Hadfield and Repatriation Commission
[2005] AATA 730
•1 August 2005
Administrative
Appeals
Tribunal
DECISION AND REASONS FOR DECISION [2005] AATA 730
ADMINISTRATIVE APPEALS TRIBUNAL )
) No V2004/771
VETERANS' APPEALS DIVISION ) Re MARY HADFIELD Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mr John Handley, Senior Member Date1 August 2005
PlaceMelbourne
Decision The decision under review is affirmed. (Sgd) John Handley
Senior Member
VETERANS’ ENTITLEMENTS – widow’s application – 83 year old veteran died from cerebral haemorrhage – pre-existing smoking and alcohol habit – hypotheses of service → smoking → lung tumour → metastasised cerebral tumour → haemorrhage → death; and smoking/alcohol → hypertension → cerebrovascular accident → haemorrhage → death; evidence of doctors did not permit findings on the probabilities of the presence of a lung tumour or cerebral tumour; quantity of alcohol did not meet SOP levels at clinical onset of hypertension; cigarette smoking not a factor in the hypertension SOP; – decision affirmed
Repatriation Commission v Deledio (1998) 83 FCR 82
Repatriation Commission v Hancock [2003] FCA 711
REASONS FOR DECISION
1 August 2005 Mr John Handley, Senior Member 1. The applicant applies to review a decision made by the Veterans’ Review Board (“the VRB”) on 16 June 2004. The VRB then decided to affirm a decision previously made by the respondent on 21 August 2003 to refuse her claim for pension.
2. Mrs Hadfield applies as the widow of the late Frederick Selby Hadfield who died on 17 February 2003 having been born on 20 May 1919. The certified cause of death was “cerebral haemorrhage – days”
3. Mr Hadfield was a Member of the Australian Army between 26 July 1940 and 8 November 1945. Part of his service was in New Guinea.
4. There was no dispute between the parties that the late Mr Hadfield consumed alcohol and smoked cigarettes during and subsequent to service. Mr Nyhof, on behalf of the respondent, conceded that those habits were acquired by reason of service. There was a dispute between the parties as to the period of time that the deceased drank and smoked cigarettes and the relevant quantities.
5. Two hypotheses were advanced by Mr Larkin on behalf of Mrs Hadfield, namely –
(i)Service caused the commencement of a smoking habit which subsequently continued after discharge from service, and was responsible for a lung cancer which metastasised into the deceased’s brain and the cerebral tumour then bled and caused death.
(ii)The consumption of cigarettes and or alcohol caused the deceased to be hypertensive which contributed to a cerebrovascular accident which was responsible for death.
6. On the first day of hearing evidence was heard from Dr Byron-Collins, a consultant pathologist, Dr Woodruff, a medical oncologist and haematologist and Dr Gilligan, a consultant neurologist. Mrs Hadfield was unwell on the first day of hearing and her evidence was subsequently heard on the second day of hearing together with Professor Cade, the Director of Intensive Care at the Royal Melbourne Hospital.
7. A number of chest x-rays and a CT scan of May 2001 and February 2003 were the subject of questioning in the evidence of all of the doctors. The radiologists’ reports of those investigations are reproduced as follows (T‑documents, pages 119, 120, 100 and 99):
CHEST 11 May 2001 (p119)
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 right hilium. 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.
CT SCAN OF CHEST 17 May 2001 (p120)
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.
CONCLUSION – There is no lung mass lesion or other evidence of malignancy noted. Mild interstitial pulmonary fibrosis in the paravertegral gutters towards both bases.
CHEST X-RAY 8 February 2003 (p100)
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 be further assessed with CT.
10/02/2003 11:43 03/6615
FINAL – General MID Report
CHEST X-RAY 10 February 2003 (p99)
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.
8. CT examinations of the brain of the deceased of 8 February 2003 and 14 February 2003 were also of significance and the radiologists’ reports of both of those interventions are also reproduced as follows (T‑documents, pages 100 and 99):
CT BRAIN 8 February 2003 (p100)
Post ictal with continuing confusion. ? Intracerebral 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 intracerbral haemorrhage which measures 4x1.5cm in diameter centred in the dee [[sic] 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
4.1.5cm 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 angiopathy.
CLINICAL NOTES 14 February 2003 (p99)
Myoclonic status post intracerebral bleed. ? Extension of haemorrhage.
