JOAN LAURIE and REPATRIATION COMMISSION
[2009] AATA 378
•25 May 2009
Administrative Appeals Tribunal
DECISION AND REASONS FOR DECISION [2009] AATA 378
ADMINISTRATIVE APPEALS TRIBUNAL )
) No 2007/5638
VETERANS' APPEALS DIVISION ) Re JOAN LAURIE Applicant
And
REPATRIATION COMMISSION
Respondent
DECISION
Tribunal Miss E A Shanahan Date25 May 2009
PlaceMelbourne
Decision The Tribunal affirms the decision under review.
(sgd) E A Shanahan
Member
VETERANS' AFFAIRS – widow’s claim for pension – kind of death – cause of death – any contributing war-caused medical conditions – hastening of death – complex hypotheses – inadvertent overdose of medication – decision affirmed
Veterans’ Entitlement Act 1986 s 8, s 11, s 120(1), s 120(3), s 120(4), s120A, s119
Statement of Principles concerning hypertension No 25 of 2003 as amended No 3 of 2004
Statement of Principles concerning ischaemic heart disease No 53 of 2003
Statement of Principles concerning ischaemic heart disease No 89 of 2007
Bushell v Repatriation Commission (1992) 175 CLR 408.
Doolitte v Repatriation Commission 21 ALD 489
McKenna v Repatriation Commission (1999) 86 FCR 144
Repatriation Commission v Codd (2007), 95 ALD 619
Repatriation Commission v Tuite (1993) 29 ALD 609
Repatriation Commission v Hancock (2003) 37 AAR 383
Repatriation Commission v Deledio (1998) 49 ALD 193
Repatriation Commission v Keeley (2000) 98 FCR 108
Repatriation Commission v Gorton (2000) 33 AAR 378
Repatriation Commission v Law (1980) 31 ALR 140
Roncevich v Repatriation Commission (2005) 222 CLR 115
East v Repatriation Commission (1987) 16 FCR 517
REASONS FOR DECISION
25 May 2009 Miss E A Shanahan 1. Mrs Joan Laurie is the widow of John Laurie who died on 27 February 2005. Mr Laurie served in the Australian Army (the Army) from 2 February 1942 to 20 September 1975 with operational service from 2 February 1942 to 30 June 1949. He was promoted to the rank of Lieutenant in 1946 and allotted to the Ordinance Corps. After a number of regimental postings, he held senior positions in the Directorate of Ordinance Services and then the Central Army Supply Agency. At the time of his death he was not in receipt of a Department of Veterans’ Affairs (Department) disability pension and had no accepted war-caused disabilities.
2. Mrs Laurie applied for a widow’s pension on 26 April 2005. Her claim was rejected by the Repatriation Commission delegate on 5 August 2005 and this decision was affirmed by the Veterans’ Review Board (VRB) on 27 September 2007. Mrs Laurie applied to the Administrative Appeals Tribunal for a review of these decisions on 21 November 2007.
3. Mrs Laurie was represented by Mr A Larkin of counsel, instructed by Williams Winter and the Repatriation Commission was represented by Mr K Rudge, an advocate of the Department. The Tribunal had before it the documents lodged pursuant to s 37 of Administrative Appeals Tribunal Act 1975 (T-documents). The parties tendered the following:
For the Applicant
·Statement of Mrs Laurie dated 16 November 2007 – Exhibit A1
·Report of Professor A Pitt dated 20 May 2008 – Exhibit A2
·Further report of Professor A Pitt dated 22 August 2008 – Exhibit A3
·Report of Dr R B Collins dated 16 April 2008 – Exhibit A4
For the Respondent
·T-Documents – Exhibit R1
·Clinical record relating to Mr Laurie’s admissions to The Valley Private Hospital - Exhibit R2
·Report of Professor R Harper dated 12 May 2008 – Exhibit R3
·Report of Professor J Cade dated 11 April 2008 – Exhibit R4
·Transcript of the Veterans’ Review Board hearing dated 27 September 2007 – Exhibit R5
4.Mr Laurie, Professor Pitt, Dr Collins, Professor Harper and Professor Cade gave evidence before the Tribunal.
BACKGROUND TO THE APPLICATION
5. Mr Laurie had been diagnosed with hypertension in 1975 although blood pressure (BP) readings dating from 1960 raised the possibility that he then suffered from labile hypertension. Treatment commenced in 1975. In March 1997 he was hospitalised with episodic chest tightness suggestive of angina pectoris. Several electrocardiograms (ECG) and serum cardiac enzyme estimations done on admission were normal, as was a subsequent thallium myocardial perfusion scan. The treating cardiologist, Dr Jack Krafchek, diagnosed mild coronary artery disease (CAD) and recommended treatment with a beta blocker (Betaloc) and aspirin, with the continuation of Renitec prescribed for the control of Mr Laurie’s hypertension. Thereafter, Mr Laurie saw his general practitioner regularly for BP monitoring and unrelated minor health problems. Poor blood pressure control led to a change in medication from Renitec to Avapro HCT. Betaloc was changed to Metoprolol (Minax 50 mg daily). The treatment achieved excellent blood pressure control. In late February 2005 Mr Laurie developed a respiratory tract infection with cough, a slightly raised temperature and a reddened throat for which the antibiotic Moxacin was prescribed on 26 February 2005.
