and proved entirely wrong at the autopsy, even on good clinical grounds. (Transcript p 27)
26. Counsel for the applicant re-examined Dr Collins on several matters raised in cross-examination. Counsel reminded the witness that it had been put to him that his opinion was dependent on supposition, to which he disagreed and said that it was an educated clinical guess. When asked the rational foundation for his opinion Dr Collins replied:
Well, the rational foundation is that we have two areas of pathology in this man; one is in the brain, and one is in the lungs if that is accepted. There is an area of haemorrhage in the brain which has a number of possibilities for its cause; one of which is related to the damage, ageing damage to the blood vessels. And if one takes only the lesion in the brain, then that would seem to be the most reasonable diagnosis. But if then one takes the lesion in the lung, then one has to seriously consider another diagnosis, or another cause of that haemorrhage, because of the known fact that, and everybody agrees to it, that the brain is a common site for metastases from the lung. Whether an individual has clinical signs and symptoms of that primary tumour is irrelevant. And therefore, is [sic] one takes those two factors together, something in the lung and something in the brain, one must, out of basic pathological reasoning, at least consider a number of causes for the intra-cerebral haemorrhage; one of which is bleeding into a secondary deposit. (Transcript p 44)
Dr Woodruff
27. Dr Roger Woodruff is a consultant physician who specialises in medical oncology, clinical haematology and palliative medicine. In 2004 he prepared reports for the applicant’s solicitors dated 16 September 2004 and 9 December 2004. He also gave evidence orally at the previous hearing. The applicant did not seek to call any further evidence from Dr Woodruff but he was made available for cross‑examination at the remitted hearing on 21 November 2006.
28. Although Dr Woodruff’s report of 16 September 2004 does not precisely identify the material supplied to him, it is clear from what he wrote that he had all of the available records and reports. To a large degree the report deals with the question of hypertension which was relevant at the time, being the basis of an alternative hypothesis, but that matter is not now being pursued and no reference need be made to the doctor’s opinion concerning it. Although not stated in the report, it appears from evidence given by Dr Woodruff at the previous hearing that he had not seen the films of the several chest x-rays and CT scans taken in 2001 and 2003 but he did have available the report of the radiologists concerned with those procedures.
29. The report of 16 September 2004 records the following under the heading medical history
This man died at St. Vincent’s Hospital in February 2003 a week after suffering an acute cerebrovasular accident. He was aged 83 years. The long history of alcohol dependence and moderately heavy tobacco consumption is noted.
His chest x-ray in February 2003 was reported to show a 2.5cm mass on the right midzone. This was not present 21 months earlier and the development of a lesion this size over this time interval makes it highly likely that it was malignant. Given his smoking history, it is likely that he had a primary carcinoma of the lung.
The CT scan of his head performed at the time of admission was reported to show an intracerebral haemorrhage in the right parietal region. It also showed evidence of previous ischemic damage and the radiologist noted that this was probably related to amyloid angiopathy, which is an age related degenerative change in the cerebral arteries and arterioles.
The lesion seen on the CT scan is most probably a primary intracerebral haemorrhage. The clinical and radiological features do not fit with a secondary haemorrhage into an ischemic stroke. It is not possible to be certain that he has not bled into a cerebral metastasis from his probable carcinoma of the lung, although solitary cerebral metastases are uncommon.
The risk factors for intracerebral haemorrhage are set out in the Statement of Principles and include increasing age, hypertension, and other vascular risk factors, most noticeably smoking.
In his second report (dated 9 December 2004) Dr Woodruff is mainly concerned to respond to comments made by Dr Gilligan concerning the hypertension issue but it also includes the following comment under the heading Possible/Probable Carcinoma of the lung;
As discussed in my previous report, this man may have died from a haemorrhage into a solitary cerebral metastasis. Also as discussed in my previous report, the only observation that is not in favour of this hypothesis is that cerebral metastases from lung cancer are solitary in only about 20% of cases.
