Lewis and Military Rehabilitation and Compensation Commission (Veterans’ entitlements)
[2015] AATA 581
•11 August 2015
Lewis and Military Rehabilitation and Compensation Commission (Veterans’ entitlements) [2015] AATA 581 (11 August 2015)
Division
VETERANS’ APPEALS DIVISION
File Number(s)
2012/0141; 2014/1712; 2014/3137
Re
Julie Lewis
APPLICANT
And
Military Rehabilitation and Compensation Commission
RESPONDENT
DECISION
Tribunal Ms Naida Isenberg, Senior Member
Date 11 August 2015 Place Sydney The decisions under review are affirmed.
...........................[sgd].............................................
Ms Naida Isenberg, Senior Member
CATCHWORDS
VETERANS’ AFFAIRS — benefits and entitlements — whether veteran suffered a service death — whether veteran suffered a service injury — whether veteran suffered an injury (including a disease) that arose out of, or in the course of, his military service or that was contributed, to a material degree, by his military service — whether veteran suffered an injury as an unintended consequence of treatment paid for by the Commonwealth — veteran died due to cardiac arrest — no causal factor relating condition to service — criteria not met — decisions under review affirmed
LEGISLATION
Military Rehabilitation and Compensation Act 2004 (Cth) ss 5, 13, 23, 24, 27, 28, 29, 335, 339, 341
Safety, Rehabilitation and Compensation Act 1988 (Cth) ss 6A, 17, 18
CASES
Brew v Repatriation Commission [1999] FCA 1246
Hay and Repatriation Commission [2009] AATA 883
Lees v Repatriation Commission [2002] FCAFC 398; (2002) 125 FCR 331
Millen and Repatriation Commission [2000] AATA 508
Re Commission of the Safety, Rehabilitation and Compensation of Commonwealth Employees v June Anne Hall [1993] FCA 129
Re Robertson and Repatriation Commission (1998) 50 ALD 668 670
Repatriation Commission v Cornelius [2002] FCA 750
Repatriation Commission v Money [2009] FCAFC 11; (2009) 173 FCR 410SECONDARY MATERIALS
Statement of Principles concerning ischaemic heart disease No. 90 of 2007
REASONS FOR DECISION
Ms Naida Isenberg, Senior Member
11 August 2015
HISTORY OF THE APPLICATION
In April 2008 Gregory Lewis (Mr Lewis), the husband of the Applicant, Julie Lewis, died of a cardiac arrest, at the age of 32, having collapsed at the family home. He had served in the Royal Australian Navy (the Navy) from 6 June 1994 until the time of his death.
On 15 August 2008 the Applicant lodged a claim for Compensation for Dependents of Deceased Members, in respect of her husband’s death which, she contended, was caused or contributed to by his military service. She claimed that “he had low potassium ever since he collapsed in 1996. The RAN knew about this and did nothing. Therefore he did not obtain appropriate clinical management”.
The Respondent, by Determination dated 12 August 2009, refused the Applicant's claim in relation to the death of her husband, on the basis that it was not liable for Mr Lewis’ death under the Statement of Principles concerning Ischaemic Heart Disease (Instrument 90 of 2007).
On review, the Veterans’ Review Board, after obtaining an opinion from a consultant cardiologist as to whether Mr Lewis was adequately monitored following his near death experience in Hawaii in 2004, affirmed the determination on 30 September 2011.
In February 2013 the Applicant also lodged a claim pursuant to the Military Rehabilitation and Compensation Act (MRC Act) for her husband’s “cardiac arrest”, and referred to her husband's ‘experiences’ in Hawaii in 2004” and that her husband 'was not adequately assessed or subsequently monitored' thereafter. Liability was denied and upon reconsideration, by reviewable decision dated 27 March 2014, the Respondent confirmed the determination.
On 13 June 2013 another claim was also lodged, pursuant to the Safety Rehabilitation and Compensation Act for “coronary events arising prior to 1 July 2004”. By determination dated 31 March 2014, the Respondent disallowed the claim which sought compensation for funeral expenses and/or entitlement following Mr Lewis’ death. Upon reconsideration the Respondent confirmed the determination on 11 June 2014.
The Applicant seeks review of the Veterans' Review Board Decision that affirmed the decision to deny liability for Mr Lewis’ death (2012/0141 ‘death claim’), and the reviewable decision in respect of ‘cardiac arrest’ (2014/1712 ‘injury claim’), and the reviewable decision in respect of ‘coronary events' (2014/3137 ‘SRC death claim’).
ISSUES
2012/0141 – death claim
·Whether Mr Lewis suffered a service death, as defined in s 28 of the MRC Act, for which liability must be accepted pursuant to s 24(1) of the Act.
2014/1712 – injury claim
·Whether Mr Lewis suffered a service injury or service disease, as defined in s 27 of the MRC Act, for which liability must be accepted under s 23(1) of the Act.
·Whether Mr Lewis suffered a service death, as defined in s 28 of the MRC Act, for which liability must be accepted pursuant to s 24(1) of the Act.
·Whether Mr Lewis suffered a service injury, service disease or service death, as defined in s 29 of the MRC Act, for which liability must be accepted under s 23(2) or s 24(2) of the Act.
2014/3137 – SRC death claim
·Whether Mr Lewis suffered an injury (including a disease) that arose out of, or in the course of, his military service or that was contributed, to a material degree, by his military service.
·Whether Mr Lewis suffered an injury as an unintended consequence of treatment paid for by the Commonwealth, such that the injury is taken to have arisen out of, or in the course of, his military service.
·Whether any injury suffered by Mr Lewis resulted in his death for which the Respondent is liable pursuant to s17(1) of the SRC Act.
APPLICANT’S EVIDENCE
In her statement dated 18 June 2012 the Applicant stated that her husband had collapsed on 16 March 1999 whilst in the military, with medical records confirming that a similar incident occurred 12 months earlier, and also on 1 October 1997 and 20 March 1999. Following these events her husband was to have “an ECG, Echo and Holter [monitor] and review ASAP”, but that no Holter monitor was put on. Her husband had difficulties maintaining his weight between 2004 and 2007, which she claimed was a direct result of stress caused by the Navy. She recalled her husband vomiting from exhaustion on several occasions due to “a gruelling exercise regime” after a failed fitness test, although she did not state when this occurred.
The Applicant relied on medical records dated 31 May 2004, 1 June 2004, 2 June 2004, 3 June 2004, 4 June 2004, 7 June 2004, and 18 June 2004, which note that her husband was “sick with stomach cramping, diarrhoea, headaches, lethargy and abdominal cramping”. The Applicant believed that no investigation was taken as to the cause of this illness.
