Learhinan and Repatriation Commission - [2000] AATA 1155

DECISION AND REASONS FOR DECISION [2000] AATA 1155

ADMINISTRATIVE APPEALS TRIBUNAL )

) No S1999/444

VETERANS' APPEALS DIVISION       )
           Re      EILEEN AGNES LEARHINAN
  Applicant
           And    REPATRIATION COMMISSION
  Respondent

DECISION

Tribunal Senior Member W.H. Eyre

Date29 December 2000
PlaceAdelaide

Decision      The Tribunal finds that Mr Learhinan's death was not war-caused and affirms the decision under review.
  (Signed)
  W.H. EYRE
  (Senior Member)
CATCHWORDS
VETERANS' AFFAIRS – whether death was war-caused – whether veteran's conceded war-caused ischaemic heart disease contributed to veteran's death from leukaemia and septicaemia – hypotheses not "reasonable"
Veterans' Entitlements Act 1986 ss.8, 120
Repatriation Commission v Bey (1997) 47 ALD 481
Byrnes v Repatriation Commission (1993) 177 CLR 564
Critch v Repatriation Commission (1996) 43 ALD 574
Re Blyth and Repatriation Commission (AAT 714, 20 May 1982)

REASONS FOR DECISION

29 December 2000 Senior Member W.H. Eyre

Mrs Learhinan, the applicant, has applied to the Tribunal for review of a decision of the respondent made on 19 November 1998 and affirmed by the Veterans' Review Board (the VRB) on 14 September 1999 that the death of her husband, Kenneth Albert Learhinan, was not war-caused.
The Tribunal has before it the documents lodged pursuant to section 37 of the Administrative Appeals Tribunal Act 1975 (the T documents), the documents tendered by the applicant (Exhibits A1-A4) and the respondent's statement of facts, issues and contentions (Exhibit R1). Mrs Learhinan gave sworn evidence. Dr Leon Zimmet, cardiologist, gave evidence on affirmation for the applicant. Mrs Learhinan was represented by Mr Pickhaver, of counsel, and the respondent by Mr Doube.
Mr Learhinan, born 17 April 1924, served in the Royal Australian Air Force from 8 June 1943 to 25 March 1949. He served outside Australia. As he had operational service, sub-sections 120(1) and (3) of the Veteran' Entitlements Act 1986 (the Act) apply.
These provide, so far as relevant, as follows:
"(1)Where a claim under Part II for a pension in respect of … the death of a veteran, relates to the operational service rendered by the veteran, the Commission shall determine that the … death of the veteran was war-caused, … unless it is satisfied, beyond reasonable doubt, that there is no sufficient ground for making that determination.
…
(3)In applying subsection (1) or (2) 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:
…
(c) that the death was war-caused or defence-caused;
… 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 … death with the circumstances of the particular service rendered by the person."
Sub-section 8(1) of the Act, so far as is relevant, provides:
"(1)Subject to this section, for the purposes of this Act, the death of a veteran shall be taken to have been war-caused if:
…
(f)the injury or disease from which the veteran died is an injury or disease that has been determined in accordance with section 9 to have been a war-caused injury or a war-caused disease, as the case may be;
Note: The effect of paragraph (f) is that, if the veteran has died from an injury or disease that has already been determined by the Commission to be war-caused, the death is to be taken to have been war-caused. Accordingly the Commission is not required to relate the death to eligible war service rendered by the veteran and sections 120A and 120B do not apply.
but not otherwise."
Mr Learhinan died on 24 May 1998 at the Repatriation General Hospital, Daw Park. The death certificate (T5/47) gives the "Cause of Death" as "Septicaemia - Days. Chronic Lymphocytic Leukaemia - Years". An autopsy was performed on 25 May 1998. It states the "Cause of Death" as (T5/48):
"1.       Direct cause:
          Chronic lymphocytic leukaemia with lymphomatous change.
2.       Other significant conditions contributing to death:
          Septicaemia."
Mr Learhinan had no accepted war-caused disabilities at the time of his death. The applicant does not contend that Mr Learhinan's chronic lymphocytic leukaemia was war-caused. Rather, the applicant contends that Mr Learhinan suffered from ischaemic heart disease, that that disease was war-caused and, had Mr Learhinan's heart not been compromised by that disease, he would have been better able to resist infection, septicaemia and the leukaemia and lived longer.
Mr Doube, for the respondent, conceded at the commencement of the hearing that Mr Learhinan did suffer from ischaemic heart disease and had he claimed that as war-caused, given his history of smoking, it would have been accepted as a war-caused disease.
The issue before the Tribunal is thus whether the evidence and material before the Tribunal points to a reasonable hypothesis that Mr Learhinan's war-caused ischaemic heart disease contributed to or hastened his death. If there is a reasonable hypothesis so pointed to, the Tribunal must allow the appeal unless satisfied beyond reasonable doubt that there is no sufficient ground for making that determination.
background
Mr Learhinan was diagnosed with chronic lymphocytic leukaemia in 1991. Mrs Learhinan's evidence is that when it was diagnosed they were told that people with that disease "had gone on for 14-15 years and longer". Mr Learhinan had undergone courses of chemotherapy and received blood transfusions fairly regularly. Mrs Learhinan told the Tribunal that her husband's last admission to the Repatriation Hospital at Daw Park was for a blood transfusion. She was not aware that he was undergoing treatment for any other medical conditions or problems at that time and thought her husband had stopped chemotherapy prior to that admission. Mrs Learhinan did mention that the general practitioner was treating her husband for clots in his legs but she did not know whether they arose from leukaemia treatment. Mrs Learhinan told the Tribunal that her husband had appeared to be all right when she left him, but about 11pm that night she had been advised by telephone that he was in intensive care. She was told that it was expected that he would "turn for the better" but this did not happen.
Mr Learhinan's last admission was on 21 May 1998. The hospital Death Summary at T2/13 under Clinical Progress states:
"This 74 year old man with known Chronic Lymphocytic Leukaemia on Chlorambucil presented with dry retching mainly during the morning and daytime, some vomiting but no blood. Some associated diarrhoea twice a day. These symptoms seemed to have occurred following his chemotherapy.
Third day of admission he developed a febrile illness and became septic. He was referred to Intensive Care Unit, however course was further complicated by a probable aspiration pneumonia. He was intubated. Blood culture started growing staph and gram negative organisms. Despite the best of care he ultimately succumbed on the 24/5/98 at 2125 hrs."