30. In the course of his cross-examination at the previous hearing it was put to Dr Woodruff that there is an argument that the veteran had a primary cancer of the lung which metastasised into the brain and that it was the metastasis that bled, to which Dr Woodruff responded;
---I’m aware that that has been advanced. I think that’s unlikely. The – one, you would have to convince me that the mass in the lung was a mass in the lung, and not a vascular shadow. Number two, if lung cancer metastasises to the brain four times out of five you will see multiple metastases. And this man’s scan did not show metastases elsewhere in the brain, so it’s rare to have a single metastasis. And when they bleed they usually bleed into the lesion. This was a described as a 4 by 1 centimetre. It was an elongated – I’m looking for the measurement, but I can’t see it – it was an elongated-type thing, which is the sort of thing you see with vascular accidents, as distinct from bleeding into tumours. Cerebral metastases are generally round or spherical and when they bleed they sort of saturate themselves inside. You get a round blood – spill of blood. So it doesn’t have the physical characteristics that would be typical of a typical cerebral metastasis with haemorrhage. It’s possible there was – I believe there was no autopsy performed, so I have to admit that this guy might have had a lung cancer, and it might have metastasised to his head, and it might have had a haemorrhage in it.
31. At the remitted hearing on 21 November 2006 Dr Woodruff confirmed that his professional opinion as to the likely cause of the veteran’s stroke remained unchanged from that expressed in his reports.
Professor Fox
32. Professor Richard Fox is an Honorary Consultant in the Department of Clinical Haematology and Medical Oncology at Royal Melbourne Hospital. He holds a PhD in medicine at the University of Sydney and is a Fellow of the Royal Australasian College of Physicians. By letter dated 5 July 2006 the Commission’s solicitors sought from Professor Fox a report addressing a series of questions concerning the death of the veteran and its surrounding circumstances. The letter set out in considerable detail the veteran’s medical history and the other material which has been referred to in these reasons and which has also been provided to other expert witnesses. In this case the witness was also provided with a copy of the reasons for decision given following the previous hearing. Professor Fox responded to the request by letter dated 16 July 2006.
33. Several of the questions posed to Professor Fox, which he answered in his report of 16 July 2006, relate to issues that were previously, but not now, relevant to the applicant’s case. To the extent that the questions and answers remain relevant they are set out below:
1.You ask am I able to find anything in the material which points to bleeding and intracerebral space occupying lesion immediately before the clinical onset of cerebrovasular accident?
My answer to this is that there is nothing in the material that suggests that there is in fact a intracerebral space occupying lesion (apart from the bleed). It has been speculated or hypothesised that such a intracerebral space occupying lesion (i.e. a lung cancer secondary) existed, but there is nothing in the material that actually points to this.
2.You ask am I able to find anything in the material that points to Mr. Hadfield having a primary malignant neoplasm of his brain.
The answer to this is essentially the as same as in the one above, no.
3.You ask am I able to find anything in the material which points to Mr Hadfield having a secondary malignant neoplasm in his brain.
My answer to that is as in 1 and 2 above, i.e. no.
4.You ask am I able to find anything in the material which points to Mr Hadfield suffering from a primary malignant neoplasm of the lung.
The only material that suggests the possibility of a lung primary is the chest x‑ray dated 8th February 2003 in which it states, as above, there is a small ovoid 2.5 cm well circumscribed opacity in the right lower zone medially. The follow up chest x-ray two days later noted that this ovoid soft tissue opacity within the right lower lung zone is less well defined.
It could be speculated that this lesion was, in fact, a primary lung cancer. That is the only material pointing to a primary malignant neoplasm of the lung.
5.(not relevant)
6.(not relevant)
7.(not relevant)
8.You ask does the material point to the cause of Mr. Hadfield’s cerebral haemorrhage being amyloid angiopathy?
I believe the most critical observation, which is not discussed in the various expert reports or in the decisions document, is the CT scan report dated 8th February 2003 in which it noted that encephalomalacia in the frontal lobes bilaterally is consistent with old bilateral anterior cerebral artery territory infarcts. It also noted that periventricular hypoattenuation is compatible with chronic small vessel deep white matter ischaemic changes.
This would suggest long standing vascular disease of his brain which would point to a cerebral haemorrhage from diseases (sic) blood vessels, i.e. the amyloid angiopathy. I use the diseased, but of course there is an age-related basis to this as well.
Professor Fox’s second report (dated 25 August 2006) deals only with issues no longer relevant and does not require further comment.
34. Subsequent to his report of 16 April 2006 Professor Fox was able to view the radiological images of the veteran’s brain and chest that were taken in February 2003. When asked by the Commission’s counsel whether his viewing of the images of the veteran’s brain affected his opinion in any way he replied:
…No, but again I must emphasise I am not a radiologist, I am not a specialist neuroradiologist, but I believe that the changes that I saw with my limitations in that area were consistent with what had been reported, and what I just said.