The Applicant described the events that occurred when her husband was in Hawaii in 2004, as she recalled them. She stated that “he worked extremely hard ... with little sleep”. On the day that he collapsed, the Applicant stated her husband had gone shopping, went out drinking with friends, and ordered a taxi to leave when he had had enough. The Applicant stated that her husband then recalled waking up at the Tripler Hospital. She stated that whenever her husband would raise the incident in Hawaii with medics at his subsequent yearly assessments, they would advise him that “there was nothing in his records that suggested his condition required any further investigation”.She recalled her husband emailing her and telling her that he was extremely ill. To her knowledge there was no medical investigation as to the cause of his illness at this time or following his recovery. She recalled being advised by the medics aboard the HMAS Newcastle, whilst still in Hawaii, that her husband’s incident would not happen again as it was caused by alcohol and that she should not worry as he would make a full recovery.
Following his return from Hawaii and during his admission to St. Vincent's Hospital, which was between 6 and 11 August 2004, it was mentioned that it would be highly likely that he would require a pacemaker as his heart had stopped nine times whilst he was under a drug induced coma, despite him being a fit and healthy man. She said that they had to consider all options as her husband did not want to jeopardise his career in the Navy. He loved the Navy, the structure, the skills, the heritage and the honour that came with being a sailor. Following a variety of tests, it was decided that a pacemaker was not required. He was led to believe that if he avoided high consumption of alcohol he would be fine.
She noted that her husband would always mention the incident in Hawaii in 2004 at his yearly medical assessments however was advised that there was nothing in his records that suggested his condition required any further investigation during the yearly check-ups.
The Applicant stated that in 2006 her husband was sick for 14 days with an illness that was allegedly not able to be diagnosed. In the eight months or so before her his death she was only aware of him suffering from a reoccurring flu. She concluded by stating that due to her husband's collapses in 1997, 1998 and 1999, his illness in June 2004, his continual low potassium, diagnosis of coronary atherosclerosis, and “knowing that his heart had stopped nine times”, the medical staff in the Navy should have considered the possibility of a serious health issue and should have investigated further. On that basis, the Applicant maintained that her husband “did not receive appropriate clinical management of his condition” and that his death was therefore linked to his military service.
In her evidence the Applicant said as to the question of whether to install a pacemaker, that the people at St Vincent's "must have been talking about it but then after all the tests it was decided that a pacemaker wasn't required", and that her husband took that advice. She also there mentioned that her husband was concerned that he would have to leave the Navy if he had a pacemaker, although "he would put his life first" if a pacemaker was required.
Her evidence was that "at home he ate pretty healthy", eating low fat meals. Her husband lost weight between 2005 and 2007; he then put on weight again. Also, the Applicant gave evidence that after the 2004 event in Hawaii he "started AFL and things...tried to get fit", adding that she knew that "he would ride to work which was 12km and vomit up the hill, trying to make it up the hill, so – everyday". She also said that he tried to go to the gym a lot because he had put on a lot of weight and that "he would do PT with some of his guys at work and he would also vomit during that". This was speaking of a period of around "2005, 2007".
In her statement she said her husband “was led to believe that if he avoided high consumption of alcohol he would be fine", although she acknowledged that she was not with him when he saw doctors and did not actually hear or receive any advice.
Mr Lewis’ medical history
Mr Lewis’ service medical records contain extensive entries of possible relevance to the claims:
·3 August 1996: “vomiting, unable to keep fluids down, stomach cramps, diarrhea”.
·An Outpatient Clinical Record dated 1 October 1997:
This 22y.o. male collapsed in the ops room, after returning from having a cigarette. Remembers feeling a hot flush and then he collapsed, has had 2/7 history of generalised abdo pain with no diarrhoea, vomiting or rebound.
·An Outpatient Clinical Record dated 2 October 1997:
… not 100% – still had mild cramping pain (R) upper quad of abdo – constant – alternating between dull to sharp.
·An Outpatient Clinical Record dated 16 March 1999:
… was found unconscious on deck of operations room...reported from workmates in ops. room that pt was sitting at his console and began to feel faint – slowly slid down out of chair...was unconscious for approximately 4 minutes … Patient transported via stores lift to sick bay– was stopped several times due to pt feeling unwell; also lost consciousness twice on route…. Approximately 12 months ago patient experiences similar occurrence–not investigated'.
A blood test was arranged.
·An Outpatient Clinical Record dated 20 March 1999 records he reported he had suffered 2 episodes of losing consciousness in the previous year. It was considered he may have had epilepsy. Investigation was planned “ASAP on RTA [return to Australia]”.
·An Outpatient Clinical Record dated 31 May 2004:
Woke up at 0930 this AM feeling Nausea. Slow progressive worsening of symptom. Light headed dizziness, feel head is 'hot', abdo cramping, vomiting, diarrhoea.
·Outpatient Clinical Records dated 4 June 2004:
… monitored daily. Urine sent for testing. Diagnosis of virus. A pathology report dated 3 June 2004 showed elevated blood lipids.Declared fit for sea.
·An Outpatient Clinical Record dated 7 June 2004: “feeling much better... Declared fit for sea. To be reviewed on return”.
·An Outpatient Clinical Record dated 18 June 2004: “reported with 2 day history of nausea/diarrhoea/cramping. Treated with anti vomiting/ anti diarrhoea medication and ordered to increase rest”.
·An Outpatient Clinical Record dated 23 July 2004: noted that a teleconference occurred between the Duty Shore Patrol and HMAS Newcastle. It was recorded
…unconscious sailor required medical attention ashore.... After exiting taxi at front gate of Pearl Harbour Naval Base, PO Lewis was seen to fall to the ground – assumed alcohol intoxication. He was unaccompanied. Ship was contacted.
He was taken by ambulance to Tripler Service Hospital, arriving at 2130.
·A consultation note from Tripler Service Hospital dated 27 July 2004 records Mr Lewis was brought into the Emergency Room with the diagnosis of acute alcohol intoxication. While at the hospital he had several cardiac arrests in the course of an hour. An echocardiogram was conducted and he was found to have a “structurally normal heart….The most likely etiology of the patient's arrest would appear to be alcohol intoxication with concomitant electrolyte abnormalities”. The notation recorded that Mr Lewis' potassium and magnesium levels should be periodically checked to ensure that he does not have a potassium wasting kidney disorder and also to ensure that his potassium levels are never low again. The notation also suggested that 'consideration should be given to placing a defibrillator when the patient returns to Australia'. The report suggests that Mr Lewis be counselled regarding alcohol use, have periodic potassium and magnesium levels checked and receive a 'work up' to ensure that he did not have a kidney disorder. On discharge he was advised to seek medical attention “if you feel chest pain, the feeling of your heart racing, or shortness of breath, or loss of consciousness, fever, chills or nausea”.
