Annette Thompson and Military Rehabilitation and Compensation Commission

[2015] AATA 171

[2015] AATA 171  

Division	GENERAL ADMINISTRATIVE DIVISION
File Number	2013/1896
Re	Annette Thompson
APPLICANT
And	Military Rehabilitation and Compensation Commission
RESPONDENT

DECISION

Tribunal	Deputy President P E Hack SC Dr M Sullivan, Member
Date	25 March 2015
Place	Brisbane

The decision under review is affirmed.

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Deputy President P E Hack SC

CATCHWORDS

COMPENSATION – where an injury to an employee results in death – rheumatic fever an accepted “injury” – contracted during military employment – evaluation of causal chain – relationship between rheumatic fever and later cardiac conditions – acute myocardial infarction – whether aortic dissection – paucity of imaging and post-mortem evidence – “uncommon condition” – decision under review affirmed

LEGISLATION

Safety, Rehabilitation and Compensation Act 1988 (Cth)

SECONDARY MATERIALS

International Registry of Acute Aortic Dissection (IRAD)

REASONS FOR DECISION

Deputy President P E Hack SC
Dr M Sullivan, Member

25 March 2015

Introduction

1. Mrs Annette Thompson is the widow of Mr Gerald Thompson.  Mr Thompson served in the Australian Army between August 1950 and February 1951.  He died in September 2008.

2. Mrs Thompson says that Mr Thompson’s death was the result of an injury suffered by him during his service in the Australian Army and that she is thus entitled to death benefits under the Safety, Rehabilitation and Compensation Act 1988 (Cth) (the SRC Act).

3. The respondent, the Military Rehabilitation and Compensation Commission, refused Mrs Thompson’s claim.  It determined that, whilst Mr Thompson suffered an “injury” in the course of his service, there was insufficient evidence to link that injury to any of the causes of his death.

4. Mrs Thompson seeks a review of the Commission’s decision to reject the claim.  For the reasons that follow we have concluded that the decision was correct and ought be affirmed. 

   Factual background

5. Mr Thompson was born in 1932.  For all of his adult life, he suffered cardiac problems commencing when he contracted rheumatic fever at 18 years of age whilst at an Australian Army Camp. There is excellent Army documentation that Mr Thompson contracted rheumatic heart disease whilst at Puckapunyal in September 1950 and was discharged as medically unfit because of that condition in February 1951.

6. Mr Thompson was operated on at Prince Charles Hospital by Dr Mark O’Brien in November 1986 after enduring reduced cardiac functioning for many years. When Dr O’Brien replaced Mr Thompson’s aortic valve, he commented in his operating notes that the mitral and aortic valve were damaged in a way that was consistent with rheumatic heart disease but he decided only to operate on the aortic valve.

7. Mr Thompson was a smoker, was hypertensive and continued to attend the Cardiology Outpatients Department at Prince Charles Hospital after his successful valve replacement because of cardiomyopathy and dilated aortic root and ascending aorta.

8. Mr Thompson died on the morning of 20 September 2008 aged 76 years.        

   The legislation

9. Given the way in which the parties approached the case no detailed analysis of the legislation is required. Mr Thompson died in 2008 and accordingly liability to pay compensation for his death arises under the SRC Act, the legislation then in force. Compensation for injuries resulting in death is dealt with in Division 2 of Part II of the SRC Act. Liability to pay compensation in the case of death is imposed by s 17(1) of the SRC Act in these terms:[1]

   This section applies where an injury to an employee results in death.

   [1]Liability to pay compensation for funeral expenses is imposed by s 18(1) of the Act in relevantly identical terms.

10. The case for Mrs Thompson is that the relevant “injury” was rheumatic fever which Mr Thompson suffered from in and around October 1950 during the course of his Army service. That brings into play the transitional provisions of the SRC Act and an earlier version of the legislation however it is unnecessary to examine those provisions given that the Commission accepts that rheumatic fever constitutes an injury for the purposes of s 17 of the SRC Act.

11. The sole issue is whether Mr Thompson’s death resulted from the rheumatic fever, i.e. whether the injury resulted in Mr Thompson’s death.

