Catherine Alice Erickson and Repatriation Commission
[2014] AATA 347
[2014] AATA 347
Division VETERANS' APPEALS DIVISION File Number(s)
2012/5575
Re
Catherine Alice Erickson
APPLICANT
And
Repatriation Commission
RESPONDENT
DECISION
Tribunal John Handley, Senior Member
Date 3 June 2014 Place Melbourne Decision The decision under review is affirmed
..................[sgd]......................................................
John Handley, Senior Member
Veterans’ entitlements - veteran engaged in operational service in WW2 - stress of service conceded - cause of death certified as respiratory failure and pneumonia - cause of death disputed - applicant pursued hypotheses of death by COPD and ischaemic heart disease - smoking history in a questionnaire completed by the veteran inconsistent with evidence of the applicant, his children and clinical entries in medical records - significant dispute between doctors interpreting the clinical evidence - whether veteran did suffer COPD - whether connection between veteran’s death and IHD - decision affirmed.
Legislation
Veteran’s Entitlements Act 1986, section 120(1)
Cases
Repatriation Commission v Deledio (1998) 88 FCR 82
Secondary Materials
Statement of Principles, Chronic Airflow Limitation, 65/1994 (revoked)
Statement of Principles, Chronic Airflow Limitation, 136/1996 (revoked)
Statement of Principles, Chronic Airflow Limitation, 73/1997 (revoked)
Statement of Principles, Chronic Bronchitis and Emphysema, 30/2004 (revoked)
Statement of Principles, Chronic Obstructive Pulmonary Disease, 37/2014
Statement of Principles, Ischaemic Heart Disease, 89/2007
REASONS FOR DECISION
John Handley, Senior Member
Standley Noel Erickson (the veteran) was a member of the Royal Australian Navy between 4 January 1940 and 14 March 1946. He was engaged in periods of overseas service between 1942 and 1944. The whole of his service constitutes operational service.
Mr Erickson died on 14 January 2012 aged 92 years. The certified cause of death was Respiratory failure-hours and Pneumonia-hours (T documents page 35).
Catherine Erickson, the widow of the veteran, is the applicant in these proceedings. She contends that a reasonable hypothesis can be raised connecting the service of her late husband and his death. Her legal representatives contend that ischaemic heart disease (IHD) and chronic obstructive pulmonary disease (COPD) should have also been recorded as causes of death.
Counsel for the applicant, Ms Ryan, said the applicant would advance two hypotheses being:
(i)Service à stress à smoking à IHD à pneumonia à death (the IHD hypothesis); and/or
(ii)Service à stress à smoking à COPD à pneumonia à death (the COPD hypothesis).
Counsel for the Respondent, Mr Rudge, did not contest the circumstances of the veteran’s service overseas as being stressful nor access to and the ready availability of cigarettes during service, as an aid to relieve the stress. Consequently, there was no challenge to the link between service and smoking
Counsel for the applicant relied on factor 6(g)(ii) and (iii) in Statement of Principles (SoP) 89/2007 in support of the IHD hypothesis and factor 5(a) of SoP 30/2004 in support of the COPD hypothesis.
Subsequent to the conclusion of the hearing, the Repatriation Medical Authority issued a SoP concerning the condition of Chronic Obstructive Pulmonary Disease (no. 37/2014). (At the date of the hearing, the SoP in support of the COPD hypothesis concerned the condition of Chronic Emphysema and Bronchitis).
The representatives were invited to make submissions on the relevance, if any, of the new Instrument.
Both acknowledged that the Instrument provides a clinical definition of COPD, which, although embracing chronic bronchitis and emphysema, also includes the condition of chronic airflow limitation. I will return to these matters later in these reasons.
The evidence
Evidence was heard from the applicant, her daughters Sue Erickson Clark and Julie Webb, and John Scanlon, the applicant’s brother-in-law. Betty Scanlon, wife of John Scanlon had lodged a statement but was in hospital on the day of the hearing and unable to give evidence. The evidence from these persons was concerned entirely with the veteran’s smoking history.
The remaining evidence was from Dr Jenkins, the veteran’s treating general practitioner, Dr Collins, a forensic pathologist who was called on behalf of the applicant and Professor Cade, an intensive care specialist who was called on behalf of the respondent.
The history and documented evidence of smoking attributable to the veteran, is located in 6 documents received as exhibits-
(a)a questionnaire completed by him on 15 November 1986 (T4 page 19) where he recorded that he commenced smoking at age 18 and was a social smoker. Between 1940 and 1946 he recorded that the quantity of cigarettes increased from 10 to 20 per day because duty free cigarettes were freely available, this being the only vice we were permitted an increase was inevitable. He recorded that he ceased smoking at age 26 (~ 1945) when he was discharged from service because on discharge tobacco rationing was in force, cigarettes were hard to obtain so I gave up smoking and have not had a smoke since.
(b)A Health Assessment dated 26 September 2005 (Exhibit A7 page 135) recording that the veteran smoked 50 years ago (~1960-1965).
(c)An entry in the clinical notes of Dr Jenkins (Exhibit A7 page 31) dated 13 May 2010 - smoker for 40 years (~1970).
(d)An entry in a report of Dr Friedman dated 3 July 2002 (Exhibit A7 page 111)-…nor had he ever been a smoker.
(e)An entry in the progress notes of Southern Health dated 19 December 2010 (Exhibit R2 page 49) – Ex smoker (army) 20 py Hx Quit 40 yrs ago (~1970).
(f)An entry in the clinical records of Southern health on 14 January 2014 - ex smoker (ceased 1960) (Exhibit R1 Page 29). This entry was made shortly prior to the veteran’s death. The source of this information is not known.
In her application to the respondent, the applicant recorded that her husband first started smoking on a regular basis about December 1942. He was then smoking about 20 cigarettes per day, he did not ever stop smoking permanently but did reduce his smoking habit in 1960 to between 5 to10 cigarettes per day (T documents pages 29 – 31).
The applicant said the questionnaire completed by her husband in 1986 was incorrect and she had no idea why he recorded that he ceased smoking in 1946.
In her statement lodged prior to the commencement of the hearing (Exhibit A4) and in her evidence she recorded that her husband was a heavy smoker when they first met in 1945, about 12 months before they married. She was a member of the Australian army and used her entitlement to a tobacco ration to supply her husband with additional cigarettes.
After they married and before the children were born – in 1959 and 1960 respectively – the applicant said her husband would have his first cigarette in bed each morning. He then smoked throughout the day and had his last cigarette, also in bed, before he went to sleep.
When the children were born she persisted in encouraging him – apparently successfully – to cease smoking inside the house and in their presence. She said he ceased smoking in the early 1960s although she has subsequently learned, because of these proceedings, that her husband was observed by her daughters smoking, on occasions, in their backyard and at other locations.
The applicant said she was surprised that Dr Jenkins had an entry in his clinical file of her husband being a smoker for 40 years.
Ms Erickson Clark and Ms Webb both recall observing their father smoking cigarettes in their backyard behind an incinerator from about the time they were in primary school until their early teens. Ms Webb recalled that the incinerator and an adjacent cubby house were later removed and replaced with a swimming pool when they were about 14 years of age. Thereafter they had no recollection of their father smoking in the backyard but they did recall occasions where he was observed smoking in a caravan with their uncle, John Scanlon at Springvale. They had also been told by their aunt, Betty Scanlon, that there were occasions when their father was seen smoking at their grandmother’s house in Clayton. Both indicated that the statement by their father of ceasing to smoke at age 26 was incorrect.