·A Restricted Medical Note from HMAS Newcastle dated 24 July 2004 recorded that the main issue was Mr Lewis' arrhythmia, which it was noted was likely due to hypokalemia and hypomagnesaemia secondary to diuresis, and was being managed with antiarrhythmic medication and electrolyte replacement.
·A Restricted Medical Note from HMAS Newcastle dated 25 July 2004, following Mr. Lewis' discharge from Tripler Hospital, recorded that he was expected to make a full recovery. On discharge his heart was normal and all biochemical tests were normal. It was noted that the ship was not due to return to Australia for another month and in discussions between the Senior Medical officer and the Director of the Tripler hospital ICU it was decided he should not return to the ship because of isolation from medical facilities should he deteriorate. There were also some compassionate issues relevant to his repatriation. A follow-up with a cardiologist was recommended on return.
·A Medical Officer's Report dated 4 August 2004 noted that at approximately 2100 on 23 July 2004, Mr Lewis “vomited and collapsed in a taxi at the Nimitz Gate to Pearl Harbour Naval Base. He was given immediate first aid at the scene by two US Military Policemen.” He was taken by ambulance to Tripler Army Medical Centre Hospital, during which he vomited many more times. At the hospital, the blood alcohol level was measured as 0.222 and
…because he was comatose due to the acute effects of alcohol, he was sedated, intubated (a tube down into his airways) and ventilated by machine. Overnight, he developed fatal heart rhythms (ventricular fibrillation) and required defibrillation (shocking) nine times... After questioning both PO Lewis and some of his shipmates, it would appear that he drank steadily for almost 24 hours, starting at the PO's function onboard on Thursday night and continuing in Waikiki for most of Friday, with the exception of a few hours on Friday morning when he slept in his bunk.. .Although PO Lewis denies a significant drinking history, anecdotal reports from his colleagues indicate that he may have a tendency to binge…
·Upon his return to Australia, Mr Lewis was admitted to Balmoral Naval Hospital where he underwent numerous tests. He was transferred to St Vincent’s Private Hospital on 6 August 2004, where he remained until 11 August 2004.
·Mr Lewis was referred to Dr David Baron, cardiologist, who reported on 10 August 2004, despite the incident in Hawaii, Mr Lewis’ chest x-ray and ECG were normal, “coronary arteries were smooth and normal”, and that Mr Lewis “doesn't have any underlying structural or electrical problem with his heart”. The doctor felt that Mr Lewis' cardiac arrest was 'probably due to a combination of factors including high blood alcohol, electrolyte disturbance, acidosis and hypoxia’. He observed that there was no underlying structural or electrical problem with his heart. He was of the view that Mr Lewis should be careful with his alcohol intake in the future.
·Mr Lewis was also referred to Dr Walker, cardiologist, who, in his report dated 12 August 2004 records that he conducted an electrophysiology study on Mr Lewis. He noted Mr Lewis' hospital admission on 24 July 2004 with severe intoxication and a blood alcohol level of 0.22. The doctor noted that Mr Lewis also suffered an episode of Torsade de Pointes and ventricular fibrillation. Dr Walker noted that Mr Lewis' family had “a strong history of coronary artery disease” however examination showed 'no evidence of structural heart disease or arrhythmic syndromes associated with sudden death'. The doctor felt that the cardiac arrest was “purely secondary to metabolic derangement with hypokalemia, acidosis and severe alcohol intoxication. There is no evidence of a potassium losing state…” He stated that Mr Lewis should be careful in the future if he develops vomiting or diarrhoea and should maintain a high potassium diet.
·Mr Lewis was offered outpatient treatment for substance abuse. A Refusal of Treatment form, dated 18 August 2004 confirmed that Mr Lewis was aware that he had been assessed as Level 2 as a result of his past alcohol use and that despite being offered outpatient treatment consisting of the Substance Abuse and Education Group, Mr Lewis formally refused treatment.
·A Balmoral Naval Hospital Discharge Summary, dated 19 August 2004 noted that Mr Lewis 'collapsed while intoxicated during a port visit in Hawaii' and had 'multiple cardiac arrests'. Following his return to Australia cardiac stress tests and angiograms were conducted by Dr Baron, cardiologist, all of which were normal. It noted he had declined counselling. A follow up with his Local Medical Officer was required.
·A pathology report dated 15 September 2004 records testing of blood collected on both 3 August 2004 and 14 September 2004, both of which showed elevated cholesterol levels.
·A Minute completed by Lieutenant Gillies on 25 October 2004 noted that Mr Lewis had attended the Substance Abuse Prevention Education Group where he had acknowledged that alcohol had been an issue for him.
·An Annual Health Assessment dated 28 July 2005 noted that the Applicant drank alcohol but was aware of responsible alcohol intake. He was advised on the “three food groups and healthy dietary intake...the positive effects of physical activity on physical and psychological well-being... [and] ways to manage stress within in the workplace and within their personal life...”
·On 4 October 2006, Mr, Lewis was admitted to the medical ward due to a headache, which was noted as a continuous, dull throbbing pain. He had taken painkillers which provided relief and then gone for a run which worsened the headache. His heart history was noted and an ECG was performed which indicated “sinus tachycardia secondary to fever and exercise”.
·An Outpatient Clinical Record dated 5 October 2006, where Mr and Mrs Lewis presented and it was noted that Mr Lewis still had a dull and constant frontal headache, with no vomiting but slight nausea. A preliminary diagnosis was made of a viral infection. He was referred to a medical officer and microbiology tests were ordered. That night both Mr Lewis and his wife attended Shoalhaven Hospital. Both were found to have thrombocytopenia and this was reported when contacted by a medical Officer the following day. They were visited at home the day after and were resting. They were visited at home again on 8 October. Further reviews occurred on the following 4 days.
·Two Outpatient Clinical Records dated 21 June 2007 noted that Mr Lewis had a day off and presented with gastro symptoms. The record states that he “woke last night with diarrhoea & vomiting”.
·An Outpatient Clinical Record dated 21 January 2008 records his attendance with a persistent productive cough.