That summary also describes "Secondary conditions as "Chronic Lymphocytic Leukaemia – diagnosed Oct 1995 (sic), Autoimmune Haemolytic Anaemia, (R) Deep Venous Thrombosis 29/8/97 – Warfarinised, Bells Palsy, Basal Cell Carcinoma, Chronic Renal Failure". The "Relevant Past History" is described as "(L) Nephrectomy for renal cell carcinoma in Feb 1993".

Mr Learhinan had previously been admitted to the same hospital on 5 May 1998. The hospital record (T2/11) states under Clinical Progress:
"This 74 year old man with known Chronic Lymphocytic Leukaemia and Autoimmune Haemolytic Anaemia was admitted through Haemotology Clinic for overnight blood transfusion. He was given 4 units of packed cells.
On examination he was jaundiced, hepatosplenomegaly, pale with tachycardia due to anaemia, but no fevers. He also had Cervical Lymph nodes, palpable on both sides.
Upon reviewing his blood picture, it is evident that his Chronic Lymphcytic Leukaemia is becoming resistant to Clorambucil. Therefore Dr Seshadri had a discussion with him for a second line chemotherapy, Fludarabine 25mg/M2 which is to commence on Monday 11/5/98."
As to Mr Learhinan's heart, Mrs Learhinan's statement (Exhibit A3) states:
"He suffered two heart attacks, one in 1950 and the other in 1956.
The heart attack that he had in 1950 occurred before we were married. He often told me that he had a lot of pain in his chest and that he had angina attacks.
He told me that his first heart attack occurred while he was at work in the mines in Broken Hill. I cannot recall if he told me about the circumstances relating to this heart attack. I do recall that he told me he obtained medical assistance and had some time off work.
After we were married we went to Broken Hill where he worked in the mines for five years. We then returned to South Australia, to Port Augusta for a short period of time before we then transferred to Adelaide where he worked for ETSA for 29 years until he retired.
I recall that he told me that when he had his first attack in 1950 that he was experiencing a lot of stress …
In 1956 he had another heart attack. He was under a lot of pressure because we had to move from Broken Hill to Port Augusta where he worked long hours in the Port Augusta Power House.
I was present when he had the second heart attack in 1956. We were working in the garden and I saw him slump down suddenly.
I rushed to my brother's home who lived close by and he took him to the hospital. We were told by the doctors that he had a hardening of the arteries and there was nothing that could be done. He was given angina tablets to take in the event of another attack.
…
I recall that he spent a lot of time going in and out of hospital since his kidney was removed in 1992. He was having a lot of blood transfusions.
He then had two weeks of chemotherapy prior to his death on the 24th of May 1998. His blood cell levels decreased and as a result he had to have a blood transfusion. During this time he contracted septicaemia and died in intensive care.
During our marriage, I recall that my husband had experienced a lot of chest pains particularly in the later years and that he was always out of breath."

