Crathern and Military Rehabilitation and Compensation Commission

[2006] AATA 1089

Administrative

Appeals

Tribunal

 

DECISION AND REASONS FOR DECISION [2006] AATA 1089

ADMINISTRATIVE APPEALS TRIBUNAL      )

)          No A2005/338

VETERANS’ APPEALS  DIVISION		)
Re		JOHN CRATHERN

Applicant

And MILITARY REHABILITATION AND COMPENSATION COMMISSION

Respondent

DECISION

Tribunal Mr S. Webb, Member

Date18 December 2006

PlaceCanberra

Decision The decision under review is affirmed.

..............................................

Mr S. Webb, Member

CATCHWORDS

COMPENSATION - liability - ischaemic heart disease - failure to diagnose Conn's Syndrome prior to myocardial infarction - treatment obtained for hypertension - multiplicity of factors contributed to heart disease - meaning of material contribution - increased risk differentiated from material contribution - mere possibility not sufficient - decision affirmed

Safety, Rehabilitation and Compensation Act 1988 ss 4, 14

Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286

Johnston v The Commonwealth (1982) 150 CLR 331

Treloar v Australian Telecommunications Commission (1990) 26 FCR 316

Comcare v Canute [2005] FCAFC 262

Comcare v Etheridge [2006] FCAFC 27

REASONS FOR DECISION

18 December 2006 Mr S. Webb, Member         

1.      John Crathern served in the Royal Australian Navy.  During the period of his service from 1987 he was treated for hypertension and high cholesterol, and was noted to be overweight.  In 1998 he suffered a myocardial infarction.  Subsequently in 2000 Conn's Syndrome was diagnosed.  Mr Crathern maintains that the failure to diagnose and treat Conn's Syndrome prior to his myocardial infarction aggravated his ischaemic heart disease.  On that basis he claimed compensation.  His claim was denied by the Military Rehabilitation and Compensation Commission and, following reconsideration, is presently before this Tribunal for review.

2.      The issue for determination is whether Mr Crathern has suffered an injury under the Safety, Rehabilitation and Compensation Act 1988 as a result of Conn's Syndrome not being diagnosed and treated prior to his myocardial infarction. 

3.      The background facts are not in dispute.  During the period of his Navy service from 1987 Mr Crathern was treated for hypertension and hypercholesterolaemia.  That treatment was provided by Navy medical officers and specialist treating doctors, including Professor Simons, Dr Hellestrand, Dr Peak and Dr Hardcastle at the Royal North Shore Hospital in Sydney.  Mr Crathern was required or encouraged to attend these doctors by his employer.  On 2 April 1998 Mr Crathern presented at the Canberra Hospital with chest pain.  His chest pain was recorded as atypical, even though his serum potassium level was noted to be low (which was treated with potassium tablets).  On 26 April 1998 Mr Crathern suffered a myocardial infarction complicated by cardiac arrest.  This event involved the total occlusion of his anterior coronary artery.  His serum potassium level was noted to be low.  Mr Crathern recovered and continued to obtain medical treatment for hypertension.  He was treated by Dr Jeffery who assessed his risk of further cardiac events as low, as only single vessel disease was present.  He was treated by Dr Schmidli from April 2000.  On or about 27 June 2000 Conn’s Syndrome was diagnosed.  Subsequently he received spironolactane treatment for Conn’s Syndrome and ongoing treatment for essential hypertension.

4.      In Mr Crathern's submission Conn's Syndrome was likely to have been present at least from 1987 and could have been diagnosed at that time or soon thereafter.  He asserts that if Conn's Syndrome had been appropriately diagnosed and treated his hypertension would have been more effectively controlled over ensuing years.  This, he says, would at least have slowed the course of his ischaemic heart disease with the result that the myocardial infarction he suffered in 1998 may have been delayed or avoided altogether.  Mr Crathern relies on the evidence of Dr Jeffrey and Dr Schmidli that the failure to diagnose Conn's syndrome increased his risk of myocardial infarction.  Dr Jeffrey’s evidence was that if Mr Crathern’s Conn's Syndrome, and in particular his hypertension, had been more effectively treated over time the myocardial infarction may have been delayed or avoided altogether.  On that evidence Mr Crathern submits that the course of his ischaemic heart disease was aggravated by the failure to diagnose and treat his Conn's Syndrome in a timely manner.