6. On 26 February 2005, according to Mrs Laurie, Mr Laurie was active, watched television in the evening and took three doses of Moxacin as prescribed. In the early hours of 27 February 2005, Mrs Laurie found him severely confused, trying to open the backdoor and endeavouring to put his socks on his head. She noted that five daily doses of his medication were missing from the dosette. She called an ambulance. After initial resuscitative procedures, Mr Laurie was transported to Monash Medical Centre (MMC). The ambulance office had coded Mrs Laurie’s call to the Metropolitan Ambulance Service (MAS) as an overdose. Both the local ambulance service and a mobile intensive care ambulance (MICA) were called and recorded that Mr Laurie was confused, combative, short of breath, hypotensive and in rapid atrial fibrillation with crackles heard in both lungs. The ambulance officers made the provisional diagnoses of severe infection or acute pulmonary oedema and confirmed that five days of medication was missing. The same provisional diagnoses were made by the medical staff in the Accident and Emergency Department at MMC, with the diagnosis of left lower lobe pneumonia favoured both clinically and radiologically. Mr Laurie remained combative and hypotensive. He was eventually sedated with Midazolam. Despite the administration of intravenous Digoxin, Amiodarone, Aramine, Lasix, intravenous fluids and antibiotics, he remained in cardiogenic shock with rapid atrial fibrillation and was found to be anuric. The family were acquainted with his poor prognosis and a not-for-resuscitation order was made. Mr Laurie died at 15.10 hours on the same day. Investigations had revealed renal failure, acidosis, a high white cell count, dehydration, blood cultures negative for septicaemia, a serum Troponin Ι of 0.46 (normal being less than 0.08 micrograms per litre) and a CRP (C-reactive protein) of 299.8 (normal being 0 to 5).
7. The hospital death certificate stated the cause of Mr Laurie’s death to be left‑sided pneumonia of day’s duration and also included a diagnosis of hypertension present for years and smoker present for years. The Bureau of Births, Deaths and Marriages’ death certificate was to the same effect
8. Professor Pitt and Dr Collins were of the opinion that Mr Laurie’s death was hastened by his coronary artery disease, the latter being contributed to by his long‑standing hypertension. Professors Cade and Harper considered Mr Laurie’s death was due to overwhelming infection with multi-organ failure, with no evidence to support contribution to, or hastening of, death by coronary artery disease.
9. The hypotheses advanced by Mrs Laurie were three-fold:
1.War-caused alcohol consumption leading to hypertension, which in turn resulted in coronary artery disease and ischaemia contributing to or hastening Mr Laurie’s death.
2.War-caused smoking leading directly or via the development of hypertension to ischaemic heart disease which contributed to his death.
3.Smoking and alcohol use leading to hypertension, which resulted in renal impairment and thereby a heightened susceptibility to the development of renal failure, contributing to Mr Laurie’s death.
10. The Repatriation Commission conceded that the number of cigarettes smoked and the volume of alcohol imbibed by Mr Laurie met the requirements of the relevant Statements of Principles (SoP) but did not accept that either habit was service‑related. Mrs Laurie met her husband late in 1946 or early 1947. She believed he had commenced smoking and drinking alcohol while serving in New Guinea and that he did so to relieve war-caused stress and anxiety.
11. It was not until the third day of the hearing of this matter and during the course of Professor Cade’s evidence, that the Tribunal noted the ambulance officer’s entries concerning the five days of medication missing from Mr Laurie’s dosette and that the call for an ambulance was logged for an overdose. Professor Cade’s opinion as to the affect of the ingestion of 1500 milligrams of Avapro, an anti-hypertensive drug was obtained. Professor Cade stated such a dose would cause severe hypotension. The Tribunal requested that the parties seek further opinions from Professors Pitt and Harper on the question of the effect of the probable overdose of prescribed medication. Both Professors agreed that the Avapro would cause hypotension. The dose of Metoprolol at 50 milligrams per day equating to an overdose of 250 milligrams in their opinion would cause hypotension but should also have slowed the heart rate. Mr Laurie was in rapid atrial fibrillation with a heart rate of 146 to 164 and therefore the bradycardia effect of Metoprolol was not evident.
ISSUES BEFORE THE TRIBUNAL
1. The cause of death and the kind of death experienced by Mr Laurie?
2.Did Mr Laurie’s operational service-related diseases contribute in any way to his death?
12. Mrs Laurie’s evidence is summarised under the heading background to the application. She later confirmed that she had called the ambulance on 27 February 2005 because of Mr Laurie’s confused state and her discovery that five days’ doses of his medication was missing.
13. Professor Pitt provided three reports (Exhibit A2 and A3 and the opinion regarding the overdose of medication after the hearing). In his written reports he had opined that a reasonable hypothesis could be raised relating Mr Laurie’s war service to the development of hypertension by way of his alcohol consumption and cigarette smoking, with this leading to the development of ischaemic heart disease contributing to cardiac failure and death. His reports were couched in terms of a reasonable hypothesis and did not address probabilities. In his evidence before the Tribunal he agreed with the assessment of Dr Krafchek in 1997, that there was no evidence of myocardial infarction at that time. He believed however that ischaemic heart disease remained likely but was probably of mild severity. Given the level of Troponin Ι recorded on 27 February 2005 as approximately six times normal, Professor Pitt was of the opinion Mr Laurie probably had a myocardial infarct on that day. Professor Pitt had discussed the relevance of such a level with Professor Schneider of the Alfred Hospital, who indicated that a level of 0.46 would be of cardiac origin. Professor Pitt believed that myocardial ischaemia short of a full thickness myocardial infarct and hypertension were sufficient to cause cardiac failure and atrial fibrillation in Mr Laurie and thereby contribute to his death.
14. Dr Collins had stated that it was reasonable to conclude, on the evidence with which he was provided, that Mr Laurie had suffered a myocardial infarct on 27 February 2005, resulting in cardiac failure and intractable pulmonary oedema. The Tribunal notes that Dr Collins had limited documentation, being provided with only the service records, the clinical notes of MMC and a copy of the death certificate. He stated:
In my opinion, it could be reasonably be opined that the late Mr Laurie’s death was due in part, or in toto, to an acute myocardial infarction, with the underlying pathological process being coronary atherosclerosis/ischaemic heart disease. (Exhibit A4)
15. Professor Harper, in his report and his oral evidence, identified the cause of Mr Laurie’s death as extensive bi-lateral pneumonia, giving rise to multi-organ failure including renal failure. In his opinion Mr Laurie’s mild pre-existing renal impairment was commensurate with his age and may have hastened death, although any acute severe illness was likely to cause renal failure. In his opinion Mr Laurie’s outcome would have been the same, even if his renal function was normal. On the data provided, Professor Harper opined that despite the presence of coronary artery disease it was not sufficient, in Mr Laurie’s case, to give rise to cardiac problems. Professor Harper agreed with Professor Pitt that the raised Troponin Ι level most probably was of cardiac muscle origin, but in his experience such levels were seen in atrial fibrillation alone. In acute pulmonary oedema levels of 20 or 30 were usual. In his opinion the severe sepsis had precipitated both the atrial fibrillation and the renal failure. He concurred with the radiologist’s opinion that the chest x-ray findings indicated that it was more likely that the lung pathology was of infective origin rather than pulmonary oedema secondary to heart failure. While the presence of hypertension over many years had been listed on the death certificate, Professor Harper believed it had not contributed to Mr Laurie’s death.