The following exchange of questions and answers then ensued:
Did you see any evidence in those images of metastases in Mr Hadfield’s brain? --- No.
Could you explain histologically what a metastasis is? --- Well, with many cancers they have the ability of cells to invade and travel in the blood stream and there re-establish themselves in other organs, and you get either a single metastasis or you can have multiple in the one organ, or multiple in many organs, and it is a relatively common progression of cancer to do so and organs that can be affected by metastasis certainly do include the brain, they include the lungs, the liver and bone, amongst other tissues.
Dr Woodruff has testified that it is rare to have a single metastasis in the brain. Do you agree with that? --- Well, it depends what you mean by the word rare, but I worked for 20 years at the Royal Melbourne Hospital which had one of the largest neurosurgical practices in Australia and they would, I would say, commonly of the order of maybe once a week or once a fortnight see patients with brain metastasis, single. So it can happen.
And the radiologist’s report of the - - -? --- But I would say they were more commonly multiple.
Any capacity to put a figure on - - -? ---I would probably say 60 or 70 per cent would be multiple. But it then depends on the stage of the disease process.
Dr Woodruff estimated 80 per cent being multiple. Would you disagree?--- Well, that is possible, I mean, it depends on the experience in a particular institute and also whether you are talking about the initial presentation of the metastatic disease or later on in the course of the disease. (Transcript p 80)
35. There are a number of other issues dealt with by way of examination-in-chief which can conveniently be summarised as follows.
· A metastasis is not usually sited deep within the white matter of the brain; they are usually more peripheral, commonly at the junction of the white matter and the grey matter;
· Sometimes it is possible to distinguish from radiological images between a primary malignant cerebral neoplasm and a solitary malignant secondary cerebral neoplasm but quite commonly radiologists do not distinguish them.
· A secondary neoplasm can bleed as the tumour progresses; some patients can have bleeds into a metastasis; it would be of the order of 10 to 20 per cent of patients that would have a bleed:
· Cerebral metastases are generally round or spherical.
· If a metastasis does bleed it saturates itself inside and you get a round spill of blood rather than the elongated spill which occurred in the veteran’s brain.
· The witness agreed with the radiologist that the ovoid soft tissue opacity seen in the right lower lung is less well defined on the x-ray taken on 10 February 2003 than was the case on 8 February 2003.
· The witness would describe what he saw on the x-ray of 10 February 2003 as an artefact.
· On the basis of the x-rays taken in February 2003 the witness did not consider the veteran to be suffering from a malignant neoplasm of the lung.
· The risk of a lifetime smoker developing lung cancer is said to be about one in eight.
· If a patient has features of chronic obstructive airways disease or emphysema they are said to be at a considerably greater risk of the development of lung cancer.
· In the witness’s opinion for the purpose of diagnosis it is important to put reliance on the report of the radiologist as to the appearance of the pathology in the brain.
36. Professor Fox was cross-examined at some length as to the availability of different x-ray techniques used in relation to the examinations carried out on the veteran in May 2001 and February 2003. Despite what were suggested to him to be inadequacies of the processes adopted, he nevertheless was of the view that the radiology did not demonstrate the existence of a mass in the veteran’s lung. The witness’s view is exemplified in the following exchanges with counsel:
If it is accepted that this man had a tumour in the lung and if it is accepted that a tumour in the lung – a site of metastases of the tumour in the lung is commonly to the brain? ---Yes.
Then that would support the proposition, would it not, professor, that despite the shape upon which you rely that there is a possibility, even a probability, that there was an underlying secondary that caused the bleed? --- Well, the problem was that the lesion in the lung in the first place – or at least the x-ray changes in the first place do not look like a lung cancer. The second problem is that you have so much other pathology going in the brain that it swings you back entirely to the primary haemorrhage without a tumour given the underlying diseases in the brain.
But you have agreed that the presence of age related degeneration and cancer are not inconsistent one with the other? --- Absolutely not. It is just in which direction you get pushed. … (Transcript p 89)
The radiology in the lung? --- In the lung. I don’t think the radiologists were as confident as you make out that there was a mass in the lung. There was an opacity. Now, unfortunately there is lots and lots of artefactual opacity that can occur and I think that is the fundamental issue. Now, if there had been a somewhat more confident diagnosis or demonstration of a mass that this might have been a primary lung cancer that is a somewhat different issue I think.