5.      As will appear I do not agree.

6.      Under the SRC Act the Commission is liable to pay compensation for an injury that results in incapacity for work, impairment or death.[1]  The word ‘injury’ is relevantly defined to mean a disease suffered by an employee or a physical injury or an aggravation of a physical injury (other than a disease) suffered by an employee that arose out of or in the course of the relevant employment.[2]  The word ‘disease’ is defined to mean any ailment or aggravation of an ailment suffered by an employee that was contributed to in a material degree by the employment.  The word ‘aggravation’ is defined to include acceleration or recurrence.  ‘Ailment’ is defined to mean any physical or mental disorder, defect or morbid condition (whether of sudden onset or gradual development). 

[1] s.14

[2] s.4

7.      Mr Crathern claimed compensation for aggravation of Conn's Syndrome and ischaemic heart disease.[3]  These conditions are ailments within the meaning of disease for the purposes of the SRC Act.  I note in passing that, in all likelihood, the myocardial infarction Mr Crathern suffered in 1998 was a sudden physiological change that is consistent with a physical injury, even though it was directly or indirectly the product of disease.[4]  However that issue is not pressed in these proceedings.

[3] T4 folio 21

[4] see Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286 at 300 and 308

8.      The leading case to which I was referred concerning the compensable aggravation of disease by delayed medical treatment is Johnston v The Commonwealth (1982) 150 CLR 331. In that case Johnston, a young seaman, experienced symptoms including rectal bleeding, which was put down to haemorrhoids. Subsequently carcinoma of the bowel was diagnosed. Unfortunately for Johnston the cancer was inoperable and ultimately caused his death. The High Court concluded that if the cancer had been detected sooner treatment could have been given which would have been effective in slowing down, if not entirely stopping, the course of the disease. The Court, in majority (Gibbs CJ, Mason and Wilson JJ), said that “the failure to diagnose and treat the cancer resulted in a worsening or aggravation of the condition when compared with the course which, given timely treatment, it should have taken”, and concluded that “compensation is payable when an employee suffers an increase in the severity of a disease and his employment contributes to that increase in severity, whether the employment so contributes by actually making the disease worse or by delaying medical treatment which would arrest the natural course of the disease”.[5]  

[5] at CLR 339-340

9.      I note that Johnston's case was decided under the Compensation (Commonwealth Government Employees) Act 1971, prior to the enactment of the SRC Act.  The SRC Act replaced the 1971 Act and brought into effect a new scheme of rehabilitation and compensation for employees within its scope, which emphasises that the contraction or aggravation of a disease is compensable as an injury if it is contributed to in a material degree by the employment.  The 1971 Act required that the employment was a contributing factor to the condition in relation to which compensation was claimed, in relation to which a Full Bench of the Federal Court said in Treloar v Australian Telecommunications Commission (1990) 26 FCR 316 at 323:

“The use of the word "material" in conjunction with the words "contributing factor" in the [1971 Act], where it has occurred in expositions of the section in other cases clearly is not intended to add to the section any significance which is not already to be found in the words used by the legislature. It has served only to emphasise that the section is not brought into play unless it be established by evidence that features of the employment did in fact and in truth contribute to the condition complained of. The causal connection must be established on the probabilities and not left in the area of possibility or conjecture. Once the link is established, however, it matters not that the contribution be large or small.”

Considering this issue under the SRC Act in the case of Comcare v Canute [2005] FCAFC 262 a subsequent Full Court (French and Stone JJ, in majority) said at paragraph 68 “the changes brought about by the enactment of the SRC Act were intended to require that the contribution be ‘more than a mere contributing factor’ and, as such, the comments of the Court in Treloar must be assessed in this light.  Content must be given to the word ‘material’ contained in the definition of disease in the legislation as it presently stands.  The inclusion of this term imposes an evaluative threshold below which a causal connection may be disregarded.”  However the Court did not proceed to consider the proper meaning of the word ‘material’. 

