MARGERY JOYCE SWINDELLS and REPATRIATION COMMISSION
[2010] AATA 482
•30 June 2010
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2010] AATA 482
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2007/6297
VETERANS’ AFFAIRS DIVISION ) Re MARGERY JOYCE SWINDELLS Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mr Egon Fice, Senior Member
Miss E A Shanahan, MemberDate30 June 2010
PlaceMelbourne
Decision
The Tribunal affirms the decision under review.
(sgd) Egon Fice
Senior Member
VETERANS’ AFFAIRS – ischaemic heart disease – contribution to veteran’s death – kind of death – pathological changes leading to death - death caused by hypercalcaemia and progressive low grade lymphoma
Veterans’ Entitlement Act 1986 ss 7, 8, 13, 120, 120A, 196B
Collins v Repatriation Commission [2009] FCAFC 90
Doolette v Repatriation Commission (1990) 21 ALD 489
Repatriation Commission v Deledio (1998) 83 FCR 82
Repatriation Commission v Hancock (2003) 37 AAR 383
Repatriation Commission v Law (1980) 31 ALR 140
Repatriation Commission v Law (1981) 147 CLR 635
REASONS FOR DECISION
30 June 2010 Mr Egon Fice, Senior Member
Miss E A Shanahan, Member1. Mrs Margery Joyce Swindells is the widow of Mr Keith Alex Swindells, who died on 25 December 2006. She lodged an application for a widow’s pension with the Department of Veterans’ Affairs (DVA) on 6 February 2007. Mr Swindells’ death was certified by Dr A Waldron, who listed the causes of death as hypercalcemia of six months duration; progressive low grade lymphoma of 10 months duration; and chronic lymphocytic leukaemia of 18 months duration. Mrs Swindells’ contended that underlying existing ischaemic heart disease, a condition which the DVA had accepted as being war-caused, contributed to her husband’s death.
2. Mr Swindells served in the Royal Australian Air Force (RAAF) from 27 January 1944 to 7 March 1945. His service constitutes eligible war service as that expression is defined in the Veterans’ Entitlements Act 1986 (the Act) because Mr Swindells served in the South West Pacific area. The Repatriation Commission (the Commission) accepted that the whole of Mr Swindells’ service was operational service.
3. On 4 April 2007 a delegate of the Commission determined that Mr Swindells’ death was not related to his war service and therefore a pension was not payable to Mrs Swindells. She sought a review of that decision by the Veterans’ Review Board (VRB). On 19 November 2007 the VRB affirmed the Commission’s decision. Mrs Swindells now seeks a review of the VRB decision by this Tribunal.
4. We are required to determine:
(a) the kind of death (cause of death) met by Mr Swindells; and
(b)whether Mr Swindells’ death was war-caused within the meaning of s 8 of the Act.
KIND OF DEATH
5. Where the death of a veteran was war-caused, the Commonwealth is, subject to the Act, liable to pay a pension by way of compensation to the dependants of the veteran in accordance with the Act (s 13). To be eligible to receive the pension Mrs Swindells must establish that her husband’s death was war-caused.
6. Section 8 of the Act provides that, for the purposes of the Act, the death of a veteran is taken to have been war-caused if, amongst other things, the death arose out of, or was attributable to, any eligible war-service rendered by the veteran. The meaning of the expression eligible war service is set out in s 7(1) of the Act. A person who has rendered operational service is taken to have rendered eligible war service while the person was rendering operational service.
7. Prior to embarking upon enquiry into the claimed connection between Mr Swindells’ death and his operational service, we must first determine the cause of death or, as it is referred to in the Act, kind of death met by Mr Swindells. As Selway J said in Repatriation Commission v Hancock (2003) 37 AAR 383 at 385:
… But in cases such as the present, the identification of the “kind of death” is the critical step in the analysis. In determining the “kind of death”, proof is on balance of probabilities: see section 120(4) of the act and see Fogerty v Repatriation Commission [2003] FCA FC 136 at [34]; Benjamin v Repatriation Commission (2001) 34 AAR 270 at 282-283 [53] – [54].