But it is a mass, an opacity, nonetheless is it not? --- It is an opacity that was seen.
Yes? --- Yes.
And an opacity is an indicator, is it not, of something that is, setting aside for the moment the possibility of shadowing, an abnormality? --- It is possibly an abnormality. I mean, he had a similar sort of phenomena in a different position in 2001 but when they did a CT scan there was no lesion there. I mean he had composite --- (Transcript p 90)
Professor Cade
37. Professor John Francis Cade is the Director of Intensive care at Royal Melbourne Hospital. His many qualifications include a PhD from the University of Melbourne in respiratory medicine and experience in practice as a thoracic specialist. Professor Cade had provided the Commission with written medical reports dated respectively 6 December 2004, 30 December 2004 and 15 April 2005, all of which were accepted into evidence.
38. In his report of 6 December 2004 Professor Cade has set out a detailed statement of the available information which he extracted from the material provided to him. He was asked to respond to several specific questions, the most relevant of which was What medical condition(s) caused death. His answer was:
The cause of death in this patient was undoubtedly the cerebral haemorrhage which had led to his hospital admission nine days previously. This is because the haemorrhage had been objectively demonstrated on CT scan and confirmed on repeat scan one week later, because the diagnosis was made by a specialist stroke unit and neurosurgical unit in a major teaching hospital, because it was severe and untreatable, because his condition was so poor that a non-for-resuscitation order was made early in his admission, and because imminent death under such circumstances is to be expected.
In turn, the cause of the cerebral haemorrhage was not identified, as it would have been inappropriate to determine the responsible vascular lesion by angiography if no treatment was contemplated. The haemorrhage was considered most likely to have arisen from fragile vessels (“amyloid angiopathy”), as there had been no apparent trauma, hypertension or antithrombotic medication. The cause of the haemorrhage was thus felt to be age-related.
There was no evidence of the presence of some other cerebral lesion, such as a tumour, which may then have bled. Such a possibility is effectively excluded by the imaging tests which were conducted.
No other conditions were diagnosed which might potentially contribute to death. In particular, no significant cardiac, respiratory, infective or metabolic comorbidities were recorded in the hospital record.
39. The report of 30 December 2004 was written in response to further documentation provided by the Department of Veterans’ Affairs. The specific nature of the further documentation is not disclosed but in the context of the material before the Tribunal, it is clear from Professor Cade’s response that it touched upon the issues presently under consideration. The report states:
I have examined the further documentation which you sent me regarding this case, and the request from the Tribunal and Mrs May Hadfield’s solicitor for clarification of the possibility that the veteran’s cerebral haemorrhage may have arisen in a cerebral metastasis.
CT scans of the brain were performed at St Vincent’s Hospital on admission on 8 February 2003 and about one week later on 14 February, three days before he died. On each occasion, they showed a large intracerebral haemorrhage, as well as more chronic changes of cerebral atrophy and ischaemic damage. No specific cause of the haemorrhage was identified, and it was attributed on the basis of probability to age-related amyloid angiopathy.
As he is an international neuroradiology expert, I have discussed the diagnostic accuracy of such imaging with the Professor of Radiology at the Royal Melbourne Hospital. Normally, a CT scan would effectively exclude an underlying lesion of greater than about 2 mm in size. Thus, while a micro-lesion could not be excluded by such a test, it would be unlikely that any such occult lesion would lead to a major haemorrhage. However, we note that the CT scans were performed in this case without added contrast, this more limited scanning technique being appropriate for the chief diagnosis sought in this case. CT scans without contrast have considerably lower resolution than those with contrast, particularly for some intracerebral lesions. Thus, although the scans in this case do not show any evidence of an underlying lesion, the possibility of such a lesion cannot be excluded definitively.
Unfortunately, this speculation does not appear to me to strengthen the proposed hypothesis in a useful way. This is because the hypothesis is based on the suggestion that the veteran may have had an undiagnosed carcinoma of the lung (smoking-related and therefore service-related). This suggestion is based on an abnormality seen on chest x-ray. However, this abnormality was later shown on CT scan of the chest not to be a mass but probably a composite vascular shadow (i.e. a non-pathological finding). The hypothesis then rests on the possibility of a lung cancer too small to be seen on CT scan but capable of metastasizing to give an undetected secondary in the brain which then fatally bled.