10.     Nevertheless, considering these authorities it is plain enough that the test of materiality requires that the contribution of the employment to the contraction or aggravation of the ailment is of sufficient significance, materially, to permit a finding that the claimed condition was in fact a consequence of the employment.  Thus the mere experience of the conditions necessary for the contraction or aggravation of the ailment in the context of employment is not sufficient.  What is required is that the employment has added its measure, materially, in contributing to cause the contraction or aggravation of the disease in relation to which compensation is claimed.  Authority for those propositions is to be found in the case of Comcare v Etheridge [2006] FCAFC 27.[6]  Even though Etheridge’s case, and the particular remarks to which I have just referred, concern the 1971 Act and antecedent legislation, there is no reason to dis-apply those principles under the SRC Act.  Thus, consistent with those principles, if Mr Crathern is to succeed in his claim there must be evidence to establish on the balance of probabilities, as distinct from mere possibility or conjecture, that his employment in the Navy materially contributed to the contraction or aggravation of his Conn's Syndrome or ischaemic heart disease.  The case as presented before me is one in which aggravation and not primary causation is alleged.  The SRC Act is a no fault compensation scheme.  Thus the relevant question is not whether Mr Crathern’s doctors should have tested for Conn’s Syndrome prior to his myocardial infarction in April 1998, but whether the Syndrome from which he suffered was diagnosed as early as it should have been.  It is to that question I now turn.

[6] see Branson J at paragraphs 44 and 45, for example

11.     In order to address the issue of liability and employment contribution to the claimed injury the following questions must be addressed.

(a)Could Mr Crathern's Conn's Syndrome have been diagnosed and treated before 2000, and especially prior to 1998?

(b)If Mr Crathern had been treated sooner for Conn's Syndrome would the progress of that Syndrome or the course of his ischaemic heart disease have been different?

(c)Did the failure to diagnose Mr Crathern’s Conn's Syndrome sooner result in the worsening or aggravation of that Syndrome, or the worsening or aggravation of ischaemic heart disease, when compared with the progress of either of those conditions if timely treatment for Conn's Syndrome had been provided?

diagnosis

12.     The weight of the medical evidence is that, in all likelihood, Conn’s Syndrome was present in Mr Crathern during the 1990’s prior to the myocardial infarction he suffered in April 1998.[7]  It is not disputed that diagnostic tests were available at that time for Conn’s Syndrome, and the Syndrome could have been diagnosed if relevant investigations (radiological investigations of the adrenal gland) had been undertaken.  However, such investigations were not undertaken in Mr Crathern’s case until June 2000, when a small adrenal adenoma was identified.

[7] Dr Jeffery, Professor O’Rourke, Dr Schmidli

13.     On the evidence of Dr Jeffery and Professor O’Rourke, if the investigations had been undertaken sooner it is likely that Conn’s Syndrome could have been diagnosed in Mr Crathern prior to his myocardial infarction. 

14.     However, the likelihood of a diagnosis being made if the appropriate test had been conducted does not necessarily conclude the matter.  The availability of a diagnostic test is merely one aspect of the process of diagnosing disease.  Essentially, diagnosis is predicated on particular signs or symptoms that are apparent in a patient.  The key indicators for Conn’s Syndrome are adrenal adenoma and reduced serum potassium levels with elevated blood pressure.  Mr Crathern’s signs and symptoms were that he was over-weight and, on testing, was found to have high levels of blood cholesterol and elevated blood pressure from 1988.  Diagnoses of hypercholesterolaemia and hypertension were made.  Importantly, the records from March 1992 and July 1995 reveal that Mr Crathern’s serum potassium level was within the normal range.[8]  Nevertheless, his blood pressure was elevated and, it appears from the subsequent contemporaneous notes, that it was difficult to control from time to time.  His serum potassium level was noted to be low in April 1998.  These factors may indicate the existence of Conn’s Syndrome prior in April 1998 and possibly in preceding months or years.  However, the timing of the onset of this Syndrome cannot be determined with any accuracy. 