16. Professor Cade found Mr Laurie’s cause of illness, as recorded in the MMC clinical notes, to be one of pneumonia, overwhelming sepsis, septic shock and multi‑organ failure. In his experience and as documented in the medical literature, this clinical scenario was associated with a 90 per cent mortality rate. In Professor Cade’s opinion, Mr Laurie’s past biochemical parameters of mild renal failure, recorded in 1997 and 2000, had no bearing on Mr Laurie’s death. Any contribution by another medical condition, including the mild clinically quiescent coronary artery disease and perhaps ischaemic heart disease would be speculative. Professor Cade attributed the raised Troponin Ι levels to sepsis and septic shock effects on the myocardium and not to ischaemic heart disease or myocardial infarction.
17. Under cross-examination by Mr Larkin, Professor Cade stated that the sudden deterioration in Mr Laurie’s condition between 10.00pm on 26 February 2005 and approximately 2.00am on 27 February 2005 was totally in accordance with severe sepsis; hypertension per se did not lead to atrial fibrillation unless there was hypertensive heart disease; renal function deterioration as measured by creatinine levels related more to age than to a masking of true levels by muscle loss associated with aging and Mr Laurie’s terminal serum creatinine and urea levels (creatinine twice normal and urea five times normal) were indicative of marked dehydration as well as degree of renal failure.
18. When informed by the Tribunal of the high probability that Mr Laurie, in his confused state, had taken five days’ dosage of drugs including 1500 milligrams of Avapro HCT, Professor Cade said that this would have caused severe hypotension.
DOCUMENTARY EVIDENCE
the death certificate
19. The death certificate for Mr Laurie was completed by Dr Mandy Li York Nan on 28 February 2005. The disease or condition directly leading to death was left sided pneumonia of days duration. Part two of the certificate refers to other significant conditions contributing to the death but not related to the disease or condition causing it stated hypertension of years duration and smoker of years duration. Dr Li did not see Mr Laurie during his admission to hospital. Both Dr Collins and Professor Harper have criticised the accuracy of the death certificate. Dr Collins was of the opinion that the death was obviously due to myocardial infarction and Professor Harper was of the opinion that while the entry regarding hypertension reflected the presence of a significant condition, this condition had not contributed to Mr Laurie’s death.
20. The Tribunal is fully aware from personal experience that in the public hospital system death certificates are completed almost exclusively by interns and resident medical officers who have never seen the deceased at any time during their hospitalisation. The entry smoker of many years duration is inappropriate as smoking is not a medical condition although nicotine addiction and withdrawal are both International Code of Disease diseases. Such entries are however often made for statistical purposes.
THE VALLEY PRIVATE HOSPITAL CLINICAL RECORD
21. Mr Laurie was hospitalised for 48 hours in March 1997, following an episode of dull central chest pain lasting 30 to 40 minutes which was relieved by Anginine obtained from a friend. His pain was initially associated with nausea, burping and shortness of breath. There was said to be no radiation of the pain. A transitory, less severe episode had occurred the previous day. Physical examination on admission was normal as were the electrocardiograph and the serum cardiac enzyme levels. Mr Laurie underwent cardiac monitoring throughout his admission and beta blockers were prescribed. He had no further chest pain during his admission. He subsequently underwent myocardial perfusion scanning and this did not reveal any evidence of myocardial ischaemia. His treating cardiologist, Dr Krafchek, reported to Mr Laurie’s general practitioner, Dr Alan Cunneen, on 26 March 1997 outlining Mr Laurie’s history and progress while in The Valley Private Hospital. He interpreted the thallium scan as showing that Mr Laurie had only mild coronary disease present, insufficient to show any perfusion defect on scanning. He recommended continuing the use of Betaloc and aspirin and better control of Mr Laurie’s hypertension. Further cardiac review was considered unnecessary unless Mr Laurie had further episodes of chest pain. During the admission to The Valley Private Hospital, Mr Laurie’s serum creatinine was elevated to a level of 156 (normal being 40 to 130) and his serum urea was 8.5 mmol/L (normal being 3.2 to 7.3). The full blood examination done at the same time showed that his packed cell volume was 54 per cent, indicating a degree of dehydration which may have contributed to the elevated levels of urea and creatinine.
monash medical centre clinical notes (T 7, p37-77)
22. Mr Laurie had attended the Accident and Emergency Department of MMC on 23 March 2004 with a lacerated forehead, sustained when he tripped on steps at home. His laceration was sutured and he was observed for a period of approximately three hours. During this time his pulse was regularly recorded, and despite the fact that he was taking Metoprolol 50 milligrams per day, his pulse rate was between 67 and 88. (T 7, p41).