Post-mortem medical evidence
The Death Certificate noted the cause of death as follows:
(1) (a) Cardiac arrhythmia
(b) Coronary atherosclerosis (left anterior descending)
(c) Possible hypokalalaemia
(d) Splenimegaly and thymic hyperplasia
(e) Active chronic gastritis (Helicobacter)
The Autopsy Report dated 14 April 2008 noted that Mr Lewis died suddenly at home when he collapsed and was unable to be resuscitated after cardio-respiratory arrest. Post mortem examination revealed “fairly severe atherosclerosis of the left anterior descending coronary artery” and “active chronic gastritis”.
The report of Dr Kenneth Hossack, cardiologist, dated 25 September 2012, recorded relevant features of Mr Lewis' medical history, from his review of the file, as follows:
·In 1998 Mr Lewis suffered an episode of unconsciousness that was not investigated.
·On 16 March 1999 he had a further episode of unconsciousness and was taken to the sick bay. On the way to the sick bay he had two further episodes of unconsciousness and was treated with intravenous fluids. Despite recommendations that he be investigated with an EEG, CT head scan, ECG, echo and holter monitor, there are no records of such investigations being undertaken.
·On 24 July 2004 (whilst Mr Lewis was in Hawaii with the Navy) he suffered a cardiac arrest and required defibrillation. Upon his return to Australia, an angiogram indicated normal coronary arteries.
·Dr David Barron, cardiologist, noted serum cholesterol was elevated at 6.1 mmol/L and HDL cholesterol was low at 0.8, both of which are consistent with dyslipidaemia.
·Lipid profile estimations in August and September of 2004 gave slightly abnormal results, with the latter result showing a total cholesterol of 6.3mrnol/L and high density lipoprotein of 0.9mmol/L, Dr Hossack felt that the results supported a diagnosis of dyslipidaemia.
·Dr Walker's assessment that Mr Lewis had noted no prior history of loss of consciousness, despite the events in 1998 and 1999 (an error that the doctor notes Professor Gutman also referred to in his report, dated 18 July 2011).
Dr Hossack considered that Mr Lewis did not receive the optimal care he required to treat his dyslipidaemia, as a result of the evaluations of Dr Baron and Dr Walker. Dr Hossack stated “it would be my opinion that failure to vigorously treat dyslipidaemia was a factor that contributed to the development of severe coronary artery disease”.The doctor also expressed his disagreement with some of the views of Professor Gutman, which is further discussed below.
In a further report dated 17 May 2013, Dr Hossack noted that he agreed with Professor Gutman that the insertion of an ICD would likely have prevented in the death of Mr Lewis in 2008. Dr Hossack noted that he did not think that sufficient weight was given to the episode of unconsciousness that occurred on 16 March 1999. Dr Hossack noted Professor Gutman's view that the death was caused by primary ventricular arrhythmia unrelated to ischaemic heart disease. Dr Hossack noted that
… the presence of significant coronary artery disease makes the heart more prone to episodes of ischaemia (lack of blood supply) that causes the myocardium to be more irritable and hence develop ventricular fibrillation.
As to what treatment he would have considered appropriate in 2004, Dr Hossack indicated that he would have recommended a low saturated fat diet, reassessment of lipid levels three to six months later and, if necessary, a small dose of statin treatment.
A Minute completed by Departmental Medical Officer, Dr Maya Kumaran on 4 November 2008 noted that following Mr Lewis's cardiac arrest in 2004, he was “extensively investigated and no abnormalities were detected”. He was treated with potassium supplements and was advised to seek treatment if he developed vomiting or diarrhoea. The doctor noted that “the clinical management so far seems appropriate”. A further Minute completed by Dr Kumaran on 6 July 2009 noted that “there is no evidence of attendance to the sick pay [sic] in the weeks prior to his death”.
A report of Associate Professor Jack Gutman dated 18 July 2011 provided an opinion following review of Mr Lewis' medical file. Professor Gutman made the following relevant findings:
·Following the incident in Hawaii in 2004 Mr Lewis was treated adequately. He had extensive investigations looking for an underlying cause of his cardiac arrest.
·Dr Gutman opines that
If a defibrillator was implanted in 2004 it may have saved his life in 2008... In 2004 many cardiologists would not have recommended the implantation of a defibrillator, especially as the cardiac event that occurred was in the setting of alcohol intoxication and abnormal electrolyte levels…
·Regular monitoring of Mr Lewis' potassium levels may not have been adequate to predict the one instant when his levels would fall to cause a cardiac arrest.
·Further ECGs would not have made any difference to management.
·If Mr Lewis had Torsades de Pointes, it may have alerted an electrophysiologist that he had an underlying predisposition to an arrhythmia.
·The two syncopal episodes in 1999 when Mr Lewis lost consciousness may have had a cardiac basis.
In a further report dated 22 April 2013, Professor Gutman noted that it is likely that Mr Lewis’ dyslipidaemia was causally connected to ischaemic heart disease, but “one cannot specify to what extent”. Professor Gutman indicated that the 2004 dyslipidaemia was not related to Mr Lewis' military service, but due to genetic factors and diet. Professor Gutman considered that Mr Lewis had received appropriate clinical management for his 2004 dyslipidaemia, which was successful in lowering his cholesterol levels to non-dyslipidaemic levels by 2006. Professor Gutman also relevantly noted that in 2004, when the dyslipidaemia was present, there was no evidence of ischaemic heart disease on coronary angiography. Professor Gutman indicated his view that Mr Lewis' death was likely caused by cardiac arrhythmia, rather than ischaemic heart disease and that the arrhythmias were of an unknown cause but not due to ischaemic heart disease.
In a further report dated 19 November 2013, Professor Gutman indicated that he was unable to make a “specific diagnosis of loss of consciousness in the late 1990s as [Mr Lewis] did not have investigations at the time”.Professor Gutman considered that Mr Lewis did not suffer an injury that arose out of or in the course of his military service, nor any disease that was contributed to, to a material degree, by his military service. Professor Gutman also considered that “there is no condition that [he had] diagnosed as an injury that was suffered as an unintended consequence of medical treatment paid for by the Commonwealth”.Moreover, Professor Gutman confirmed that “there is no causal relationship between any condition that [he had] diagnosed and Mr Lewis' death”. Professor Gutman stated that Mr Lewis' death was “not a consequence of medical treatment paid for by the Commonwealth”.Professor Gutman observed that Mr Lewis had apparently had a normal echocardiogram in 2004, which would have included normal left ventricular function. He considered that the coronary artery disease found in the autopsy of 30-40% stenosis and a 60-80% stenosis was not sufficient to cause or contribute to the death in 2008. Professor Gutman also noted that clinical guidelines for treatment of dyslipidaemia and target lipid levels were not relevant to Mr Lewis. Professor Gutman stated that they were relevant to patients with clinical evidence of coronary artery disease, which Mr Lewis did not have. As such, Dr Hossack's comment that he would reassess the lipid values three to six months after dietary control and if the LDL cholesterol was greater than 2mmot/L a small dose of statin “is not supported by PBS guidelines or clinical guidelines in someone who does not have evidence of clinical coronary artery disease”.