John Scanlon described his brother-in-law, the deceased, as a sneaky smoker. He said the applicant was not aware that her husband had been smoking cigarettes. He said he was also aware that the veteran had told the applicant that he stopped smoking, but he was smoking on the sly. He recalled occasions when he was smoking with the veteran when they were constructing a swimming pool in their backyard and on another occasion when they when he was constructing a brick garage. He recalled the last time he observed the veteran smoking was on the occasion of the birth of the first grandchild of Julie Webb (Ms Webb had said earlier that occasion was in 1992).
Betty Scanlon, who did not give evidence but lodged a statement (Exhibit A2) recorded that she recalled the veteran was a heavy smoker until he stopped smoking in front of both his daughters when they were young children, but heard from others that he continued to smoke and was observed by his daughters to be smoking when they were teenagers. Until he stopped smoking in their presence he seemed to almost constantly have a cigarette in his hand.
Medical evidence
Dr Paul Jenkins
Dr Jenkins is a general practitioner who first saw the veteran in April 2002 and on many subsequent occasions. He completed two reports on behalf of the applicant dated 2 May 2012 (T documents page xi) and 31 March 2014 (Exhibit A6).
On 16 December 2005, Dr Jenkins received a copy of a CT report (T documents page 103) which found that there was consolidation present in the lower lobe of the veteran’s right lung with minor changes in the base of the left lung with associated atelectasis. (The deceased had been admitted to Peninsula Private Hospital on 15 December 2005 and remained as an inpatient until 23 December 2005. In a report of 13 January 2006, Dr Alexander Friedman, a consultant physician and cardiologist who had also been treating the deceased from 1997 reported that the deceased was admitted initially to the Frankston Hospital and later to the Peninsula Private Hospital because of increasing breathlessness, angina and collapse at home. During his admission the deceased underwent angioplasty and stenting of his right coronary artery).
Dr Jenkins explained that consolidation is an indicator of pneumonia and atelectasis is a term describing collapse. He was satisfied that the images on the CT pointed to pneumonia in the right lung and collapse of the base of the left lung which he said would be consistent with [the diagnosis of COPD] but not diagnostic of it. He said a person with COPD is prone to infection and collapse of the lung is also associated with infection (Transcript page 5). He said the clinical onset of COPD was in 2005 when consolidation was found on the CT films of 16 December 2005 (Transcript page 12).
On 12 July 2010 (Exhibit A7 page 155) a radiologist reported consolidation present in the mid and lower zones and the middle and lower lobes of the veteran’s right lung. The radiologist interpreted the films as indicating pneumonia in the right middle and lower lobes. Dr Jenkins reaffirmed that COPD would make it more likely that he would have developed severe lung infections including pneumonia (Transcript page 9).
During the years the veteran was under the care of Dr Jenkins he also presented on a number of occasions with a cough, the first being 14 June 2007, when a diagnosis of acute bronchitis was made. A chest x-ray taken on 15 June 2007, the day following the consultation above, demonstrated hyperinflation of both lungs and minor patchy consolidation in the lower right lung. The radiologist concluded that the films demonstrated a presumed infective exacerbation of COPD (Exhibit A7 page 50)).
Dr Jenkins said the presence of hyperinflation indicated emphysema. It was his opinion that a person suffering COPD has difficulty exhaling and their lungs take on an appearance of being enlarged. He said the presence of hyperinflation, in the context of recurring chest infections is strong presumptive evidence of COPD (Transcript page 6).
On 14 January 2012 the veteran was admitted to Southern Health Emergency (Monash Medical Centre) at 2am. The attending doctor recorded the deceased presented with shortness of breath, a past medical history of previous pneumonia, cardiac failure, AF (atrial fibrillation) and HTN (Exhibit A7 page 195).
Dr Jenkins said he was unfamiliar with the expression HTN. He said the reasons recorded for presentation are consistent with a person who suffers COPD. He was also satisfied, and recorded in his report of 31 March 2014 that the antecedent cause of the pneumonia included COPD and IHD (Transcript page 11).
Dr Jenkins said there was a connection between IHD and pneumonia by the presence of COPD. He said a person’s heart and lungs must work in tandem. If lungs are deficient, the heart has a greater strain imposed on it. Alternatively if a person’s heart is not operating efficiently, a strain is then placed upon a person’s lungs. He said the applicant was known to have suffered IHD for some years. Accordingly, a person suffering from COPD and IHD will have a buildup of fluid in their lungs which causes or contributes to infection which then leads to pneumonia (Transcript page 12).
Dr Jenkins was taken to a report, dated 3 July 2002 (Exhibit A7 page 111), sent to him from Dr Friedman, which recorded that a Persantin Thallium test taken in August 1997 showed reversible ischaemia in the anterolateral wall…. Dr Jenkins said that finding is consistent with a clinical diagnosis of IHD in August 1997 (Transcript page 13).Earlier, he said IHD was developing for a while before the veteran had surgery in 2005 when his right coronary artery was stented (Transcript page 12). Dr Szto, the treating cardiologist reported on 23 December 2005 the veteran had a past medical history of IHD (Exhibit A7 page 140).
In a report to Dr Jenkins of 20 December 2011 (Exhibit A7 page 191), Dr Friedman reported that the deceased had been treated on 20 November 2011 as an emergency patient at the Sandringham Hospital where a pleural effusion was found and drained but he developed probable pneumothorax bilaterally, it was transudate there was no growth. Dr Friedman thought the pleural effusion was probably secondary to heart failure.
Dr Jenkins understood that report to mean that the veteran was admitted with heart failure rather than an infective cause (Transcript page 11).
Dr Jenkins said the contribution by IHD to the pneumonia was by the mechanism of the pleural effusion leading to the pneumothorax (Transcript page 13).
The deceased suffered a number of falls, one of which caused him to be admitted to the Cabrini Hospital on 30 October 2011. He was found to be in atrial fibrillation and had suffered considered considerable weight loss. A CT scan of the deceased’s chest and abdomen did not reveal the presence of any tumour. The principal diagnosis made at discharge from the Cabrini Hospital (Exhibit A7 page 160 – 161) was of syncope secondary to bradycardia (fainting due to reduced heart rate). The Hospital noted that the deceased had a history of IHD, atrial fibrillation and hypertension.
In cross examination, Dr Jenkins agreed there is no reference made by the hospital (or in a report of that admission by Dr Friedman-Exhibit A7 page 162) to a diagnosis of COPD nor were the medications issued for treatment of respiratory disease (Transcript pages 19-20).
Dr Jenkins’ attention was drawn to an aged care assessment completed by the Kingston Aged Care Assessment Service (Kingston) which reported on 6 January 2012 (Exhibit A7 pages 192 – 193) that the veteran was admitted to the Sandringham Hospital as an emergency patient on 20 November 2011 following a fall at home. Dr John Cade who reported on a medico legal basis for the respondent (26 July 2013) understood the deceased suffered rib fractures in the fall (Exhibit R6). Both he and the clinician from Kingston reported the deceased also suffered secondary pneumonia.