Non Contrast axial scans have been performed from skull base to vertex.
Hyperdense right parietal lesion, consistent with haematoma, is unchanged in dimensions. There is 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 4 x 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
Haematoma size unchanged. No significant increase in surrounding oedema.
No definite subfalcine/tonsillar/uncal herniation. No increase in ventricular size. No evidence of re-bleed.
dr richard byron-collins
9. Dr Byron-Collins is a forensic pathologist who provided two reports dated 12 August 2004 and 26 May 2005.
10. In his first report he opined that the features of the parietal lobe found upon CT scans were not definite and such features could be produced either by an intracerebral haemorrhage or by bleeding into a pre-existing lesion, being either primary or secondary. He thought that it was worth noting the opinion of the radiologist that the lesion at CT on 14 February 2003 was “consistent with haematoma”.
11. Dr Byron-Collins was of the opinion that there was a reasonable hypothesis that the deceased suffered a primary malignant lung tumour which metastasised to the brain which subsequently bled causing hospital admission and subsequent death. He noted that the X-rays of 2001 and the subsequent CT scan in the following week did not then confirm the presence of a tumour of the lung. However the appearances of the 2.5cm mass in 2003 were suggestive of a lung tumour.
12. In his second report, Dr Byron-Collins noted that the location of the “vascular shadowing” of May 2001 (initially thought to potentially be a tumour) had a different location to the mass found at X-ray in 2003. It therefore followed that it was more than likely that at 2003 the deceased did suffer a primary tumour in his right lung which could have metastasised to the brain.
13. In evidence, Dr Byron-Collins said that the findings on X-ray of 8 February 2003 of “well circumscribed opacity in the right lower zone medially” meant that there was a distinctly visible, well defined area in the lower zone of the lung. He said that the area of 2.5cm was of “reasonable size” and an X-ray of the lung – as opposed to a CT scan – would have been undertaken, because the deceased was then in a terminal phase and investigations were being undertaken to determine whether there was any infective process then present.
14. Dr Byron-Collins said that the chest X-ray of May 2001 was arranged by the deceased’s general practitioner because Mr Hadfield then had respiratory difficulty. The CT scan of 17 May 2001 discounted the presence of any tumour and the description “vascular shadow” was of no significance.
15. Dr Byron-Collins said that from an advisory opinion of the Disability Compensation Branch of the Department of Veterans’ Affairs (No. 13 of 2000), he observed that there was a 70 per cent likelihood of a primary lung tumour metastasising into the brain. On balance therefore, he was satisfied that the appearances at chest X-ray in 2003 suggested the presence of a primary lung tumour which ultimately metastasised into the deceased’s brain and bleeding then occurred within that secondary tumour. He said the mechanism for bleeding is the weakening of the walls of blood vessels as they grow within a tumour and surrounding tissue then is affected by the haemorrhaging. This is apparent upon CT scan.
16. Dr Byron-Collins was reluctant to comment upon the second hypothesis with respect to alcohol, because the quantities of alcohol consumed by the deceased did not meet applicable factors within the Statement of Principles (“SOPs”) according to the material that he had read.
17. In cross-examination, Dr Byron-Collins confirmed that the CT scan of 2001 excluded the presence of any tumour in the deceased’s right lung. He acknowledged that there appeared to be a shadow within the lung, and it was more likely than not that a tumour was not then present.
18. It was his opinion that the X-rays of the lungs in February 2003 clearly demonstrated a lesion in a different part of the lung to the shadow that appeared at the CT scan of 2001. He said that the appearance in 2003 was of a well defined and obvious lesion and the presence of a tumour then could not be excluded. He noted that the deceased had been admitted to hospital and was being treated for his cerebral bleeding and a chest X-ray would have been undertaken to determine whether there was any infective process. In those circumstances the treating doctors would not have considered a CT scan of the chest and lungs to be warranted.
19. Dr Bryon-Collins acknowledged that the cause of the cerebral haemorrhage remains unknown but a reasonable hypothesis exists that there had been a metastasis in the brain from the lungs which had haemorrhaged. He acknowledged that that opinion could not be expressed with any certainty nor upon the balance of probabilities but said that it was more than a possibility that a secondary tumour had bled.