The Statement of Principles (SoP) concerning Ischaemic Heart Disease (Instrument No. 140 of 1996, as amended by No. 77 of 1997 and No. 37 of 1998) provide (since 29 May 1998):
"'death from ischaemic heart disease' in relation to a person includes death from a terminal event or condition that was contributed to by the person's ischaemic heart disease;";
…
"'terminal event' means the proximate or ultimate cause of death and includes:
a)         pneumonia;
          b)        respiratory failure;
          c)        cardiac arrest;
          d)        circulatory failure; or
          e)        cessation of brain function.".
The Tribunal notes that the definition of death from ischaemic heart disease is an "includes" definition and that it, in the Tribunal's opinion, contemplates that death may be from a "condition" or from a "terminal event" and that the contribution from ischaemic heart disease may be either to the "condition" or to the "terminal event".
The Tribunal has already referred to the causes of death stated on the death certificate and autopsy report (paragraph 6 above). The autopsy report (T5/48) gives as "Major Pathological Findings", the following:
"1.Extensive lymphadenopathy involving mediastinal, cervical, para-aortic and mesenteric groups of lymph nodes. Lymph nodes measuring up to 50mm in diameter.
2. Pulmonary infarct in the right lower lobe of the right lung.
3.Hepatosplenomegaly, both liver and spleen having a mottled appearance, and a splenic infarct."

Under "Cardiovascular System" appear the following findings:
"The heart weighed 440g. There was fibrotic scarring of the anterior wall of the left ventricle, typical of old myocardial infarction. The heart chambers were normal in size and there were no valvular lesions. No fluid was present in the pericardial cavity. The coronary arteries showed a mild degree of atherosclerosis. The thoracic and abdominal aorta showed a moderate degree of atherosclerosos with calcified plaques."

Under "Reticulo-Endothelial System" the doctors observe:
"…
Extensive lymphadenopathy was present involving the mediastinal, cervical, para-aortic and mesenteric groups of lymph nodes. The lymph nodes measured up to 50mm in diameter and the mediastinal nodes were compressing the superior vena cava."

Under "Clinicopathological Correlation" Dr Somers and Dr Rozenbilds note:
"Mr Kenneth Learhinan was a 71 (sic) year old man with chronic lymphocytic leukaemia. During his admission for treatment of anaemia he became febrile and progressively deteriorated. Gram negative septicaemia was confirmed on blood cultures. Autopsy findings showed extensive lymphadenopathy, with mediastinal lymphadenopathy resulting in SVC obstruction. Histological examination confirmed lymphomatous change with infiltration of the liver and spleen. The findings of pulmonary and splenic infarction with ischaemic changes in the kidney and lymph nodes indicates that abnormal proliferation of lymphoid cells resulted in hyperviscosity of the circulating blood and subsequent widespread hypoperfusion.
Mr Kenneth Learhinan died as a result of chronic lymphocytic leukaemia with lymphomatous change and septicaemia."

dr zimmet's evidence

Dr Zimmet is a specialist cardiologist with 27 years experience. He did not treat or examine Mr Learhinan but was given, prior to the hearing, various documents prepared for the VRB hearing which included the autopsy report (T5).
In Dr Zimmet's report of 16 March 2000 (Exhibit A2) he states:
"…
Although I can see no reference to a previous myocardial infarct in his past medical history, significantly at autopsy it was noted that there was fibrotic scarring of the anterior wall of the left ventricle, typical of an old myocardial infarction.
Thus on the basis that this gentleman had a past myocardial infarct, it is possible that this myocardial infarct may have rendered him more susceptible to the effects of an overwhelming septicaemia with sudden death and in view of this it is possible that the previous damage to the heart from this myocardial infarct may have been a factor in his subsequent death."

