DAVID GILKINSON and REPATRIATION COMMISSION
[2012] AATA 467
•24 July 2012
[2012] AATA 467
Division VETERANS’ APPEALS DIVISION File Number(s)
N2006/0296
Re
DAVID GILKINSON
APPLICANT
And
REPATRIATION COMMISSION
RESPONDENT
DECISION
Tribunal Mr RP Handley, Deputy President
Dr H Haikal-Mukhtar, MemberDate 24 July 2012 Place Sydney The decision of the Repatriation Commission dated 30 March 2005 refusing Mr Gilkinson’s claim for a disability pension in respect of sleep apnoea is set aside and a decision substituted that Mr Gilkinson’s sleep apnoea is war-caused. The date of effect of this decision in terms of the payment of pension is 14 June 2004. The matter is remitted to the Repatriation Commission to determine the rate of pension payable to Mr Gilkinson.
.............[sgd]...........................................................
Mr RP Handley, Deputy President
CATCHWORDS
VETERANS’ AFFAIRS – disability pension – operational service – whether sleep apnoea war-caused – decision under review set aside
LEGISLATION
Veterans’ Entitlements Act 1986 ss 5D, 6C, 9, 13, 196B
Statement of Principles concerning Sleep Apnoea, Instrument No.13 of 2005
CASES
Gilkinson v Repatriation Commission (2008) 104 ALD 406; [2008] FCA 1441
Gilkinson v Repatriation Commission (2011) 197 FCR 102; [2011] FCAFC 133
Kaluza v Repatriation Commission [2010] FCA 1244
Re Gilkinson and Repatriation Commission [2008] AATA 364
Re Gilkinson and Repatriation Commission [2010] AATA 23
Repatriation Commission v Crane (2004) 81 ALD 608
Repatriation Commission v Deledio (1998) 83 FCR 82Repatriation Commission v Knight [2012] FCAFC 83
Repatriation Commission v Stoddart (2003) 134 FCR 392REASONS FOR DECISION
Mr RP Handley, Deputy President
Dr H Haikal-Mukhtar, Member24 July 2012
The Federal Court set aside the Tribunal’s previous decision in this matter and remitted it to the Tribunal to be decided again according to law either with or without the hearing of further evidence. The proceedings concern Mr Gilkinson’s claim for a pension in respect of sleep apnoea, a condition which he contends is “war-caused” in terms of the relevant provisions of the Veterans’ Entitlements Act 1986 (the Act).
BACKGROUND
Mr Gilkinson (the Applicant) was born in 1949 and is now aged 63. He joined the Navy on 10 July 1965, aged 16, and was discharged on 9 July 1977, having served for 12 years. From 15 February 1970 to December 1972, Mr Gilkinson served on HMAS Sydney during which time he had ten periods of “operational service” on voyages between Australia and Vietnam, as follows:
16 February 1970 to 5 March 1970
21 October 1970 to 12 November 1970
15 February 1971 to 4 March 1971
26 March 1971 to 8 April 1971
13 May 1971 to 1 June 1971
20 September 1971 to 16 October 1971
26 October 1971 to 18 November 1971
24 November 1971 to 17 December 1971
14 February 1972 to 9 March 1972
1 November 1972 to 30 November 1972
While not relevant for these proceedings, Mr Gilkinson also had “defence service” from 7 December 1972 to 9 July 1977.
The Repatriation Commission (the Commission) notes that Mr Gilkinson’s operational service was not continuous and there were significant gaps between the periods of operational service: for example, between 5 March 1970 and 21 October 1970 (seven and a half months), 12 November 1970 to 15 February 1971 (three months), 1 June 1971 and 29 September 1971 (nearly four months), and between 9 March 1972 and 1 November 1972 (nearly eight months).
On 14 September 2004, Mr Gilkinson lodged a claim for pension in respect of sleep apnoea and for an increase in the rate of his pension based on his previously accepted disabilities. On 30 March 2005, a delegate of the Commission refused his claim, a decision that was affirmed by the Veterans’ Review Board (VRB). Mr Gilkinson applied for a review of this decision by the Tribunal which, on 6 May 2008, affirmed the decision: Re Gilkinson and Repatriation Commission [2008] AATA 364. The Federal Court then set aside this decision and remitted the matter to the Tribunal to be determined in accordance with the law and the reasons of the Court: Gilkinson v Repatriation Commission (2008) 104 ALD 406; [2008] FCA 1441. Rares J said at [30]:
It [the Tribunal] did not advance a reason for negating beyond reasonable doubt Dr Volker’s hypothesis that shift work could have caused or contributed to Mr Gilkinson’s eating or not exercising. Instead, the tribunal simply stated a conclusion which indirectly may have rejected the hypothesis. But, it had to make a finding of fact as to whether that hypothesis had been disproved beyond reasonable doubt. Since Dr Volker put forward the hypothesis that shift work contributed to the eating disorder, the tribunal had to make findings which negated any causal effect of shift work on the obesity of Mr Gilkinson first observed in 1971 after he had completed 92 days of operational service for his country.
His Honour found that the Tribunal made an error of law by not considering the correct questions and failing to consider a relevant consideration.
On the remittal, the Tribunal again affirmed the decision under review: Re Gilkinson and Repatriation Commission [2010] AATA 23. On appeal to the Full Federal Court from the decision of a single judge of the Federal Court, the Court ordered that the Tribunal’s decision be set aside and remitted to the Tribunal “to be decided again according to law either with or without the hearing of further evidence”: Gilkinson v Repatriation Commission (2011) 197 FCR 102; [2011] FCAFC 133 (the Full Court decision). The error of law identified by the Court was that the Tribunal had failed to address the application of s 196B(14)(b) of the Act which it found to be different in its application to that of s 196B(14)(d) on which the Tribunal relied in making its decision.
Mr Gilkinson no longer challenges the decision of the Commission to assess his pension at 80% of the General Rate based on the previously accepted disabilities. Moreover, there is no dispute that Mr Gilkinson suffers from the condition sleep apnoea which was diagnosed in April 2001. The only live issue before the Tribunal is, therefore, whether his sleep apnoea is war-caused.