    The medical background

12. That question falls to be determined on the basis of the views of two highly qualified cardiologists, Dr Kenneth Hossack, called by Mrs Thompson, and Dr Adam Cannon, called by the Commission. They, and we, had the benefit of a considerable body of medical evidence including extensive notes of Mr Thompson’s treatment at the Caloundra Hospital in the hours prior to his death. From those notes it emerges that Mr Thompson was taken by ambulance to the Caloundra Hospital Emergency Department on the night of 19 September 2008.

13. He was complaining of central chest pain which radiated to his back. His blood pressure was low, he was sweaty and distressed. The initial diagnosis was an acute coronary syndrome but aortic dissection was considered as very possible. Like all blood vessels, the aorta is a tube which has many concentric layers. If there is a tear in the inner lining of the aorta, blood can to be forced along the other tissue planes of the multiple layers causing severe central chest pain. Ultimately this will block off the blood supply that the aorta carries to the rest of the body and if the blood tracks into the sac (known as the pericardium) surrounding the heart, the heart is not able to contract fully. Aortic dissection is common in those with high blood pressure and other connective tissue disease which affect the integrity of the aorta. The diagnosis is really only confirmed by medical imaging such as CT, MRI or echocardiography, or post-mortem examination.

14. As Mr Thompson had had previous cardiac surgery and ongoing cardiac consultations at Prince Charles Hospital, that hospital was contacted on the night of his presentation. Information was relayed that Mr Thompson had dilated cardiomyopathy and a dilated aortic root of the ascending aorta as well as the previous aortic valve replacement.[2]

    [2]Exhibit 2, page 234.

15. A CT scan at the Nambour General Hospital to confirm the diagnosis was arranged as Mr Thompson’s chest X-ray did not show any mediastinal widening which is a strong but not absolute indicator of an aortic dissection. The CT scan was not able to be performed prior to Mr Thompson’s death. From the notes at Caloundra Hospital[3] it appears aortic dissection as a diagnosis was discussed with the family and the poor prognosis in Mr Thompson’s case was explained.

    [3]Exhibit 2, page 237.

16. Mr Thompson’s troponin level rose. Troponin levels in the blood rise when the heart muscle is damaged. There is a relationship between the amount of troponin and the amount of damage. It is highly indicative of a myocardial infarction but some other cause of damage to the heart can cause it to rise. The ECG was consistent with an inferior myocardial infarction.

17. There is, in the material, evidence of Mr Thompson’s haemoglobin levels in the period prior to his death. We should say immediately that there are two types of results, results determined after an analysis at a laboratory and “calculated haemoglobin”, a rapid assessment on a blood gas machine.[4] It is material to note, first, that a laboratory test of Mr Thompson’s haemoglobin was undertaken on 10 September 2008 providing a reading of 80g/L.[5] There is no reason to doubt the accuracy of that reading. The reading is low but it is consistent with a further laboratory test on a sample taken at 9 pm on 19 September 2008 when Mr Thompson was in the Caloundra Hospital which showed a reading of 78g/L.[6] A calculated haemoglobin test performed, presumably in the Emergency Department, on a sample collected at 9.54 pm gave a reading of 102g/L. Given the earlier reading, laboratory analysed, of 78g/L and the consistency with the 10 September 2008 result, the 9.54 pm result must be open to considerable doubt. Dr Cannon thought that result quite odd and difficult to explain. Dr Hossack seemed not to disagree in his oral evidence but made the point that what was needed was a comparison within test types. Finally, another calculated haemoglobin test was undertaken on a sample taken at 8.52 am on 20 September 2008, shortly prior to Mr Thompson’s death. It showed a reading of 75g/L. It is also material to note that blood was ordered through the night for Mr Thompson and he was given two bags of packed cells and also some IV fluids in the early hours of the morning.

    [4]It was described in this way in the hearing by Dr Cannon however the clinical notes (see, for example, page 156 of exhibit 2) suggest that it was a different device, an i-STAT machine. The difference seems not to matter.

    [5]Exhibit 2, page 387.