[8] See T13 folio 164

15.     It is not reasonable to conclude with the benefit of hindsight that a condition was able to be diagnosed if no signs or symptoms of the specific condition were apparent at the time.  In Mr Crathern’s case his persistently elevated blood pressure in the years prior to 1998 may have pointed to a cause of hypertension other than those then considered, however serum potassium levels that were within the normal range in 1992 and 1995 tended to contraindicate Conn’s Syndrome at that time.  Nevertheless his serum potassium levels were recorded as low prior to the myocardial infarction in April 1998.  Thus, on balance I find that Conn’s Syndrome was reasonably able to be diagnosed at some point in the period from 1995 to 1998.

course of disease

16.     Mr Crathern says that the course of his ischaemic heart disease and the related myocardial infarction would have been different if Conn’s Syndrome had been diagnosed and treated earlier. 

17.     However, I am not satisfied as a matter of probability rather than mere possibility that the course of Mr Cratherns’ heart disease would have been different if Conn’s Syndrome had been diagnosed and treated earlier.

18.     Mr Crathern’s ischaemic heart disease is multifactorial.  Factors include hyperlipidaemia, hypertension, family history and lifestyle.  I accept Professor O’Rourke’s evidence that Conn’s Syndrome may also have been a minor factor insofar as that Syndrome is associated with hypokalaemia (low serum potassium) and may have contributed to Mr Crathern’s hypertension.

19.     It is asserted that earlier treatment of Conn’s Syndrome would have had a positive effect on Mr Crathern’s hypertension.  Even if that was likely, and I make no such finding, the evidence is that other operative factors and their effect on the course of Mr Crathern’s heart disease would have continued unaffected.

20.     Mr Crathern’s hypertension was diagnosed and treated from 1988.  There is no question about the quality of the treatment he received at the hands of the doctors he was required to attend by the Navy.  His medical records reveal his blood pressure levels from 1988.[9]  His treating doctors monitored and managed his hypertension, and adjusted his treatment and medications from time to time. 

[9] T5, folio 117-118, for example.

21.     Professor O’Rourke gave evidence that Mr Crathern’s hypertension and blood pressure levels were effectively managed by the treatment and medications he received over time.  Doctor Jeffery gave evidence that Mr Crathern’s hypertension and blood pressure could have been more easily and effectively managed if his Conn’s Syndrome had been diagnosed and treated sooner with spironolactone medication.  Considering Dr Jeffery’s evidence it would be reasonable to expect to see improvement in Mr Crathern’s blood pressure levels and hypertension following commencement of the spironolactone treatment for Conn’s Syndrome.  The key point is whether Mr Crathern’s blood pressure and hypertension were better controlled, that is in terms of lability and level with reference to the normal range, following commencement of spironolactone treatment.  Professor O’Rourke’s evidence was that difficulties controlling Mr Crathern’s blood pressure persisted despite treatment with spironolactone and that treatment for essential hypertension (to be distinguished from blood pressure elevation as a result of Conn’s Syndrome) continued thereafter.  That evidence is consistent with the contemporaneous blood pressure records and is to be preferred.[10]   Nevertheless I accept that Mr Crathern’s hypertension was easier to manage than previously and there was no recurrence of hypokalaemia.[11] 

[10] See, for example, 130/90 on 3 August 2000 (T5 folio 71), 116/90 on 30 August 2000 (T5 folio 70), 140/70 on 23 November 2000 (T5 folio 67), 148/94 on 6 March 2001 (T5 folio 64) , 140/85 on 31 May 2001 (T5 folio 60), 118/82 on 21 September 2001 (T5 folio 136), 114/80 on 12 December 2001 (T5 folio 57), 139/78 on 6 December 2001 (T5 folio 55), 116/84 on 7 June 2002 (T5 folio 53), 140/75 on 9 July 2002 (T5 folio 52).