8. The Full Court of the Federal Court (Mansfield, Stone and Edmonds JJ) in Collins v Repatriation Commission [2009] FCAFC 90 dealt comprehensively with how the expression kind of death should be interpreted. They said, at 287-288:
Sections 8 and 13 [VE Act] look to the “death” of a veteran, but do not use the term “kind of death”. Similarly, s 120 refers to the relationship of a veteran’s death with the operational service of the veteran. It also does not use the term “kind of death”. The term “kind of death” is introduced by ss 120A(2) and (4) and 196B(2) in the expression “particular kind of injury, disease or death”. That expression refers to the circumstances in which a Statement of Principles may be determined and then applied to decide whether an hypothesis connecting an injury or disease or death is reasonable as assessed under ss 120(1) and (3) as informed by s 120A(3).
The proper construction of those different terms was not a matter of debate on the appeal. It was common ground that, where the word “death” appears in ss 8 and 13 it means the medical cause of the death.
9. As the Full Court said, the question regarding the nature of the death of a veteran is anterior to and distinct from the relationship of the death to the service of the veteran and the extent of entitlement to benefits under the Act in respect of that death. As to determination of the first question, the Full Court said, at 288:
In our view, the word “death” used in s 8, and in the phrase “injury, disease or death” in s 13 has the same meaning, that is the nature of the condition which causes the death. To be more precise, it is the medical cause or causes of the death.
10. The fact that there may be more than one medical cause for a veteran’s incapacity or death was recognised by the Full Court of the Federal Court (Bowen CJ, Brennan and Lockhart JJ) in Repatriation Commission v Law (1980) 31 ALR 140. That decision was upheld on appeal to the High Court of Australia (147 CLR 652). The Court said, at 151:
It seems clear that the expression “attributable to” in each case involves an element of causation. The cause need not be the sole or dominant cause: it is sufficient to show “attributability” if the cause is one of a number of causes provided it is a contributing cause.
11. Relying on the above expression regarding attributability of cause, O’Loughlin J, in Doolette v Repatriation Commission (1990) 21 ALD 489, at 492, said:
I see no reason to consider that expression “was attributable to” appearing in the present legislation should be interpreted differently. In addition, the Learned Deputy President pointed out, and I agree, that if death is hastened because of the accelerated progress of a disease, which acceleration was itself caused by a war‑caused condition, the proper conclusion would be that death was attributable to war service: Re Blyth and Repatriation Commission (1982) 4 ALN N147.
12. Although it might be thought that Doolette stands for the proposition that simply hastening death by the acceleration of progress of a disease could properly be regarded as causative of the death of a veteran, the Full Court in Collins’ case made it clear that this did not necessarily follow from the legislation. Mansfield and Stone JJ dealt with the contention that, where a medical condition contributes to the death of a veteran only by affecting its timing, it is an error of law on the part of the Tribunal to conclude that, for the purposes of ss 8, 13, 120 and 120A of the Act, the death (a medical cause of death) or the kind of death does not include that medical condition. Their Honours said, at 291:
The contention necessarily carries with it the proposition that any particular effect upon the time of death must as a matter of law be a death and a kind of death.
13. However, after close examination of the sections dealing with death and kind of death, their Honours said it is clear that the sections ask a causative question. They then said, at 296:
Those provisions support the conclusions that the enquiry about the death or the kind of death for the purposes of the VE Act is, in essence, a question of fact about the medical cause or causes of the death. It does not support the proposition on behalf of Mrs Collins that there is a legislative intention that any medical condition which hastens the time of death of a veteran by a measurable period, even a short one, where in medical terms another medical condition is clearly the medical condition which accounts for the pathological changes leading to death, is itself a medical cause of death.
14. Mr Swindells suffered an acute myocardial infarct (heart attack) in 1991 and was hospitalised for eight days. Following that event, he commenced the regime of medication that is standard for such events. He ceased smoking. From 1997 he received a disability pension for his ischaemic heart disease, amongst other conditions. The ischaemic heart disease was attributed to cigarette smoking which he commenced during operational service.
15. In October 2004 Mr Swindells applied for a review of his pension, with a view to increasing it to 100 per cent of the general rate. At that time one of his treating general practitioners, Dr Ong, assessed his exercise tolerance at 3 to 4 METS, indicating he became short of breath on mild to moderate exertion such as walking at 5 km per hour, pulling a golf buggy, mowing with a power mower, and vacuuming. Mr Swindells was diagnosed with hypertension in 2001 and was treated with various medications.
16. Mr Swindells’ medical history from 2000 to 2006 has been taken from the clinical notes relating to Mr Swindells’ treatment by his general practitioner Dr Waldron; St Vincent’s Hospital medical records; and the Echuca Regional Health Hospital records. There was no dispute about the facts set out in those records.