23. The MMC medical record contains the reports of the Wheelers Hill division of the MAS and that of the MICA Unit, both of which attended following Mrs Laurie’s call for assistance. Her call was received at 4.29am and both ambulance crews coded the call as an overdose. The notes of the ambulance officers record that Mr Laurie was being treated for a chest infection, was confused, combative and that his antihypertensive drugs were missing from his dosette. On examination they noted that he was short of breath and on auscultation of the chest, crackles were heard in both lungs. His blood pressure at that time was recorded as 100 systolic, the respiration rate at 40 per minute and the heart rate on ECG monitor was that of atrial fibrillation at 164 beats per minute. A diagnosis of possible acute pulmonary oedema or chest infection was made. The MICA officers inserted an intravenous line and administered morphine without effect. They gave him oxygen at high flow rates. The ambulance officers forewarned MMC Accident and Emergency Department of Mr Laurie’s clinical status and transported him to the hospital, arriving at 5.30am. On his arrival at the hospital, Mr Laurie was assessed by a resident medical officer, Dr Chanpur, who obtained the same history or transcribed that obtained by the ambulance officers; with the exception that there is no notation of the possible inadvertent taking of excessive medication (Mr Laurie was not accompanied by family members and he was not capable of giving a history). The examination findings were the same as those described by the ambulance officers. The neurological examination was essentially normal. Dr Chanpur made a diagnosis of septicaemia, acute pulmonary oedema and rapid atrial fibrillation. A barrage of investigations was commenced and Mr Laurie was sedated with intravenous Midazolam. Intravenous Digoxin and Amiodarone were administered in order to control the heart rate and Aramine was given in an effort to raise the blood pressure. The latter action was of short-lived benefit.
24. By 5.55am the results of the critical investigations were to hand, revealing acidosis, renal failure, left lower lobe and left mid-zone lung consolidation with changes also in the right mid-zone, considered by the radiologist to represent pneumonia as opposed to acute pulmonary oedema. The Troponin level of 0.46 was also to hand. An ECG confirmed the presence of rapid atrial fibrillation. At 5.55am Dr Chanpur spoke with Mrs Laurie and her family, advising them of Mr Laurie’s poor prognosis. After discussion, a not-for-resuscitation order was made. Attempts to control the heart rate and increase the blood pressure were then abandoned. At 7.15am Mr Laurie was assessed by the Medical Registrar, Dr Chahadi and a diagnosis of pneumonia and sepsis was made. Dr Chahadi also spoke with Mrs Laurie and confirmed the family wishes that he not be resuscitated; that is, he was not to be intubated and ventilated, admitted to the Intensive Care Unit or given cardiopulmonary resuscitation. Antibiotics were to be continued for a period of 24 hours. Morphine was administered intravenously on a regular basis. Mr Laurie was transferred to a medical ward at 12.50pm, although ward records state he arrived at 2.30pm. There are discrepancies in relation to the time of death between the nursing notes and the medical notes. The intern who saw Mr Laurie recorded that death occurred at 2.10pm, although the nursing notes state that this was 3.00pm. These discrepancies were reviewed by another Resident Medical Officer after death and it was concluded that the intern had entered the incorrect time of death, death having occurred at 3.10pm.
GENERAL PRACTITIONERS CLINICAL NOTES CONCERNING MR LAURIE (T 13, P86-106)
25. Dr Alan Cunneen had been Mr Laurie’s general practitioner and his notes from 1 May 1989 until 17 October 2006 were provided. Mr Laurie attended on a regular basis for monitoring of his blood pressure and minor illnesses unrelated to this claim. On 3 March 1997 he had presented to Dr Cunneen with what was said to be chest pain, although Mr Laurie pointed to his epigastrium as the site of pain. He was subsequently admitted to The Valley Private Hospital for investigation and treatment of this symptom.
26. Mr Laurie attended the clinic on 26 February 2005 with cough, mild fever and a reddened throat. A diagnosis of chest infection was made and the antibiotic Moxacin was prescribed. A chest x-ray was requested but not performed on the day.
27. The records reveal that on 14 March 2000, Mr Laurie’s serum urea was 8 (mmol/L) which was within the then normal range and his creatinine was 0.013 mmol/L, at the upper limit of the normal range, normal being 0.11. This particular specimen was haemolysed and thus does not present an accurate picture of his electrolyte status and renal function at that time. A repeat estimation of serum electrolytes and urea on 17 March 2000 was normal with respect to the levels of urea and creatinine although the serum potassium remained elevated. The latter was attributed to probable technical faults in collection.
RELEVANT LEGISLATION
28. Section 8 of the Act provides that the death of Veteran is war-caused if:
(1)Subject to this section and section 9A, for the purposes of this Act, the death of a veteran shall be taken to have been war-caused if:
(a)the death of the veteran resulted from an occurrence that happened while the veteran was rendering operational service;
(b)the death of the veteran arose out of, or was attributable to, any eligible war service rendered by the veteran;
(c)the death of the veteran resulted from an accident that occurred while the veteran was travelling, while rendering eligible war service but otherwise than in the course of duty, on a journey to a place for the purpose of performing duty or away from a place of duty upon having ceased to perform duty;
(d)in the opinion of the Commission, the death of the veteran was due to an accident that would not have occurred, or to a disease that would not have been contracted, but for his or her having rendered eligible war service or but for changes in the veteran’s environment consequent upon his or her having rendered eligible war service; or
(e)the injury or disease from which the veteran died:
(i) was suffered or contracted while the veteran was rendering eligible war service, but did not arise out of that service; or
(ii) was suffered or contracted before the commencement of the period, or last period, of eligible war service rendered by the veteran, but not while the veteran was rendering eligible war service;
and, in the opinion of the Commission, the injury or disease was contributed to in a material degree by, or was aggravated by, any eligible war service rendered by the veteran, being service rendered after the veteran suffered that injury or contracted that disease; or …
29. In determining the kind of death and the relationship of the death to contributing war-caused diseases, the standard of proof is one of reasonable satisfaction as outlined in s 120(4) of the Act:
…
(4)Except in making a determination to which subsection (1) or (2) applies, the Commission shall, in making any determination or decision in respect of a matter arising under this Act or the regulations, including the assessment or re-assessment of the rate of a pension granted under Part II or Part IV, decide the matter to its reasonable satisfaction. …
30. As Mr Laurie had operational service the standard of proof is in terms of a reasonable hypothesis attracted by s 120(1) and s 120(3) of the Act which state:
(1)Where a claim under Part II for a pension in respect of the incapacity from injury or disease of a veteran, or of the death of a veteran, relates to the operational service rendered by the veteran, the Commission shall determine that the injury was a war-caused injury, that the disease was a war-caused disease or that the death of the veteran was war-caused, as the case may be, unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
Note:This subsection is affected by section 120A.