Dr Zimmet was asked in examination-in-chief:
"In terms of the operation of the heart, what does fibrotic scarring in lieu of normal tissue mean to the heart condition and function?"

and answered:

"Well, I guess that there is (sic) two affects. It really depends on how much scarring there is but when you do have a scar on the heart, you are certainly more liable at times to develop various rhythm disturbances because that area where the scar tissue and the normal cardiac tissue meet, as it were, can be a little unstable which may make the heart rhythm susceptible to arrhythmia or abnormal rhythms and if it is a large area of scar tissue, they may be more susceptible to develop heart failure where the heart pump is not as efficient as normal."

Later in his evidence-in-chief Dr Zimmet stated:
"… I guess having developed septic shock, the mechanism of ultimate death is not immediately apparent from what I can see although often people, of course, die in this situation from what we call cardiac arrhythmia where the heart goes out of rhythm, they develop fibrillation. In the setting of a scarred heart you would be more likely than not to develop fibrillation than if the heart were normal."

In cross-examination Dr Zimmet was asked:
"… the myocardial infarct has been dated to 1956 and the veteran has continued since that time with no treatment for heart irregularities in the interim. That is not an uncommon finding in someone who has had a heart attack a long time ago, is it?"

Dr Zimmet replied:

"I think he is fortunate, I mean, with actual history of heart disease is that if he had 40 years of good health following an infarct would be fortunate for him, suggesting that the infarct was not a great infarct, again, he still does have scar tissue there."

The Tribunal sets out the following from Dr Zimmet's examination-in-chief:
"Q: Am I right also – again this is a lay question – is it necessary for the body to efficiently distribute these T cells throughout the body by means of the heart, veins and arteries?
A: Well, yes. I guess the cardiac output is responsible for distributing the blood around the body, yes.
Q: … what affect is there on that distribution if the heart has fibrotic scarring?
A: I mean, it depends on how much fibrotic scarring there is. If the cardiac output is reduced, well, then the delivery of blood cells to the rest of the body is also reduced.
…
Q: I will come to the issue of septic shock in a minute but if the distribution of the blood is reduced, as you are suggesting, does that mean his ability to withstand the infection is also reduced?
A: Yes"
Dr Zimmet was clear that Mr Learhinan had developed septicaemia and then septic shock. He explained septic shock as "really a condition where you develop quite severe, I guess, general organ failure related to the severe infection. The bacteria produce a lot of toxic substances which have affect on blood pressure, on the heart, on the brain and really on almost all organs of the body".
Dr Zimmet was asked:
"If his heart had not had the fibrotic scarring, can you give the Tribunal any guidance as to how he may have coped with the infection?"

He replied:

"Well, again I think, in an overwhelming infection, occasionally even if the heart is normal, you know, if the infection is so overwhelming the blood pressure can also drop in that situation as well, so it [sic] there is a relative difference between a scarred heart and a normal heart with severe septic shock. I mean, the condition that is getting a lot of publicity at the moment, of course, is meningococcal infection which often occurs in younger people also can cause quite overwhelming septic shock and impair peripheral circulation."