17. Dr Waldon’s clinical notes disclose that until March 2005 Mr Swindells regularly attended for blood pressure checks and for repeat prescriptions for his cardiac and osteoarthrosis drugs and anti-hypertensives.
18. On 1 March 2005 Mr Swindells complained of a two month history of dry nocturnal cough and was found to have crepitations (a crackling sound) over the right upper lobe of the lung. A chest X-ray revealed slight widening of the mediastinum (the area behind the breast bone), then thought to be due to vascular ectasia (dilatation), and minor areas of collapse (atelectasis) in the left lower lobe of the lung. While his cough improved, it persisted. A routine full blood examination on 26 April 2005 (his previous blood examination was in September 2003) revealed a markedly elevated lymphocyte count and the blood film suggested chronic lymphocytic leukaemia. Lymphocyte surface markers performed on 16 May 2005 confirmed the diagnosis of chronic B-cell lymphocytic leukaemia (CLL). An urgent referral to a haematologist was arranged and he was seen by Dr A Dowling. A decision was made to observe and not to actively treat the CLL.
19. A CT scan of the chest was performed on 17 October 2005. This revealed enlarged mediastinal lymph nodes and nodular opacification (becoming opaque) in part of the left lower lobe of the lung. Mr Swindells was referred to a consultant respiratory physician, Dr G Russell. Dr Russell performed lung function tests on 23 January 2006 which showed very minimal air flow limitation, that is, mild chronic obstruction pulmonary disease (COPD). Dr Russell diagnosed asthma.
20. In late January 2005 Mr Swindells developed right posterior chest wall pain that progressively worsened. He also developed pain in the right upper quadrant of his abdomen. A CT scan of his abdomen on 16 February 2006 revealed retroperitoneal lymph node enlargement, enlargement of the spleen and a right basal pleural effusion (fluid in the thoracic cavity). By 26 April 2006 the right effusion was described as huge and Mr Swindells was short of breath. A small left pleural effusion was also noted on X‑ray. On 1 May 2006 a right enlarged cervical (neck) lymph node was noted. Repeat CT scanning showed wide spread lymph node enlargement. The right pleural effusion was drained on 17 May 2006, 2.5 litres of fluid being removed. Arrangements were made for Mr Swindells’ transfer to St Vincent's Hospital for a pleurodesis. Chemotherapy with Chlorambucil, given orally, was commenced following the pleurodesis. Despite this treatment, Mr Swindells' peripheral blood lymphocytes initially remained over 50,000, the norm being 1,000 to 4,000.
21. Mr Swindells was admitted to St Vincent's Hospital on 4 June 2006 for a video assisted thoracoscopy (VATS) and talc pleurodesis (surgical adhesion) to relieve the right pleural effusion. On admission, Mr Swindells completed a pre-admission assessment in which he answered a number of questions. He answered No to the question regarding whether he experienced any chest pain or angina. Dr C Tippett, who conducted his pre-anaesthetic assessment, recorded Mr Swindells had a myocardial infarct in 1991 and had not had any chest pain since that date.
22. At the VAT procedure, 1200mls of pleural fluid was removed. The pleura (membrane enfolding both lungs) was grossly abnormal and biopsies were taken. Talc was instilled to effect pleurodesis. The histopathology of the pleural biopsies showed pleura infiltrated by a small cell lymphoma. On full blood examination, lymphocyte counts were now of the order of 60,000. The veteran's post-operative recovery was uncomplicated and he returned home on 10 June 2006.
23. The hospital records disclose a chest X-ray of 26 May 2006 showing the heart size to be normal and a CT scan of 25 May 2006 disclosed a marked increase in the intrathoracic, abdominal and iliac chain lymphadenopathy and bilateral pleural effusions.
24. In September 2006 Mr Swindells again complained of posterior chest and right upper quadrant abdominal pain. Investigations ordered this time (22 September 2006) revealed a markedly elevated serum calcium, elevated urea and creatinine. The serum calcium had never before been estimated.
25. Despite ongoing treatment with Mabthera, a monoclonal antibody, Mr Swindells continued to deteriorate with his serum calcium levels remaining high, his haemoglobin low but renal function, as measured by urea and creatinine levels, slightly improved. His abdominal pain increased and MS Contin (slow release morphine) was commenced on 2 November 2006. On 17 November 2006 Dr Zenel recorded that Mr Swindells was dyspnoeic (short of breath) but there was no evidence of cardiac failure. From early December Mr Swindells was described as stable but slowly fading. Two weeks later he was described as fading but comfortable.