THE RELEVANT LAW AND ISSUES
Section 13(1) of the Act provides that where a veteran is incapacitated from a war-caused disease, the Commonwealth is liable to pay compensation to the veteran in the form of a pension. The word “disease” is defined in s 5D(1) as including “any physical or mental ailment, disorder, defect or morbid condition (whether of sudden onset or gradual development)” or the recurrence of such a condition, but does not include the aggravation of such a condition. Section 5D(2) provides that unless a contrary intention appears, “a reference to the incapacity of a veteran from a war-caused injury or a war-caused disease … is a reference to the effects of that injury or disease and not to a reference to the injury or disease itself”.
Section 9(1) provides that a disease contracted by a veteran shall be taken to be a war-caused disease if it “resulted from an occurrence that happened while the veteran was rendering operational service” (s 9(1)(a)), or “arose out of, or was attributable to, any eligible war service rendered by the veteran” (s 9(1)(b)). Section 6C(1) refers to the relevant operational service being “continuous full-time service”.
The questions that the Tribunal must address in its decision are those set out by the Full Federal Court in Kaluza v Repatriation Commission [2010] FCA 1244 (Kaluza), which follows the Full Federal Court decision in Repatriation Commission v Deledio (1998) 83 FCR 82 (Deledio).
As stated above, there is no dispute that Mr Gilkinson suffers from the condition sleep apnoea, which was diagnosed in April 2001. There is also no dispute that Mr Gilkinson rendered ‘operational service’ as defined in s 6C(1).
The matters that must be addressed by the Tribunal, identified by the Court in both the Deledio and Kaluza decisions, comprise the following four steps:
(1) The Tribunal must consider all the material before it and determine:
(a) whether the material points to some fact(s) (the raised facts) which support a hypothesis connecting the disease with the circumstances of the operational service; and
(b) whether that hypothesis can be regarded as reasonable if the raised facts are true.
(2) If the raised facts point to a hypothesis of a connection, is there a Statement of Principles (SoP) in force in respect of the kind of disease from which the veteran suffers?
(3) If a SoP is in force, the Tribunal must determine whether, in its opinion, the hypothesis is reasonable, meaning is it consistent with the “template” found in the SoP? In particular, does the hypothesis raised contain one or more of the factors that the Repatriation Medical Authority has determined to be the minimum that must exist and be related to the veteran’s service?
In Repatriation Commission v Knight [2012] FCAFC 83, the Full Federal Court said there are two discrete issues at play in considering whether there is a reasonable hypothesis:
(i)does the material before the Tribunal point to the factor relied upon; and
(ii)does the material also point to that factor being related to the veteran’s operational service (s 196B(14))?
Section 196B(14) sets out the circumstances in which a “factor causing, or contributing to, an injury, disease or death is related to service rendered by a person” which relevantly include (b) where “it [the injury, disease or death] arose out of, or was attributable to, that service”, and (d) where “it was contributed to in a material degree by, or was aggravated by, that service”.
The Full Federal Court in its reasons for remitting this matter to the Tribunal held that paragraph (d) is not a broader test that necessarily subsumes the paragraph (b) question of whether a factor arose out of, or was attributable to, that service. The meaning of “arose out of, or was attributable to” in s 9(1)(b) and s 196B(14)(b) is the same and requires a contributory cause that need not be the sole or dominant cause: see the Full Court decision, Perram J at [6-7] and [13], and Nicholas and Robertson JJ at [37]-[38].
(4) If the hypothesis is reasonable, the Tribunal must be satisfied beyond reasonable doubt that the incapacity did not arise from the war-caused disease. (Any fact finding must only be made at this final stage in the process.)
DISCUSSION
Step 1: does the material before the Tribunal point to some fact(s) (the raised facts) which support a hypothesis connecting the disease with the circumstances of the operational service; and can that hypothesis be regarded as reasonable if the raised facts are true?
Mr Gilkinson joined the Navy on 10 July 1965. He gave evidence that in 1968 or 1969, he had a minor snoring problem. It was in about 1970 or 1971, when serving on Sydney, that he started getting a “fair few” complaints about his snoring, with people waking him up and telling him to turn over (transcript 7 April 2008, p 13). At that time, he also began experiencing daytime sleepiness such that, depending on the shifts he was working, he would nap nearly every day during working hours on the upper deck and the side; this gradually got worse over the years (transcript 7 April 2008, pp 15-16). In his report dated 10 June 2006, Professor ABX Breslin, Consultant Thoracic Physician and Clinical Associate Professor of Respiratory Medicine, took a history of Mr Gilkinson starting to snore about three years after he joined the Navy: therefore, in approximately 1968. Professor Breslin expressed the opinion that it is likely that Mr Gilkinson’s sleep apnoea “dates back to his time in the Navy”.
Mr Gilkinson’s evidence is that he was drinking heavily during the time that he had operational service. In reply to the question why he and his group used to go and get drunk at every opportunity, Mr Gilkinson said it was “Just the stress, trying to get the mind clear” (transcript 7 April 2008, p 15). The Department of Defence Medical Records for Mr Gilkinson indicate that he also put on a significant amount of weight during this time and record that he was classified as ‘obese’ in 1971. He said that he started putting on a lot of weight in 1970/71, partly due to a lack of proper diet and too little exercise (transcript 7 April 2008, p 17). Alcohol consumption may also have had an influence on his weight. Further, he stated that while at sea, he was working in the ship’s engine room where he was exposed to fumes and solvents and experienced nasal stuffiness, for which he used nasal sprays. He had started using the sprays from the end of 1968 or 1969 to clear a blocked nose (transcript 7 April 2008, p 11). He described the nose stuffiness as being always there and getting worse over these three to four years, but “sometimes worse” than at other times (transcript 7 April 2008, p 12).
As the Commission pointed out, and as the periods of Mr Gilkinson’s operational service set out above show, there is no one continuous period of operational service but a series of ten shorter periods between February 1970 and November 1972, comprising sea voyages to and from Vietnam. The Commission submits that the evidence must show a connection between Mr Gilkinson’s sleep apnoea and his operational service, relevantly that his sleep apnoea arose out of, or was attributable, to that service (s 9(1)(b)). The Applicant acknowledges that there are gaps between the periods of operational service but contends that nothing turns on that.