…
(3)In applying subsection (1) or (2) in respect of the incapacity of a person from injury or disease, or in respect of the death of a person, related to service rendered by the person, the Commission shall be satisfied, beyond reasonable doubt, that there is no sufficient ground for determining:
(a)that the injury was a war-caused injury or a defence-caused injury;
(b)that the disease was a war-caused disease or a defence-caused disease; or
(c)that the death was war-caused or defence-caused;
as the case may be, if the Commission, after consideration of the whole of the material before it, is of the opinion that the material before it does not raise a reasonable hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person.
31. As the claim was lodged after 1 June 1994, s 120A is attracted. Section 120A provides for the testing of the reasonableness of a hypothesis against Statement of Principles (SoP) determined by the Repatriation Medical Authority (RMA) in accordance with s 196B. S120A(3) directs the Tribunal to determine the existence of any relevant SoP concerning the kind of death.
32. In the Repatriation Commission v Deledio (1998) 49 ALD 193 the Full Federal Court adopted a four-step process for the testing of a hypothesis against the SoP. This Tribunal is bound to follow the steps promulgated, which are:
1.The Tribunal must consider all the material which is before it and determine whether that material points to a hypothesis connecting the injury, disease or death with the circumstances of the particular service rendered by the person. No question of fact finding arises at this stage. If no such hypothesis arises, the application must fail.
2.If the material does raise such a hypothesis, the Tribunal must then ascertain whether there is in force an SoP determined by the Authority under s 196B(2) or (11). If no such SoP is in force, the hypothesis will be taken not to be reasonable and, in consequence, the application must fail.
3.If an SoP is in force, the Tribunal must then form the opinion whether the hypothesis raised is a reasonable one. It will do so if the hypothesis fits, that is to say, is consistent with the "template" to be found in the SoP. The hypothesis raised before it must thus contain one or more of the factors which the Authority has determined to be the minimum which must exist, and be related to the person's service (as required by ss 196B(2)(d) and (e)). If the hypothesis does contain these factors, it could neither be said to be contrary to proved or known scientific facts, nor otherwise fanciful. If the hypothesis fails to fit within the template, it will be deemed not to be "reasonable" and the claim will fail.
4.The Tribunal must then proceed to consider under s 120(1) whether it is satisfied beyond reasonable doubt that the death was not war-caused, or in the case of a claim for incapacity, that the incapacity did not arise from a war-caused injury. If not so satisfied, the claim must succeed. If the Tribunal is so satisfied, the claim must fail. It is only at this stage of the process that the Tribunal will be required to find facts from the material before it. In so doing, no question of onus of proof or the application of any presumption will be involved.
SUBMISSIONS
33. Mr Larkin addressed the Tribunal on the required standard of proof to be applied in determining the kind of death or cause of death, that being to the Tribunal’s reasonable satisfaction (Repatriation Commission v Hancock (2003) 37 AAR 383) and that any contribution by war-caused diseases is all that is required and not that the death could be attributed to the disease.. (Repatriation Commission v Law (1980) 31 ALR 140, Doolette v Repatriation Commission 21 ALD 489 and Roncevich v Repatriation Commission (2005) 222 CLR 115). Mr Larkin submitted that the late veteran’s smoking habit and alcohol intake were war-caused and derived from stress he experienced during his service in New Guinea. The Respondent had conceded that the quantities of cigarettes smoked and alcohol imbibed met the requirements of the relevant Statements of Principles. Mr Larkin argued that the smoking and alcohol consumption were war-caused on the basis that Mr Laurie had enlisted at the age of 19 when the legal age for drinking alcohol was 21, he had experienced stressful events while serving in New Guinea and had told his wife that these habits related to his service. The applicant relied on the beneficial nature of the Act, in particular s 119 and the finding of the Federal Court in Repatriation Commission v Tuite(1993) 29 ALD 609, wherein the relationship between service and smoking was considered to be more than temporal and arose from all the incidents of service.
34. Three hypotheses were advanced to link Mr Laurie’s death with his war service. The third hypothesis was first raised during the course of the hearing and sought to link Mr Laurie’s known hypertension to the development of renal failure or impairment, which in turn had contributed to his death, one feature of his final illness being acute renal failure. As there was no SoP for renal failure, Mr Larkin contended that this relationship would need to be determined by the application of s 120(1) and s120(3) as interpreted by the High Court in Bushell.
35. Mrs Laurie relied on the reports of Professor Pitt, who was of the opinion that during Mr Laurie’s final illness there was evidence of myocardial ischaemia but not infarction and this was pointed to by a near six-fold rise in the level of serum Troponin Ι. She also relied on the opinion of Dr Collins, who had concluded that Mr Laurie’s death was due in part or in toto, to myocardial infarction.
36. Mr Larkin submitted that the requirements of Factor 5(a) or Factor 5(e)(iii) of the SoP concerning ischaemic heart disease (Instrument N° 53 of 2003) was met; or, in the alternative, Factor 6(a) or Factor 6(g)(iii) of the SoP concerning ischaemic heart disease (No 89 of 2007) were met. With respect to Mr Laurie’s development of hypertension, Factor 5(b) of the SoP concerning hypertension (No 35 of 2003 as amended by No 3 of 2004) was met.
37. Mr Rudge contended that the cause of death was overwhelming sepsis which was said to carry a mortality rate of 90 per cent. Mr Laurie’s development of atrial fibrillation and renal failure were merely manifestations of the overwhelming sepsis. The Respondent while conceding the quantities of cigarette smoked and alcohol imbibed as meeting the SoP requirements, did not accept that these habits were war-caused.
