ANDREW and REPATRIATION COMMISSION
[2011] AATA 624
•5 September 2011
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2011] AATA 624
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2009/2682
VETERANS' APPEALS DIVISION ) Re DIANNE DOROTHY ANDREW Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Mr John Handley, Senior Member Date5 September 2011
Place Melbourne
Decision The Tribunal affirms the decision under review. (sgd) John Handley
Senior Member
VETERANS’ AFFAIRS – widow’s application – veteran died in a motor vehicle accident ‑ kind of death – alcohol consumption during service caused hypertension – whether hypertension caused heart disease resulting in a mini blackout which caused the accident – medical cause of death – whether attributable to veteran’s service
Veterans’ Entitlements Act 1986 (Cth) s 8(1), s 8(1(b), s 8(1)(d), s 13, s 120(1), s 120(3), s 120A(3), s 196B(2) s 196B(11)
Collins v Repatriation Commission (2009) 177 FCR 280
Collins v Repatriation Commission [2008] FCA 1982
Doolette v Repatriation Commission (1990) 21 ALD 489
Repatriation Commission v Hancock [2003] FCA 711
Repatriation Commission v Law (1980) 47 FLR 57
Repatriation Commission v Deledio (1998) 83 FCR 82
REASONS FOR DECISION
5 September 2011
Mr John Handley, Senior Member
1.Mrs Andrew, the applicant in these proceedings, is the widow of the late Peter Donald Andrew.
2.Mr Andrew was a member of the Australian Army between 26 February 1969 and 26 February 1990. He was engaged in operational service in Vietnam between 20 January 1971 and 16 December 1971.
3.For reasons which are unknown, Mr Andrew lost control of a motor vehicle he was driving on 28 August 2007 on Urana Road Jindera in southern New South Wales. Mr Andrew died as a result of injuries he then suffered.
4.Mrs Andrew made a claim on 2 May 2008 for a pension under the Veterans’ Entitlements Act 1986 (the Act). She claimed, with the assistance of a Legacy Advocate, that there was a contribution to her husband’s death by hypertension and ischaemic heart disease (IHD). In an appendix to the claim form, she contended that the deceased’s service was responsible for his excessive consumption of alcohol post service, which caused his hypertension and IHD. As a result of the IHD, it was contended the deceased suffered a mini black out which was responsible for him losing control of his vehicle (T11, p 59).
5.The hearing commenced in Wodonga on 26 August 2010. Evidence was then heard from Mrs Andrew and her daughter, Tamara.
6.A hypothesis of a potential connection between service and diabetes emerged during the first day of hearing. Investigation of that disease and its connection with service was subsequently required. Mrs Andrew did not pursue that hypothesis when the hearing resumed in Melbourne on 17 and 18 March 2011.
7.Mr Rudge who appeared on behalf of the Repatriation Commission (the respondent), made a number of concessions (which, l am satisfied were properly made) on the basis of the clinical and other material lodged, namely:
(i)The deceased did suffer hypertension.
(ii)The clinical onset of hypertension was either in 1974 or 1977.
(iii)The deceased did consume at least 300g of alcohol per week for a continuous period of at least six months before the clinical onset of hypertension (Instrument No 11 of 2008).
(iv)A connection does exist between the operational service of the deceased, his alcohol consumption and hypertension.
8.The hearing, on resumption, was therefore confined to an inquiry into the kind of death of Mr Andrew.
LEGISLATION
9.A dependent of a deceased veteran is eligible for payment of a pension if death is war-caused (s 13 of the Act).
10.The death of a veteran shall be taken to have been war-caused within the meaning of s 8(1) of the Act, if the death of the veteran arose out of, or was attributable to, eligible war service (s 8(1)(b)) or the death of the veteran was due to an accident that would not have occurred, or to a disease that would not have been contracted, but for his … having rendered eligible war service … (s 8(1)(d)).
11.The respondent is obliged to determine that the death of a veteran was war-caused unless it is satisfied beyond reasonable doubt that there is no sufficient ground for making that determination (s 120(1) of the Act). The respondent will reach that conclusion if a reasonable hypothesis has not been raised connecting death with service (s 120(3)).