In Repatriation Commission v Crane (2004) 81 ALD 608, where the veteran had three short periods of operational service totalling 74 days between December 1967 and April 1968, the Full Federal Court, at [76], noted that despite the veteran being exposed to asbestos for almost the whole of his period of service in the Navy (from 9 October 1966 to 31 December 1973), this included exposure during operational service so that the veteran’s anxiety about asbestos was attributable in part to operational service. In Repatriation Commission v Stoddart (2003) 134 FCR 392, where the veteran worked as a stoker/engineer, the Full Federal Court referred to the Tribunal’s finding that the veteran had been undertaking his normal duties. The Court’s discussion, at [37] to [39], pointed to the need to establish a connection between the relevant factor in the SoP and the veteran’s operational service, albeit that this might be subjectively perceived.
With respect to the short periods of operational service in Mr Gilkinson’s case, in a report dated 5 July 2009, at p 4, Associate Professor T Gill, Principal Research Fellow and Scientific Programs Manager at the Institute of Obesity, Nutrition and Exercise at the University of Sydney, stated his opinion that “Despite anomalies in his records, there is sufficient evidence to suggest that Mr Gilkinson was obese … during his period of operational service”. Professor Gill said, at p 9: “a pattern of shiftwork duties such as that undertaken by Mr Gilkinson’s [sic] during operational service may have had some impact on his diet and physical activity patterns … the size of that effect is likely to have been moderate”. In oral evidence, he described the scale as “ranging from mild, moderate, severe to very severe” and said he had given what he believed to be “an appropriate but conservative opinion”. He said that he had taken into account that Mr Gilkinson’s periods of operational service were just short bursts of operational service and their disjointed nature (transcript 17 December 2009, pp 14 and 16).
Dr DH Volker, Consultant Dietician, who provided reports dated 15 June 2007 and 7 October 2009, was aware of Mr Gilkinson’s limited periods of operational service while serving on HMAS Sydney, when expressing an opinion about his obesity. In her later report, at p 5, she stated: “There is convincing evidence that David Gilkinson became obese during his period of 30 weeks of operational service (16/02/1970-30/11/1972).”
The Tribunal is satisfied that the raised facts – in particular, Mr Gilkinson’s alcohol consumption, stuffy nose, obesity and snoring – support a hypothesis connecting Mr Gilkinson’s sleep apnoea with the circumstances of his operational service. While Mr Gilkinson’s operational service between February 1970 and November 1972 comprises ten periods of between 14 and 30 days, sometimes with significant gaps in between, the material before us points to the relevant facts being at least partly attributable to Mr Gilkinson’s operational service in so far as they are connected to his being on board ship. These facts point to his sleep apnoea arising out of or being attributable to his service and, in our view, the hypothesis can be regarded as reasonable if the raised facts are true.
Step 2: is there a Statement of Principles (SoP) in force in respect of the kind of disease from which the veteran suffers?
The relevant SoP is Instrument No. 13 of 2005 (SoP No 13). Clause 2(b) states:
(b)For the purposes of this Statement of Principles, “sleep apnoea” means sleep disordered breathing characterised by periods of cessation or reduction in airflow at the nose and mouth, leading to arousals from sleep (disrupted sleep architecture), together with significant clinical consequences such as excessive daytime sleepiness, impaired memory, difficulty concentrating, morning headache, pulmonary hypertension, right heart failure or respiratory failure.
Clause 5 of the SoP states relevantly:
5.The factor that must as a minimum exist before it can be said that a reasonable hypothesis has been raised connecting sleep apnoea or death from sleep apnoea with the circumstances of a person’s relevant service is:
(a)having chronic obstruction of the upper airways at the time of the
clinical onset of sleep apnoea; or
(b)being obese at the time of the clinical onset of sleep apnoea; or
…
(j)having chronic obstruction of the upper airways at the time of the clinical worsening of sleep apnoea; or
(k)being obese at the time of the clinical worsening of sleep apnoea; or
…
(s)consuming an average of at least 30 grams of alcohol per day for at least the six months before the clinical worsening of sleep apnoea; or
...
Clause 6 states:
6.Paragraphs 5(j) to (t) apply only to material contribution to, or aggravation of, sleep apnoea where the person’s sleep apnoea was suffered or contracted before or during (but not arising out of) the person’s relevant service.
Clause 8 of SoP No 13 provides that:
“alcohol” is measured by the alcohol consumption calculations utilising the Australian Standard of ten grams of alcohol per standard alcoholic drink;
…
“being obese” means an increase in body weight by way of fat accumulation which results in a Body Mass Index (BMI) of thirty or greater.
The BMI = W/H2 and where:
W is the person’s weight in kilograms and
H is the person’s height in metres;
“chronic obstruction of the upper airways” means ongoing obstruction at the level of the nose, nasopharynx, oropharynx, hypopharynx or larynx;
Step 3: the Tribunal must determine whether, in its opinion, the hypothesis is reasonable, meaning is it consistent with the “template” found in the SoP? Thus, (i) does the material before the Tribunal point to the factor(s) relied upon in clause 5; and (ii) does the material also point to the factor(s) being related to the veteran’s operational service (s 196B(14))?
The Applicant relies on five factors in clause 5 of SoP No 13: factors (a), (b), (j), (k) and (s). The first issue that must be addressed, as required by the clause 5 factors, is the date which the material before the Tribunal points to as being the date of clinical onset of Mr Gilkinson’s sleep apnoea.
Clinical Onset
As stated above, Mr Gilkinson’s evidence is that in 1968 or 1969 he had a minor snoring problem but he started receiving a lot of complaints about his snoring in about 1970 or 1971 at the time he was serving on Sydney, and also experienced daytime sleepiness nearly every day which gradually got worse over the years. This is consistent with the history Professor Breslin took of Mr Gilkinson’s snoring gradually becoming worse and of his waking unrefreshed, dating “…back to his time in the Navy” (report dated 10 June 2006, p 3). In giving evidence in 2008, Professor Breslin said “it’s more probable than not that his [Mr Gilkinson’s] sleep apnoea started with his snoring [in about 1968], not with excessive daytime sleepiness [in about 1970/1971]”, but he accepted that it could have begun with increased sleepiness “because not everybody that snores has sleep apnoea” (transcript 8 April 2008, p 106).