Evidence given at the Hearing
Professor Gutman and Dr Hossack gave evidence concurrently at the Hearing. Professor Gutman and Dr Hossack agreed that the cause of death was cardiac arrhythmia. That started at least in 2004 and is likely to be the cause of the syncopal/unconscious episodes in 1997 and 1999, although that had not been proven. The essential difference between their evidence was that Professor Gutman attributes the death to predisposition to cardiac arrhythmias, whereas Dr Hossack believed that coronary artery disease played a role.
Professor Gutman explained why he did not consider the incidental coronary artery disease of the Applicant to have a role in his death. He explained that he would not expect ventricular arrhythmia to be caused by partial blockage of such a small artery as referred to in the autopsy report. Professor Gutman later referred to this 60-80% blockage of a small vessel of less than 1mm as having no role in causation and said that the chance that "the blockage was contributory was probably close to 0%".
Professor Gutman further explained why the report of the pathologist who performed the autopsy did not lead him to any other conclusion, explaining that a pathologist does not have expertise or experience in "whether a blockage is of physiological significance and causing myocardial ischemia", adding that doing autopsies on people that have died does not give knowledge of whether a blockage is causing myocardial ischemia. Professor Gutman said (with respect to the pathologist's findings):
it was a tiny diagonal vessel with a 60-80% stenosis, and I would, you know, adamantly say that the pathologist would have no idea whether that lesion or that blockage in that tiny vessel would cause ischemia to cause his demise… I can't understand that someone would think that - a pathologist seeing a 60-80% stenosis in a tiny diagonal vessel is enough to cause ischemia. I don't know how you can make that conclusion.
Professor Gutman did not agree that a defibrillator should have been installed in 2004. He noted that there were other explanations available for ventricular arrhythmias at that time – "biological causes and alcohol" and that, 10 years ago, opinion would have been divided as to whether to install a defibrillator. Professor Gutman further explained that in 2004 some aggressive cardiologists may have installed a defibrillator and more conservative ones would not – "fifty-fifty would put in a defibrillator". Professor Gutman also pointed to the disadvantages of implanting a defibrillator that need to be weighed. He referred to:
·the possibility of "inadvertent shocks", where "the patient gets shocked when there is not a ventricular arrhythmia", risk of infection;
·the complications of inserting the device eg the heart can be perforate the heart and cause a patient's death (rare), or bruising and bleeding into the chest wall on insertion.
·There was also the need to come back for battery checks every 6 months and the replacing of the defibrillator when the battery life expires, making the insertion “a lifelong event".
Despite first arguing that a defibrillator should have been implanted in 2004, Dr Hossack eventually conceded that implantation of a defibrillator in 2004 was something that some cardiologists may have decided to do, and other cardiologists may not have decided to do, "each acting competently".
Initially, it was assumed by the doctors (incorrectly in the Respondent's submission – a point to which I will return) that Mr Lewis was given no advice in relation to diet and exercise. There was also a conflict of evidence between Professor Gutman and Dr Hossack both as to whether cholesterol had a role in Mr Lewis’ death and as to whether statins (for cholesterol) should have been prescribed. Professor Gutman’s evidence was that cholesterol did not play a part in Mr Lewis’ death. In any event, his evidence was that he would not have prescribed statins given the guidelines that were in place at the relevant time.
Professor Gutman remarked that "most patients, especially if they have been given the advice, know what to eat and what not to eat". The principal point in relation to diet and exercise, however, is that in this case, death was not as a result of coronary artery disease (including such matters as weight or cholesterol) but rather because he "was prone to primary ventricular arrhythmias of unknown cause."
The doctors disagreed as to the impact of diet and exercise and the prescription of statins would have made upon the event of 2008. Professor Gutman thought it would have no impact and the event would have occurred anyway, because he was not satisfied that there was any connection between coronary artery disease and Mr Lewis’ death. Dr Hossack suggested that, absent implantation of a defibrillator, he
would argue that perhaps if he had exquisitely good treatment of high cholesterol, then there may have been some delay in the progression of coronary artery disease…and the event may not have occurred in 2008, but it may have occurred at a later date.
Dr Hossack complained that "a programmed ventricular stimulation" was not undertaken. Professor Gutman did not say that such a step should have been taken. He did not agree that Mr Lewis should have had ongoing echocardiograms, noting that he had echocardiograms that were normal. He also gave evidence that "putting a holter monitor on for 24 hours would not have likely shown any arrhythmia to account for his collapses in 1997 and 1999".
Dr Hossack conceded that Mr Lewis could simply have told Dr Walker, in answer to questions, that he did not have such symptoms as the doctor described as presyncope, syncope or exertional symptoms.
CONSIDERATION
2012/0141 – death claim
The Applicant's primary position was that s 29(3) of the MRC Act applies in that Mr Lewis received treatment under the regulations made under the Defence Act 1903 (which was conceded by the Respondent), and, as a consequence of that treatment, he died. The Respondent submitted that Mr Lewis’ death at home on 12 April 2008 was not as a consequence of that treatment.
The Respondent submitted, and there appeared to be no issue, that "treatment", in s 29(3), has the meaning given the meaning in s 13(1) by s 5 of the MRC Act:
Treatment provided, or action taken, with a view to:
(a) restoring a person to physical or mental health or maintaining a person in physical or mental health; or
(b) alleviating a person's suffering; or
(c) ensuring a person's social well-being.
The Applicant submitted that there need only be a causal link between the treatment and the death, but it was not entirely clear what particular treatment is being relied upon by the Applicant. I accept though that it concerned treatment as a result of the events in Hawaii in 2004. The Applicant did not identify any deficiency in her husband’s treatment in Hawaii, nor was there any evidence to the effect that it was deficient. Indeed, the report from Tripler Hospital suggested a high level of care, especially as Mr Lewis received treatment in the ICU.
As to treatment on return to Australia after the event, the Applicant referred to the failure to insert a defibrillator. The evidence was that the recommendation, which Mr Lewis accepted, was not to install a pacemaker.