26. Mr Swindells was admitted to the Echuca Hospital on 21 December 2006 with a five to seven day history of constipation, shortness of breath and increased frequency of micturition (voiding of urine). When he was examined it was found that air entry was reduced over the left lower lobe of the lung, crepitations were present, as was pitting oedema (swelling due to fluid collection associated with impaired venous drainage) of the ankles. On 22 December 2006 he became confused. Dr Waldron ordered palliative care only and directed that Mr Swindells was not to be resuscitated. Mr Swindells continued to deteriorate. All medication was ceased on 24 December 2006 and he was given morphine injections regularly. He died on 25 December 2006.
27. Mr Swindells had previously been admitted for a course of intravenous Mabthera, given weekly over a period of four weeks. He was also admitted on several occasions for blood transfusions when his haemoglobin fell to 9 grams per litre. When he was admitted as a day case for Mabthera and blood transfusions, it was noted that he had responded to the extent that his circulating lymphocytes fell to a normal level but his haemoglobin and calcium levels remained unchanged. His urea and creatinine levels varied but the trend was toward normal.
28. Dr Burns was nominally Mr Swindells' treating oncologist but as most treatment took place in Echuca, Dr Dowling was frequently involved. Dr Dowling saw Mr Swindells initially on 1 June 2005 and advised a conservative, wait and see approach, given the lack of symptoms. A four-monthly review was advised and Dr Dowling continued the follow up until mid-February 2006. Dr Burns saw Mr Swindells on 15 September 2005, on 27 April 2006, in June 2006 when Mr Swindells was hospitalised at St Vincent's Hospital, on 19 August 2006 and, for the last time, on 14 September 2006.
29. Treatment for CLL/lymphoma was commenced in June 2006 after Mr Swindells had undergone pleurodesis. Dr Burns' letters to Dr Waldron indicated Mr Swindells was responding to treatment as his lymphocyte count had fallen. On 29 June 2006 Dr Burns reported the physical findings of bilateral pleural effusions or pleural thickening and an enlarged right cervical lymph node.
30. In August 2006 the cervical node had decreased markedly in size and the right pleural effusion/thickening was less marked. A repeat CT scan was to be performed in September 2006. When he saw him on 14 September 2006, Dr Burns described Mr Swindells as quite well with lessening cough but persisting abdominal pain. The CT scan in September revealed a persisting left pleural effusion and generalised lymphadenopathy. Treatment with Chlorambucil was to continue. This was the last time Dr Burns saw Mr Swindells. Dr Dowling was the oncologist who diagnosed progressive disease from CT scanning with associated hypercalcaemia. He initiated treatment with Mabthera.
31. Dr Burns provided two reports, dated 2 December 2008 and 20 July 2009, which were admitted into evidence. The salient points in the first report were:
· Mr Swindells’ CLL was reasonably well controlled at the time of his death.
· The development of Non-Hodgkin's Lymphoma may have been related to his earlier diagnosed CLL.
· It was possible that ischaemic heart disease contributed to the right pleural effusion.
· Dr Burns considered it likely that Mr Swindells' ischaemic heart disease and COPD significantly hastened his death.
· There was evidence of congestive cardiac failure on Mr Swindells’ admission to Echuca Hospital on 21 December 2006 in the form of shortness of breath, decreased air entry over the right lower lobe and bilateral crepitations (the clinical notes state that the air entry was decreased over the left lower lobe of the lung and that there were basal crepitations, not bilateral crepitations).
· A CT scan prior to admission showed a left pleural effusion which had increased sequentially over several months.
· Dr Burns believed the signs of the left pleural effusion, crepitations and ankle oedema favoured congestive cardiac failure rather than progressive low grade lymphoma, CLL or hypercalcaemia.
· The hypercalcaemia had been present over preceding months and was unlikely to be a primary cause of death.
32. Dr Burns’ report dated 20 July 2009 was in response to the reports and opinions of Professors Cade and Fox. Dr Burns' opinion was unchanged by these reports. He agreed with Professor Cade that chest imaging throughout 2006 did not show any evidence of cardiac enlargement or pulmonary congestion but rejected Professor Cade's opinion that Mr Swindells' peripheral oedema was due to venous obstruction. His rejection was based on a CT scan of 15 September 2006 which showed the inferior vena cava to be patent (blood flowing) although displaced by the enlarged retroperitoneal lymph nodes. Dr Byrne’s also rejected Professor Fox's attribution of the left pleural effusion and leg oedema to a low serum albumin.