20. Dr Byron-Collins was aware of the opinions expressed by Professor Cade. He acknowledged that the deceased probably did have some degree of amyloid angiopathy being an age related cerebral disease process. Nonetheless it was his opinion that bleeding within a tumour remained as more than a possibility.
dr woodruff
21. Dr Woodruff is a haematologist who provided two reports dated 16 September 2004 and 9 December 2004.
22. In his first report he noted that the SOP with respect to hypertension defined it as a “usual blood pressure” of a systolic reading greater than or equal to 140mmHg and or the diastolic reading greater than or equal to 90mmHg. Upon the blood pressure readings that he located within the T‑documents commencing in December 1993, it would appear that the deceased had been mildly hypertensive.
23. Dr Woodruff reported upon the history of the deceased’s alcohol consumption and noted that it was a risk factor in persons who were hypertensive. He also noted that the deceased had smoked cigarettes, and whilst acknowledging that cigarette smoking does not cause hypertension, it was his opinion that there was strong evidence that smoking caused damage to blood vessels. And in the case of persons who are hypertensive, they are at risk of cerebrovascular accident.
24. In evidence Dr Woodruff said that despite the first blood pressure reading that he could locate, being December 1993, it was unlikely that the deceased then became hypertensive. When he learnt of a blood pressure reading taken in 1945 of 140/70 at discharge from service, he thought that the deceased had then subsequently been mildly hypertensive.
25. In cross-examination, Dr Woodruff said that he was aware of the opinions expressed by Professor Cade but said that he would prefer to observe the films of the X-rays and CT scans of the deceased’s lung before he adopted the opinions that had been expressed. Conversely he said that what sometimes appears on X-ray to be a tumour, is “a shadow”. The belief by the radiologist in 2001 that “vascular shadowing” then found to be present at CT scan, would not have required any further investigation.
26. It was the opinion of Dr Woodruff that the intracerebral haemorrhage suffered by the deceased was caused by his chronic hypertension and the increased risk of haemorrhage due to the deceased’s prior cigarette habit. He said that cigarette smoking will not cause hypertension but significantly increases the risk of cerebral haemorrhage in persons who are hypertensive. He also noted that consumption of alcohol is a risk factor for hypertension.
27. Dr Woodruff thought that it was unlikely that there was any tumour in the deceased’s right lung. It therefore followed, that it was unlikely that there had been any metastases from the lung into the deceased’s brain. He said in his experience a cerebral metastases originating from a lung is more likely to cause multiple tumours. Additionally, any haemorrhaging from cerebral tumours having metastasised from the lung are more likely to be “round” in appearance upon CT scan. He said that from the documents he read, there was nothing that pointed to the deceased having any tumour in his lung.
28. When he was asked to consider the radiologist’s observations of the lungs in 2001 and 2003, ‑ noting also that the findings at 2003 were of 2.5cm in size – Dr Woodruff was of the opinion that a lung tumour did then exist, having regard to the history of cigarette smoking. Nonetheless he remained of the opinion that it was unlikely that a tumour of the lung would metastasise into the brain by a single lesion only. He reaffirmed his earlier opinion that any bleeding from a cerebral lesion would be round in appearance, whereas the radiologist reported that the haemorrhage was “elongated”.
29. Dr Woodruff also said that in his experience a metastases in the brain from the lung would produce multiple tumours in 80 per cent of cases.
30. In re-examination Dr Woodruff was asked to consider that if there was a 20 per cent chance of a single cerebral metastasis originating from the lung, whether he would regard that as being “absurd”, “ridiculous” or ”fanciful”. He said that if it was accepted that there was a tumour in the deceased’s lung in 2003 (having regard to its size and the absence of an apparent tumour in 2001), that by reason of the cerebral haemorrhage suffered by the deceased, there would have to be consideration of Mr Hadfield having suffered a haemorrhage into a cerebral tumour which had metastasised from the lung.
dr bernard gilligan
31. Dr Gilligan is a neurologist who prepared three reports dated 15 September 2004, 12 January 2005 and 13 May 2005.
32. In his first report he concluded that the cerebral haemorrhage suffered by the deceased was not related to hypertension associated with smoking or alcohol. However, the appearances upon chest X-ray in February 2003 could have represented a lung tumour, associated with prior smoking, and the cerebral haemorrhage could have occurred within a secondary tumour from the possible lung cancer. He reported that he regarded the latter hypothesis as being reasonable.