TRIBUNAL’S DELIBERATIONS
38. Mrs Laurie is the widow of John Laurie, who died on 27 February 2005. The veteran had operational service in the Army from 1942 to 1947. Mrs Laurie meets the preliminary criteria for consideration of her claim for widow’s pension (Hancock per Selway J).
THE KIND OF DEATH
39. The Tribunal finds, to its reasonable satisfaction, that the cause of Mr Laurie’s death was pneumonia leading to overwhelming sepsis with septic shock and multi‑organ failure, complicated by a probable inadvertent overdose of prescribed medication.
40. The term kind of death is a legal not a medical concept. There is considerable precedent dealing with the concept in the setting of widows’ claims for pension. In Repatriation Commission v Codd (2007), 95 ALD 619 Gordon J said:
[39] On the proper construction of the VE Act, consistent with its evident statutory purpose and existing authority, the “kind of death met by the [veteran]” that is to be considered is the question of medical causation or the kind of death, being a medical cause of death, including the contributing or underlying medical cause of death.
41. Mr Laurie’s death certificate states the cause of death to be left-sided pneumonia, with contributing factors listed as hypertension and smoker. Dr Collins considered the death certificate inaccurate in that it made no mention of myocardial infarction; and Professor Cade criticised the insertion, under part two of the certificate relating to contributing factors, of the term smoker. Smoking is not a disease; it is a habit unless it has progressed to the state of nicotine addiction. The Tribunal notes that the death certificate was completed on 28 February 2005 by a resident medical officer, probably an intern, who had not been involved with Mr Laurie’s medical treatment during his final hospitalisation on 27 February 2005.
42. It is well established that any contribution by a disease to the death is sufficient to satisfy the requirements of the Act and the death does not need to be attributable to the war‑caused disease. In Repatriation Commission v Law (1980) 31 ALR 140 the Full Court of the Federal Court said at 151:
It seems clear that the expression “attributable to” in each case involves an element of causation. The cause need not be the sole or dominant cause: it is sufficient to show “attributability” if the cause is one of a number of causes provided it is a contributing cause.
43. In Roncevich v Repatriation Commission (2005) 222 CLR 115 the majority of the High Court held at paragraph 27:
… A causal link alone or a causal connexion is capable of satisfying a test of attributability without any qualifications conveyed by such terms as sole, dominant, direct or proximate.
THE ISSUE
44. The issue for the Tribunal is whether any war-caused condition contributed to Mr Laurie’s death. Mr Laurie was diagnosed with hypertension in 1975, there being sporadic recordings of elevated blood pressure from 1961 onward, which was suggestive of labile hypertension. The hypotheses raised by Mrs Laurie were based on the existence of hypertension and/or ischaemic heart disease. The Respondent has conceded that the quantities of alcohol imbibed and cigarettes smoked by the veteran meet the requirements of the relevant SoPs but did not concede that these habits were war‑caused.
45. The Tribunal accepts that it is more probable than not, that Mr Laurie’s alcohol and smoking habits were war-caused. Mr Laurie was 19 years old when he enlisted in the Army in 1942, a time when the legal drinking age was 21; Mrs. Laurie believes that he commenced these habits in the Army and that he did so to relieve service related stress; and that both habits were well established when she met him in late 1946 or early 1947. He ceased smoking in 1980 but only reduced his alcohol intake in the late 1990s, when he developed gout.
The medical evidence
46. Dr Collins was of the opinion that Mr Laurie suffered a myocardial infarct on 27 February 2005 and that this hastened his death. The Tribunal is satisfied, based on the MMC clinical records and the opinions of Professors Cade, Pitt and Harper, that there is no evidence to support such a diagnosis although myocardial ischaemia short of causing infarction was probably present in the setting of documented atrial fibrillation and lowered cardiac output, both of which reduce coronary artery blood flow, regardless of the presence or absence of coronary artery disease.
47. The medical experts dealt with each of the clinical manifestations of Mr Laurie’s final illness, namely poor cardiac function, hypotension, atrial fibrillation, radiological chest x-ray findings, renal function impairment and terminal renal failure and serum Troponin levels. These factors were dealt with in regard to their diagnostic significance when seen in isolation. For example, Professor Harper said hypertension can cause hypertensive heart disease (left ventricular (LV) hypertrophy and strain leading to ventricular dilatation and dysfunction), precipitating atrial fibrillation but there was no evidence of cardiac enlargement in Mr Laurie’s case. Professors Harper and Cade addressed the medical evidence in a holistic manner and were of the opinion that, in combination, all of the clinical parameters pointed to overwhelming sepsis and septic shock and this diagnosis adequately explained all the separate clinical manifestations. The Tribunal accepts and agrees with their conclusion. It must however consider the contrary opinion of Professor Pitt, who was of the opinion that a degree of myocardial ischaemia short of causing a myocardial infarct had contributed by hastening Mr Laurie’s death. All the expert witnesses agreed that Mr Laurie would, at the age of 82, have CAD and a degree of IHD described by Professor Pitt as mild, by Professor Cade as quiescent and considered by Professor Harper to be asymptomatic and non-contributory.
48. It appears extremely likely that in his confused mental state, Mr Laurie took five days’ doses of his prescribed medication. Both Professors Harper and Pitt commented on the absence of bradycardia that would result from excess beta blocker medication. Mr Laurie was in rapid atrial fibrillation. The Tribunal notes that despite taking 50 mg of Metoprolol per day for many years, Mr Laurie’s pulse rate was monitored by MMC in March 2004 at between 67 and 88 (normal levels). The manufacturers of Metoprolol, in their product information, recommend that the daily dose of this drug should not exceed 320 mg. If Mr Laurie did take 250 mg on 27 February 2005 this would not be outside what is considered a therapeutic dose. In contrast 1500 mg of Avapro is well outside the therapeutic range and such a dose according to Professors Cade, Pitt and Harper would produce severe hypotension.