Dr Jenkins said he did not believe the deceased suffered fractured ribs but acknowledged he did not have any correspondence from the Alfred Hospital. He acknowledged that rib fractures, if present, may have affected the veteran’s lungs but said if you’ve got COPD then it takes a lot less damage to cause major problems for your breathing than if you’ve got nice, healthy lungs (Transcript page 15). However he acknowledged that a rib fractures are a common cause of a pneumothorax. (Evidence of bilateral ribs fractures is found in the Kingston triage report – Exhibit R2 page 1)
Dr Friedman completed a number of medical reports commencing in May 2003 and concluding in December 2011 and which are located in Dr Jenkins clinical file (Exhibit A7).
Between 16 May 2003 and 20 July 2010, Dr Friedman consistently reported that the deceased’s chest sounded clear. He did not report that the deceased suffered shortness of breath. Dr Jenkins agreed that on the basis of those reports, Dr Friedman did not find any respiratory or pulmonary disease. He thought it was surprising that Dr Friedman would report on 14 July 2010 (Exhibit A7 page 156), two days after a chest x-ray (Exhibit A7 page 155) reported right middle and lower pneumonia that chest sounded clear. He noted Dr Friedman again reported on 20 July 2010 (Exhibit A7 page 157) that chest sounded clear but with an additional comment Rapid improvement. CXR much improved 19/07. Chest auscultation improved. Dr Jenkins said if the veteran had improved it had to be not perfect at the time. He acknowledged the veteran recovered well from an acute episode but said it could also be the actions of a gentleman who understated his symptoms and wanted to get away from medical care (Transcript page 19).
Dr Jenkins acknowledged that CT scans of 16 December 2007 and 25 October 2011 and x-rays of 16 June 2007, 15 February 2010 and 12 July 2010 make no reference to COPD. He disagreed with a proposition put to him that COPD was a doubtful diagnosis. Dr Jenkins said he had no doubt about the diagnosis, simply from the look of the man who – really he looked like he had COPD, and he stated to me that he been a smoker for 40 years. I guess he might have seen Dr Friedman – he saw Dr Friedman twice a year – he might have seen him mostly on his good days, but I saw him with recurrent chest infections towards the end of his life and I’m confident of my diagnosis (Transcript pages 21-22).
When he was asked to consider an opinion expressed by Professor Cade that any chronic lung disease which was too subtle to be identified on chest imaging could not be expected to contribute to morbidity, Dr Jenkins said if the veteran had minimal or minor COPD… [it would not be] the cause of pneumonia. In his opinion, the veteran had significant COPD and it was a probable or a possible cause of pneumonia. He said he did not see the veteran after 27 October 2011 and therefore had no subsequent clinical involvement with him (Transcript pages 22-23).
Dr Jenkins performed a spirometry assessment of the veteran on 13 May 2010. The results were interpreted by Doctor Jenkins as indicating severe limitation of lung function. He concluded that the veteran had COPD (Transcript page 8). However it was suggested to him that an interpretation of the data would not be reliable if the veteran was then affected by bronchitis. The clinical notes taken on the day of testing record the veteran attended with a history of cough-clear sputum, and the recorded reasons for visit are COPD, infective exacerbation.
Dr Jenkins said the results during an episode of bronchitis would be worse than normal. But if one had normal lungs you wouldn’t expect it to be as bad, or nearly as bad as it was (Transcript page 21).
In relation to the hypothesis involving IHD, Dr Jenkins was informed of an opinion also expressed by Professor Cade that IHD would have contributed to death via an arrhythmia, an ischaemic attack or cardiac failure for which there was no clinical evidence. Dr Jenkins said that in the absence of obvious heart failure demonstrated radiologically, he would defer to the opinion of Professor Cade (Transcript page 23).
In re-examination Dr Jenkins said the veteran had lost weight in the last six months of his life, he was very thin and his chest was a bit on the over expanded size which is what you expect with COPD (Transcript page 23).
During the last two years of the veteran’s life he said his 40 year smoking habit finally caught up with him and the damage to his lungs showed up at that stage with recurrent infections and chronic cough. And poor spirometry based on the investigation I did in 2010-13 May 2010.
Dr Byron Collins
Dr Collins is a consultant forensic pathologist who provided two reports at the request of the applicant’s solicitors dated 23 August 2013 and 4 April 2014 (Exhibits A8 and A9 respectively).
In his first report Dr Collins recorded that IHD, COPD and atrial fibrillation should have been recorded on the death certificate as causes of death. It was his opinion that IHD and COPD could have the very real potential to significantly contribute to the deceased’s immediate cause of death, by a variety of pathophysiological mechanisms involving particularly a predisposition to the development of an acute lung infection such as (i) cardiac failure (IHD), (ii) altered respiratory tree anatomy (COPD).
Dr Collins was asked to comment, for the purposes of his second report, on a report of an x-ray of the deceased taken on 15 June 2007 (Exhibit A7 page 50). (In evidence he said he had not seen the films). He noted that the radiologist found that the deceased’s lungs were hyperinflated and had concluded that there was a presumed infective exacerbation of COPD. It was his opinion, contrary to a reported opinion of Professor Cade, that the absence of clinical reporting of the deceased having hyperinflation elsewhere did not negate its presence nor support an inference which he said could be drawn from the opinions expressed by Professor Cade concerning the clinical severity of any chronic lung disease.
In evidence (Transcript pages 3-4) Dr Collins was asked to comment on a report of an x-ray taken on 15 December 2005 at the Frankston Hospital (Exhibit R4) reproduced as follows;
Previous films are not available for comparison. Appearances on the left side suggest a pneumothorax but this appears to be due to a skin fold since there are lung vascular markings projecting beyond the apparent pleural line. Basal fibrotic changes are identified with some bullous change suggesting underlying airways disease.
The clinical notes completed when the deceased was examined in the emergency Department of Frankston Hospital on 15 December 2005 record that he had collapsed earlier that day whilst at home, there was a history of having collapsed on two occasions in the preceding six months, and had been producing phlegm and had had a cough within the preceding two years. On examination, bilateral basal crackles with basal pleural rub were detected.
Dr Collins said that the clinical presentation and the history obtained was consistent with chronic bronchitis and the presence of the basal crackles and the basal pleural rub indicated the presence of fluid in the lungs with possible inflammation or infection. He said the findings in the x-ray report of basal fibrotic changes are consistent with fibrous tissue or scarring in the base of the lungs, most commonly the result of a previous chest infection and the reported bullous changes were suggestive of the deceased developing emphysema or COPD. He agreed with the conclusions of the radiologist that the findings suggested an underlying airways disease.
When he was cross-examined (Transcript pages 14-15), Dr Collins indicated that he was aware that a CT scan was undertaken of the applicant on 16 December 2005, the day after the above x-ray. He said he had read the report of it but had not seen the films. The report is found in the clinical file of Dr Jenkins (Exhibit A7 page 41) and is reproduced as follows
Consolidation is present within the right lower lobe involving particularly the posterobasal segment. Peribronchial changes are also noted extending into the left lower lobe and there is atelectasis at the left lung base posteriorly. No definite mass lesion is seen. The lung fields are otherwise clear. A 1cm pre-carinal lymph node is noted. No lymphadenopathy is noted elsewhere within the chest. The adrenal glands bilaterally are normal in appearance.