33. In his second report, Dr Gilligan thought that the opinion of Professor Cade of the deceased having amyloid angiopathy was a reasonable diagnosis, but the possibility of a secondary neoplasm existing in the brain having originated by a primary lung tumour was not excluded. He reported that the ovoid opacity found at X-ray on 8 February 2003 could possibly have been a primary lung tumour, and in the absence of an autopsy, this hypothesis was reasonable and could not be disproved.
34. In his third report, Dr Gilligan commented upon the opinions expressed by Professor Cade. He noted that it was the opinion of Professor Cade that the CT scan of 2001 dismissed the presence of any tumour but rather it gave the appearance of a “composite vascular shadow”. Whilst acknowledging that could be the explanation for the appearance, Dr Gilligan said that it could not be “proved”.
35. In the absence of any lesion having been found in the deceased’s lungs, Dr Gilligan said that the most likely diagnosis would be a primary intracerebral haemorrhage from amyloid angiopathy.
36. In evidence, Dr Gilligan confirmed his opinion that a possibility existed of the deceased having suffered a lesion in his right lung which could have metastasised into his brain. Whilst acknowledging that Dr Woodruff had given evidence concerning the probable shape of cerebral bleeding within a secondary cerebral tumour, he said that in his experience the “shape” as apparent upon X-ray or CT scan, would be either circular, ovoid, irregular or multi lobed. Additionally he said that a secondary metastases from the lung could either be single or multiple.
37. In cross-examination, Dr Gilligan expanded this theme and said that it could not be said with any degree of certainty that the deceased only suffered from a single cerebral tumour. He said that within the haemorrhage there could have been more than one cerebral tumour and it would be impossible to be confident that only a single tumour existed. Additionally he said that a CT scan, if taken, would not have necessarily shown the presence of all tumours.
38. Dr Gilligan said that it was possible that the appearance in the deceased’s right lung in 2003 was related to the appearance at 2001 because both appearances were in the same zone of the right lung. Later he said that whilst the radiologist in 2001 referred to the “mid zone” and the radiologist in 2003 referred to the “lower zone”, he acknowledged that it was possible that there were two separate lesions or there had been a growth of the lesion of 2001 from 6mm to 2.5cm in size, thereby extending it from one zone to another. Alternatively, there had been an inadequate description by the radiologists of the particular zones of the lung where the lesions existed.
39. Dr Gilligan said that it was not possible, on the balance of probabilities, to find that there was a tumour in the deceased’s lung. However, he noted that the radiologist concluded after a CT scan of 2001 that a tumour did not exist, but “something” was present upon chest X-ray in 2003. He said the presence of a tumour could not then be excluded and a reasonable hypothesis did exist; the deceased having been engaged in service, taking up a smoking habit, developing a lung tumour which metastasised to his brain which ultimately bled and which caused death.
40. Dr Gilligan was of the opinion that if a tumour in 2001 was excluded or if it was considered as being present but being 6mm in size only, a 2.5cm tumour in 2003 was highly suggestive – against the history of chronic cigarette smoking – of a malignant lesion then being present.
41. When the hearing resumed on 21 July 2005, Professor Cade and Mrs Hadfield both gave evidence.
professor cade
42. Professor Cade is the Director of Intensive Care at the Royal Melbourne Hospital (“RMH”). He provided three reports in this matter dated 6 December 2004, 30 December 2004 and 15 April 2005. All of the reports were received into evidence.
43. Professor Cade said that he had read the reports of Doctors Byron-Collins, Woodruff and Gilligan and whilst he agreed “broadly” with some of their conclusions, it was his opinion that upon either hypotheses advanced, no relationship with service existed. In his reports, he concluded that the deceased died from a cerebral haemorrhage but by reason of amyloid angiopathy, being an age related state of fragile blood vessels. In his report of 6 December 2004, he said it was “most likely” that amyloid angiopathy was responsible for the cerebral haemorrhage and he found no evidence of any other cerebral lesion such as a tumour – either primary or secondary – being responsible for the haemorrhage. Additionally he dismissed the other hypothesis advanced in this application; namely, an association between service, hypertension and death, because in his opinion, and upon the LMO notes, the deceased was not hypertensive.