Asked "Are you able to say whether a person with an unimpaired or undamaged heart … is better able to withstand septic shock", Dr Zimmet replied "Certainly. I think if the heart is normal, you would expect a better prognosis than if you had had a previous heart attack".
Later Dr Zimmet said: "I would say that the effect of the low blood pressure and reduced diffusion to the heart because of septic shock, the scarred heart would be more at risk than the normal heart" and agreed that "Mr Learhinan was more likely to succumb to the septic shock than if he had had a normal or non compromised heart". Dr Zimmet said: "Although, as I have said, people with severe septic shock who had normal hearts can die from septic shock but I think having a damaged heart would suggest that the chances of survival are reduced". Dr Zimmet also said that a normal heart would respond better to drugs used to stimulate the heart and raise blood pressure which the Tribunal understands to be part of the usual treatment for septic shock.
In cross-examination Dr Zimmet agreed that septicaemia was a life threatening condition and particularly so in a person whose immunity was reduced and whole system impaired by leukaemia. He said:
"… the hypothesis that has been put forward is the fact that it is possible this gentleman was going to die anyhow from his overwhelming septicaemia but the fact that he had a previous myocardial infarct possibly rendered him more likely than not. I mean the pathologists are really giving us the main cause of death which, of course, related to the overwhelming septicaemia he got because he had leukaemia, but the actual mechanism of his final death one would assume related to his severe low blood pressure and, as I have said, a compromised heart, a damaged heart, is going to be at more risk of coping with septicaemia than a normal heart."