49. The Tribunal notes that upon Mr Laurie’s arrival in the Accident Emergency Department at MMC a definitive diagnosis was not made. The resident medical officer made provisional diagnoses of pneumonia or acute pulmonary oedema and instituted treatment in a very active manner to address both these possibilities. Within 30 minutes of Mr Laurie’s arrival the results of all major investigations were to hand and the decision was made that Mr Laurie was not for resuscitation. Thereafter, treatment was directed at making him comfortable. Intravenous antibiotics and Digoxin were continued but inotropic agents aimed at increasing blood pressure and cardiac output were ceased. The immediate cause of death was certified as left sided pneumonia. It is difficult to envisage that treatment would have been reduced in this manner if myocardial ischaemia or reversible acute renal failure, both of which are treatable conditions, had been considered a major contributory factor.
50. The Tribunal accepts that Mr Laurie at age 82 had mild ischaemic heart disease probably dating from 1997 but asymptomatic thereafter.
the hypotheses raised
51.In Repatriation Commission v Codd (2007), 95 ALD 619, Gordon J said at para 11:
The threshold question posed by s 120(3) is whether the whole of the material before the decision raises a reasonable hypothesis connecting the veteran’s death with the circumstances of his service,
and at para 12:
A reasonable hypothesis within s 120(3) of the VE Act is a hypothesis that is pointed to by the material before the decision-maker, and not merely left open (or not excluded) by that material.
In contrast the test posed in Bushell and East was couched in terms of some fact or facts (the ‘raised facts’). The raised facts have been interpreted on many occasions to be those supporting the hypothesis, with those opposing the hypothesis being considered under s120(1). The judgement of Brennan CJ in Repatriation Commission v Owens is said to have assuaged these conflicting interpretations when he stated the question is answered in reference to the whole of the material before the Administrative Appeals Tribunal.
53.Matters continue to be argued before this Tribunal based on the raised facts or fact and when unsuccessful, frequently succeed on appeal to the Federal Court. The correct approach remains a dilemma for the Tribunal. In the matter under consideration there is one fact which points to a reasonable hypothesis if one follows Bushell but fails in terms of being pointed to by the whole of the material.
54. The Tribunal is satisfied on the balance of probabilities that the hypothesis connecting pre-existing renal impairment or chronic renal failure to the development of acute renal failure on 27 February 2005 is flawed in that pre-existing chronic renal failure or renal impairment is not supported by the evidence before the Tribunal. On two occasions Mr Laurie had elevated creatinine levels; the first in 1997 when he was admitted to the Valley Private Hospital with chest pain and the second in the year 2000. On both occasions there were other factors contributing potentially to such an elevation in creatinine levels, on the first occasion he was obviously dehydrated and on the second occasion the pathology service reported technical faults with the blood sample. Subsequent estimations of serum urea and creatinine levels were normal. While there is no SoP relating to chronic renal failure, the RMA has defined chronic renal failure in the SoP concerning ischaemic heart disease Instrument No 53 of 2003 as:
“chronic renal disease” means renal injury of a sustained nature that is not reversible and leads to destruction of nephron mass and is associated with a demonstrable functional abnormality of the kidney which raises the level of creatinine
and in Instrument No 9 of 2004 concerning ischaemic heart disease, Instrument No 89 of 2007 concerning ischaemic heart disease and Instrument No 35 of 2003 concerning hypertension the definition has changed to:
“chronic renal failure” means irreversible kidney damage which leads to impaired renal function
Mr Laurie’s documented renal function tests do not meet these criteria as it was reversible. The Tribunal will not consider this hypothesis further.
52. Of the remaining hypotheses, one is complex in that it contains a sub‑hypothesis and in accordance with the decision of the Full Federal Court in McKenna v Repatriation Commission (1999) 86 FCR 144. The Tribunal must consider each sub‑hypotheses in order to assess the reasonableness of the hypothesis advanced.
APPLICATION OF THE STEPS IN DELEDIO
53. The Tribunal is required to test the hypothesis in accordance with the steps laid down by the Full Federal Court in Deledio.
STEP ONE OF DELEDIO
54.Two hypotheses were raised by Mrs Laurie.
55. The first is based on the acceptance of Mr Laurie’s alcohol consumption being war-caused leading to hypertension; the hypertension in turn resulted in the development of ischaemic heart disease and the latter contributed to his death. The second hypothesis related Mr Laurie’s cigarette smoking to the development of ischaemic heart disease; which in turn resulted in a myocardial infarction or ischaemia contributing to his death on 27 February 2005. Having examined all the material before the Tribunal, some of the material, namely the finding of the serum Troponin 1 level six times that of normal, points to a hypothesis connecting the disease and death with the circumstances of the service rendered by Mr Laurie. However, a consideration of the whole of the material does not support such a hypothesis.
Step Two Of Deledio
56. The Repatriation Medical Authority (RMA) has made determinations based on sound medical/scientific evidence that indicate that hypertension and death from hypertension and ischaemic heart disease and death from ischaemic heart disease can be related to relevant service rendered by a veteran.
57. Where such SoPs exist, the primary decision maker is required to apply the relevant SoP in force at the time of the application for pension. In Mrs Laurie’s case, these are the SoP relating to ischaemic heart disease (Instrument No 53 of 2003 as amended by Instrument No 9 of 2004) and the SoP concerning hypertension (Instrument No 35 of 2003 as amended by Instrument No 3 of 2004)
58. The Tribunal is required to give consideration to any relevant SoP determined by the RMA prior to the date of its decision. (Keeley, Gorton) New SoPs have been promulgated for hypertension and ischaemic heart disease since Mrs Laurie’s application. However, these do not substantially alter the factors that must as a minimum be related to any relevant service rendered by the Veteran. Instrument No 11 of 2008 (concerning hypertension) does increase the required quantity of alcohol consumed per week from 200 grams to 300 grams but Mr Laurie’s consumption meets this level and that of the earlier SoP.