Conclusion: Consolidation is present posteriorly within the right lower lobe and there are minor changes also at the left lung base with associated atelectasis.
Dr Collins said that in a broad sense the CT images would have a higher resolution and a clearer view than a chest x-ray. He accepted that there was no comment in the CT report of the lungs being hyperinflated and said but that doesn’t mean to say it’s not there. He said the radiologist may have concentrated on the location of the consolidation and may have left out other findings that may well be present. He said the x-ray taken on the day previous would have been focusing on the deceased’s lungs but the CT may have been undertaken for a different purpose. He suggested the radiologist was looking for any underlying malignancy that may have been a cause of chest infection. He said that would not be an unreasonable explanation for a radiologist to focus on a particular area because malignancy of the lungs is not all that uncommon. He said it could well be that the radiologist at x-ray was looking for a cause of the chest infection, for example pneumonia, chronic bronchitis or emphysema but the radiologist at CT may have seen something but not necessarily comment on it. He said that would not have been an extraordinary oversight on the part of the radiologist.
On 19 January 2006, being the month after the above x-ray and CT scans, the veteran was admitted as an emergency patient to the Frankston Hospital. The attending doctor recorded he had a community acquired pneumonia of the right middle lobe and queried whether there was ongoing recurrent syncope because a history was obtained of the veteran having collapsed without loss of consciousness when he got out of bed, of being increasingly unwell over the previous two days and having an increased cough. Clinical investigations included a chest x-ray which revealed RML (right middle lobe) pneumonic changes. A clinical examination of the veteran’s chest was recorded as revealing air entry equal. Mild creps rll (right lower lobe).
Dr Collins said that those findings and presentation are consistent with COPD.
On 14 June 2007 the veteran consulted with Dr Jenkins who found on examination (Exhibit A7 page 24) Creps present. Rhonchi present. The following day Dr Jenkins arranged for him to have an x-ray which was reported by the radiologist as demonstrating the lungs being hyperinflated and patchy consolidation in the right lower lobe. The radiologist concluded that there was a presumed infective exacerbation of COPD.
Doctor Collins said that the most common cause of hyperinflation, if generalised, is COPD. He agreed with a description given by Doctor Jenkins that the veteran’s appearance with an over expanded chest would suggest he suffered COPD.
The entries in an assessment report of the veteran completed at Southern Health on 6 January 2012 (approximately 1 week before his demise) which recorded his health status as having reduced mobility; emphysema/reduced endurance were interpreted by Dr Collins as clinical indications of the presence of COPD.
Dr Collins said that he was satisfied on the basis of the clinical findings described above that the deceased was properly diagnosed with COPD and a causal relationship existed between it and the terminal pneumonia.
In relation to the point of difference between himself and Professor Cade, concerning the absence from x-rays and CT scans and other clinical references for a number of years of the presence of chronic lung disease, Doctor Collins said that he was satisfied that there was some degree of COPD. The absence of features consistent with COPD on later x-rays were noted but, he explained, that doesn’t mean to say that it is not present. Dr Collins said that the bullous changes found in x-ray on 15 December 2005 do not heal (Transcript pages 7 – 9).
In relation to the IHD hypothesis, Dr Collins was asked to comment on a report of a chest x-ray taken of the deceased on the day of his death (T documents page 72). The report is reproduced as follows:
Even allowing for the projection the heart size appears at least borderline. Focal airspace opacities are identified in the left upper to mid zone with some airspace infiltrate also present in the right lower zone likely the right middle lobe. Small pleural effusion is identified on the right. No evidence of significant underlying pulmonary venous congestion, these findings may reflect infective consolidation, follow-up chest x-ray post-treatment is recommended to ensure resolution. A 1 cm nodule is projected over the anterior aspect of the 6th right rib, this may represent a nipple shadow however an intrapulmonary nodule cannot be excluded as such close follow-up imaging is again indicated.
Dr Collins said, contrary to an opinion expressed by Professor Cade in his reports that the x-ray report does not exclude left heart failure.
Dr Collins noted that the radiologist reported that there was no evidence of significant underlying pulmonary venous congestion. He said the word significant indicated that pulmonary venous congestion was not excluded. He said by the time the x-ray had been taken, the deceased had been treated for congestive cardiac failure by the administration of medication. In his opinion, rather than focus on the reasons for the absence of reporting the presence of pulmonary venous congestion, it may well be that he had more significant pulmonary oedema or congestive cardiac failure in the days leading up to his admission than was diagnosed either clinically and/or radiologically. (Transcript pages 9-10).
Dr Collins was asked to consider contents of the report of Dr Friedman dated 7 November 2011 (Exhibit A7 page 162) recording that the deceased had suffered a number of falls in October 2011 requiring admission to the Cabrini Hospital. He also noted from the report that the medication prescribed to the deceased was changed and he had improved heart rate without any further episodes of syncope.
Dr Collins said that if those episodes of collapse were related to a form of cardiac malfunction being either atrial fibrillation and/or a slow ventricular rate, then he has chronic heart disease, most likely ischaemic in origin, and it may well have contributed to the development of congestive cardiac failure.
In another report completed by Dr Friedman on 20 December 2011 (Exhibit A7 page 191) he noted that the deceased had been admitted to the Sandringham Hospital on 20 November 2011 were a pleural effusion was found. It was drained but a bilateral pneumothorax developed and he was admitted to the Alfred Hospital. The effusion was transudate, there was no growth and was considered to be probably secondary to heart failure.
Dr Collins said the history given in the report above from Dr Friedman pointed to evidence of congestive cardiac failure. He said the deceased’s lungs had become leaky and fluid had collected in the pleural space within the chest cavity. He thought the pleural effusion noted by the radiologist on 14 January 2012 may have had a similar cause, that is, an infection and leaking of fluid. If the effusion was not indicative of cardiac failure it was, in his opinion, indicative of pneumonia.
In cross-examination Dr Collins acknowledged that the radiologist who reported the x-ray on 14 January 2012 made no reference to heart failure or chronic bronchitis or emphysema. He said the use of the word significant indicated, possibly, that there were features present that were less than significant (Transcript pages 15 – 16).
Dr Collins agreed that a report of a CT scan of 25 October 2011 (Exhibit A7 page 77) made no findings of COPD or emphysema. He said however that it was obvious that the radiologist was attempting to ascertain why the deceased was losing weight and there was a focus on whether there was a malignant lesion was within the lungs (as an explanation for the weight loss). He acknowledged that there were references made by the radiologist to the presence of lymph nodes, a small right side pleural effusion and right-sided basal collapse or consolidation and it could fairly be assumed that the radiologist was not focused on the malignancy only. He also acknowledged although the CT did not make any finding of COPD or emphysema or heart failure, he said well, it says there is a pleural effusion; and that may be consistent with heart failure. It may not be. (Transcript page 16-17)
Doctor Collins acknowledged that a report of a chest x-ray taken on 15 February 2010 (Exhibit A7 page 64), which, whilst reporting that there was some linear atelectasis in the right lung base, also reported the remainder of the [veteran’s] lungs appeared clear and are not congested. He agreed the radiologist made no finding of COPD or emphysema or any sign of congestive cardiac failure.