12.Section 120A(3) of the Act provides that a hypothesis connecting the death of a veteran with service will only be reasonable if there is in force a Statement of Principles (SoP) determined pursuant to s 196B(2) or (11) that upholds the hypothesis.
13.In order to comprehend the relevance of the expression kind of death, it is necessary to progress through the above sections which leads to s 196B of the Act. Section 196B establishes the Repatriation Medical Authority (RMA) which in part, has a responsibility to determine SoPs. It will do so if there is sound medical – scientific evidence indicating that a particular injury, disease or death can be related to (in this case) operational service.
14.If the RMA does form the view that by reason of sound medical – scientific evidence available, it is more probable than not that a particular kind of … death can be related to eligible service, it must determine a SoP in respect of that kind of … death … before it can be said that, on the balance of probabilities, … death of that kind is connected with the circumstances of that service (s 196B(3) of the Act).
15.In Collins v Repatriation Commission (2009) 177 FCR 280, the Full Court of the Federal Court unanimously dismissed an appeal against a decision of the Federal Court which upheld a decision of the Tribunal. The Tribunal accepted that the veterans’ IHD may have hastened his death. However, it decided that the veteran died from pulmonary embolism (the kind of death) which was not war-caused. In dismissing the appeal, the Court discussed the meaning and application of the concept of kind of death.
16.The Full Court in Collins decided that the kind of death for the purpose of s 120A(2) and (4) of the Act refers to the medical cause or causes of death (at [45-47]). The kind of death (or the cause of death) is a question of fact based on the medical evidence and is to be determined on the balance of probabilities (at [45]). When the cause of death is identified, the decision-maker must then determine whether the death was war-caused in accordance with the principles set out in Repatriation Commission v Deledio (1998) 83 FCR 82 (at [47]). Therefore, an enquiry into the kind of death is made independently of s 120, s 120A or any SoP. A determination about the medical cause or causes of death is anterior to, and unrelated to, whether the death is war-caused (at [50]).
17.When considering the meaning of death arising of out or being attributable to service in s 8(1)(b) of the Act, particularly where there are multiple causes of death, the Full Court referred to Repatriation Commission v Law (1980) 47 FLR 57. In Law, the Full Court considered the meaning of these words in the now repealed s 101(1)(b) of the Repatriation Act 1920. The Court said that arising out of requires a consequential relationship between death and service. However, something less proximate than caused by or results from will suffice, provided that it is not fanciful (at 67-68). When considering the words attributable to, the Court in Law said at 68:
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…
18.The decision in Law was followed by O’Loughlin J in Doolette v Repatriation Commission (1990) 21 ALD 489. His Honour held (at 492):
… 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.
19.Having reviewed the authorities, the Full Court in Collins acknowledged that there may be more than one cause of death. In the event that there is more than one medical cause, the Full Court said at [84]:
… we do not consider that as a matter of law any medical condition which may affect the time of death of a veteran by a measurable period, but does not otherwise play any real role in the pathological changes leading to the death (which are medically ascribed to another medical condition), is a death (that is a medical cause of death) or a kind of death under the VE Act…
20.Edmonds J in Collins delivered separate reasons. His reasons did not depart from those delivered by Mansfield and Stone JJ. In dismissing the appeal, Edmonds J substantially adopted the conclusions of Emmett J in Collins v Repatriation Commission [2008] FCA 1982. He agreed that there was no error of law by the Tribunal and significantly, it may be that there is really no question of law raised (at [17]).
21.In summary, Mrs Andrew will be entitled to the widow’s pension if her late husband’s death was war-caused. It will be war-caused if his hypertension played a real role in the pathological changes that resulted in his death so as to qualify as the kind of death. The kind of death or the cause of the veteran’s death will be a question of fact determined on the basis of the medical evidence before the Tribunal.
EVIDENCE
22.Dr Oxbrow performed a post-mortem examination on the late Mr Andrew and concluded that the direct cause of death was extensive fractures of the skull with brain injury and haemorrhage (Report dated 30 August 2007 at [5] found within the Coroner’s file (Exhibit R4)). The cause of death recorded on the death certificate is in identical terms (T11, p 61).
23.If not apparent from the foregoing, Mrs Andrew disputes that the kind of death was as recorded by the Coroner.