    [6]Exhibit 2, page 153.

18. Mr Thompson died on the morning of 20 September 2008. The death certificate, signed by Dr G van Wyk on 23 September 2008,[7] gave as the cause of death:

    [7]Exhibit 2, page 124.

    1(a) Dilated cardiomyopathy

    1(b) Aortic valve disease

    1(c) Mitral valve disease

    1(d) Ischaemic heart disease

    2     COPD [chronic obstructive pulmonary disease]

    This death certificate was later amended by the same doctor who then recorded the causes of death as:[8]

    1(a) Aortic dissection

    1(b) Aortic valve disease

    1(c) Ischaemic heart disease

    1(d) Dilated cardiomyopathy

    1(e) Mitral valve disease

    2     COPD

    Dr van Wyk had been in attendance at Caloundra Hospital during Mr Thompson’s final illness. There is no information available about the reason for the amendment of the death certificate and the addition of aortic dissection as primary cause of death.

    [8]Exhibit 2, page 123.

    The medical opinions

19. Dr Hossack and Dr Cannon provided reports and gave concurrent evidence about the relationship between Mr Thompson’s rheumatic heart disease and his death on 20 September 2008. Both agree that Mr Thompson died from an inferior myocardial infarct but the cause and precipitants of the infarction is in dispute.

20. Dr Hossack said that the differential diagnosis of aortic dissection causing chest pain on 19 September 2008 was correct and consistent with Mr Thompson’s clinical picture.

21. In his opinion, Mr Thompson had an extension of the aortic dissection to the origin of the right coronary artery (cutting off the blood flow), which then caused an inferior myocardial infarction giving the characteristic ECG changes on Mr Thompson’s tracing and his rising troponin levels. The consequence, he says, was that the inferior myocardial infarction was the direct result of an aortic dissection which came about from damage to the wall of the aorta from years of disturbed functioning of the heart and heart valves.

22. The episode of rheumatic fever in 1950 caused the damage to the aortic and mitral valves and over many years also to the wall of the aorta predisposing Mr Thompson to an aortic dissection as he aged and, ultimately, an inferior myocardial infarction.

23. Dr Hossack was satisfied that the last presented report of moderate aortic root and ascending aorta dilation in the Prince Charles Department of Cardiology letter of 9 January 2006[9] most likely came from damage which started before the replacement of the affected aortic valve and continued after the aortic valve replacement.

    [9]Exhibit 2, page 200.

24. For Dr Hossack, the damage to, and disturbed functioning of, the heart valve was a direct consequence of contracting rheumatic fever whilst serving in the Army. The ongoing documented weakening of the aortic root and ascending aorta has its origins in the changed haemodynamics and stress on the integrity of the aorta. This, he considers started at 18 years of age.

25. Dr Hossack summarises his opinion in this way:[10]

    I am convinced that the pre-existing history of cardiac surgery, dilated aortic root, dilated ascending aorta, abnormal chest X-ray, ECG evidence of inferior infarction, Troponin elevation and evidence of blood loss indicates that Mr Thompson died as a result of complications from an aortic dissection.

    [10]Exhibit 5, page 8.

26. Dr Cannon in his final report of 24 September 2014 sums up his opinion with the comment that the clinical picture,

    … does not definitively exclude a possible aortic dissection but the absence of any corroborating positive clinical features makes that diagnosis very difficult to sustain. There is however incontrovertible evidence of a classic inferior ST elevation myocardial infarction.

    Dr Cannon says that an aortic dissection is highly unlikely to have occurred and, if it did, then other factors are responsible for its occurrence. Dr Cannon, in oral evidence, stated that once a diseased aortic valve is replaced, haemodynamic factors do not continue to weaken and dilate the aorta. He stated that this was supported by current research.

27. According to Dr Cannon, Mr Thompson’s age, long term history of smoking and hypertension are satisfactory reasons for his continued aortic dilatation. Furthermore, Dr Cannon stated that the cardiac surgeon, Dr Mark O’Brien, made no mention of aortic dilatation in his operating notes.