Thus, a speculative metastasis from a speculative primary cancer does not seem to me to provide the basis for a plausible hypothesis. Moreover, I understand that the standard of proof for the diagnosis of conditions leading to death in such cases is one on the balance of probabilities. In this regard, as previously discussed, there is already a most likely aetiology for the fatal cerebral haemorrhage, namely amyloid angiopathy, which is age-related and which cannot be considered service-related by any known mechanism.
40. In March 2005 Professor Cade was provided with copies of reports from Drs Woodruff and Gilligan. The former was obviously concerned with an issue that is no longer before the Tribunal. In response to Dr Gilligan’s reports, Professor Cade wrote in his report of 15 April 2005:
I agree with Dr Gilligan that, although the CT scan of the brain did not show any pre-existing intracerebral lesion, such a lesion could not be definitively excluded as the cause of this patient’s cerebral haemorrhage.
Where we disagree relates to the nature of any such lesion. Dr Gilligan suggests that this could have been an occult metastasis from a primary cancer of the lung, and he bases this suggestion on a lesion consistently seen on plain chest x-ray. However, this lesion was shown on CT scan of the chest in 2001 not to be a mass at all but probably to be a composite vascular shadow. There is therefore no evidence of a potential lung cancer in this patient.
Thus, although a pre-existing cerebral lesion cannot be definitively excluded in this case, there is no evidence suggesting what the nature of any such lesion might be. As I concluded previously, “a speculative metastasis from a speculative primary cancer does not seem to me to provide the basis for a plausible hypothesis”.
41. In his oral testimony before the Tribunal Professor Cade reaffirmed the opinions previously expressed in his written reports.
Associate Professor Mitchell
42. Associated Professor Peter John Mitchell is a radiologist and Director Neuroradiology and Neurointervention at Royal Melbourne Hospital. He is a Fellow of the Royal Australasian College of Radiologists. The Commission’s solicitors requested an expert report regarding the death of the veteran and provided copies of medical reports from Drs Collins, Woodruff and Gilligan and Professors Cade, Davis and Fox in addition to the other material that has been referred to in relation to the veteran. Associate Professor Mitchell’s response is contained in a written report dated 25 October 2006.
43. Associate Professor Mitchell’s report responds to a series of specific questions posed to him. Helpfully he has stated each question as asked and responded to it. The questions and answers are as follows:
…
1.You ask am I able to find anything in the material which points to “bleeding within an intracerebral space occupying lesion immediately before the clinical onset of cerebrovascular accident”?
My answer is no. The hypothesis presented raises the possibility of the right cerebral intraparenchymal haematoma being secondary to any underlying malignancy. This hypotheses cannot be completely excluded particularly on a non-contrast enhanced CT scan. However on the balance of probabilities, in the presence of frontal lobe white matter hypo density, periventricular hypo density related to likely small vessel ischemia, a lobar haemorrhage in absence of significant hypertension is almost certainly secondary to underlying amyloid angiopathy. There are no specific features on the CT scan to suggest otherwise.
2.You ask am I able to find anything in the material which points to Mr Hadfield having a primary malignant neoplasm of his brain?
No. The answer is essentially the same as the first question and that is there are no features on the CT scan that suggests an underlying primary malignant neoplasm as the cause for the haemorrhage, but in the presence of a haemorrhage it is impossible to absolutely exclude such a lesion.
3.You ask am I able to find anything in the material which points to Mr Hadfield having a secondary malignant neoplasm of his brain?
No. The answers above apply to this question as well.
4.You ask if I am able to find anything in the material which points to Mr Hadfield suffering from a primary malignant neoplasm of the lung?
The density seen on the chest x-ray 8/2/2003 has been described as less clearly evident on 10/2/2003, and was not further characterised by a lateral chest x-ray at the time of his last admission. I note the history of a 6mm density in the right mid zone investigated by CT scan of the chest in 2001 at which time a conclusion of confluent vascular shadows was made with no evidence of a pulmonary mass. This does not exclude the abnormality we are seeing on the chest x-ray representing a pulmonary mass as this could have developed in the interim. However on the single chest x-ray available there is no evidence that the mass lies within the chest and could easily lie on the patient’s skin, but could also represent a confluent shadow. A primary malignant neoplasm of the lung cannot be excluded.