44. Professor Cade discussed the X-rays and CT reports of 2001 and 2003. He said the radiologist who conducted the chest X-ray on 11 May 2001 was suspicious that the deceased did have a primary carcinoma because of the presence of a “6mm rounded opacity in the right mid zone” and recommended that a CT scan be undertaken. That was conducted on 17 May 2001 and a lesion was not found. The radiologist reported that the “previously suspected mass on the plain film is probably due to composite vascular shadowing”. Professor Cade said that the appearance of a suspected lesion at X-ray was probably caused by the angle of the image, this being common in X-rays. He said that a CT scan depicts a 3D image which excludes “shadowing” but often demonstrates overlapping blood vessels. He said that the CT scan of 17 May 2001 dismissed the presence of any lesion.
45. Professor Cade noted that a CT scan of the deceased’s lungs was not performed at all following admission to hospital in February 2003 but it was a chest X-ray on 8 February that reported a “small ovoid 2.5cm well circumscribed opacity” in the right lower zone. Professor Cade said that the right zone is adjacent to the mid zone being the zone where a lesion was suspected in the X-rays of May 2001. Professor Cade said that by comparison of the X-rays of May 2001 and February 2003, he had assumed that the lesion first thought to exist, and again thought to have existed in 2003, was in the same zone. He noted that the radiologist in February 2003 recorded in the body of the report that previous films would be needed to exclude any neoplastic process. Professor Cade thought that the X-ray of 10 February 2003 may have been taken by a mobile machine whilst the applicant was immobilized in bed and thought that film obtained by such a process was “satisfactory but had limitations”.
46. Professor Cade concluded that on the balance of probabilities the deceased did not have a lesion in his right lung. It therefore followed that the lung could not have been the primary site for a metastases in the deceased’s brain and he remained of the view that the cause of death was amyloid angiopathy. He also confirmed an opinion expressed in his report of both 30 December 2004 and 15 April 2005, that in the absence of a lesion in the lung and the absence of any evidence of a metastases in the brain, a “speculative metastases from a speculative primary cancer does not seem to me to provide the basis for a plausible hypothesis”. He acknowledged that the possibility for such a hypothesis existed but it did not amount to a probability. Additionally he said that if there was one metastases only in the deceased’s brain, it was unlikely that it had its primary origin in the right lung. That is to say, a primary lung tumour having metastasised into a person’s brain is more likely to produce multiple tumours.
47. In cross-examination Professor Cade explained that his description of the cause of death by amyloid angiopathy as “most likely” (as he reported on 6 December 2004), was a description used by him in the absence of post-mortem. He said all the clinical signs and information made available to him, dismissed the probability of a pre-existing lung tumour having metastasised to the brain. Rather, having regard to the deceased’s age and the absence of the radiologist observing any cerebral tumours, amyloid angiopathy was most likely to have been the cause of death.
48. Professor Cade conceded that Dr Woodruff had become suspicious of the presence of a lesion in the lung because in 2001 the mass was then observed to be 6mm in size, whereas, in February 2003 it was 2.5cm in size. However Professor Cade said that a CT scan in 2001 had excluded the presence then of a tumour and in the absence of a CT scan of the lung in 2003 there was no clinical data which would then establish the presence of a tumour, on the balance of probabilities. Additionally, he noted that the language used by the radiologist in 2003 was similar to the language of the radiologist in 2001 suggesting to him that the radiologist was observing shadowing and held no more than a suspicion of the existence of a tumour. It was also noted that previous films were not available for comparison.
mary catherine hadfield
49. Mrs Hadfield is the widow of the late Frederick Selby Hadfield. She provided a report with the assistance of her solicitors on 29 June 2004 which was received into evidence.
50. Mrs Hadfield said that she met her husband in 1940 and married him on 11 August 1942. She recalled that her husband served in New Guinea but did not speak about his service nor about any illnesses that he may have suffered. Mrs Hadfield said that she did not know whether her husband was hypertensive or had been treated for hypertension. She said that there were “lots of things he didn’t tell me about and if he did go to the doctor he would keep it to himself”. She said that her husband did consume Dilantin medication following a head injury he suffered in the 1950’s.
51. Mrs Hadfield said that her husband consumed alcohol to excess. She said that he drank every day of the week except on Sundays and was frequently drunk when he arrived home from work. She said there was conflict between her and her husband because of the quantity of cigarettes that he smoked and the quantity of alcohol that he drank. She said that he drank less alcohol after his retirement in 1982 and until the mid 1990’s he was drinking three or four stubbies of beer per day. She said that in his last years he was very unwell and did not drink daily. She said that in the last twelve months of his life he would drink “a can occasionally”.
conclusion and reasons for decision
52. In the present application there was agreement between both parties that the cause of death of the late Mr Hadfield was a cerebral haemorrhage. This is consistent with the certified cause of death found within the Death Certificate found at page 24 of the T‑documents. The issue in this review was whether there was a connection between the service of the deceased and the cause of his death.