As to whether, in applying the standards that were applicable at the time, the advice not to have a pacemaker was appropriate, Professor Gutman did not agree that a defibrillator should have been installed in 2004. At that time, opinion was divided as to whether to install a defibrillator in circumstances such as Mr Lewis’. Dr Hossack conceded that implantation of a defibrillator in 2004 was something that competent cardiologists may or may not have decided to do.
I do not consider there to have been a causal link between the treatment provided, namely the failure to insert a defibrillator, and Mr Lewis’ death. There was no evidence that his death was as a consequence of the failure to have a defibrillator inserted.
In the alternative, the Applicant submitted that the medical treatment relating to Mr Lewis’ pathology results, and in particular his elevated cholesterol levels – dyslipidaemia – was a direct cause his death. The Autopsy report stated that there was "fairly severe atherosclerosis of the left anterior descending coronary artery and probably sufficient to cause myocardial ischemia leading to arrhythmia and death". The Applicant referred to the pathology results of 3 August 2004 which indicated a 6.1 cholesterol level. Cardiologist Dr Baron on 10 August 2004 considered these results when treating Mr Lewis. Further pathology results on 14 September 2004 indicated his cholesterol level had increased to 6.3. Both pathology results state that there is an increased risk of coronary heart disease (CHD) when cholesterol levels are above 6. The Applicant claimed that neither Dr Walker or Dr Baron took action in relation to the increased cholesterol reading on 14 September 2004, but there was no evidence that either had treated Mr Lewis after that date.
The Applicant also submitted that service medical personnel also failed to treat or advise or take any action in relation to Mr Lewis’ increased cholesterol readings as at 14 September 2004, which were initialed by a medical officer.
Mr Lewis was prescribed diet and exercise and at his annual health assessment in July 2005 it was noted that he was “advised on those matters as well as stress management”. Dr Hossack agreed that “he would have recommended a low saturated fat diet”. Professor Gutman gave evidence that he did not consider that statin therapy was indicated or that it would have been supported by PBS guidelines at the time.
I note that there was no evidence of elevated cholesterol levels after 2004. I do not accept the Applicant’s contention that Mr Lewis’ cholesterol level remained untreated between September 2004 and his death nearly four years later or that his death was a consequence of the treatment of advice as to diet and exercise and the failure to prescribe statins.
In the alternative, the Applicant submitted that the claim could be dealt with under s 24(1) and s 28, of the MRC Act. Section 335(3) provides that, for non-warlike service, the Respondent (and therefore the Tribunal on review) is to decide the matter to its reasonable satisfaction. Section 339(3) sets out the appropriate standard of proof for a death that relates to non-warlike service, that standard may only be found to have been satisfied if:
·There is a connection between the death and some particular aspect of the Applicant's service: s 339(3)(a)
·There is a Statement of Principles (SOP) in force (or a determination under s340(3) of the Act): s 339(3)(b)(i) and
·Applying the SOP, the death is, on the balance of probabilities, is connected with that service: s339(3)(c).
Section 341 of the MRC Act provides that the current SOP as at the time of the decision must be applied by the Tribunal. The current SOP concerning Ischaemic Heart Disease is Instrument 90 of 2007, as amended.
The Applicant relied on Factors 6(f), 6(v) and 6(gg), which provide.
(f) having dyslipidaemia before the clinical onset of ischaemic heart disease
(v)having dyslipidaemia before the clinical worsening of ischaemic heart disease
(gg) inability to obtain appropriate clinical management for ischaemic heart disease.
The first question is whether Mr Lewis suffered ischaemic heart disease, and, if so, when was the clinical onset of the condition. Dr Hossack considered Mr Lewis suffered ischaemic heart disease. Professor Gutman accepted that Mr Lewis had some minor ischaemic heart disease, and atherosclerosis was found at autopsy, although Professor Gutman was critical of the autopsy results, referring to the difficulty in diagnosis. I am prepared to accept that Mr Lewis suffered ischaemic heart disease. There was, however, no evidence as to the date of clinical onset of ischaemic heart disease, although I note that the autopsy found there to be “fairly severe atherosclerosis of the left anterior descending coronary artery”, which might suggest the condition had been present for some time. The events of 2004 did not give rise to a diagnosis of ischaemic heart disease, and, in the intervening years, there were no symptoms which enabled a doctor to say that the disease was present at that time: per Re Robertson and Repatriation Commission (1998) 50 ALD 668 670 and Repatriation Commission v Cornelius [2002] FCA 750 and Lees v Repatriation Commission [2002] FCAFC 398; (2002) 125 FCR 331.
Neither was there evidence as to the date of clinical onset of dyslipidaemia, although there was evidence that Mr Lewis had dyslipidaemia in 2004. To satisfy factor 6(f) the person must have had dyslipidaemia before the clinical onset of ischaemic heart disease. As ischaemic heart disease was not found in 2004, it is reasonable to conclude that the dyslipidaemia preceded the ischaemic heart disease. However, clause 5 provides that, "subject to clause 7, at least one of the factors set out in clause 6 must be related to the relevant service rendered by the person". Therefore the dyslipidaemia must itself be related to Mr Lewis’ service. Professor Gutman considered that Mr Lewis’ dyslipidaemia was not related to his military service, but was due to genetic factors and diet. There was no evidence connecting Mr Lewis’ dyslipidaemia with his service. Accordingly, Mr Lewis’ dyslipidaemia is not related to Mr Lewis' service so as to satisfy clause 5 of the SOP.
As to factor 6(v), the Applicant submitted that the worsening or aggravation of Mr Lewis’ ischaemic heart disease led to her husband’s death. However, there was no evidence that Mr Lewis’ ischaemic heart disease had worsened.
Factor 6(gg) refers to an "inability to obtain appropriate clinical management for ischaemic heart disease". The Applicant contended that her husband was not adequately monitored given previous health concerns outlined in his medical documents.
As discussed above, the date of clinical onset of ischaemic heart disease is unclear. Consequently any consideration of its management is problematic. In those circumstances Dr Hossack's opinion that Mr Lewis' dyslipidaemia should have been more “vigorously” treated does not support a finding that Mr Lewis failed to obtain appropriate clinical management for ischaemic heart disease. Even if the treatment of Mr Lewis' dyslipidaemia were relevant, appropriate clinical management does not mean perfect or optimal clinical management. In any event, Professor Gutman's view was that Mr Lewis' dyslipidaemia had been adequately treated in 2004. According to Professor Gutman, there was, in any event, no failure of Mr Lewis to obtain appropriate clinical management for his ischaemic heart disease. Professor Gutman considered specifically what best practice was at the time and found that there had been no deficiency. Dr Hossack frequently referred to Mr Lewis’ "sub-optimal" care. The Applicant referred to Dr Hossack's suggestion that appropriate assessment was not made in 2004 insofar as "significant prior history was not elicited", "specific recommendations regarding the management of dyslipidaemia were not made" and "a specific follow up of mild ventricular dysfunction was not recommended".