5.You ask does the material point to the cause of Mr Hadfield’s cerebral haemorrhage being amyloid angiopathy?
My answer is yes. I believe that a lobar haemorrhage on the background of moderate to severe periventricular hypo density consistent with chronic small vessel ischemia, and the changes in the frontal lobe make the most probably diagnosis – a haemorrhage secondary to amyloid angiopathy. On the CT findings alone I would have to include hypertensive haemorrhage as a possible cause, as even though it is not in a classic site, up 10% of hypertensive haemorrhages lie outside those classic sites. The determination as to whether the patient had hypertension is beyond my area of expertise and I would take the advice of relevant medical experts.
44. Associate Professor Mitchell gave oral evidence on 16 April 2007. He was subjected to a searching examination-in-chief and cross-examination during which the written opinions of the previous witnesses and their oral evidence were discussed. For the most part he agreed with the other opinions that had been advanced. When asked to clarify his opinion as to the likelihood of amyloid angiopathy versus bleeding within an intracerebral space occupying lesion being the cause of the veteran’s cerebrovascular accident he replied:
I believe it is almost certain that amyloid angiopathy and a haemorrhage related to amyloid angiopathy explains the CT findings. My choice of the term “on the balance of probabilities” was really saying that a 99 per cent to one per cent kind of balance of probabilities. I was not implying a 50/50 sort of balance of probabilities. I am convinced on the imaging available that the – far and away the most likely explanation would be of haemorrhage related to amyloid angiopathy. I also state that it is impossible to absolutely exclude the hypothesis that there was an underlying tumour without further imaging, and even then it would be impossible to absolutely exclude it, but I think that extremely unlikely. (Transcript p 110)
When in cross-examination the passage from Dr Collins’ evidence reproduced at paragraph 26 was put to him he said:
--- I would agree that you would have to consider all those possibilities but not with the haemorrhage that we’ve got. If there was a tumour in the brain, an enhancing lump in the brain and there was that shadow on the lung, I would agree that the most likely explanation would then shift to that tumour, however, what we are seeing in the brain isn’t anything that I can link to a lung cancer in any real likelihood. I haven’t seen a haemorrhage like that ever from a lung cancer metastasis.
So, on the probabilities, you would set your face against that? --- Yes. (Transcript p 129)
And in re-examination, in the same context the witness said:
---I – the proposition that if there is a lump in the lung and there is something in the brain, that you have to at least consider all possibilities, I agree with. Yes, always consider all those possibilities, but I – looking at that haemorrhage, I can say that in my years of practice I have not seen a lung carcinoma secondary to the brain produce that size haemorrhage and I think it extremely unlikely that a haemorrhage of the particular size, shape, appearance – without any obvious underlying lump that I can see – would be due to a lung carcinoma secondary to the brain. I think it extremely unlikely. (Transcript p 130)
Professor Davis
45. Professor Stephen Misha Davis is a consultant neurologist and is Director of the Division of Neurosciences, Department of Neurology at Royal Melbourne Hospital. Reference has been made earlier to some aspects of the opinions he expressed in a written report dated 24 July 2006. Most relevant for present purposes are paragraphs numbered 3 and 4 of the report in which he stated:
3.I would conclude that this haemorrhage was almost certainly due to amyloid angiopathy, a condition which is not related to hypertension or smoking but where there is an excessive deposition of beta-amyloid in the walls of cerebral vessels, cause unknown. The condition is associated with advancing age and often associated with dementia. It is always considered when a patient has a lobar haemorrhage, particularly in the context of dementia, in an elderly individual and where blood pressure readings have not indicated significant hypertension (as in this case).
4.I am not convinced that there is any evidence that this patient had lung cancer and certainly no evidence that he had metastatic brain disease. It appears that there was some right lung lesion two years before the patient’s demise and that this was thought probably to have been vascular artefact, rather than tumour based on a CT scan of the chest performed in 2001. If indeed this had represented lung cancer, one would have expected significant further evolution before 2003.
46. Professor Davis gave oral evidence before the Tribunal in the course of which he was questioned at length both by way of examination-in-chief and cross-examination. In his answers he was at pains to avoid expressing conclusive opinions in respect of matters not within the scope of his professional expertise. One issue that was put to him had to do with the diagnostic value of a CT scan without contrast compared with a CT scan with contrast. In this context the following exchange with counsel took place by way of re‑examination which can fairly be said to summarise the overall thrust of the witness’s evidence.