Dr Collins was then examined in relation to the reports completed by Dr Friedman. He was asked to consider the recurring comment in all of his reports that following an examination of the deceased, his chest sounded clear.
Dr Collins said that that comment does not necessarily mean that it was referable to COPD or emphysema. He said it would be reasonable to conclude that the comment was made in relation to whether the deceased had congestive cardiac failure.
Dr Collins said that if Dr Friedman was concerned with treatment and management of COPD, he would have made comment upon it. He said the absence of any comment in relation to the presence of severe chronic obstructive airways disease doesn’t necessarily mean to say that it wasn’t there in some form. He acknowledged Dr Friedman would have examined the deceased’s chest. Whilst he did not doubt the finding that he made that the chest sounds were clear, he maintained his belief that the expression chest sounded clear was Dr Friedman’s clinical finding in relation to congestive cardiac failure and it may be that when he was examining the late Mr Erickson that he was indeed in controlled cardiac failure with the therapy that he was being given (Transcript pages 18 – 19).
Dr Collins was aware that a chest x-ray of 12 July 2010 was reported by the radiologist as indicating right middle and lower lobe pneumonia however Dr Friedman, who examined the deceased on 14 July 2010, recorded that the x-ray showed left lower lobe pneumonia and again recorded that on examination chest sounded clear (Exhibit A7 pages 155 and 156).
He said the radiologist or Dr Friedman may have made an error in recording the presence of pneumonia in either the left or the right lung. However, irrespective of which lung was affected, he said if the chest sounds were clear, that is, there was no sound detected or heard through his stethoscope, a finding of a clear sound would be inconsistent with the presence of pneumonia.
Professor John Cade
Professor Cade is the principle specialist in intensive care at the Royal Melbourne Hospital. He completed 2 reports at the request of the respondent, dated 26 July 2013 and 17 September 2013 (Exhibits R6 and R7).
In his first report, Professor Cade, having reviewed the extensive clinical material exhibited in this review noted that the deceased was diagnosed with atrial fibrillation in 1972 or 1973 and was subsequently treated appropriately with medication. He also noted that the deceased had been under the care of Dr Friedman, a cardiologist from 1997.
The first clinical entry of pneumonia was found in the notes of the Peninsula Private Hospital in 2005 when the veteran underwent angiography and his right coronary artery was stented. During that admission the deceased developed right lower lobe pneumonia.
The next clinical entry recording pneumonia was in the notes of the Como Private Hospital in July 2011 where the veteran was admitted under the care of Dr Friedman.
Another entry recording the presence of pneumonia, (secondary to bilateral pneumothoraces following rib fractures after a fall at home) was diagnosed in December 2011 (in the month prior to his death) during admission to Sandringham Hospital where the veteran also had a pleural effusion.
On 14 January 2012, the veteran was admitted to the Monash Medical Centre where he was found to have pneumonia, severe sepsis, hypotension and respiratory failure. Professor Cade reported that the recorded cause of death as respiratory failure and pneumonia was accurate.
Professor Cade reported that the clinical notes recorded the veteran was well prior to his terminal presentation but with acute shortness of breath. However, the pneumonia found on admission indicated to him that it had been developing over a few days.
He noted the veteran had previously been diagnosed with other conditions which had the potential to cause or contribute to death being IHD, atrial fibrillation hypertension and renal impairment.
It was noted that the IHD was demonstrated at angiography in 2005 however Doctor Friedman had reported the veteran suffering from angina since 1985, which satisfied Professor Cade that the clinical onset of IHD then occurred. He acknowledged in his report that the mechanism by which IHD could have potentially contributed to death was by an arrhythmia but there was no evidence of it during the eight hour period that the veteran was a patient at the Monash Medical Centre before his demise. He also noted that a chest x-ray taken at the hospital excluded left heart failure. It was his expectation that septic shock from which the veteran suffered would have rapidly caused the deceased’s demise, irrespective of his cardiac function. He noted that atrial fibrillation and been present for about 40 years but appears to have been well-controlled, was uncomplicated and would not have been responsible for the death nor could it be related to prior service.
Hypertension was noted to have been present for 25 years but it was well-controlled and without complication but may have contributed to renal impairment.
Professor Cade reported that he could find no reference in the clinical files to a diagnosis of COPD. He inspected x-rays and CT reports, particularly a CT scan in 2006. He recorded any form of chronic lung disease too subtle to be identified on sophisticated chest imaging or referred to in detailed hospital notes could not be expected to be able to contribute materially to patient morbidity (Exhibit R6 page 4).
Professor Cade conceded that the possible presence of COPD should be considered because if it was related to his prior service it could have predisposed the deceased to chest infections including his terminal pneumonia. However the only entries in the clinical files where pneumonia was diagnosed were in 2005 when the deceased had coronary artery stenting and in July and December 2011 because of complications from his traumatic pneumothoraces.
In his second report, Professor Cade noted that Dr Collins interpreted the findings of the radiologist who performed the chest x-ray on 14 January 2012 as not excluding the presence of left heart failure. Dr Collins reported that the clinical findings of the deceased having creps and wheeze in his chest were consistent with pulmonary oedema (Exhibit A 8 page 3 paragraph 3). Professor Cade reported that the chest x-ray of that date specifically excluded left heart failure. Whilst he noted that pneumonia was present (bilateral consolidation) there was no sign of acute pulmonary oedema. In his opinion the creps and wheeze were non-specific, were due to extensive pneumonia and were not an indication of cardiac failure.
Professor Cade agreed with a comment in the first report of Dr Collins (Exhibit A8 page 3 paragraph 4) that the existence of COPD was somewhat tenuous.
In evidence he confirmed that the clinical onset of IHD was in 1985 yet the reports completed by Dr Friedman indicated that that condition was stable and the notes of the Monash Medical Centre do not indicate any cardiac component for his presenting illness. Professor Cade remained adamant that the illness of septic shock would have and in fact did cause the death.
In relation to the chest x-ray taken during that admission, Professor Cade said that a possible mechanism of IHD contributing to death would be via an arrhythmia. He said the deceased would have been in a controlled and monitored environment and nothing indicated his heart was out of rhythm. The x-ray would be expected to confirm the presence of pneumonia and it would also show whether there was cardiac failure, by the presence of acute pulmonary oedema, which was absent (Transcript page 23).
When he was informed that Dr Collins had said in evidence that the radiologists had not reported the presence of COPD on chest x-rays and CT scans because they might have been looking for something else, Professor Cade said that was an unusual comment. He said as a clinician he would be shocked if a radiologist overlooked an obvious diagnosis. Additionally, it was his opinion that COPD was not overlooked, the radiologist had looked for it and it was not present. In relation to the chest x-ray taken on 14 January 2012, shortly before the deceased died, he dismissed the opinion of Dr Collins that the treatment with Lasix and morphine would have denied the heart failure from being observed. He said if there had been such a wonderful response to the medication, the IHD would not have contributed to death. He said more than likely it would have been many hours, perhaps more than a day before the medication consumed would have ablated the radiological findings of cardiac failure (Transcript page 24).