I mention this because the Applicant made extensive submissions in the context of Mr Lewis’ “inability to obtain appropriate clinical management” in relation to the appropriateness of the treatment. The focus of the factor is upon "inability to obtain" and does not invite an inquiry as to the appropriateness of the clinical management: see Millen and Repatriation Commission [2000] AATA 508 at [22] and Hay and Repatriation Commission [2009] AATA 883 at [35].
There was, however, no evidence of deterioration occasioned by an inability to obtain appropriate clinical management such as to link his condition with his death.
In Repatriation Commission v Money [2009] FCAFC 11; (2009) 173 FCR 410 (Money), Finn, Dowsett and Edmonds JJ commented, at [43]:
...However, we do not on the material before us accept that the expression "appropriate clinical management" envisages only positive treatment of the disease. Both the Tribunal and Dr Waring expressed opinions consistent with the propositions that advice properly could and should be given to a patient in the proper course of providing a prognosis that he or she desist from certain activities (eg to stop smoking) or take other steps (e,g, to lose weight or to cease to work on submarines) as measures designed to preclude exacerbation of the disease's inexorable progress. We are satisfied that the making of prudential recommendations as to the taking of or refraining from, courses for the purpose of thereby foreclosing the possible impacts of extraneous causes that might be likely to accelerate the progress of the disease may, in appropriate circumstances, properly be regarded as falling within appropriate clinical management for cl 5(a) purposes. In expressing this view, we agree with the primary judge's conclusion that providing advice as part of the appropriate clinical management of a condition in relation to factors not mentioned in the SoP does not undermine the regime of SoPs.
For factor (gg) to apply therefore, there must have been either an objective or subjective barrier to Mr Lewis obtaining appropriate medical treatment for a condition, which is dependent on the facts.
The Applicant understood that her husband was led to believe that if he avoided high consumption of alcohol he would be fine. Dr Hossack was critical of Dr Walker for not searching for (and finding) evidence of prior syncope episodes in 1997 and 1999. Mr Lewis also denied suffering dizzy spells, fits or fainting, which, according to his medical documents, was clearly false. In my view, Dr Walker was entitled to rely upon the history given to him by Mr Lewis.
The Applicant also contended that "a specific follow up of mild ventricular dysfunction was not recommended". Professor Gutman and Dr Hossack did not agree that "lack of investigation into the late veteran's condition was below the standard of care for someone with a relevant medical history [at] that time". Professor Gutman did not say that such a step should have been taken. He did not agree that Mr Lewis should have had ongoing echocardiograms, noting that he had echocardiograms that were normal. He also gave evidence that a Holter monitor would not have likely shown any arrhythmia to account for Mr Lewis’ collapses in 1997 and 1999.
The meaning of “inability to obtain appropriate clinical management” was considered in Brew v Repatriation Commission [1999] FCA 1246 (Brew) and Repatriation Commission v Money [2009] FCAFC 11, to which the Applicant referred. In Brew the Federal Court confirmed that appropriate clinical management must be measured by the standards of clinical management available at the relevant time and then regarded by the medical profession as appropriate.
The Applicant contended that during Mr Lewis’ service, despite there being some form of clinical management that may have been effective in preventing the deterioration or reducing the progress of deterioration of the condition which led to his death, he was not able to obtain such clinical management. Not being able to obtain such clinical management worsened the condition which led to the death. The circumstances of Mr Lewis’ service prevented him from being able to obtain the clinical management so as to prevent the deterioration or reduce the progress of the deterioration of the condition which led to his death. However in my view this misconstrues the factor. There was no evidence that Mr Lewis had an inability to obtain appropriate clinical management in the sense that he was unable to, or prevented from, obtaining such clinical management.
Accordingly, factor 6(gg) of the SOP concerning ischaemic heart disease is not met.
For completeness, I address the Applicant’s alternative submission that in the event I had preferred Professor Gutman’s evidence that Mr Lewis' death was caused by cardiac arrhythmia, rather than ischaemic heart disease, and that the two conditions are unrelated.
There is in force a SOP concerning atrial fibrillation – Instrument 20 of 2003, which defines atrial fibrillation for the purposes of the SOP as “a paroxysmal, persistent or permanent arrhythmia arising in the atria of the heart, causing disorganised atrial activity and an irregularly irregular ventricular response”.Professor Gutman described Mr Lewis’ arrhythmia as “primary ventricular arrhythmias”, which is a different medical phenomenon from atrial fibrillation. Accordingly, the SOP concerning atrial fibrillation does not apply.
The Applicant contended that, if, in accordance with the report of Professor Gutman’s evidence, no SOP applies, in this case I must be reasonably satisfied whether the condition from which Mr Lewis died can be categorized as a service death pursuant to s. 28 of the MRC Act.
As no SOP applies in relation to ventricular arrhythmia, the Respondent will be liable for that condition if the definition of ‘service death’ in s 28 applies or if the condition was a 'service injury or disease' under s 27 of the MRC Act, which caused Mr Lewis' death. In circumstances where Professor Gutman considered that the arrhythmias were of an 'unknown cause' and the Applicant was not actually rendering military service at the time of his death, but was at home, there is no basis to conclude that the condition is a 'service death' pursuant to s 28 or was caused by a 'service injury or disease' pursuant to s 27 of the MRC Act.
The MRC Act 2004 Injury Claim
The Applicant submitted that on 14 September 2004 Mr Lewis suffered an aggravation of his ischemic heart disease, which, more probably than not, can be related to the failure by Dr Walker, and/or Dr Baron, and/or other service medical personnel to treat his increasing cholesterol: s 340 of the MRC Act. The Applicant submitted that in 2004 her husband suffered a service injury under the MRC Act.