53. There was no contest that the deceased did consume cigarettes and alcohol in his lifetime subsequent to service. The respondent conceded a connection between service and cigarette consumption and between service and alcohol consumption. Additionally, it was conceded that if a primary lung tumour was found to have existed, that it would have, as its cause, the pre-existing smoking habit.
54. One of the hypotheses advanced by the applicant was that a war-caused smoking habit precipitated the presence of a primary right lung tumour which metastasised into the deceased’s brain and which ultimately haemorrhaged and was responsible for death.
55. In the alternative, the pre-existing cigarette and alcohol habit was responsible for hypertension which contributed to a cerebrovascular accident which precipitated the cerebral haemorrhage and death.
56. In Repatriation Commission v Hancock [2003] FCA 711 (“Hancock”) Selway J decided to apply a decision of the Full Federal Court in Repatriation Commission v Deledio (1998) 83 FCR 82 (“Deledio”) in order to decide whether there was a proof of any entitlement under the Veterans’ Entitlements Act 1986 (“the Act”). However His Honour additionally decided that there were pre-existing matters which required attention before there was any focus on the four steps found within the Deledio principles. Whilst acknowledging that some of those pre-existing steps were self-evident, namely, that the deceased was a veteran, that he was deceased and that his widow was the applicant, it was necessary to identify the “`kind of death' suffered by the veteran”. Further, His Honour decided that whilst in most cases the “kind of death” will be obvious, the identification of the “kind of death” is by proof on the balance of probabilities. At paragraph 11 in Hancock His Honour then discussed the stages of analysis in order to determine whether a reasonable hypothesis existed. His Honour decided that having determined the “kind of death” on the balance of probabilities, SOPs, if any, were to be identified and the Deledio methodology was to be invoked.
57. The four stages of analysis in Deledio are reproduced as follows:
1. The tribunal must consider all the material which is before it and determine whether that material points to a hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person. No question of fact finding arises at this stage. If no such hypothesis arises, the application must fail.
2. If the material does raise such a hypothesis, the tribunal must then ascertain whether there is in force an SoP determined by the authority under s 196B (2) or (11). If no such SoP is in force, the hypothesis will be taken not to be reasonable and, in consequence, the application must fail.
3. If an SoP is in force, the tribunal must then form the opinion whether the hypothesis raised is a reasonable one. It will do so if the hypothesis fits, that is to say, is consistent with the "template" to be found in the SoP. The hypothesis raised before it must thus contain one or more of the factors which the authority has determined to be the minimum which must exist, and be related to the person's service (as required by ss 196B (2) (d) and (e)). If the hypothesis does contain these factors, it could neither be said to be contrary to proved or known scientific facts, nor otherwise fanciful. If the hypothesis fails to fit within the template, it will be deemed not to be "reasonable" and the claim will fail.
4. The tribunal must then proceed to consider under s 120 (1) whether it is satisfied beyond reasonable doubt that the death was not war-caused, or in the case of a claim for incapacity, that the incapacity did not arise from a war-caused injury. If not so satisfied, the claim must succeed. If the tribunal is so satisfied, the claim must fail. It is only at this stage of the process that the tribunal will be required to find facts from the material before it. In so doing, no question of onus of proof or the application of any presumption will be involved.
58. In the present application there is material which points to both hypotheses raised by the applicant and there are applicable SOPs. The first two stages accordingly are satisfied.
59. In relation to the third stage, the applicable SOP with respect to cerebrovascular accident, being the precipitator of death in this application was Instrument No. 52 of 1999 being the only relevant SOP for that injury within the assessment period. Factor 5 (a) concerns the presence of hypertension before the clinical onset of cerebrovascular accident, factor 5 (e) refers to the consumption of alcohol before the clinical onset of cerebrovascular accident and 5(m) (v) refers to bleeding within an intra cerebral space occupying lesion immediately before the clinical onset of cerebrovascular accident. The SOPs with respect to hypertension within the assessment period relevantly are Nos 35 of 2003 and No 3 of 2004. Factor 5 (b) in the earlier Instrument refers to the consumption of at least 200gms of alcohol per week which cannot be decreased to less than an average of 200gms per week at the time of clinical onset of hypertension. The latter Instrument revoked that factor and substituted a factor of consumption of an average of 200gms per week of alcohol for a continuous period of at least six months immediately before the clinical onset of hypertension which cannot be decreased to less than an average of 200gms per week.