At the hearing on 22 June 2012, Professor Breslin said that sleep apnoea is a condition causing a person to stop breathing for short episodes in their sleep (transcript 22 June 2012, p 7). Most people with sleep apnoea snore, but not all snorers have sleep apnoea. Nevertheless, if a person is a snorer, the chances of them having sleep apnoea are high. Professor Breslin noted that both Mr Gilkinson’s parents snored and said that with Mr Gilkinson snoring in 1968, the chances of him having obstructive episodes and therefore sleep apnoea were greater than 50 per cent (transcript 22 June 2012, p 28). It was on this basis that Professor Breslin expressed his opinion that the clinical onset of Mr Gilkinson’s sleep apnoea was in 1968. However, Professor Breslin agreed that it was also possible that the clinical onset could have been in 1971 when Mr Gilkinson said his snoring got worse and he began experiencing daytime sleepiness.
Professor Breslin distinguished clinical onset from clinical worsening of sleep apnoea. He said clinical worsening occurs when the obstructive episodes become worse or more frequent (transcript 22 June 2012, p 9). Clinical worsening need not, however, be permanent. For example, the number of obstructive episodes may increase with excessive use of alcohol or with increased weight, but can decrease in number if a person moderates their alcohol use or loses weight. It depends on whether the weight gain or increase in alcohol use is permanent. In Mr Gilkinson’s case, there was a gradual worsening of his condition as he got older and put on weight. Professor Breslin said he was unable to put a date on exactly when that worsening was clinically relevant but it certainly became relevant about 15 years before diagnosis (which was in April 2001) (transcript 22 June 2012, p 16).
Professor Breslin was asked about other symptoms of sleep apnoea such as waking at night choking, excessive daytime sleepiness, impaired memory and concentration, and morning headaches. He said a diagnosis of sleep apnoea and an assessment of the degree of severity is made on the basis of clinical symptoms (transcript 22 June 2012, p 17). He agreed that Mr Gilkinson’s evidence of daytime sleepiness could also be a symptom of clinical worsening (transcript 22 June 2012, p 18).
Professor Breslin was referred to the definition of sleep apnoea in clause 2(b) of SoP No 13, which states that sleep apnoea means “sleep disordered breathing … together with significant clinical consequences”, of which it gives examples including excessive daytime sleepiness but not including snoring. He said, “Most people defining sleep apnoea would have snoring in the definition” (transcript 22 June 2012, p 20). Professor Breslin agreed that there is no objective evidence that Mr Gilkinson had chronic obstruction of the upper airways in 1968 except the fact that he was snoring (transcript 22 June 2012, p 22). He agreed that Mr Gilkinson did not then have a history of the sort of symptoms that the SoP requires.
With regard to Mr Gilkinson’s evidence that his snoring got worse in 1971 and that he was experiencing daytime sleepiness, Professor Breslin agreed that the clinical onset could have been in 1971 (transcript 8 April 2008, p 106). At the most recent hearing, he said: “Whether it was clinical onset or not, one couldn’t say, but it certainly would point to clinical worsening” (transcript 22 June 2012, p 28). He also agreed that it is a reasonable hypothesis that Mr Gilkinson’s increase in weight and his drinking may have led to a clinical worsening of his sleep apnoea which, the evidence suggested, was permanent.
Professor Breslin was also asked about Mr Gilkinson’s evidence that the nasal stuffiness he experienced became worse in the Navy due to exposure to fumes and toxins. Professor Breslin said this is consistent with Mr Gilkinson experiencing rhinitis. There is a medical record of his being diagnosed with rhinitis on 7 July 1968 when a history of many years of “stuffiness” and “inflamed mucosa” was noted and the medication ‘Avil Retard’ was prescribed. Mr Gilkinson recalled that he also started to use nasal sprays at about this time (transcript 7 April 2008, p 11).
The Tribunal notes that snoring may or may not be a symptom of sleep apnoea, and is not a significant clinical consequence of the condition. As Professor Breslin said (transcript 22 June 2012, p 7):
…you can snore without having sleep apnoea. Sleep apnoea means that you stop breathing in your sleep and actually as a consequence of that your sleep is fragmented and because of that you’re tired during the day. Snoring doesn’t make you tired during the day, which the – which is excessive daytime sleepiness, it’s the obstruction to the upper airway which causes you to fragment your sleep that makes you tired during the day.
By contrast, Professor Breslin opined that excessive daytime sleepiness is a significant clinical consequence. In answer to Mr Colborne’s question, “… is it the case that you would say that the excessive daytime sleepiness has a significant clinical consequence?”, Professor Breslin responded (transcript 22 June 2012, pp 20-21):
Sure. And it has for him. … The excessive daytime sleepiness means you can have car accidents. It means you can fall into the machinery you’re working with, or whatever it might be, and so that’s a pretty important clinical consequence.
Further, Professor Breslin described a collection of clinical features that are relied on when making an assessment of the clinical onset of sleep apnoea: snoring, waking choking at night, partner noticing that they have stopped breathing in their sleep, waking up with morning headaches and feeling unrefreshed, having impairment of memory and concentration and excessive daytime sleepiness and, often, a family history. He said (transcript 22 June 2012, pp 11-12):
Not everybody who snores has sleep apnoea. It’s the obstructive episodes associated with the snoring that cause the choking at night, the apnoeas, the waking unrefreshed, the poor memory and concentration, the morning headaches and the daytime sleepiness. Often worse – often a family history.
Notwithstanding this evidence, Professor Breslin based his opinion of the onset of sleep apnoea dating back to 1968 solely on one symptom, that of snoring (which may or may not be a symptom of sleep apnoea), and on a family history of snoring, not of sleep apnoea. He noted that: “… sleep apnoea really has only been diagnosed in terms of mechanisms and the use of a CPAP [Continuous Positive Air Pressure] machine since the early 1980s” (transcript 22 June 2012, p 12).
Professor Breslin agreed that there is no objective evidence that Mr Gilkinson had chronic obstruction of the upper airways in 1968 except the fact that he was snoring (transcript 22 June 2012, p 22). At the first hearing, Professor Breslin also noted that there was no objective evidence of Mr Gilkinson being obese in 1968 (transcript 22 June 2006, p 23).
Further, while sleep apnoea is not strictly speaking within Dr Volker’s expertise, we note her opinion regarding the onset of Mr Gilkinson’s obesity and sleep apnoea during his operational service in a report dated 15 June 2007, at pp 10-11:
There is objective evidence that the veteran was obese in 1971 and sleep apnoea would have developed clinically in 1971 and not in 1968-1969 when snoring was caused by allergens and toxins.