24.The hypotheses advanced by Mrs Andrew were of a service related alcohol habit precipitating hypertension which in turn was responsible for IHD or hypertensive heart disease (HHD). Either or both of those diseases precipitated or was responsible for an arrhythmia which caused the deceased to suffer a decrease in his conscious state (a blackout), lose control of his vehicle and then suffer fatal injuries.
25.Specialist medical evidence was heard from Dr Byron Collins, a forensic pathologist, Professor Richard Harper, a consultant and interventional cardiologist and Professor Douglas Lording, an endocrinologist.
26.Mrs Andrew lodged two statements prior to the commencement of the hearing (Exhibits A1 and A2).
27.In the first statement dated 6 July 2009, Mrs Andrew recorded that her husband was often very tired, he would fall asleep at the dinner table and he often seemed to be exhausted in the mornings after he had slept well. She stated that he would fall asleep whilst she was talking with him. These episodes were increasing in frequency prior to his death and because they were so unusual, she classed them as blackouts (Exhibit A1).
28.In her second statement, Mrs Andrew described occasions when her husband would suddenly black out. On one occasion, she recalled that he had been sitting on a stool at a breakfast bar at home when he fell to the floor. He was unconscious for about 30 seconds and when he eventually opened his eyes, she noticed that they were glazed and his hands had a gentle tremor. On another occasion, she heard him fall in another room of the house and found him unconscious. His recovery on that and on a third occasion was similar to the first occasion. She recorded that each blackout had occurred between 10.30am and 11.30am (Exhibit A2).
29.Tamara Andrew, the daughter of Mr and Mrs Andrew, prepared a statement on 6 July 2009. She referred to many occasions where she noticed that her father was exhausted, frequently sleeping during the day and falling asleep at the dinner table (Exhibit A3).
30.In her evidence, Tamara said that her mother told her of occasions when her father had suffered blackouts at home. She said on one occasion, she had seen her father after he had suffered a blackout and recalled that he had a mark across his face. When she asked him about it, he told her that he had another fall (Transcript of 26 August 2010, p 40).
31.Dr Collins said that the descriptions given by Mrs Andrew of her husband’s black outs were, if reliable, evidence of a loss of consciousness or a decreased conscious state as a consequence of an abnormal cardiac rhythm (Transcript of 17 March 2011, p 7).
32.It was his opinion, having regard to the findings at autopsy, that the deceased suffered IHD, a feature of which would be abnormal cardiac rhythm as a consequence of diminished blood supply to the heart. If in turn there is also a decrease in blood supply to other organs, especially the brain, a person would then be at risk of cerebral hypoxia which may then precipitate a change in the conscious state of that person (Transcript, p 7-8).
33.The alteration in cardiac rhythm and arrhythmia, is, according to Dr Collins a well-recognised consequence of IHD or HHD. Contrary to an opinion expressed in a report of Professor Harper, Dr Collins said an arrhythmia may occur in the absence of IHD. He said that in his experience, an arrhythmia may occur when HHD alone is present, although the presence of IHD will increase the likelihood of an arrhythmia occurring (Transcript, p 11).
34.Dr Collins was adamant that the deceased did suffer from IHD. He said the post-mortem report recorded the deceased as suffering from moderate coronary atherosclerosis and his interpretation of the pathology slides demonstrated a 30 to 40 per cent narrowing of the coronary arteries. Those findings, he said, were typical in a person suffering from IHD.
35.Additionally, Dr Collins said the deceased was found at autopsy to have a grossly enlarged heart of 657 grams which, despite the weight and height of the deceased, pointed to the diagnosis of HHD and/or IHD. He said the heart was sufficiently enlarged for the reasonable possibility of the generation of a significant cardiac rhythm to occur (Transcript, p 11).
36.Dr Collins did not exclude the possibility that the deceased may have fallen asleep when driving his vehicle on the day of the accident but added there is a perfectly satisfactory and reasonable set of pathological conditions which could also explain the event (Transcript, p 11).
37.Professor Lording is an endocrinologist who was engaged by Mrs Andrew’s solicitors, primarily to give an opinion on the relationship, if any, between the veteran’s service, cigarette smoking, diabetes and ultimately his death. As recorded earlier, that hypothesis was not pursued. Nonetheless, despite him qualifying himself as a physician and not as a cardiologist, Professor Lording said a consequence of an ischaemic event could be either a heart attack or an arrhythmia. He said a sudden loss of consciousness and falling is a presentation of acute arrhythmias. I don’t think that description fits someone falling asleep (Transcript, p 25-26).