33. In his oral evidence, Dr Burns maintained his opinions as expressed in his written reports but acknowledged that the CLL and B-cell lymphoma were part of the same lymphoproliferative disorder and not separate entities. He also agreed that the hypercalcaemia was due to this malignancy. He said that while the CLL was incurable, it was treatable. In his opinion, the CT scan in September 2006 showed stable disease and it was not until mid-November 2006 that scanning showed progression necessitating a change of treatment. Dr Burns considered Mr Swindells' death to be unexpected.
34. Under cross-examination by Mr Purcell of counsel, who appeared on behalf of the Commission, Dr Burns attributed Mr Swindells’ right pleural effusion to the lymphoma but considered the left pleural effusion more likely to be due to cardiac failure. He agreed that the heart size had been radiographically normal throughout 2006. Although Ms McMahon of counsel, who appeared on behalf of Mrs Swindells, suggested that a chest X-ray of 5 June showed cardiac enlargement, the Tribunal pointed out that this was a portable chest film performed after Mr Swindells’ VATS and, as it was an anterior – posterior rather than a posterior – anterior film, it could not be used to assess cardiac size. Dr Burns considered the hypercalcaemia to be treatable and did not consider the underlying CLL/lymphoma as refractory (resistant) to treatment prior to Mr Swindells’ death.
35. The Tribunal posed several questions to Dr Burns. Dr Burns had attributed Mr Swindells’ anaemia to his medication with Chlorambucil but when informed of Mr Swindells’ blood iron studies, agreed that the CLL/lymphoma had been the cause of the anaemia. Based on the CT scan of 15 September 2006, which showed free fluid in the abdomen (ascites) and oedema of the peritoneum, he said this also could be caused by the lymphoma; as could the leg oedema, given that the external iliac lymph nodes were enlarged.
36. The Tribunal asked Dr Burns about the likelihood of the right pleural effusion (acknowledged as being due to lymphoma), which was an exudate with a protein content greater than 30 grams per litre, and the left effusion, being a transudate, that is, protein less than 30 grams per litre, being found in the same patient. His answer was I don't know. Dr Burns did not consider himself appropriately expert to comment on whether Mr Swindells’ cardiac medications were routine therapy for individuals who had suffered a myocardial infarct rather than being indicative of ongoing cardiac dysfunction.
37. We asked what further treatment Dr Burns envisaged after Mabthera failed to arrest the lymphoma's progress. Dr Burns stated he would have continued to treat the hypercalcaemia but not the underlying lymphoma.
38. Professor Fox was the Professor of Haematology and Oncology at the Royal Melbourne Hospital until recently. He holds several government health board appointments and is the Vice-President of the Victorian Cancer Council. He continues to do research at St Vincents Hospital.
39. Professor Fox provided a report dated 13 March 2009 which was admitted into evidence. His opinion was based on papers provided by the Commission.
40. In his opinion the development of high serum calcium level was evidence of advanced disease. He attributed the veteran's left pleural effusion and leg oedema to the low serum albumin.
41. In answer to specific questions put by the Commission’s legal advisors, Professor Fox agreed with the causes of death as certified although he said CLL and lymphoma were the same condition. He said he found no evidence of congestive cardiac failure. In his opinion, the contemporaneous clinical notes and all of the features of Mr Swindells’ final illness represented sequelae of his chronic lymphocytic leukaemia, including the left pleural effusion and leg oedema secondary to low serum albumin.
42. Professor Fox's oral evidence was to the same effect. He disagreed with Dr Burns that Mr Swindells’ pleural effusion was due to cardiac failure. He attributed the shortness of breath and ankle oedema to the lymphoma and said while anaemia could affect cardiac function, Mr Swindells’ anaemia had been corrected by frequent blood transfusions. In Professor Fox's opinion, the death of Mr Swindells from lymphoma had been inevitable since June of 2006 when the malignant right pleural effusion was diagnosed. Professor Fox said that while Dr Burns was surprised by Mr Swindells’ death, the other oncologist treating Mr Swindells obviously thought differently and had commenced treatment with Mabthera, this being a rescue or last ditch therapy.