28. Therefore, for Dr Cannon, Mr Thompson’s continuing aortic dilatation is not related to his rheumatic valvular disease and replacement, and any putative aortic dissection brought about by aortic dilation is not related to rheumatic heart disease. Dr Cannon said that there was no objective evidence that Mr Thompson suffered an aortic dissection. There was no definitive radiological imaging and no post-mortem examination. He disputed that the chest X-ray of the night of 19 September 2008 showed anything other than the expected unfolding of the aorta and that there was no widening of the mediastinum which would point towards an aortic dissection.

29. He rejected the view of Dr Hossack that Mr Thompson’s lack of change in his haemoglobin after being given two units of packed cells was proof of an aortic dissection. Dr Cannon said that the picture of Mr Thompson’s haemoglobin levels on the night and early morning when he died was complicated by the fact that Mr Thompson was also given intravenous fluids. He considered that the haemoglobin result of the test on the sample taken at 9.54 pm on 19 September 2008 (102g/L) was likely to be incorrect given the laboratory result of 78g/L from the test of the sample taken a little earlier at      9 pm and given that one week earlier Mr Thompson’s haemoglobin, when ordered by his general practitioner, was 80g/L. He felt that the consistency between these results did not suggest that bleeding was occurring at the time.

30. In his oral evidence, Dr Cannon believed that the documented aortic dilatation, which continued after Mr Thompson’s aortic valve replacement, was not due to rheumatic valvular disease. He stated that Mr Thompson’s aorta measured only 40mm in 1986 when his aortic valve was repaired. The dilatation in the aorta was most likely due to hypertension and smoking. Dr Cannon’s opinion was that once an aortic valve was repaired, haemodynamic forces adversely affecting the wall of the aorta ceased.

31. He dismissed a coronary angiogram in 1998 at Prince Charles Hospital, which showed no coronary artery disease, as being too old to be of relevance. Dr Hossack’s view was that this proved there was not likely to be any ischaemic changes to the heart predisposing Mr Thompson to a heart attack.

32. Dr Cannon also referenced research which was presented in documents of the International Registry of Acute Aortic Dissection (IRAD).[11] In oral evidence, he pointed out that evidence from American research is that the incidence of aortic dissection has best been estimated at 5 to 30 per one million per year and the incidence of myocardial infarction has been estimated at 4400 per one million per year. In his report of 24 September 2008,[12] Dr Cannon showed for Australian figures that myocardial infarction is 300 times more common than a dissection. In that same report, Dr Cannon suggests that aortic dissection is an uncommon event and an aortic dissection extending to a flap affecting the right coronary artery is a further subset of an already infrequent clinical event. That being so, he said:

    … then there is approximately 1 chance in 15,000 that Mr Thompson suffered an acute myocardial infarction caused by a dissection of the ascending aorta producing coronary occlusion.[13]

    [11]Exhibit 2, page 60.

    [12]Exhibit 8.

    [13]Exhibit 8, page 4.

33. Dr Cannon’s view was that a myocardial infarction in a man of 76 years of age who smoked for a long time,[14] and who had hypertension was a common event with a significant mortality. Mr Thompson had a classic picture of chest pain, elevated troponin levels and ECG changes all pointing to a myocardial infarction.

    [14]In November 1986, Mr Thompson was reported as having given up a 10-cigarette-a-day smoking habit 6 months earlier (Exhibit 2, page 447). However, his general practitioner’s clinical notes (Exhibit 2, page 304) record him as smoking at the same level some years later.

34. Dr Hossack agreed with Dr Cannon that the final agonal event was an acute inferior myocardial infarction. However, he believes that this was precipitated by an aortic dissection in Mr Thompson’s case. In his report of 3 November 2014,[15] he compared the result of 78g/L from the sample taken at 9 pm on 19 September 2008 with the result of 75g/L from the test the following morning. The failure of the haemoglobin to rise significantly over that period following the giving of two bags of blood was suggestive of internal blood loss. In his oral evidence, and somewhat differently to the approach in his report, Dr Hossack emphasised the need to compare between similar samples and pointed to the comparison between the results of the calculated haemoglobin tests, results of 102g/L at 9.54 pm on 19 September 2008 and 75g/L at 8.52 am on 20 September 2008. That drop, especially given the transfusion of two units of blood, was strongly suggestive of blood loss resulting from an aortic dissection.