38.In cross-examination, Professor Lording said if a CT scan or an ultrasound reported a patient as having a 30 per cent narrowing in an artery, despite the presence of atheroma, it would be a non-significant finding and IHD would not be diagnosed (Transcript, p 27). Professor Lording said there can be a narrowing of arteries which will not interfere with blood flow to the heart. Whilst he would need to take some advice on the likely percentage of narrowing of an artery that would be regarded as critical, he thought 30 per cent was fairly trivial (Transcript, p 30).
39.Professor Lording said Professor Harper is well respected by his colleagues and his patients. He was aware that Professor Harper had expressed an opinion, based on the autopsy findings, that the deceased did not suffer IHD and that it was more likely that he suffered from HHD.
40.Professor Lording said his expertise as an endocrinologist did not permit him to be comfortable giving an opinion that the extent of HHD, as found by Professor Harper was not of sufficient severity to cause arrhythmias.
41.Professor Harper has practised as a cardiologist for 35 years. He prepared a report dated 11 May 2010 at the request of the respondent (Exhibit R10). From the documents made available to him, including the post-mortem notes, he was satisfied that cardiac enlargement and myocardial fibrosis was indicative of HHD. Despite the presence of coronary atherosclerosis, he thought it was mild and did not cause coronary obstruction. For that reason, he was satisfied the deceased did not suffer IHD. He also reported that serious arrhythmias such as ventricular tachycardia or ventricular fibrillation would usually only occur where there is advanced HHD or where IHD is also present. He concluded that IHD was not present and the extent of HHD, as described in the post-mortem notes, was not severe enough to be a likely cause of ventricular arrhythmias, although he said, that possibility could not be discounted (Exhibit R10 and Transcript of 18 March 2011, p 28-29)).
42.Professor Harper concluded in his report that there was a strong possibility that the deceased may have fallen asleep whilst driving his motor car. However, he also acknowledged that had the deceased suffered a serious transient cardiac arrhythmia, he could have lost consciousness and veered off the road. On balance, he thought that the extent of his HHD was not sufficient to cause cardiac arrhythmias. He concluded that falling asleep was a more likely cause of the accident than a cardiac arrhythmia but he did not exclude that possibility (Exhibit R10, p 3).
43.In evidence Professor Harper said there would need to be a 70 per cent obstruction in an artery before there would be interference with blood supply. IHD would only be diagnosed in those circumstances. Professor Harper was aware that Dr Collins had given an opinion of a 30-40 per cent obstruction in the coronary arteries based on microscopic slides that had been prepared and retained following the autopsy. Professor Harper said an estimation of narrowing can be made if the slides were properly prepared. He said there was no way of knowing whether they were or they weren’t. On the basis that the slides were properly prepared and if the estimation by Dr Collins of a 30 ‑ 40 per cent occlusion was accurate, it will not physiologically, will not cause deprivation of blood supply and ischaemic heart disease (Transcript, p 45).
44.Professor Harper also disagreed with an opinion expressed by Dr Collins that the presence of coronary atherosclerosis and myocardial fibrosis pointed to a diagnosis of IHD. He said if the atherosclerotic plaques do not cause significant obstruction then they don’t cause ischaemic heart disease. However, the pathologist at post-mortem reported that there was no significant obstruction in the coronary circulation and in those circumstances, without significant obstruction, IHD could not be diagnosed (Transcript, p 43).
45.Additionally, it was his opinion that myocardial fibrosis is a symptom of, and typically found in persons who are diagnosed with HHD. Professor Harper said that the findings as reported by the pathologist are typical in persons who suffer HHD. If there had been a finding of a discrete large area of fibrosis, it may point to a previous heart attack which may in turn permit a diagnosis of IHD (Transcript, p 44).
46.Professor Harper preferred the diagnosis of HHD which he acknowledged was a risk factor for atrial fibrillation. He said there was no evidence the deceased had suffered an arrhythmia. He said that arrhythmias are more likely to occur in the presence of HHD where there had previously been a large amount of damage to the heart by a previous heart attack. He said there was no evidence of that having occurred nor found at autopsy (Transcript, p 46).