43. When questioned by the Tribunal, Professor Fox said that both the right and left effusions could have been malignant and that patients with CLL can decompensate rapidly when Richter's conversion to lymphoma occurs.
44. Professor Cade was the Director of Intensive Care at the Royal Melbourne Hospital until recently. He continues to work part-time as a consultant in this unit. He provided three reports, all of which were admitted into evidence. In the first of these, dated 26 August 2008, he reiterated the known history. He noted that there were no cardiac symptoms following the 1991 myocardial infarct. In addition, lung function tests performed in 2006 had shown minimal chronic obstructive pulmonary disease (COPD) and Dr Russell had made a diagnosis of asthma. Radiological records documented bilateral pleural effusions since 19 May 2006. He agreed with the causes of death as listed in the death certificate. He said there was no evidence of congestive cardiac failure provided in the clinical records nor were there any symptoms of ischaemic heart disease. From the medical reports, there was no evidence of clinical cardiac failure: nor was it present on the chest X-ray or CT scans.
45. Professor Cade's report dated 2 March 2009 was in response to Dr Burns’ reports and opinion. While he had no doubt that Dr Burns' report was kindly meant, Dr Burns and his colleague’s contemporaneous documentation never mentioned any evidence of cardiac disease. Multiple chest X-rays in 2006 had not shown pulmonary congestion or oedema indicative of left ventricular failure, left ventricular failure being the feature of ischaemic heart disease. Professor Cade was of the opinion that on the available evidence, cardiac failure was excluded as a cause of death.
46. Dr Burns had suggested the CLL/lymphoma was insufficiently advanced to cause the veteran's death. Professor Cade's opinion was that Mr Swindells’ clinical condition and the sequential CT scanning showed progressive lymph node enlargement. Also, the pleural effusion on the right was caused by CLL and both the right and left pleural effusions, as they increased without evidence of cardiac failure, must be considered malignant.
47. Professor Cade was sent additional documentation for comment. He reported on 21 September 2009. It had been suggested that COPD had also contributed to Mr Swindells’ death. Once more Professor Cade pointed out that lung function testing in early 2006 revealed minimal obstructive disease.
48. In his oral evidence, Professor Cade said his opinion was unchanged. Under cross-examination by Ms McMahon, Professor Cade agreed that the presence of crepitations and peripheral oedema were signs of congestive cardiac failure but he maintained that in Mr Swindells’ case, there was another explanation i.e. CLL/lymphoma. He agreed that anaemia could have an adverse effect on heart muscle function. However, contrary to Dr Burns’ opinion, Professor Cade said that based on the evidence, the malignancy was advanced, extensive and refractory; that is, it was out of control. Although the leukaemic phase of the disease appeared controlled, based on the lymphocyte count in the peripheral blood, the solid phase, that is the lymphoma, greatly increased and was the cause of the hypercalcaemia.
49. Ms McMahon put to Professor Cade Mrs Swindells’ evidence that her husband suffered from chest pain, shortness of breath on exertion and nocturnal shortness of breath. Once more, he attributed all the signs and symptoms to CLL/lymphoma, as there was no evidence of cardiac failure documented at any time.
50. There was no issue about the fact that Mr Swindells suffered from ischaemic heart disease. This was attributed to his cigarette smoking which commenced during his operational service. It was a condition accepted by the Commission and for which he was receiving a pension. Mr Swindells ceased smoking after he suffered an acute myocardial infarction in 1991.
51. Mrs Swindells gave evidence that her husband complained of chest pain and shortness of breath quite frequently in the period leading up to his death. She said she also noticed that his feet were swollen and she had difficulty when assisting him to put his slippers on.
52. Mr Swindells was diagnosed with CLL following a full blood examination in April 2005 as a result of investigation for a persistent cough. His previous full blood examination was in September 2003. Therefore, the CLL developed at some time in that 18 month interval. Although it was suggested that Mr Swindells was asymptomatic, his cough was present from December 2004 and persisted throughout his illness. His chest x-ray of March 2005 disclosed mediastinal widening which was later proven on CT scanning to be due to lymph node enlargement, particular the subcarinal nodes. Such subcarinal lymph node enlargement can cause persistent cough.
53. Other than Mrs Swindells’ evidence about her husband experiencing chest pain and shortness of breath, the only documented chest pain between 2000 and 2006 was right posterior chest wall pain first reported in January 2005. This was most likely due to intra-pleural lymphoma.