In relation to the contribution if any to the death by COPD Professor Cade said he found no reference to any of the clinical material from his local GP, the hospitals or from the deceased’s specialist (Dr Friedman) that that condition was present. He said it was unlikely that the deceased, who was admitted to a premier hospital with pneumonia would fail to mention any underlying COPD. He otherwise confirmed a comment in his first report that the absence of it being detected on radiology could not be explained or it was so mild that it would not have contributed to death. He dismissed comments from Dr Collins that the absence of a reference to COPD in radiology reports was not evidence that it was present. Professor Cade said that it was almost inconceivable and would be incredible if the radiologists missed an obvious important diagnosis (Transcript pages 25-26).
In cross-examination, Professor Cade dismissed a proposition put to him that the deceased’s history upon admission to the Frankston Hospital in December 2005 of having collapsed twice in the previous six months, having a cough and phlegm for two years, the presence of right basal crackles and a basal pleural rub could suggest the presence of COPD. He said however the pathology was confined to one lung only and was suggestive to him of either a chest infection or cardiac failure. He noted that an x-ray taken on that date (Exhibit R4) suggested a pneumothorax but the radiologist reported that it appeared to be due to a skinfold because the lung vascular markings projected beyond the pleural line. He also noted that the radiologist reported that basal fibrotic changes are identified but some bullous change suggesting underlying airways disease, however in his experience it was unusual for bullous changes to be basal, they are normally apical and when prominent they become generalised. Professor Cade said the report of the radiologist, alone, may have suggested the presence of COPD however bullous changes have not been reported in subsequent radiology (Transcript page 27).
He noted a report of a CT examination on the following day, 16 December 2012 (Exhibit A7 page 41) did not report the presence of bullae. He said a CT scan provides sophisticated imaging, it takes precedence over an x-ray and whilst it was valid for the radiologist to report his impression of bullous changes, the CT scan demonstrated they were not present (Transcript page 34).
Professor Cade said that he was aware of an aged care assessment completed at Kingston on 6 January 2012 recording the veteran’s current health status as including emphysema (Exhibit R2 page 20). He said the assessment report would have been completed to determine appropriate respite care. He said he had not found any reference in any of the clinical material to a finding of emphysema (Transcript page 28).
Professor Cade said the evidence given by Dr Jenkins of the veteran having recurring chest infections, a poor result from a spirometry test, his observations of that the veteran looked like a man with COPD, having creps and wheezes and having an over expanded chest would be significant in a COPD diagnosis however he could not locate that diagnosis having been made within his clinical file and it bothered [him] that nobody else seemed to agree (Transcript pages 28 – 29). (In re-examination Professor Cade doubted the value of the spirometry results obtained by Dr Jenkins. He said if testing is undertaken whilst a patient is impaired by suffering acute illness, including pneumonia, bronchitis or cardiac failure the result does not give a true reflection of an underlying basal condition. He said it was a rule of lung function testing that spirometry should only be undertaken when a patient is well so that the results have some validity – Transcript page 35).
Professor Cade disagreed with a proposition put to him that if the veteran had suffered from COPD or emphysema he would have been predisposed to terminal pneumonia. He noted that two of the three reported episodes of pneumonia involved admission with rib fractures and the other occasion associated with cardiac failure. That occasion was in July 2011 when he was admitted to the Como Hospital under Dr Friedman who didn’t give us a clue that left lower lobe pneumonia might have been predisposed by any underlying lung disease (Transcript page 30).
Professor Cade said he was not aware of a chest x-ray taken on 12 July 2010 which reported the presence of consolidation in the right middle and lower lobes and a diagnosis made by the radiologist of pneumonia. He noted that Dr Friedman, in a report of 14 July 2010 – two days later – recorded that on admission to the Como Hospital the veteran gave a history of three weeks of cough, had felt weak whilst in the shower and had fallen. He recorded that a chest x-ray had showed left lower lobe pneumonia and the deceased’s chest sounded clear. He acknowledged the discrepancy between the radiologist’s report and the report of Dr Friedman. He said it was a little surprising that the chest was clear and there were no basal creps at the site of the pneumonia. He said it was unlikely that a cardiologist having listened to the chest would miss creps if they’re there and my conclusion was that the pneumonia has resolved (Transcript pages 30 and 37).
In relation to the hypothesis involving the contribution to the veteran’s death by IHD, Professor Cade acknowledged in his reports and in evidence that Dr Friedman had reported on 20 December 2011 that the deceased, upon admission to the Sandringham Hospital on the previous day, had been found to have a pleural effusion which was transudate and was regarded as secondary to heart failure.
He acknowledged that the pleural effusion was indicative of cardiac failure and whilst there was a remote possibility that the pleural effusion found upon x-ray on 14 January 2012 indicated continuing cardiac failure, the pneumonia was by far the most likely culprit of a pleural effusion. That is, a pleural effusion in the presence of pneumonia is almost certainly going to be secondary to the pneumonia (Transcript page 31).
Professor Cade noted a CT scan taken on 25 October 2011 (Exhibit A 7 page 77), approximately one month before admission to Sandringham Hospital did not report the presence of bullae, hyperinflation or changes in the parechymal where COPD, if at all, would be expected to have been found.
Professor Cade was asked, to comment on the reports of Dr Friedman who had consistently recorded chest sounded clear. He said Dr Friedman is very well regarded as a physician and a cardiologist. He said the consistency of him reporting chest [sounds] clear means on examination at the time there is no evidence of either lung disease or cardiac disease that is clinically detectable and as far as what it means, it’s inconceivable to me that a consultant physician and cardiologist examining a patient over years would miss a diagnosis of significant COPD… (Transcript page 36).
I asked Professor Cade whether the absence of any finding by the radiologist of COPD at CT examination on 25 October 2011 could mean that it was previously present as the radiologist reported at x-ray on 15 December 2005. He said both CT examinations – on 16 December 2005 and 25 October 2011 failed to show the presence of COPD. He said it is not a condition that comes and goes, it doesn’t disappear and as it was not shown on any other x-rays I’ve taken it that the CT’s take precedence – take evidentiary precedence in this matter and that there is no support radiologically for diagnosis of COPD (Transcript page 38).
Conclusion and reasons for decision
Prior to his death, the veteran suffered from pneumonia, ischaemic heart disease, atrial fibrillation, renal impairment and hypertension. All of these conditions are well documented in the extensive clinical information exhibited in this review. Both parties acknowledge the existence illnesses. On the balance of probabilities I am satisfied that the veteran did suffer these illnesses.
Before the hypotheses advanced by the applicant are considered, it is necessary to make the above findings. Equally it is necessary to determine whether the veteran did suffer from COPD. For reasons which follow I am satisfied, on the balance of probabilities, that he did not suffer that illness.
The illness of COPD was the subject of considerable debate amongst the doctors who gave evidence. The clinical information, particularly the results of x-rays and CT scans, were also subjected to interpretation and analysis.
Unfortunately, I found the evidence of Dr Collins to be unhelpful and, on occasions, to be speculative. His opinions in support of the presence of COPD rarely reached a level of any probability.