Professor, you were also asked a question regarding the resolution of CT scans and it was then put to you that the imaging did not identify any underlying amyloid angiopathy and you said, correct, needs qualification. Could you now provide that qualification? --- Thank you. Well, amyloid angiopathy is a pathological diagnosis. It’s a diagnosis made by examining the walls of the cerebral vessels and staining them with a particular stain looking for evidence of beta amyloid, which is this abnormal protein which is deposited in the walls of the vessels. So there is a newly described experimental technique with positron emission tomography where possibly the diagnosis can be made in life but in generally, it’s a pathological diagnosis. So the diagnosis in life is made as I indicated before, on the basis of the location of the haemorrhage, on the history of age, strengthened by lack of hypertension, the location of the haemorrhage not being in the hypertensive regions of the brain but more peripherally in the lobes of the brain and by the lack of any evidence of any other underlying cause and further strengthened by evidence of dementia which I was given the information that there was in the deceased’s case. So I think in relation to the imaging, had two scans, non-contrast scans a week apart. When we evaluate patients for stroke, until very recently, contrast is not given and it’s not given because in the great majority of cases, it doesn’t alter diagnosis. Unenhanced CT is extremely diagnostically valuable in cerebrovascular disease and in acute stroke. In this particular case, the person had two CTs six days apart and there is no evidence of any underlying pathology that’s been revealed. So for the positive reasons of the clinical factors, the location of the haemorrhage, the shape of the haemorrhage, the lack of any underlying disease, I think there’s an overwhelming likelihood of amyloid angiopathy. One cannot be 100 per cent certain that it wasn’t haemorrhage into a metastasis but I think exceedingly unlikely (Transcript p 153, lines 17-41)
CONCLUSIONS
47. The Tribunal has heard a considerable volume of evidence from a range of medical specialists drawn from a number of disciplines. Each has relied upon his training and experience as the basis for formulating the opinions that have been expressed. For the most part the witnesses have been careful not to stray beyond the scope of their own speciality but there is a general consensus that in medical science there are few certainties. It is however common ground with all of the witnesses that the veteran died as the result of cerebral haemorrhage.
48. Central to the case is the interpretation of the evidence disclosed by the several chest x-rays and brain scans and in this context the Tribunal prefers the opinion of the only specialist radiologist to give evidence, Associate Professor Mitchell, whose specialist training and experience equips him to assess and interpret the radiological evidence. This is not to say that the Tribunal disregards the evidence of the other witnesses, much of which is entirely consistent with Associate Professor Mitchell’s but rather, in his own field of expertise, Associate Professor Mitchell’s evidence is entitled to be accorded considerable weight.
FINDINGS
49. The overwhelming weight of the evidence points to the conclusion that the veteran’s death from cerebral haemorrhage was related to amyloid angiopathy and whilst it is generally conceded that it is impossible to absolutely exclude the hypothesis that there was an underlying tumour, there is no evidence, apart from speculation, that this was the case. On the balance of probabilities the Tribunal finds that the veteran’s death resulted from cerebral haemorrhage related to amyloid angiopathy. The Tribunal also finds that on the balance of probabilities the veteran did not suffer from lung cancer. It follows that none of the factors identified in paragraph 6(p)(vi) of SoP 51/2006 are met nor are any of the relevant factors in the previous SoPs referred to in paragraph 14 above.
50. The Tribunal, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the death of the veteran with the circumstances of the particular service rendered by him.
51. Having regard to its finding as to the cause of the veteran’s death and the absence of a reasonable hypothesis connecting the death of the veteran with the circumstances of the service rendered by him, the Tribunal is satisfied, beyond reasonable doubt, that there is no sufficient ground for making a determination that the death of the veteran was war-caused.
DECISION
52. The Tribunal affirms the decision under review.
I certify that the fifty-two (52) preceding paragraphs are a true copy of the reasons for the decision herein of
The Hon Howard Olney AM QC, Regina Perton and
Dr K. BreenSigned: Dianne Eva
ClerkDates of Hearing 21/11/2006, 16/4/2007, 30/4/2007
Date of Decision 18 July 2007
Counsel for applicant Mr N. Green SC, Ms J. Bornstein
Solicitor for applicant William Winter
Counsel for respondent Ms J. MacDonnell
Solicitor for respondent Australian Government Solicitor
0
0
0