54. In the course of questioning by the Tribunal, Dr Burns agreed that the clinical notes showed clear evidence that Mr Swindells’ right sided pleural effusion was an exudate. That is, it had high protein content, some 39 grams per litre. Although he also had a left pleural effusion at the same time, the left pleural effusion was not drained. However, Dr Burns agreed that cardiac failure results in a transudate effusion. Therefore, the Tribunal put to Dr Burns that it would be most unusual to see a unilateral exudate with a unilateral transudate in the same patient.
55. According to Dr Burns, the findings of basal crepitations, increasing left plural effusion and leg oedema were more in keeping with signs of congestive cardiac failure than progressive low grade lymphoma, CLL or hypercalcaemia. That led Dr Burns to the view that congestive cardiac failure was related to Mr Swindells’ ischaemic heart disease which significantly contributed to and hastened his death. In other words, as we understood Dr Burns, his opinion was that Mr Swindells’ accepted ischaemic heart disease indirectly caused pathological changes leading to his death.
56. Dr Waldron was not called to give evidence. However, a brief statement he made on 28 February 2007 was in evidence. He said that he believed that the manner and timing of Mr Swindells’ death was also contributed to by his underlying existing ischaemic heart disease and that this had a definite impact on his haematological condition and his final illness.
57. The problem for Mrs Swindells is that some of the signs her husband exhibited prior to his death, such as shortness of breath, basal crepitations, increasing left pleural effusion and leg oedema, are equivocal. Because there is nothing in the clinical notes which refers to the possibility of congestive cardiac failure, those features could equally represent the sequelae of his CLL. As Professor Fox said in his report, Mr Swindells’ low serum albumin would have been the cause of the pleural effusion (associated with infiltration of the leukaemia into the pleura), and the leg oedema could result from low osmotic pressure reflecting the low serum albumin.
58. Professor Cade also referred to the lack of recording of any clinical features of cardiac disease. There was no mention of it during various specialist consultations and hospital admissions in the last months of Mr Swindells’ life. Although Professor Cade agreed that the observation of lower leg oedema made on Mr Swindells’ admission to hospital in December 2006 could, in some circumstances, represent cardiac failure, he did not agree that this occurred in Mr Swindells’ case. This was because chest imaging repeatedly excluded left heart failure and because isolated right heart failure is not a feature of ischaemic heart disease in the absence of right ventricular infarction, for which there was no evidence. In fact, Professor Cade attributed Mr Swindells’ lower limb oedema to lymphadenopathy which became so marked as to cause documented renal tract obstruction and, by implication, local venous obstruction.
59. Dr Burns was also of the opinion that Mr Swindells’ malignancy was insufficiently advanced to have caused his death in its own right. As Dr Burns said, his death was unexpected. However, as Professor Cade reported, in May 2006 Mr Swindells’ chest CT scan reported showing pleural effusions and enlarging para‑aortic and pelvic lymph nodes with hydronephrosis (renal tract obstruction) due to obstructive pressure.
60. Also, as Dr Anthony Dowling reported on 9 November 2006, chemotherapy (chlorambucil) was no longer effective even though it had reduced Mr Swindells’ total white cell count. Dr Dowling said that a new line of therapy was required for what he described as Mr Swindells’ low grade lymphoma, although Dr Burns had by that time noted generalised lymphadenopathy. Dr Dowling elected to treat Mr Swindells with Mabthera. Furthermore, as a 15 November 2006 CT scan disclosed, there was a significant increase in the size of mediastinal, retroperitoneal and periportal lymph nodes. The report concluded that the findings were in keeping with progressive tumour bulk within the areas described. Dr Dowling also reported that Mr Swindells was frail, elderly and hypocalcaemic despite treatment at this time and was suitable only for Rituximab therapy.
61. It is, in our opinion, also significant that Mr Swindells’ death certificate was completed by Dr Waldron, who had been closely involved in his care for the six years prior to his death. While Dr Waldron provided a brief, single paragraph, letter in February 2007 to the effect that we have referred to above, he was not called to give oral evidence or to provide a further written statement in this matter. The only conclusion we can draw from this is that Dr Waldron’s evidence would not have assisted Mrs Swindells in this case.
62. In our opinion, the objective radiological evidence in this matter precludes a finding that congestive heart failure contributed to Mr Swindells’ death. Although shortness of breath, crepitations and peripheral oedema are signs of congestive cardiac failure, for the reasons given by Professor Cade and Professor Fox, it is more likely that these symptoms were caused by Mr Swindells’ CCL/lymphoma. Accordingly, we find that, on the balance of probabilities, the kind of death met by Mr Swindells was as stated on his death certificate. His ischaemic heart disease did not contribute to his death. It did not account for the pathological changes which led to Mr Swindells’ death.