Dr Volker concluded, at p 11:
David Gilkinson’s OSA [Obstructive Sleep Apnoea] can be linked to his being obese. There is an objective record of this in 1971. Some expert reports suggest that OSA commenced in 1968 when the veteran was reported to snore. This episode of snoring can be related to the veteran’s nasal problems and workplace conditions. A reasonable hypothesis can be made connecting sleep apnoea with the development of obesity. Factors contributing to the development of obesity were shift work, nasal congestion leading to low exercise tolerance and alcohol use.
In 1971, Mr Gilkinson was receiving a lot of complaints about his snoring and was experiencing daytime sleepiness, the latter being identified as a significant clinical consequence of sleep apnoea. In our view, this points to the clinical onset of Mr Gilkinson’s sleep apnoea being in 1971 rather than in 1968, and not to 1971 being just a clinical worsening of sleep apnoea. The effect of this is that it is only factors 5(a) and 5(b) that are relevant to this case because the material before us points to any clinical worsening of Mr Gilkinson’s sleep apnoea not being connected to his operational service, thereby excluding factors 5(j), (k) and (s) for which clinical worsening forms a part of the description. While the parties also gave further consideration to factors 5(j), (k) and (s) in their submissions, we have chosen not to do so in these Reasons, having concluded that only factors 5(a) and (b) are relevant.
Factor 5(a): having chronic obstruction of the upper airways at the time of the clinical onset of sleep apnoea
As stated above, “chronic obstruction of the upper airways” is defined in clause 8 as meaning “ongoing obstruction at the level of the nose, nasopharynx, oropharynx, hypopharynx or larynx”. Mr Gilkinson’s evidence points to his having a chronic obstruction of the upper airways in about 1971 at the time of the clinical onset of his sleep apnoea: he was receiving a lot of complaints about his snoring which had become worse, and he was experiencing daytime sleepiness leading him to take naps on the upper deck whenever he could (transcript 7 April 2008, pp 13 and 16). Mr Gilkinson also said his stuffy nose became worse when he was working in the engine room “with the heat and the fumes and solvents and everything like that” (transcript 7 April 2008, p 11). This is consistent with the history Professor Breslin took that Mr Gilkinson “had rhinitis most of his life including as a child but he thinks it was worse in the Navy and has been variable since” (report dated 10 June 2006, p 4).
Professor Breslin was of the opinion that “many years of stuffy nose”, noted in Mr Gilkinson’s Navy Medical Records on 7 July 1968, fits the definition of chronic obstruction of the upper airways (transcript 8 April 2008, p 95), although he noted that the 1976 report of the nose being clear showed that the “nasal obstruction comes and goes” (transcript 8 April 2008, p 97).
When asked to explain what stuffiness meant, Professor Breslin stated that stuffiness meant rhinitis, meaning that the nasal mucosa has become swollen causing intermittent or permanent obstruction to the nasal passages (transcript 22 June 2012, p 29). Professor Breslin agreed that Mr Gilkinson’s account of getting a stuffy nose working in the engine room is consistent with rhinitis (transcript 22 June 2012, p 30). However, his opinion is that in Mr Gilkinson’s case the obstruction was intermittent (transcript 22 June 2012, p 29), noting “no evidence of nasal abnormality on examination by an ENT Surgeon on the 12th of August 1976” (report dated 10 June 2006, p 7). Professor Breslin also distinguished between sinusitis and rhinitis, stating that one could have sinusitis without rhinitis and that “Sinusitis is generally not considered relevant to obstructive sleep apnoea” (transcript 22 June 2012, p 30).
In summary, Professor Breslin appears to be saying that Mr Gilkinson may have had chronic obstruction of the upper airways in 1968 based on his long history of having a stuffy nose. There is, however, no objective evidence of this, Professor Breslin recognises that such nasal obstruction can be intermittent, and the effect of this is only that “when the nasal mucosa is swollen, it makes any tendency to sleep apnoea worse at the time” (transcript 22 June 2012, p 29).
Professor Breslin differed in his opinion from Dr J Scoppa, Ear, Nose and Throat (ENT) Physician who, in a report dated 25 August 2006, at p 5, stated:
… in my opinion Mr Gilkinson’s chronic sinusitis is one of the causes contributing to his sleep apnoea, and the chronic sinusitis would have caused chronic obstruction of the upper airways at the time of clinical onset of sleep apnoea during the early 1970s.
In Dr Scoppa’s opinion, the notation in the medical records of Mr Gilkinson’s nose being “normal” in reference to the ENT examination on 12 August 1976 and 25 May 1977 “do not exclude the diagnosis of chronic sinusitis because in most cases the diagnosis of chronic sinusitis is a radiological rather than a clinical one”.
Dr Scoppa attributes Mr Gilkinson’s chronic sinusitis to a genetic and environmental contributing cause, the latter being the fumes and toxins he has been exposed to (report dated 25 August 2006, p 3). He also says that “sinusitis is almost invariably associated with rhinitis – indeed many standard ENT textbooks and articles prefer the term ‘rhinosinusitis’ instead of ‘sinusitis’” (report dated 27 January 2008, p 2). The Tribunal notes that although Dr Scoppa considered that SoP No 21 of 2003 on Sinusitis to be the most appropriate SoP in Mr Gilkinson’s case, his comments are relevant to our discussion in relation to SoP No 13.
In particular, Dr Scoppa describes rhinosinusitis or chronic sinusitis as part of the definition of chronic obstruction of the upper airways at the level of the nose and nasal pharynx. In answer to counsel’s question whether rhinosinusitis or chronic sinusitis fit the definition of chronic obstruction of the upper airways, Dr Scoppa answered, “Well you would at the level of the nose and nasal pharynx, because it’s the lining which is involved” (transcript 8 April 2008, p 128).
Dr Scoppa described Mr Gilkinson’s symptoms as “variable” rather than intermittent. He stated: “it is well documented in standard ENT literature that chronic rhinitis is a condition that typically varies in severity, ranging from periods of clinical inactivity to periods of severe symptomatology” (report dated 27 January 2008, p 2). He noted that this variable nature is consistent with Professor Breslin’s report of 10 June 2006, Mr Gilkinson’s evidence and the medical records of Dr Hakam, his general practitioner. In particular, Dr Scoppa notes that “Mr Gilkinson’s history of aggravation of symptoms of rhinitis during Navy service is documented in Dr Hakam’s clinical notes on folios 57 and 62” (report 27 January 2008, p 3).