Mr Doube referred Dr Zimmet to the fact that there was no mention at all of the ischaemic heart disease on the admission notes or death certificate. Dr Zimmet responded:
"No. I think there's, you know, this is getting to the situation whereby there's obviously a difference from the medical point of view and the medico-legal point of view whereby the cause of death is overwhelming infection which, of course, is related to his chronic lymphatic leukaemia. What hasn't been added, of course, is the possibility what other contributions may have contributed to his death."
Asked whether there was any evidence of heart failure, Dr Zimmet replied:
"Hard to say because heart failure really is more of a clinical condition. They don't mention any fluid. Well, the lungs we congested which may suggest there might have been fluid in the lungs which may – could be a heart failure, but heart failure is more a diagnosis one tries to make during life rather than pathologically, but congestion of the lungs would be consistent with heart failure."
Asked whether the lung condition was the final event, Dr Zimmet replied that this was possible but noting the comment in the autopsy report that no pulmonary emboli were present he said: "I guess where it plays a part in the death it's hard to delineate". Later he indicated that it was possible that Mr Learhinan died of acute heart failure because of clots on the lung – "The heart has not been able to pump blood into the lungs because of the clots that have developed within the lungs, so they develop acute right heart failure and die because of that".
Dr Zimmet was asked: "Is there anywhere in that report that indicates what was occurring just prior to death?". He replied: "No, not that I've got hold of".
Dr Zimmet, in response to a question from the Tribunal said that Mr Learhinan had "chronic renal failure so certainly that kidney, that left nephrectomy which he obviously would appear to have impaired his renal function would also I guess be a factor in his demise".
Mr Doube put to Dr Zimmet at the conclusion of his evidence to the Tribunal: "and when you were talking about the possibilities the conjecture for these sorts of things, you are not saying that the evidence here supports one ahead of the other, are you? You are talking about these as (or "are") possibilities?". Dr Zimmet replied: "Yes".
the applicant's submissions
The applicant referred the Tribunal to Repatriation Commission v Bey (1997) 47 ALD 481, distinguishing it on the facts, and pointing to the approach taken by the majority at p484, the now well established method of applying sub-sections 120(1) and (3). Mr Pickhaver pointed to the passage at p485 that "In some cases the hypothesis may assume the occurrence or existence of a "fact". That does not itself make the hypothesis unreasonable : Byrnes v Repatriation Commission (1993) 177 CLR 564 at p570 and Critch v Repatriation Commission (1996) 43 ALD 574 at p577.
The applicant also referred the Tribunal to the judgment of Nicholson J in Bey at p492-493:
"…
In my view, a proper understanding of the application of s 120(3) as enunciated by the High Court in Bushell and Byrnes is clouded by the negative characterisation of evidence as "a mere possibility". That description leaves unexplained what constitutes such evidence. It is preferable to approach the application of the subsection in the manner made apparent in the decisions of the High Court, that is, by searching for "material" which "raises" a reasonable hypothesis.
There may be circumstances in which evidence of a hypothesis by a suitably qualified expert founded upon some grounds whether in medical literature or experience may adduce evidence being material from which a reasonable hypothesis can be found to arise. Such evidence may be capable of description as being a "mere possibility", yet may raise a hypothesis within the principles stated in Bushell and Byrnes. That is why the general description of evidence as "a mere possibility" is not helpful in that it clouds the distinction between a hypothesis raised by the material and a hypothesis of which there is evidence that it cannot be excluded but which is not otherwise raised.
…"
Later, in summary at p493, Nicholson J expressed his referred approach thus:
"…
(1) A "mere possibility", in the sense of a hypothesis advanced, for example, by a medical practitioner speaking within the ambit of his expertise, will ordinarily raise a reasonable hypothesis. The evidence of expertise will provide the acceptability or credibility to the hypothesis even if the evidence is the hypothesis cannot be excluded : Bushell at CLR 414 and 430. While eminence in such field alone, in a case where the medical opinion is no more than to the effect the possibility of causation of the morbid condition by the nature of the service cannot be excluded, is close to a hypothesis unsupported by any evidence, it will, however, be a matter of judgement whether the eminence is such as to give rise to raised facts.
(8) A "mere possibility", in the sense of a hypothesis unsupported by any evidence of a witness with appropriate expertise to give it acceptability or credibility, cannot qualify as a reasonable hypothesis – it will not be a hypothesis "raised by the facts".
…"
Mr Pickhaver, for the applicant, also referred the Tribunal to Re Blyth and Repatriation Commission (AAT 714, 20 May 1982) a decision of the Tribunal comprised by Morling J Deputy President), Mr Mahony and Dr Garlick at p22 per Morling J:
"If the applicant's death was hastened because of the accelerated progress of his cancer, which acceleration was itself caused by war-related ill health, we think that the proper conclusion would be that his death was attributable to his war service within the meaning of s 101(1)(b) of the Act."
The Act there referred to was the Repatriation Act 1920. Nonetheless the Tribunal would accept that "acceleration" would amount to a "contribution" as the SoP provides.
Mr Pickhaver submitted that Dr Zimmet's evidence raises as a reasonable hypothesis that Mr Learhinan's death was hastened by the consequences of myocardial infarction from war-caused ischaemic heart disease. If Mr Learhinan had not had a heart compromised by ischaemic heart disease, by previous myocardial infarction, he would have been better able to resist the septicaemia and lived longer. He specified three factors as part of an hypothesis, namely that Mr Learhinan would have had more capacity to prevent or resist septic shock, more capacity to counter the effect of reduced circulation by lowered blood pressure caused by septic shock or that the treatment given to him would have been more effective had his heart not been compromised. He invited the Tribunal to find any one or more of these as sufficient to amount to a reasonable hypothesis.
respondent's submissions