WAS MR SWINDELLS’ DEATH ATTRIBUTABLE TO ELIGIBLE WAR SERVICE?
63. Mr Swindells’ death must be taken to have been war-caused if his death arose out of, or was attributable to, any eligible war service which he rendered (s 8 of the Act).
64. Mrs Swindells also relied on s 8(1)(f) of the Act, which provides that the death of the veteran shall be taken to be war-caused if:
(f)the injury or disease from which the veteran died is an injury or disease that has been determined in accordance with section 9 to have been a war-caused injury or a war-caused disease, as the case may be;
Note:The effect of paragraph (f) is that, if the veteran has died from an injury or disease that has already been determined by the Commission to be war-caused, the death is to be taken to have been war-caused. Accordingly the Commission is not required to relate the death to eligible war service rendered by the veteran and sections 120A and 120B do not apply.
but not otherwise.
65. Although Mr Swindells had a number of accepted war-caused medical conditions, hypercalcaemia and CLL or progressive low grade lymphoma where not amongst those conditions. Accordingly, we find that s 8(1)(f) of the Act has no application in this case. Therefore, we are required to apply the standard of proof set out in s 120 of the Act.
66. Section 120(1) of the Act requires a finding, where the veteran has rendered operational service, that the injury, death or disease of the veteran was war-caused, unless the Commission is satisfied beyond reasonable doubt that there is no sufficient ground for making that determination. Because Mr Swindells rendered operational service, s 120(1) applies to his claim for the purposes of establishing the causal connection between his war service and his hypocalcaemia and CLL transforming to a lymphoma.
67. Section 120(3) of the Act, which must be considered when applying s 120(1), requires the Commission, and therefore the Tribunal, to be satisfied beyond reasonable doubt that there is no sufficient ground for determining that an injury, disease or death was war-caused if, after considering the material before it, the Commission is of the opinion that the material does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the veteran.
68. To determine whether the hypothesis is reasonable, where claims are made on or after 1 June 1994, the Tribunal must apply s 120A of the Act. In particular, s 120A(3) provides that, for the purposes of s 120(3), a hypothesis connecting an injury, disease or 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) or (11) of the Act, which upholds the hypothesis. Section 120A(3) does not apply to a claim for incapacity resulting from injury or a disease or the death of a person where the Repatriation Medical Authority has neither determined a SoP under s 196B(2), nor declared that it does not propose to make a SoP.
69. The method by which s 120(1), s 120(3) and s 120A(3) are to be applied was explained by the Full Court of the Federal Court of Australia in Repatriation Commission v Deledio (1998) 83 FCR 82. In that case, the Court set out four steps which should be followed in order to properly apply those sections of the Act. We need not set all of them out in full, because there was no evidence before us linking any of the conditions stated on Mr Swindells’ death certificate with his operational service. The first step described by the Court is 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.
70. Because there was no evidence before us which links the cause of death stated in Mr Swindells’ death certificate with his eligible war service, Mrs Swindells’ claim must fail. Accordingly, we find, beyond reasonable doubt, that the cause of Mr Swindells’ death was not connected with his eligible war service.
CONCLUSION
71. We have found that the cause of Mr Swindells’ death was as stated on his death certificate. We do not accept that a contributing cause to his death was congestive cardiac failure, which in turn could be attributable to his ischaemic heart disease, which the Commission had accepted as being war-caused.
72. Furthermore, there was no material before us linking Mr Swindells’ stated causes of death with his eligible war service. Therefore, the decision made by the VRB on 19 November 2007 refusing Mrs Swindells’ claim for a War Widow’s pension was correct. We affirm that decision.
I certify that the seventy-two [72] preceding paragraphs are a true copy of the reasons for the decision herein of
Mr Egon Fice, Senior Member and
Miss E A Shanahan, Member(sgd): Leah Berardi
ClerkDates of Hearing 9 March 2010, 13 April 2010
Date of Decision 30 June 2010
Counsel for the Applicant Ms Ann McMahon
Solicitor for the Applicant Williams Winter
Counsel for the Respondent Mr Gerald Purcell
Advocate for the Respondent Department of Veterans’ Affairs
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