    [15]Exhibit 5, page 6.

    Consideration

35. The first question we need address is the cause of Mr Thompson’s death. Was it, as Dr Hossack suggested, aortic dissection or was it, as Dr Cannon suggested, acute myocardial infarction.

36. There is no hard evidence such as imaging or a post-mortem examination to establish a diagnosis of an aortic dissection. As it seems to us, it is important to recognise that, as a matter of pure statistics, a diagnosis of acute myocardial infarction is far more likely. Dr Cannon spoke of an aortic dissection as a one in a million possibility whereas myocardial infarction was a 4,000 in a million possibility. It is undoubtedly correct that aortic dissection was a possibility but we accept, as Dr Cannon said, that it was highly improbable.

37. While recognising and acknowledging Dr Hossack’s considerable clinical expertise, we remain not satisfied that his clinical judgement in the present case elevates the likelihood to probable. The indications to the contrary, set out in Dr Cannon’s report of 24 September 2014,[16] satisfy us that myocardial infarction is far more likely to have been the cause of Mr Thompson’s death.

    [16]Exhibit 8.

38. Dr Hossack places considerable weight on the apparent drop in the calculated haemoglobin levels between 9.54 pm on 19 September 2008 and 8.52 am on 20 September 2008. That drop, he says, especially given the transfusion of two units in the meantime, suggests blood loss. We think the better explanation is that the calculated haemoglobin level at 9.54 pm was unreliable. The consistency between the laboratory result on the 9 pm 19 September 2008 sample and the 10 September 2008 sample not only suggests an absence of bleeding on presentation they also tend to suggest that the 102g/L result at 9.54 pm cannot be correct. If it is ignored the 8.52 am reading, albeit by a different testing regime, is quite consistent with the other laboratory results.

1. Whilst there certainly was some consideration on the night of his presentation that Mr Thompson could have had an aortic dissection, the death certificate did not initially list it as a cause of death. It was later amended to add it as a cause, however, it is difficult to place much weight on this factor given we have no direct explanation for the change. Ultimately we place no reliance on either the differential diagnosis or the death certificate.

2. In any event, even if an aortic dissection had occurred and then, as a consequence, an acute myocardial infarction occurred, it must be related to damage to the aorta from aortic valvular disease. Dr Hossack’s theory must also demonstrate that the dissection resulted from the effects of rheumatic heart disease. There is no clinical evidence (such as post-mortem histological examination of the wall of the aorta) to know what the actual pathological process was that caused the aortic wall to weaken and dilate.

3. Mr Thompson’s aortic dilatation seems to have come to the attention of his medical attendants after his valve replacement. He was a smoker, obviously for a considerable time, and suffered from hypertension (although there is evidence that it was well controlled from at least 2004). Both of these conditions could be responsible for an aortic dilatation.

4. Dr Hossack is obviously a thoughtful, experienced clinician but his hypothesis is hindered by the fact that Mr Thompson died at a small peripheral hospital without sophisticated imaging. Dr Hossack gives a medically interesting clinical scenario but there is a paucity of imaging evidence and no post-mortem. We think the evidence of Dr Cannon is to be preferred. It deals more adequately with the probabilities in the absence of evidence of the types of tests that are capable of demonstrating an aortic dissection and his opinion provides a likely and plausible alternative explanation for Mr Thompson’s death.

5. The result is that we will affirm the decision under review.

I certify that the preceding 43 (forty-three) paragraphs are a true copy of the reasons for the decision herein of Deputy President P E Hack SC and  Dr M Sullivan, Member

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Associate

Dated 25 March 2015

Date of hearing	18 December 2014
Counsel for the Applicant	Mr M Black
Solicitors for the Applicant	Maurice Blackburn
Counsel for the Respondent	Mr CJ Clark
Solicitors for the Respondent	Moray & Agnew