47.Professor Harper said there were many reasons which might explain the deceased having lost consciousness, for example, hypoglycaemia or a vasovagal episode. He acknowledged the possibility of an arrhythmia but also acknowledged that the apparent obesity of the deceased may have contributed to poor sleep patterns which could be responsible for him being tired and easily falling asleep. Neurological problems or brain tumour could also account for a loss of consciousness but no such phenomena were found at post-mortem.
48.In cross-examination, Professor Harper acknowledged that he was not aware the deceased had only travelled 9kms from home when the accident occurred just after 10.00am and then shortly after he consumed a cup of coffee. When asked whether that scenario changed his opinion about the possibility of falling asleep, Professor Harper said:
… it makes it less likely perhaps, than before. … but statistically I would still think that falling, falling – people fall asleep at any time during the day and I think it – I would still say it is more likely than the alternative possibility. But it is perhaps, I am less strong with that evidence that you provided to me than I was previously, because I wasn’t aware of that scenario. But … statistically it was more likely that he fell asleep [Transcript, p 47].
49.When asked whether 70 per cent obstruction was the absolute standard for a diagnosis for ischaemic heart disease, Professor Harper said that 70 per cent is a generalisation and there can be occasions where a narrowing of a lesser per cent could cause ischaemia. When an angiogram points to narrowing of about 60 or 70 per cent, a stress test is usually undertaken to see whether the narrowing is capable of causing ischaemia. In his experience, ischaemia will not be demonstrated in arteries with less than 70 per cent obstruction. He said such a phenomenon would be extremely rare. He acknowledged that lesions can change abruptly and explained that a person with a 30-40 per cent obstruction could suffer a clot which might then cause a 70 or 80 per cent obstruction, or indeed a complete occlusion. However, on the material available to him, no such event had occurred to the deceased during his lifetime and there was no evidence at post-mortem to suggest that such an event was responsible for his death (Transcript, p 48).
50.Professor Harper acknowledged that the deceased did have a significantly enlarged heart which would be an indication of relatively advanced HHD. In turn, the deceased would have been at risk of arrhythmias which could occur in the absence of IHD. He agreed with an opinion expressed by Professor Lording that an arrhythmia would not necessarily show up on post-mortem.
51.On balance, Professor Harper remained of the view that it is more likely that the deceased fell asleep, despite it having occurred in the morning and without any evidence of the deceased’s sleep pattern during the previous evening. He said that falling asleep is common in the older age group, particularly when people are overweight. Professor Harper acknowledged that an episode of ventricular tachycardial fibrillation may have been a cause. However, such an episode, unlike falling asleep, is pretty rare. He said the deceased had risk factors for falling asleep, I would attribute it to that, but I can’t be sure. Equally he conceded that the deceased did have risk factors for cardiac arrhythmias (Transcript, p 50-51).
CONCLUSIONS
52.The cause of the motor vehicle accident will probably never be known.
53.It can be said with certainty that the deceased was not affected by alcohol. A certificate of analysis prepared for the Coroner did not detect the presence of alcohol in the blood of the deceased.
54.During the hearing, the medical witnesses referred to other possible causes of the deceased losing control of his vehicle, namely, hypoglycaemia, a vasovagal episode, sleep apnoea, myocardial infarction and (if the deceased did lose consciousness) a neurological catastrophe. There was no material which pointed to any of those possibilities.
55.The focus by Mrs Andrew, as recorded earlier, was of the deceased having suffered a blackout as a consequence of an arrhythmia which had its origin either in IHD and/or HHD. Dr Collins was satisfied that the deceased suffered from IHD. Without resiling from that opinion, Ms Bornstein submitted on behalf of Mrs Andrew that the deceased suffered an arrhythmia which arose out of his HHD. Having regard to the evidence of Professor Lording and particularly that of Professor Harper, Ms Bornstein’s approach was sound. Professor Harper is a reputable cardiologist with extensive experience. Although Professor Lording is not a cardiologist, he confirmed the evidence of Professor Harper. I accept their evidence is sound and based on their experience as clinicians.