The almost total absence from the radiologists’ reports of any finding of COPD did not deter him because in his opinion that doesn’t mean to say that it is not present on the particular x-ray or CT scan. He said if a radiologist had a particular focus or direction the report may not include other findings. He said this is a normal practice… and I think that that is a reasonable explanation as to why the particular finding of hyperinflated lungs or more importantly bullous emphysema had not been noted each time and to some extent if there is an infective process those features may – of chronic obstructive airways disease may well be somewhat clouded by the overlying infection (Transcript page 8, 14 and 15).
When pressed on this issue in cross examination he said the radiologists may not have made an oversight in reporting their findings, rather they may have not made comment. For example, during a time when a suspected malignancy in the veteran’s lungs was being considered, he said the radiologist may have focused entirely on whether such a malignancy was present rather than reporting on any other pathology depicted by the films (Transcript page 15 and 16).
When he was asked to comment on the consistent reporting by Dr Friedman that the veteran’s chest sounded clear, Dr Collins disagreed that COPD and emphysema had been excluded, because that entry may then have been a reference to congestive cardiac failure being an illness within the expertise of Doctor Friedman. Again he said the absence of any comment by Doctor Friedman of the presence of COPD doesn’t necessarily mean to say that it wasn’t there in some form (Transcript page 18).
The clinical data recorded the veteran having had ten x-rays between 2 November 2003 and 14 January 2012. Within that period he also had three CT scans.
The contents of the radiology reports, concerning the enquiry into whether the veteran suffered COPD are important in the determination, which I make, that that condition was not suffered.
The dates of the x-rays and their respective exhibit references are as follows - 2 November 2003, R1 page 51; 15 December 2005, R4 fifth (unnumbered) page; 15 June 2007 A7 page 50; 12 July 2007 A7 page 155; 15 February 2010 A7 page 64; three x-rays on 19 December 2010 R1 pages 48-50; 20 December 2010 R1 page 46; and 14 January 2012 R1 page 44.
The dates of the CT scans and their respective exhibit references are as follows - 16 December 2005 A7 page 41; 20 December 2010 R1 page 47 and 25 October 2011 A7 page 77.
Except for the x-ray of 15 December 2005 which reported that basal fibrotic changes were identified with some bullous change suggesting underlying airways disease, without reference to whether the pathology was specific to one unidentified lung or both, every other x-ray (excepting the x-ray described at the conclusion of this paragraph) reported the presence of either fibrosis or consolidation or atelectasis (inflammation) in the right lung. The x-rays taken at 8:57 PM and 10:15 PM on 19 December 2010 reported patchy consolidation in the base of the right lung. An x-ray taken on the following day at 10:31 PM, by the same radiologist at the same location (Monash Medical Centre) also reported that there was interval development of a focal area of consolidation in the left lower zone. I doubt the accuracy of this finding. It was not considered by the witnesses in their reports or their evidence.
The x-ray of 15 December 2005 reported the presence of bullous change suggesting underlying airways disease however that finding is not contained in any other report of x-ray or CT scan. Dr Collins said bullous changes (the breakdown of tissue in the internal walls of a lung) do not heal or repair - once they are there, they are there (Transcript page 8). The CT scan taken on the following day did not report the presence of bullae. (The radiologist on this occasion did report the presence of atelectasis in the left lower lobe but described them as minor changes).
The only indication in the radiology of the veteran’s lungs being hyperinflated is found in the x-ray of 15 June 2007.
Dr Collins and Professor Cade said that hyperinflation and bullous changes were strong indicators of the presence of COPD.
The absence of reporting by the radiologists in all but one x-ray of bullous changes and in all but one x-ray of hyperinflation points to the absence of COPD. The radiologist who reported the bullous change also reported that it was suggesting underlying airways disease. The absence of it being reported at CT on the following day and in every other x-ray and CT scan satisfies me that bullous changes, as a fact, were not a feature of the veteran's pathology.
The radiologist who reported that the veteran’s lungs were hyperinflated at x-ray on 15 June 2007 also reported that there was a presumed infective exacerbation of COPD. The presence of pathology pointing to COPD was not reported by any other radiologist, before or after this date.
I agree with the comments made by Professor Cade (Transcript pages 25-26), that in the virtual absence of reporting bullous changes, hyperinflation and COPD it would be almost inconceivable with a proper radiology department. It would be incredible if they missed obvious important diagnoses. I therefore dismiss the opinion of Dr Collins that the absence of reference is not evidence that it wasn’t there.
In concluding this part, the consistency of reporting by Doctor Friedman of chest sounded clear should not be understood as confining himself to congestive cardiac failure only and the treatment of it. As a competent and well respected cardiologist, if signs or symptoms of COPD were present, they would have been reported.
An issue emerged during the hearing of the radiologist’s report dated 12 July 2010 finding pneumonia in the right middle and lower lobes and Dr Friedman reporting, two days later of those findings being present in the left lower lobe (Exhibit A7 pages 155 and 156). Irrespective of whether the reported presence of pneumonia was in the right or the left lung, on examination on both 14 and 20 July 2010 (Exhibit A7 page 156), Dr Friedman reported chest sounded clear. Additionally he reported on the latter date that there had been Rapid improvement. CXR much improved 19/07. Chest auscultation improved. (I cannot locate the report of any x-ray of 19 July 2010 in the clinical material).
I am satisfied that had the veteran ever demonstrated any symptom or sign of COPD between August 1997 and November 2011 being the period during which Dr Friedman treated, that he would have reported it. It would be inconsistent with his experience and reputation not to have done so.
Dr Jenkins treated the veteran for many years prior to his demise. He favoured a diagnosis of COPD – his clinical file records COPD on 13 May 2010, (and COAD) on 27 May 2010 and 13 December 2010 – however many of his opinions were inconsistent with the radiology. He was satisfied the veteran suffered hyperinflation because of his appearance. The cover sheet to his clinical file does not record COPD under the subheading of Past History nor do any of his referral letters to any of the specialists to whom he referred the veteran, including Doctor Friedman between 18 May 2005 and 28 October 2011 (Exhibit A7 pages 93-107).
The most recent SoP-No. 37/2014 - defines COPD as comprising chronic bronchitis, emphysema and chronic airflow limitation. That condition was not embraced by the definition in the SoP (No.30/2004) existing at the date of the hearing (although it was the subject of previous SoP’s (Nos. 73/1997, 136/1996 and 65/1994 which have all been revoked).
The condition of chronic airflow limitation is defined in paragraph 3 of the most recent SoP as:
chronic airflow limitation means persistent post-bronchodilator spirometry values of :
i) forced expiratory volume in one second (FEV1) of less than 80 per cent of the normal predicted value for a person of the same age, height and sex; and
ii) a ratio of FEV1 to forced vital capacity of less than 70 per cent;
which are not attributable to another disease.
The only evidence of spirometry in this review is found in the clinical entry of Dr Jenkins made on 13 May 2010 (Exhibit A7). The results of the assessment are recorded. However, irrespective of the recorded results, that sole assessment does not meet the requirement of the definition of persistent post bronchodilator spirometry values as prescribed.
In these circumstances I am unable to find that the veteran suffered the condition of chronic airflow limitation – and therefore does not satisfy the definition of COPD.
For all of the above reasons I am satisfied, on the balance of probabilities, that prior to his death, the veteran did not suffer COPD.