60. In the present application the hypotheses raised are reasonable because they are consistent with the template of the SOPs.
61. It is only at the fourth stage of Deledio that fact finding is required.
the service → smoking → lung → tumour → cerebral tumour → haemorrhage → death ypothesis
62. The hypothesis of connection between service and smoking involved the development of a primary lung tumour which metastasised to the deceased’s brain causing haemorrhage and death. There was an intra cerebral haemorrhage without doubt, but I am not satisfied on the balance of probabilities that it had its origin in a secondary tumour which had metastasised from a primary lung tumour. I make this finding on the basis that I am not satisfied on the balance of probabilities that a primary lung tumour did exist.
63. Dr Byron-Collins said that a “reasonable hypothesis existed of a primary tumour in the lung” in his report of 12 August 2004. In his report of 30 May 2005, he reported that there was a possible “duality of lesions” when the chest X-rays of 2001 and 2003 were considered and compared. He concluded that a right lung lesion existed. That opinion was not put on the balance of probabilities and, having regard the evidence of Professor Cade in particular, and upon observation of the CT result of the chest in 2001, I cannot be satisfied on the balance of probabilities that the suspicious appearance at chest X-ray in 2001 was in fact a primary tumour. On the evidence of Professor Cade, the language of the radiologist in 2003 was similar to the language used in 2001, suggesting, that in 2003, the radiologist was again observing “shadowing”. A CT scan was not taken of the deceased’s lung in 2003 and a diagnosis of a lung tumour by CT procedure could not be concluded.
64. Dr Gilligan in his report of 15 September 2004 was suspicious that the chest X-ray taken at St Vincent’s Hospital did have features which could have been a lung tumour, not diagnosed, and thought that a reasonable hypothesis existed between the presence of a lung tumour metastasising as a secondary tumour into the deceased’s brain. In his report of 13 May 2005, he stated that it could not be disproved that the shadowing in 2001 was not a tumour then existing. This theory, in my view, is deficient because it does not acknowledge that the CT scan of the deceased’s chest in the following week excluded the presence of a lung tumour.
65. Having regard to the evidence of Dr Byron-Collins, Dr Gilligan and the evidence of Professor Cade in these proceedings, I could not on the balance of probabilities find, as a fact, that a lung tumour existed. The history of cigarette smoking would ordinarily cause a suspicion of a lung cancer. But the pathology does not support such a diagnosis. At best, the evidence put the presence of a lung tumour as a possibility. Professor Cade thought it was speculative.
66. Additionally, I cannot be satisfied, on the balance of probabilities that a cerebral tumour existed, even assuming that it was primary or originating from the lung. The evidence of the doctors referred to a primary or multiple tumours or the possibility of tumours not being seen by reason of the haemorrhaging.
67. Dr Byron-Collins said that the haemorrhage in the deceased’s brain would have either been by reason of a metastatic tumour having its origin in the lung or by a “pure intra cerebral tumour”. The deceased did suffer from an intra cerebral haemorrhaging, and upon the evidence of the treating doctors at St Vincent’s Hospital, as well as Professor Cade, the most likely cause of this cerebral haemorrhage was amyloid angiopathy. Dr Gilligan was of the opinion that in the absence of a metastasised cerebral tumour, the most likely cause of death was amyloid angiopathy. He said the size and site of the haemorrhage alone pointed to amyloid angiopathy (refer report 15 September 2004).
the service → alcohol/cigarettes → hypertension → cerebrovascular accident → haemorrhage → death hypothesis
68. The remaining hypothesis with respect to hypertension was of some controversy. Professor Cade said that the deceased was not hypertensive. In a report of 25 July 2003, the deceased’s LMO recorded that he had “normal blood pressure”. Dr Woodruff however summarised clinical data and found 13 references to blood pressure readings between December 1993 and October 2002. He recorded those readings in his first report. The only other blood pressure reading that I could locate within the T‑documents was of the deceased in his discharge medical examination being found then (in 1945, when aged 26 years) to be 140/70.