In his report dated 25 August 2006, at p 4, Dr Scoppa refers to a statement by Dr J Bradshaw, Mr Gilkinson’s General Practitioner in Grafton, in a referral letter to Dr S Prince (neither of which was provided to the Tribunal) that Mr Gilkinson had a history of “long term nasal obstruction”. Dr Geoffrey Williams, Thoracic Physician (Coffs Harbour Sleep Disorders Clinic), in a report dated 16 September 2005, stated:
In addition he relates having nasal obstruction and stuffiness most of his life. This was aggravated during naval service from his work in dusty environments, such as the engine room of ships etc. …
David also reports that his nasal problem was aggravated by naval service. This may also have contributed to his development of the Obstructive Sleep Apnoea Syndrome.
The Tribunal is satisfied that the material before it, discussed above, including the weight of medical evidence, points to Mr Gilkinson having chronic obstruction of the upper airways at the time of the clinical onset of sleep apnoea in 1971.
Factor 5(b):being obese at the time of the clinical onset of sleep apnoea
The clause 8 definition of “being obese” is set out above. Essentially, a person is classified as obese if they have a Body Mass Index (BMI) of 30 or more. The summary of the service records referring to Mr Gilkinson’s weight prepared by Mr Colborne provides the following information:
Date Age Weight Height BMI Reference 12/05/1965 15 126 lb 57.15 kg 67 in 170 cm 19.7 Tab 55 p 617 09/07/1969 20 180 lb 81.65 kg Tab 55 p 601 05/12/1969 20 187 lb 84.82 kg Tab 55 p 596 29/01/1970 21 193 lb 87.54 kg Tab 55 p 594 02/12/1970 21 192 lb 87.01 kg Tab 55 p 592 07/06/1971 22 “Obese” Tab 55 p 661 25/05/1977 28 95 kg 177 cm Tab 55 p 587
No specific weight was recorded in the Department of Defence Medical Record for Mr Gilkinson dated 7 June 1971. The Record merely states that Mr Gilkinson is “obese”. As Mr Colborne pointed out, this suggests the finding may have been based on appearance rather than on a measurement of Mr Gilkinson’s weight. However, the fact that such a comment had not previously been made in his Medical Records, suggests that he may have put a significant amount of weight in the previous six months.
One of the difficulties with Mr Gilkinson’s service records is that many of these do not record his height. Dr Dianne Volker, a consultant dietician and nutritional scientist who prepared a nutritional report for the proceedings, gave evidence that the Department of Health considers that males and females reach their adult height and weight at the age of 18 (transcript 8 April 2008, p 150). Medical reports for Mr Gilkinson for 1977 record his height as being 177 cm, that is, 69.685 inches or 5 foot 9½ inches. This accords with Mr Gilkinson’s evidence that the maximum height that he reached was 5 foot 9 inches (transcript 7 April 2008, p 19).
On the basis that his height at the age of 18 was 177 cm, one can assume that on 29 January 1970 (at the age of 20) he would also have been 177 cm in height. A weight of 87.54 kg gives a BMI of 27.94, and on 2 December 1970 (at the age of 21), with a weight of 87.01 kg, his BMI would have been 27.78, not far short of a BMI of 30 (the point at which a person is classified as “being obese” according to the definition in clause 8 of the SoP. The Tribunal notes there was a slight decline in Mr Gilkinson’s weight between 29 January 1970 and 2 December 1970 of one pound (0.53 kg). Minor fluctuations in weight are not unusual and the Tribunal does not consider this significant in relation to Mr Gilkinson being described as “obese” on 7 June 1971. On that day the material points to his description as “obese” closely according with the clause 8 definition. Thus, the Tribunal is satisfied that the material before it points to Mr Gilkinson being obese during operational service.
In her report dated 7 October 2009, at pp 5-6, Dr Volker said:
There is convincing evidence that David Gilkinson became obese during his period of 30 weeks of operational service (16/02/1970-30/11/1972). … Given that the shift work evidence is contentious, there is sufficient evidence that adverse health outcomes were developing for this sailor. Metabolic syndrome risk factors were becoming more pronounced, stress reactions cited by David Gilkinson together with shift work (not quantified) all contribute to his poor health outcomes.
Professor Gill’s opinion is also relevant (report dated 5 July 2009, p 4):
Despite anomalies in his records, there is sufficient [evidence] to suggest that Mr Gilkinson was obese under the currently defined criteria (BMI ≥ 30) during his period of operational service.
Even taking into consideration the confusion around his true height, it is clear that Mr Gilkinson’s weight exceeded the definition of obesity set out in the Australian Naval Order existing at the time of his operational service (Writeway Research Report, 2009). It would appear that actions set out under this order were not instigated at this time to address Mr Gilkinson’s weight problems.
When reviewing Mr Gilkinson’s height measurements, dietary and alcohol intake, physical activities and shift work during operational service, Dr Volker’s opinion was that “One factor is convincing, David Gilkinson’s weight increased to an obese level during his operational service” (report dated 7 October 2009, p 4).
The next question is whether there is material before the Tribunal pointing to Mr Gilkinson’s operational service contributing to his weight gain (s 196B(14)). The Applicant contends that the shift work undertaken by Mr Gilkinson while on operational service, the alcohol consumption and the lack of physical activity all contributed to his obesity. The Respondent submits that the available evidence does not point to a nexus between weight gain and operational service.
In relation to whether there is a nexus between Mr Gilkinson’s operational service and his weight gain, the Tribunal notes that Professor Breslin, when asked whether Mr Gilkinson’s weight and drinking may have led to clinical worsening of his sleep apnoea, answered ‘yes’ and in relation to “whether it was permanent worsening or not, the evidence would suggest it probably was” (transcript 22 June 2012, p 29).
In a report dated 17 May 2009, Captain John Macdonald Rtd for Writeway Research Service Pty Ltd, identified the work undertaken by Mr Gilkinson on board Sydney during his periods of operational service as mostly “double bottoms”, that is being a member of the fuelling and fuel tank party working a normal day shift. Captain MacDonald said, at [31], that the extent of Mr Gilkinson’s watchkeeping (requiring shift work) was limited:
On the basis of the Veteran’s employment records, which show his primary duties over the period of operational service in HMAS SYDNEY were as part of the Double Bottoms (DB) Party and the recollections of Marine Engineering Officers serving in SYDNEY at that time, it seems that the extent of his ‘watchkeeping’ would have been limited, not continuous and not excessive overall. However, in his DB role he would have been required, in the course of his duties, to move about the very lowest decks of the ship, regularly climbing up and down ladders to access confined and uncomfortably hot compartments containing the tank tops or the sounding tubes for measuring the level of fuel in the tanks.