56.I acknowledge that the deceased appeared to have, at least from the findings at post-mortem, a degree of arterial narrowing. Dr Collins was of the opinion that the extent of narrowing would have been in the vicinity of 30-40 per cent. Professor Lording thought a 30 per cent narrowing of a coronary artery which would be fairly trivial (Transcript, p 30). Professor Harper said that a 30-40 per cent occlusion can never be an indicator or a symptom of [IHD] (Transcript, p 48).
57.I prefer the evidence of Professor Harper on this issue and I am satisfied and find as a fact, that the deceased did not suffer from IHD. It follows that if the deceased suffered an arrhythmia, it was not precipitated by IHD.
58.Dr Collins together with Professors Lording and Harper all agreed that the deceased suffered HHD.
59.Dr Collins was of the opinion that a person with HHD alone with an enlarged left ventricle could experience an arrhythmia in the absence of IHD (Transcript, p 11). In his opinion, the presence also of IHD increases the likelihood of an arrhythmia. Professor Harper reported that HHD alone can be responsible for arrhythmias but usually where there is advanced disease or where both HHD and IHD are present. It was his opinion that the clinical material did not indicate that the extent of HHD was sufficient to cause arrhythmias, although he did not discount that possibility (Transcript, p 49).
60.The opinions of Professor Harper were based on his clinical experience and practice as a well-respected senior cardiac clinician. His opinions, in my view, are sound and to be preferred. He did not discount the possibility of an arrhythmia precipitating a loss of consciousness by HHD but it was more likely that such an episode would occur where HHD was extensive. Having perused the post-mortem notes and the clinical notes of the deceased’s treating doctor, Professor Harper said that there was no evidence to point to extensive disease. I accept that the deceased suffered HHD. However, l am not satisfied that the extent of HHD was sufficient to precipitate an arrhythmia.
61.When determining the kind of death, the standard of proof is the balance of probabilities (Repatriation Commission v Hancock [2003] FCA 711 at [8]).
62.Having found as fact that the deceased did not suffer IHD, l therefore find that it could not be responsible for an arrhythmia. In the absence of IHD, it also follows that an arrhythmia did not arise because of the combined effects of IHD and HHD. While HHD was present, it was not sufficiently advanced to cause an arrhythmia.
63.Professor Harper said unless HHD was extensive, any connection between HHD and an arrhythmia leading to loss of consciousness would be no higher than a possibility. Dr Collins reported that a connection between HHD, arrhythmia and loss of consciousness would be entirely reasonable to hypothesise (Exhibit A5) or likely due (Exhibit A6) or was a very real possibility (Exhibit A7). Professor Lording was reluctant to express an opinion on this issue because of his confessed lack of expertise in the area (Transcript, p 29).
64.There is no evidence on the probabilities connecting the kind of death with an arrhythmia having its genesis in IHD or HHD. For reasons stated above, I prefer the evidence of Professor Harper. In any event, from the evidence heard in these proceedings any connection between an arrhythmia and the death of Mr Andrew is no more than a possibility.
65.It follows that l cannot be satisfied on the balance of probabilities that IHD or HHD was the cause of death or the kind of death met by Mr Andrew. It also follows that the kind of death is not connected with his operational service.
66.Dr Collins used the word likely in his report (Exhibit A6) which may approach the necessary standard of proof. However, Dr Collins used the word in the context of hypertensive/ischaemic heart disease. Having regard to my previous findings, his opinion no longer has relevance.
67.The kind of death in these circumstances was the injuries certified by the Coroner, namely extensive fractures of the skull with brain injury and haemorrhage. For reasons stated above, I am not satisfied that IHD or HHD played any real role in the pathological changes leading to Mr Andrew’s death (Collins at [84]).
DECISION
68.For all of the above reasons, the decision under review is affirmed.
I certify that the sixty-eight [68] preceding paragraphs are a true copy of the reasons for the decision herein of:
Mr John Handley, Senior Member
Signed: Olympia Sarrinikolaou
Legal Assistant
Dates of Hearing 26 August 2010 and 17-18 March 2011
Date of Decision 5 September 2011
Counsel for the Applicant Ms J. Bornstein
Solicitor for the Applicant Williams Winter Solicitors
Counsel for the Respondent Mr R. Douglass (26 August 2010) and Mr K. Rudge
Solicitor for the Respondent Department of Veterans’ Affairs
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