69. The definition of hypertension within the SOP is of a “usual” blood pressure reading of a systolic reading greater than or equal to 140mmHg or a diastolic reading greater or equal to 90mmHg.
70. The blood pressure readings recorded by Dr Woodruff, together with the reading at the discharge medical examination, are the only readings available. Except for the word “usual” in the definition of hypertension within the applicable Instrument it would appear that the deceased, at least from 1993, was hypertensive. This would satisfy factor 5 (a) of the cerebrovascular accident SOP but there would need to be satisfaction of a sub-hypothesis, being factors existing as a minimum before it could be said that hypertension was related to service. In the present case the only applicable factors within the two hypertension Instruments existing within the assessment period, concern the consumption of alcohol of at least 200gms per week, either at the time of the clinical onset of hypertension or at least six months before the clinical onset.
71. In evidence and in her statement, Mrs Hadfield recorded that her husband retired in 1982 and thereafter considerably reduced his consumption of alcohol. She said in the last five or ten years of his life he was drinking not more than one or two small cans of beer “per drinking session” and in his last 12 months he would drink “a can occasionally”.
72. “Alcohol” is defined within Instrument No 35 of 2003 as being measured by a standard of 10gms per standard alcoholic drink.
73. Two hundred grams of alcohol would amount to 20 standard drinks per week. On the evidence of Mrs Hadfield, her husband was not consuming alcohol at that level after 1982.
74. Between the discharge of service of Mr Hadfield in 1945 and the blood pressure reading reported by Dr Woodruff in December 1993, nothing is known as to whether the deceased was hypertensive. There are no other records available, Mrs Hadfield did not know whether her husband was hypertensive and the LMO said that the deceased had “normal blood pressure”.
75. I cannot find as a fact that between 1945 and November 1993 that the deceased was hypertensive. There was no evidence which would permit such a finding on the balance of probabilities. Hypertension as defined, is a reference to the “usual” blood pressure. The “usual” blood pressure of the deceased before 1993 other than the solitary reading in 1945 is not known. It is unlikely that the deceased suddenly became hypertensive in 1993 but whether he was hypertensive in 1982 is unknown.
76. It would appear that the deceased was heavily consuming alcohol prior to his retirement in 1982. There is nothing which points to him being hypertensive at or about that time. Accordingly I cannot find that factor 5 (b) of Instrument No 35 of 2003 or factor 5 (b) as amended by Instrument No 3 of 2004 is satisfied. In making these findings I cannot find the clinical onset of hypertension was in 1982.
77. I am therefore unable to find as a fact that the deceased was consuming 200gms of alcohol per week at the time of the clinical onset of hypertension or for a continuous period of at least six months before the clinical onset of hypertension. On the clinical data I would be obliged to find the clinical onset occurred in December 1993.
78. Mr Larkin conceded that the Mrs Hadfield could not satisfy factor 5 (e) of the cerebrovascular accident Instrument because it could not be established as a fact that the deceased consumed 250gms alcohol per week immediately before the clinical onset of cerebrovascular accident. Indeed in the last year of his life very modest quantities of alcohol were consumed which did not approach the level dictated by this factor. Accordingly factor 5 (e) cannot be satisfied. Additionally, factor 5 (m) (v) could not be satisfied because any intracerebral bleeding must have a connection with the circumstances of service. For the reasons given earlier, I cannot make such a finding.
79. Dr Woodruff said there was an association between smoking and hypertension by an adverse affect on blood vessels, putting persons at risk of cerebrovascular accident. Whatever might be thought of this hypothesis, there is no factor within the hypertension SOPs which refers to smoking and the cerebrovascular accident SOP refers to smoking only in the case of cerebral ischaemia and not in the case of intracerebral haemorrhage.
80. On the balance, I am satisfied beyond reasonable doubt that there is no sufficient ground to determine death of the late Frederick Selby Hadfield was war‑caused.
I certify that the 80 preceding paragraphs are a true copy of the reasons for the decision herein of ‑
Mr John Handley, Senior MemberSigned: Alice Beattie
AssociateDates of Hearing 1 June and 21 July 2005
Date of Decision 1 August 2005
Counsel for the Applicant Mr A Larkin
Solicitor for the Applicant Williams Winter
Departmental Advocate Mr E Nyhof
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