In a statement dated 29 June 2009, in which he commented on Captain Macdonald’s report, Mr Gilkinson said while he worked normal working hours (8.00 am to 4.30 pm), he also had to undertake fuel oil pumping duties. Six crew, working in teams of two, were on a 24 hour roster for four to six hourly pumping duties which would take one and a half to two hours; this would involve him working nearly every night (transcript 16 December 2009, p 15). The Tribunal notes that these rostered duties are referred to by the expert witnesses as shift work although technically not shift work in the usual sense. In the discussion that follows, we also have referred to rostered duties as shift work since the distinction is not of any significance to our decision.
Dr Volker stated that “Shift work has been linked with weight gain” and opined that “lack of physical exercise, heavy drinking and ample supply of food” all contributed to Mr Gilkinson’s obesity (report dated 15 June 2007, p 2). Captain Macdonald said “the quality and quantity of meals in HMA ships were of a high order” (report dated 17 May 2009, at [25]). Mr Gilkinson’s evidence (statement dated 29 June 2009, at [4]) indicates that food was plentiful. Dr Volker thought Mr Gilkinson’s shift work, which would have interrupted his circadian rhythm, would have had a moderate effect on his weight gain (transcript 17 December 2009, p 4). Bearing in mind that Mr Gilkinson’s operational service comprised “just short bursts”, Professor Gill considered the impact of Mr Gilkinson’s pattern of duties on his diet and physical activity patterns was likely to be moderate (transcript 17 December 2009, p 14).
Apart from the contribution from shift work and diet, the Applicant contends that operational service contributed to his increased consumption of alcohol because of his anxiety about what might happen in Vietnam, and that this in turn contributed to his weight gain and his being obese. Specifically, the anxiety arose from working in the engine room, in the centre of the ship, which was the main target for enemy mines or bombs (transcript 7 April 2008, p 41). While at sea on board the Sydney and not involved in operations, sailors were allowed to purchase 26 ounces (750 ml) of beer on most nights (transcript 7 April 2008, p 38; Macdonald report dated 17 May 2009, at [27]) which is equivalent to approximately three standard drinks or 30 grams of alcohol. However, Mr Gilkinson’s evidence is that it was while in port, en route to and from Vietnam, he and his mates would go and “get drunk”, consuming about 20 middies of beer. Mr Gilkinson said that on “the way up” to Vietnam, Sydney would stop at one of Kuala Lumpur, Singapore or Hong Kong and, it appears that on the way back, Sydney would stop at Fremantle or Adelaide for a few days before returning to Sydney (transcript 7 April 2008, pp 40 – 41).
Commenting on Captain Macdonald’s evidence that sailors were generally permitted 750 ml of beer a day while at sea, Dr Volker said: “This level of intake during operational service would not have had a major influence on excessive energy intake, however in port consumption; [sic] given the naval culture of binge drinking would have had more impact” (report 7 October 2009, p 5).
Professor Gill commented (report dated 5 July 2009, p 6):
The alcohol issue at sea during Mr Gilkinson’s operations service could have made a contribution to the excess energy intake that lead [sic] to his weight gain but this contribution is likely to be minor.
The culture of excessive and binge drinking that lead [sic] to periods of very heavy alcohol consumption during his service may have made a larger contribution to Mr Gilkinson’s weight problems and to his other health problems.
The Applicant also contends that lack of physical activity contributed to his weight gain while on operational service. Mr Gilkinson’s evidence is that when aboard Sydney, his duties sometimes involved a lot of going up and down ladders, but at other times just involved watching a machine; the only capacity to exercise was to walk around the upper deck or flight deck provided the army was not on board in which case “it was choc a block” (transcript 7 April 2008, p 18). In his report dated 17 May 2009, at [32], Captain Macdonald noted that Sydney, “Being a converted Aircraft Carrier, with a large hangar space and a flight deck, … had ample room onboard in which to conduct physical training exercises and walking or jogging exercises”.
We are satisfied that the above material points to Mr Gilkinson being obese at the time of the clinical onset of sleep apnoea and to his obesity being attributable to his operational service (s 196B(14)(b)). The material before us in turn points to the weight gain being contributed to by the shift work, diet, lack of physical activity and alcohol consumption during Mr Gilkinson’s operational service.
In conclusion in relation to step 3, the Tribunal is satisfied that the material before us points to factors 5(a) and (b) of the factors on which the Applicant is relying and to those factors being related to Mr Gilkinson’s operational service. Thus, we are satisfied that the hypothesis is reasonable in so far as it is consistent with factors 5(a) and (b) in SoP No 13.
Step 4: If the hypothesis is reasonable, the Tribunal must be satisfied beyond reasonable doubt that the incapacity did not arise from the war-caused disease. (Any fact finding must only be made at this final stage in the process.)
As stated above, there is no dispute that Mr Gilkinson suffers from sleep apnoea. He was diagnosed following a sleep study in April 2001. Equally, there is no dispute that he rendered operational service while on board Sydney during the period February 1970 to November 1972. The Tribunal having found that the material before us points to the clinical onset of Mr Gilkinson’s sleep apnoea being in 1971, the question is whether there is evidence from which we are satisfied beyond all reasonable doubt that his incapacity did not arise from the sleep apnoea. The answer to that question is ‘No’. While Professor Breslin’s evidence is that the deterioration of Mr Gilkinson’s sleep apnoea was gradual and not sudden, and almost certainly associated with weight gain (report dated 10 June 2006, p 7), we are not satisfied beyond reasonable doubt that Mr Gilkinson has not suffered incapacity as a result of his sleep apnoea.
While Mr Gilkinson was not diagnosed with sleep apnoea until 2001, we note that Professor Breslin’s evidence at the time of Mr Gilkinson’s operational service, diagnosis of sleep apnoea in terms of its mechanisms and treatment with CPAP were not available (transcript 22 June 2012, p 12).