59. The application is considered under the earlier SoP referred to above.
60. Mrs Laurie relies upon Factor 5(b) in Instrument No 35 of 2003.
consuming an average of at least 200 grams per week of alcohol which cannot be decreased to less than an average of 200 grams per week, at the time of the clinical onset of hypertension;
Mrs Laurie also relies upon Factor 5(a) in Instrument No 53 of 2003:
(a)the presence of hypertension before the clinical onset of ischaemic heart disease; …
(e)…
(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;
61. Mrs Laurie’s reliance on Factor 5(a) in Instrument No 53 of 2003 (the ischaemic heart disease SoP) is dependent upon the hypertension being caused by excessive alcohol consumption. It is a complex hypothesis involving both SoPs (McKenna).
STEP THREE OF DELEDIO
62. The Tribunal is required to determine whether the hypotheses raised are reasonable in terms of their consistency with the template to be found in the SoP. The Tribunal finds that the hypotheses raised fit the templates of the SoPs, there being present one or more factors which the authority has determined to be the minimum which must exist to relate the Veteran’s service to his death. While there are doubts regarding the presence of ischaemic heart disease the Tribunal at this point is not to indulge in fact-finding.
STEP FOUR OF DELEDIO
63. Mr Laurie’s hypertension has been well documented and in existence from at least 1975 and the requirement regarding alcohol consumption is met.
64. With respect to the diagnosis of ischaemic heart disease, the expert witnesses and his treating cardiologist agree that Mr Laurie had coronary artery disease. The evidence with respect to the existence of ischaemic heart disease is controversial. A degree of confusion has arisen from the use of these two terms synonymously. Professor Harper drew the distinction in his evidence between coronary artery disease and ischaemic heart disease. He explained that coronary artery disease is an anatomical description of the presence of atheromatous deposits (soft plaque) or atherosclerosis (hard plaque) in the coronary arteries. It was to be expected that an 82 year old male of average height and weight, who had smoked and consumed alcohol for decades, would have evidence of coronary artery disease. Coronary artery disease is a degenerative disorder which has been shown to commence as early as 18 years of age and in the majority of persons in western civilisation increases with the passage of time. SoP No 53 of 2003 defines ischaemic heart disease as a cardiac disability characterised by insufficient blood flow to the muscle tissue of the heart due to atherosclerosis, thrombosis, or vasospasm of the coronary arteries.
65. Thus ischaemic heart disease is a physiological concept relating to reduced coronary artery blood flow. Such blood flow does not decrease until there is stenosis or narrowing in the arteries greater than 70 per cent. (Bernoulli’s and Venturi’s Theories of Flow as applied to tubular structures).
66. The material before the Tribunal records that Mr Laurie suffered central chest and epigastric pain on two consecutive days in 1997 and was never again reported to experience this symptom. The treating cardiologist, Dr Krafchek, diagnosed coronary artery disease but not ischaemic heart disease, although he did initiate cardio protective drug therapy. All the expert witnesses considered it possible that the pain described by Mr Laurie could have been gastrointestinal or cardiac in origin. Investigation at the time showed no evidence of myocardial infarction and on thallium scanning there was no evidence of ischaemia.
67. If Mr Laurie did have ischaemic heart disease, it was quiescent in the opinion of Professor Cade and not present in 1997 in the opinion of Professor Harper. Professor Pitt considered Mr Laurie did have ischaemic heart disease but that it was probably mild.
68. Dr Collins in his oral evidence resiled from his written opinion that Mr Laurie had suffered a myocardial infarct. On reconsideration, he considered it probable that Mr Laurie experienced the lesser physiological insult of myocardial ischaemia. Dr Collins is a forensic pathologist. He is not a clinician. As such, and with due respect to him, his opinion does not carry the weight of the cardiologists and intensivists who are involved on a daily basis with the treatment of severely ill, decompensated patients. They have all opined that there was no evidence of myocardial infarction during Mr Laurie’s final illness. Such a diagnosis was not raised or even contemplated as a possibility in the MMC medical record.
69. The question is therefore whether there is evidence of myocardial ischaemia, that is reduced coronary artery blood flow, contributing to Mr Laurie’s death. There is evidence of cardiac muscle insult or reduced perfusion as reflected in the elevation of the serum Troponin Ι level, this test being specific for such damage. Professor Pitt quoted the opinion of Professor Schneider, who had advised that a level of 0.46 micrograms per litre was likely to be of cardiac origin.
70. The Tribunal accepts that Mr Laurie did suffer from ischaemia; but when his illness is viewed in the totality of the clinical setting, this ischaemia is the result, not the cause, of Mr Laurie’s cardiac decompensation, which in turn was a component of the multi-organ failure documented. Professors Cade and Harper both referred to their experience of seeing levels of Troponin Ι at 20 to 30 micrograms per litre in intensive care patients with serious life-threatening illnesses unrelated to a primary cardiac event.
71. The clinical picture present by Mr Laurie’s final illness was that of uncontrolled infection and septic shock affecting cardiac, renal, pulmonary and hepatic function, as indicated by a high white cell count and elevated CRP (C-reactive protein, an inflammatory marker), severe acidosis and the chest x-ray findings of pneumonia. The probable inadvertent overdose by Mr Laurie of his normal medication would have further contributed to hypotension resistant to treatment.
72. The Tribunal is satisfied beyond reasonable doubt (S120(1) of the Act) that any myocardial ischaemia suffered by Mr Laurie in his final illness was a result of overwhelming sepsis, not underlying mild ischaemic heart disease as defined in the SoP. Therefore, his death was not contributed to by any war-caused disease. It follows that the Tribunal must affirm the decision under review.
I certify that the seventy-two (72) preceding paragraphs are a true copy of the reasons for the decision herein of
Miss E A ShanahanSigned: ..Dianne Eva
ClerkDates of Hearing 10 March, 11 March & 23 March 2009
Date of Decision 25 May 2009
Counsel for the Applicant Mr A Larkin
Solicitor for the Applicant Ms U Noyé, Williams Winter Solicitors
Advocate for the Respondent Mr K Rudge, Department of Veterans' Affairs
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