The Applicant's contention was that on 14 September 2004 (the date of the blood test report, and not the date of the cardiac arrest at Pearl Harbour), her husband suffered an "aggravation of his ischaemic heart disease", which was said to be "caused by the unintended consequence of failing to take any action in relation to Mr Lewis’ increasing cholesterol levels, with that disease process commencing prior to 1 July 2004...” The 2004 pathology results regarding cholesterol have already been described. There are none in evidence before or after 2004. A change from 6.4 on 3 June 2004 to 6.3 on 14 September 2004 is not, the Respondent submitted, an increase and there is no measure showing a subsequent increase. It is not shown by the Applicant when her husband first had high cholesterol. In short, the Applicant has shown neither "increasing cholesterol levels" nor "aggravation of Mr Lewis’ ischaemic heart disease". The Applicant made a broad reference to the alleged "failure by Dr Walker, Dr Baron and/or other service medical personnel to treat his increasing cholesterol". The Applicant has not shown evidence of any "aggravation of ischaemic heart disease" on 14 September 2004 or otherwise. Again, there is also the difficulty for the Applicant that, accepting the evidence of Professor Gutman, cholesterol did not play any role in her husband's death.
Also, Dr Walker’s role was to provide “electrophysiological studies", not to treat cholesterol. With respect to Dr Baron, his report refers to the events in Hawaii involving cardiac arrest "probably due to a combination of factors including high blood alcohol, electrolyte disturbance, acidosis and hypoxia". It notes family history of diabetes, no significant findings on physical examination or ECG, records the cholesterol readings (from a test, apparently conducted on 3 August 2004, showing cholesterol of 6.1, high density lipids of 0.8 and low density lipids of 4.8 – all of which are recorded in the 15 September 2004 report. Dr Baron's report also comments upon a cardiac catheterisation that had been performed on the 6 August 2004, observing that the "coronary arteries were smooth and normal and there was no coronary anomaly". The report goes on to also state that an echocardiogram and an electro physiological study were both normal and that the deceased "doesn't have any underlying structural or electrical problem with his heart". The report noted to the GP that Mr Lewis’ needed to be careful with alcohol in the future. There was no evidence of what Dr Baron may have said to Mr Lewis.
Moreover even if the advice given to Mr Lewis was deficient, I do not accept that there was evidence that the deficiency itself caused "aggravation of ischaemic heart disease". Further, I have found that Mr Lewis’ death was not causally related to elevated cholesterol in 2004, or to ischaemic heart disease.
Accordingly, Mr Lewis did not suffer a service injury or disease, or any aggravation, as a result of treatment funded by the Commonwealth. Mr Lewis also did not suffer a service death as a result of Commonwealth treatment.
The SRC Act – Death Claim – (Syncopal injury claim)
Section 18 of the SRC Act provides that Comcare is liable to pay the cost of the employee's funeral to the person who paid the cost of the funeral. The Applicant has paid the cost of the funeral and seeks such an order.
Liability is dependent on the Tribunal being satisfied that Mr Lewis had suffered an "injury", as defined in the SRC Act, which resulted in his death. The Applicant submitted that pursuant to s 6A of the SRC Act Mr Lewis suffered an injury under the SRC Act – an aggravation of his ischaemic heart disease – which was caused by the unintended consequence of failing to take any action in relation to the deceased's increasing cholesterol levels, with that disease process commencing prior to 1 July 2004 and therefore falling within the ambit of the SRC Act.
As previously discussed, it is not correct to say that no action was taken in relation to Mr Lewis’ cholesterol. Importantly, there is no evidence that his cholesterol levels increased, or that that was the result of any medical advice received, or that any deficiency in such advice contributed to any "aggravation of ischaemic heart disease". Furthermore, as I have found, Mr Lewis’ death was not related to his cholesterol or to ischaemic heart disease.
The Applicant also relied on Dr Hossack's report which had contended that further weight should have been given to Mr Lewis' prior episodes of unconsciousness on 1 October 1997 and 16 March 1999. The Applicant submitted that these two episodes of her husband collapsing prior to 1 July 2004 constitute 'injuries' pursuant to s l4 of the SRC Act due to the sudden physiological change, but did not, as far as I could see, particularise that submission. The evidence is inconclusive as to the nature of those incidents of loss of consciousness. In evidence both Dr Hossack and Professor Gutman agree, in retrospect, they were probably caused by atrial fibrillation resulting in Mr Lewis suffering syncopal episodes whilst at work. However, the nature and cause of the episodes were not identified at the time, and has not been identified since, although Professor Gutman considered they 'may have had a cardiac basis'. I accept the Respondent’s submission that, even if, with the benefit of hindsight, it is assumed that those incidents were indicative of Mr Lewis’ underlying tendency to arrhythmia, there is no evidence that either of those two incidents, as opposed to the underlying propensity (not itself compensable) had any causal connection with Mr Lewis’ ultimate death. Whatever the nature of the episodes Mr Lewis did not sustain an injury (including a disease) within the meaning of the SRC Act.
The Applicant also contends that Mr Lewis did not receive adequate medical treatment, as further investigations ought to have been conducted at the time, and therefore Mr Lewis suffered an injury as an unintended consequence of treatment funded by the Commonwealth, pursuant to s 6A of the SRC Act. There is no evidence that would support a finding that the treatment received at the time of the two episodes was inadequate or, specifically, that a diagnosis of any underlying cardiac condition could or should have been made in 1997 or 1999. Furthermore, there is no evidence of any treatment that reasonably ought to have been undertaken to prevent any worsening of any condition. Indeed, investigations undertaken in 2004 showed a structurally normal heart.
Any aggravation or acceleration suffered as an unintended consequence of medical treatment must itself cause the death. It is not sufficient for the injury to have accelerated a condition for it to have resulted in death if the acceleration is 'spent' before the death: Re Commission of the Safety, Rehabilitation and Compensation of Commonwealth Employees v June Anne Hall [1993] FCA 129.
In order for liability to exist under s 17 of the SRC Act an injury must be found to have resulted in Mr Lewis' death. There is no evidence that the episodes in 1997 and 1999, or treatment received after those episodes resulted in Mr Lewis' death.
Professor Gutman confirmed that 'there is no causal connection between any condition I have diagnosed and Mr Lewis' death'. Professor Gutman also considered that Mr Lewis' death was caused by cardiac arrhythmia and that the cardiac arrhythmia was of an 'unknown cause'.
DECISION
The decisions under review are affirmed.
I certify that the preceding 81 (eighty -one) paragraphs are a true copy of the reasons for the decision herein of Ms Naida Isenberg, Senior Member ...........................[sgd].............................................
Associate
Dated 11 August 2015
Date(s) of hearing 21 November 2014 Date final submissions received 9 January 2015 Counsel for the Applicant D Richards Solicitors for the Applicant KCI Lawyers Counsel for the Respondent G Johnson SC Solicitors for the Respondent Moray & Agnew
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