We note the result of a medical examination of Mr Gilkinson on 12 August 1976 by an ENT specialist, Dr H D Raffan, who reported “Nose and throat clear”. The focus of Dr Raffan’s examination seems to have been the assessment of possible hearing loss and, in any event, Professor Breslin’s evidence is that “nasal obstruction comes and goes” (transcript 8 April 2008, p 97). Moreover, in a report dated 25 August 2006, at p 5, Dr Scoppa comments that the entry for 12 August 1976 and another entry, dated 25 May 1977, that Mr Gilkinson’s nose was “normal” just before discharge:
… do not exclude the diagnosis of chronic sinusitis because in most cases the diagnosis of chronic sinusitis is a radiological rather than a clinical one. Furthermore it is clear that not all entries in the service medical record are consistent.
Dr Scoppa said:
… in my opinion Mr Gilkinson’s chronic sinusitis is one of the causes contributing to his sleep apnoea, and the chronic sinusitis would have caused chronic obstruction of the upper airways at the time of the clinical onset of sleep apnoea during the early 1970s.
In the light of the above evidence, the Tribunal cannot be satisfied beyond reasonable doubt that factor 5(a), “having chronic obstruction of the upper airways at the time of the clinical onset of sleep apnoea” during operational service, is negated.
With respect to whether Mr Gilkinson’s significant alcohol consumption was contributed to by stress while on operational service, including when in port en route to and from Vietnam, we note the report from Dr Robert Delaforce, Forensic Psychiatrist, dated 15 May 2001. When assessing Mr Gilkinson following his claim in respect of “Sleeping Problems” and “PTSD” (Post Traumatic Stress Disorder), Dr Delaforce recorded, at p 1:
When I inquired about any stressful periods during those trips to and from Vietnam he indicated there was not, except for the worry that something stressful might happen at Vung Tan Harbour. However, nothing of significance happened. When I inquired about any significant stressors at other times during service he referred to difficulty putting up with “idiots”, the “over–educated authority figures” in the navy.
On the other hand, Dr Ian Hayes, Psychiatrist, who assessed Mr Gilkinson in September 2006, but whose report is undated, stated in relation to Mr Gilkinson:
He is not haunted by any specific memories of his Vietnam days or other experience. He does however report a general sense of anxiety and tension, and concern about what might happen. This relates to him being a crew member in the engine room of the Sydney on 10 trips to Vietnam.
During this time there was clear threat from enemy floating mines or divers, and a recognition that if the engine room was holed, that he would be trapped in with other crew as the hatches would be locked.
This is consistent with Mr Gilkinson’s oral evidence when asked by Counsel for the Respondent about the stress he said he was suffering while on Sydney which lead to his drinking more. Mr Gilkinson replied that he was (transcript 7 April 2008, p 41):
Worrying about what was happening, what could happen mainly and working in the engine room which were in the centre of the ship was the main target for any enemy with mines or bombs or whatever.
In relation to Mr Gilkinson’s alcohol consumption and its contribution to his “being obese” during operational service, Professor Gill commented (report dated 5 July 2009, p 6):
The alcohol issue at sea during Mr Gilkinson’s operations service could have made a contribution to the excess energy intake that lead [sic] to his weight gain but this contribution is likely to be minor.
The culture of excessive and binge drinking that lead [sic] to periods of very heavy alcohol consumption during his service may have made a larger contribution to Mr Gilkinson’s weight problems and his other health problems.
We also note Professor Gill’s opinion with regard to the naval diet and opportunities for physical activity (report dated 5 July 2009, pp 5-6). Professor Gill commented with respect to diet:
In the absence of consistent information, further speculation is of little value in defining the composition of Mr Gilkinson’s diet during his operational service and thus it is not possible to make judgement about its potential to contribute to the development of obesity.
And with respect to physical activity:
It is likely that Mr Gilkinson maintained a reasonable level of physical activity during his operational service on HMAS Sydney, but there is insufficient evidence to make a firm judgement on the overall physical activity levels of Mr Gilkinson during this period.
Mr Gilkinson’s duties were physically demanding when he was at sea and there is some evidence that suggests that sailors were encouraged to be physically active outside of work hours. However, there were considerable periods during Mr Gilkinson’s operational service where he was not required to undertake his physically demanding tasks and there is not sufficient evidence to make a judgement on the opportunities to be physically active and exercise aboard HMAS during these times.
However, Professor Gill commented in relation to shift work and its impact on diet and physical activity (at p 9):
It is my opinion that a pattern of shiftwork duties such as that undertaken by Mr Gilkinson’s during operational service may have had some impact on his diet and physical activity patterns but that the size of that effect is likely to have been moderate.
Professor Gill said he took into account that Mr Gilkinson’s operational service was not a continuous period and that there were just a “short bursts” of operational service (transcript 17 December 2009, p 14).
In the light of Professor Gill’s and Dr Volker’s opinions referred to above and Mr Gilkinson’s account of a lack of physical activity during operational service, of his excessive alcohol intake and the impact of his rostered fuel oil pumping duties, the Tribunal cannot be satisfied beyond reasonable doubt that factor 5(b), “being obese at the time of clinical onset of sleep apnoea” as a result of shift work, lack of physical activity and excessive alcohol consumption during operational service, is negated. Thus, in relation to factors 5(a) and (b) of SoP No 13, the Tribunal is not satisfied beyond reasonable doubt that the hypothesis that Mr Gilkinson’s sleep apnoea is war-caused is negated.
DECISION
The decision of the Repatriation Commission dated 30 March 2005 refusing Mr Gilkinson’s claim for a disability pension in respect of sleep apnoea – is set aside and a decision substituted that Mr Gilkinson’s sleep apnoea is war-caused. The date of effect of this decision in terms of the payment of pension is 14 June 2004. The matter is remitted to the Commission to determine the rate of pension payable to Mr Gilkinson.
I certify that the preceding seventy seven (77) paragraphs are a true copy of the reasons for the decision herein of Mr RP Handley, Deputy President and Dr H Haikal-Mukhtar, Member ........[sgd]................................................................
Associate
Dated 24 July 2012
Dates of hearing 21-22 June 2012 Counsel for the Applicant C Colborne Solicitor for the Applicant Veterans’ Advocacy Service, Legal Aid NSW Counsel for the Respondent K Eastman Solicitor for the Respondent Australian Government Solicitor
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