The respondent submitted that Dr Zimmet's evidence was of mere possibilities, of conjecture. Mr Doube submitted that on the evidence available it is not possible to say one way or another whether the conjecture occurred or not. Mr Doube referred to the lack of references to Mr Learhinan's heart or heart condition in the material before the Tribunal pertaining to Mr Learhinan's hospital admissions, in the Repatriation Hospital clinical notes from 17 March 1992 to January 1995 in T14, and to noted "complications" in respect of his final and penultimate admissions. He submitted that the autopsy findings in relation to Mr Learhinan's heart were essentially incidental and that there was nothing to suggest Mr Learhinan's previous infarct was a significant factor contributing to his death.
Mr Doube referred to Dr Zimmet's evidence, particularly that set out at paragraph 36 above, as putting forward only possibilities and conjecture. He submitted that an hypothesis merely left open cannot be a "reasonable" hypothesis and that this was the situation here. Mr Doube argued that given the overwhelming nature of septicaemia on a person whose condition was severely compromised by leukaemia, whether or not Mr Learhinan had a good or uncompromised heart, he was unlikely to have survived. Mr Doube submitted that the evidence suggested that any contribution from ischaemic heart disease fibrotic scarring was de minimis. Nowhere in the hospital or autopsy documents is there any mention of Mr Learhinan's impaired heart in the progress of the condition that caused his death. Nor is there any material indicating what was happening either as to treatment or physical signs just before Mr Learhinan's death.
the hypotheses
There is no shortage of hypotheses in this matter. In addition to those referred to in paragraph 4 above, Dr Zimmet also raised the hypothesis of arrhythmia and if the fibrotic scarring was extensive of heart failure.
are any of the hypotheses reasonable, pointed to by the evidence?
As the Tribunal understands the authorities, including Bey, the fact that an expert medical practitioner testifies as to possible causes does not make an hypothesis reasonable unless the evidence taken as a whole points to, that is points to some (albeit very slight) degree to the presence of the hypothesised cause in the particular case.
As mentioned above there is no material which indicates what was happening, in terms of detailed treatment or physical signs, just before Mr Learhinan's death. Dr Zimmet stated that "the mechanism of ultimate death is not immediately apparent from what I can see". In cross-examination he stated that "the actual mechanism of his final death one would assume related to his severe low blood pressure". It is also clear from his evidence that "septic shock is a condition where you develop quite severe organ failure related to the severe infection. The body produces a lot of toxic substances which have an effect on blood pressure, on the heart, on the brain and really on almost all organs of the body".
The Tribunal finds that the material before it does not point to any one or more particular "terminal events" in Mr Learhinan's case. Accordingly, the Tribunal finds that the hypotheses relating to "death from a terminal event contributed to by Mr Learhinan's ischaemic heart disease "are not reasonable".
The definition of "death from ischaemic heart disease" is defined by the SoP to include "death from a … condition that was contributed to by the person's ischaemic heart disease". Mrs Learhinan has testified that her husband told her that he had had angina attacks and she stated he "had experienced a lot of chest pains particularly in the later years and that he was always out of breath". Without reflecting in any way on Mrs Learhinan's credibility, there is nothing by way of medical opinion or hospital notes that raise connection between angina and Mr Learhinan's death. The connection that has been propounded is based on Mr Learhinan's old myocardial infarction and the resultant fibrotic scarring.
The Tribunal agrees with the respondent's submission that the cause, the "contribution", that must be pointed to by the evidence must be a contribution that is more than a de minimis contribution.
The Tribunal accepts Dr Zimmet's view that the omission of any mention of Mr Learhinan's heart condition on admission details is not something which should be given much weight. Nonetheless, it appears from the evidence, that Mr Learhinan's ischaemic heart disease was not having any obvious affect on him in his last years. Also, the extent of the fibrotic scarring is not known and the autopsy report does not propound Mr Learhinan's heart as a cause of his death.
The applicant acknowledges that Mr Learhinan's leukaemia was a much greater factor in his death than his compromised heart, but submits that the material, the fibrotic scarring and Dr Zimmet's evidence based on that, points to Mr Learhinan's compromised heart as a factor in his death. The applicant acknowledges that issues relating to Mr Learhinan's lung may or may not have been a factor in his death. Dr Zimmet acknowledged that Mr Learhinan's chronic renal failure would have played some part.
The Tribunal must find the evidence before it points to Mr Learhinan's compromised heart, his war-caused ischaemic heart disease, as having had a role to play whether by way of its effect on circulation, on the septic shock or on the ability to withstand that shock, or on Mr Learhinan's ability to respond to drugs apparently given to maintain his circulation before it can find these hypotheses (or any of them) to be "reasonable".
The Tribunal has closely considered the evidence, particularly Dr Zimmet's. At the end of the day the Tribunal's conclusion is that the hypotheses are not pointed to – rather they are possibilities left open by the evidence. Given the overwhelming nature of the septicaemia and the leukaemia it is the Tribunal's conclusion that the evidence does not point to Mr Learhinan's ischaemic heart disease having contributed to his death other than at most to a de minimis extent with other factors. In the Tribunal's opinion this does not signify as a "reasonable" hypothesis connecting his death to his ischaemic heart disease.
The applicant has not pursued Mr Learhinan's leukaemia as war-caused. For completeness, having regard to the applicable SoP, the Tribunal finds that Mr Learhinan's chronic lymphoid leukaemia was not war-caused.
For the reasons given above, the Tribunal finds that Mr Learhinan's death was not war-caused and affirms the decision under review.
I certify that the 56 preceding paragraphs are a true copy of the reasons for the decision herein of Senior Member W.H. Eyre
Signed:         .....................................................................................
  Personal Assistant
Date/s of Hearing  20 October 2000
Date of Decision  29 December 2000
Counsel for the Applicant        Mr Pickhaver
Solicitor for the Applicant         Mr G. Hemsley
Counsel for the Respondent    Mr G. Doube
Solicitor for the Respondent    DVA