The hypotheses
The focus now turns to whether the death of the veteran was related to his operational service. That will be decided, eventually, after consideration of the four stages of analysis determined by the Full Federal Court in Repatriation Commission v Deledio (1998) 88 FCR 82 at 95.
The applicant advanced two hypotheses, which she asserted were reasonable, connecting the service of her husband and his death. The first included the illness of IHD. I am satisfied that the material points to such a hypothesis. The other links making up the chain of connection between service and death, namely, stress by service precipitating smoking and the illness of pneumonia were not disputed by the respondent. I am not deciding at this stage that the hypothesis is reasonable.
The other hypothesis connecting service and death included the illness of COPD. For reasons given above I have found that the deceased did not suffer that illness in his lifetime. The chain of connection between service and the cause of death must exist. COPD is a missing link. I cannot be satisfied that there is material pointing to a connection between service and death involving the illness of COPD.
There is a SoP in force in relation to IHD being Instrument 89 of 2007. The applicant relied on factor 6(g)(ii) and (iii) reproduced as follows
The factor that must as a minimum exist before it can be said that a reasonable hypothesis has been raised connecting ischaemic heart disease or death from ischaemic heart disease with the circumstances of a person is relevant service is:
…
(g) where smoking has ceased prior to the clinical onset of ischaemic heart disease:
(ii) smoking at least 5 pack years but less than 20 pack years of cigarettes or the equivalent thereof in other tobacco products, and the clinical onset of ischaemic heart disease has occurred within 15 years of smoking cessation; or
(iii) smoking at least 20 pack years of cigarettes or the equivalent thereof in other tobacco products, before the clinical onset of ischaemic heart disease;
The third Deledio stage requires me to form an opinion whether the raised hypothesis is reasonable. It will be reasonable if it is consistent with a factor within the SoP which must exist as a minimum and be related to the veteran’s service. I am satisfied, at this third stage that the hypothesis fits with the SoP and is reasonable.
Only at the fourth and final Deledio stage will findings of fact be made. I am required to determine, pursuant to s.120(1) of the Veteran’s Entitlements Act 1986, whether I am satisfied beyond reasonable doubt that the veteran’s death was not war caused. If I am not so satisfied, the application will succeed. If I am satisfied, the application will not succeed.
I am satisfied and find as a fact that the clinical onset of IHD, consistent also with the evidence of Professor Cade, was in 1985, when the veteran was diagnosed with angina.
I am satisfied that a connection exists between smoking and service. The veteran commenced smoking on a regular basis because of the stress of service (T documents page 30). The issue now to be determined is when, as a fact, he ceased smoking.
I have never heard an application, concerning a smoking hypothesis where a veteran or a veteran’s widow or family members have ever given evidence about smoking habits with some degree of certainty or at least confidence. It is also not unusual for a smoking questionnaire completed by a veteran in his lifetime to be found, on the basis of evidence, to contain information which is false or incorrect. On the basis of the evidence of the applicant and her daughters, which I accept, I am satisfied that the contents of the smoking questionnaire completed by the veteran, does contain incorrect information. The history also taken by Dr Friedman of the deceased not ever having been a smoker is also incorrect.
The applicant said her husband commenced smoking on a regular basis in 1942, at 20 cigarettes per day until the early 1960’s when he then reduced smoking to between 5 and 10 cigarettes per day. The applicant said she asked her husband to cease smoking after the children were born, in 1959 and 1960, which she understood he did. However, she learnt after discussion with her daughters that they observed their father smoke cigarettes in the backyard and elsewhere, when they were young teenagers which would have been in the first half of 1970.
The applicant said her husband was a heavy smoker when she first met him in 1945 and she understood he had been smoking regularly since December 1942 and then at 20 cigarettes per day. She also gave evidence of her husband smoking inside the house commencing when he awoke each morning (and whilst in bed) and last thing at night, in the bedroom, before he went to sleep. That evidence suggests that the veteran was a heavy smoker and did smoke at least 20 cigarettes per day.
Dr Jenkins (Exhibit A7 page 31) had a history, taken in 2010, of the veteran smoking for about 40 years. The progress notes of Southern Health (Exhibit R2 page 49), also made in 2010, record the veteran ceasing to smoke 40 years previously which would have been about 1970. If the veteran did commence to smoke in 1942 and thereafter 20 cigarettes per day he would smoked for at least 20 pack years.
The health assessment record found at Exhibit A7 page 135, completed in 2005 recorded a history of smoking 50 years ago which would approximate ceasing in about 1960 but does not give any indication of the quantity of cigarettes the veteran had been smoking. This information could not as a fact be accepted with any precision and some latitude must be given to the data. It would not be unreasonable to conclude that the deceased smoked less than or more than 50 years earlier and therefore ceased smoking before or after 1960. Another entry in the notes of Southern Health (Exhibit R1 page 29) record the veteran ceasing to smoke in 1960.
On the basis of the above information, which I again acknowledge causes difficulty reaching any conclusion, I am satisfied that the veteran did smoke for at least 20 pack years (defined as an average of 20 tailor-made cigarettes per day) between the early 1940s and the early 1960s. Factor 6(g)(iii) of the SoP is satisfied.
However, although I am satisfied that the veteran did suffer IHD, I am not satisfied that a connection exists between it and the death of the veteran.
The notes on admission to the Monash Medical Centre on the day of the veteran’s death record that he was profoundly hypotensive, was suffering from respiratory distress and in septic shock (Exhibit R1 page 29). There is no clinical data pointing to the deceased suffering an arrhythmia or cardiac failure.
The chest x-ray taken on 14 January 2012, in the opinion of Professor Cade, was suggestive of the deceased suffering pneumonia and the absence of any reporting of pulmonary oedema excluded any finding of left ventricular failure. It was his opinion that whilst the deceased did have impaired cardiac function, his demise, inevitably, was by the combined effects of the pneumonia and the septic shock, especially the latter, having regard to the veteran’s age and his frail state.
I cannot find, on the balance of probabilities, as suggested by Dr Collins that the medication administered to the deceased prior to the chest x-ray denied a cardiac catastrophe being observed. Consistent with the evidence of Professor Cade, if the medication had relieved any cardiac pathology – and therefore not observed by the radiologist – death would not have occurred by IHD.
Professor Cade acknowledged that the finding by the radiologist on 14 January 2012 of pleural effusion, was more likely to be a consequence of pneumonia, rather than cardiac failure.
I am satisfied and find on the balance of probabilities that the veteran died from the combined effects of respiratory failure, pneumonia and septic shock. I am not satisfied that IHD caused or contributed to death. A link in the hypothesis connecting service and death is missing, namely the absence of contribution by IHD.
It follows that I am not satisfied beyond reasonable doubt that the death was not war caused.
Decision
The decision under review is affirmed.
I certify that the preceding 155 (one hundred and fifty-five) paragraphs are a true copy of the reasons for the decision herein of John Handley, Senior Member ........................[sgd]................................................
Associate
Dated 3 June 2014
Date(s) of hearing 7 - 8 April 2014 Date final submissions received 15 May 2014 Counsel for the Applicant Ms F. Ryan Solicitors for the Applicant Williams Winter Solicitors Counsel for the Respondent Mr K. Rudge Solicitors for the Respondent Department of Veterans' Affairs Advocacy Section
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