[11] Dr Jeffery and Dr Schmidli

22.     Thus, even though I accept that Mr Crathern’s hypertension was easier to manage following commencement of the treatment for Conn’s Syndrome, I am not satisfied that the effect of that treatment was sufficient to have materially changed the course of his ischaemic heart disease if it had commenced sooner.  Mr Crathern suffered from hypertension before and after the commencement of treatment for Conn’s Syndrome.  I am satisfied that any change in Mr Crathern’s hypertension and blood pressure levels following treatment of his Conn’s Syndrome is at the margin.  The hypertension and his blood pressure levels were multifactorial.  They were monitored, treated and managed, with varying degrees of difficulty from 1988.  I accept that Mr Crathern’s hypertension was but one factor in the matrix of factors contributing to Mr Crathern’s heart disease and myocardial infarction.  It does not follow that because Mr Crathern’s hypertension was easier to manage following commencement of the spironolactone treatment, hypertension is to be discounted from the matrix of operative factors associated with Mr Crathern’s heart condition, nor does it follow that previous treatments were not effective in controlling his hypertension, albeit with greater difficulty.[12]   I am satisfied that they were, and so find.  I am not persuaded by the evidence of Dr Jeffery and Dr Schmidli that the effect of the spironolactone treatment for Conn’s Syndrome was sufficient to change the course of Mr Crathern’s hypertension and, in consequence, his ischaemic heart disease if it had commenced sooner. 

[12] Professor O’Rourke

23.     Hypertension is but one aspect of Conn’s Syndrome symptomatology.  It is also necessary to consider the effect of the spironolactane treatment for Conn’s Syndrome on Mr Crathern’s hypokalaemia in the present matrix of factors affecting the course of his heart disease.  I accept that Mr Crathern’s serum potassium levels were easier to maintain within the normal range following commencement of the treatment for Conn’s Syndrome.  However, there is no contemporaneous evidence that his serum potassium levels were below the normal range prior to 2 April 1998, albeit at the low end of the range.  On the contrary, the available evidence from 1995 and 1992 indicates that his serum potassium levels were within the normal range at those times.  There is some evidence (Dr Jeffery and Dr Schmidli) that low serum potassium levels may be associated with arrhythmia and even cardiac arrest in cases of myocardial infarction.  However, it is not clear that this is what occurred in Mr Crathern’s case.  The contemporaneous notes and Professor O’Rourke’s evidence indicate that low serum potassium may have been associated with diuretic medication at the time.  On the available evidence it is possible that hypokalaemia may have been a factor in the complications Mr Crathern experienced during his myocardial infarction.  However, I am not satisfied on the balance of probabilities that hypokalaemia related to Conn’s Syndrome materially contributed to cause or aggravate Mr Crathern’s arrhythmia or cardiac arrest in April 1998.  Even if it did the fact is that Mr Crathern received treatment for reduced serum potassium on 2 April 1998 and subsequently, and there is no evidence that those treatments were not effective in managing his serum potassium levels at the time.  On that basis there is insufficient evidence on which to conclude on the balance of probabilities that treating Conn’s Syndrome sooner would have altered the course of Mr Crathern’s hypokalaemia or the Syndrome itself, or his ischaemic heart disease.

24.     If Conn’s Syndrome had been diagnosed and treated earlier, prior to April 1998, it is possible that Mr Crathern would not have suffered a myocardial infarction when he did.  That is a possibility.  However, the evidence on which Mr Crathern relies and particularly the evidence of Dr Jeffery and Dr Schmidli, all of which I have carefully examined and taken into account, does not persuade me, to the requisite reasonable satisfaction standard of proof, on the balance of probabilities, that the course of his heart disease would have been different if the delay had not occurred.  I am not satisfied, therefore, on the balance of probabilities, that the course of Mr Crathern’s ischaemic heart disease, or the course of his Conn’s Syndrome, or the occurrence of his myocardial infarction, would have been different if his Conn’s Syndrome had been diagnosed and treated earlier.  I so find. 

25.     Mr Crathern’s case is to be distinguished from Johnston’s case.[13]  Johnston did not receive timely treatment of the condition that ultimately led to his death.  The evidence was that if such treatment had been provided the course of his disease would, at least, have been slowed, and the High Court so ruled.  Mr Crathern was treated for the operative factors that materially contributed to his ischaemic heart disease, including the symptoms (low serum potassium and hypertension) that may have been related to Conn’s Syndrome.  Unfortunately for Mr Crathern, the evidence in his case does not establish the probability of any change in the course of his ailments and disease if earlier treatment for Conn’s Syndrome had been provided.

[13] supra

the question of aggravation

26.     Mr Crathern asserts that his ischaemic heart disease was aggravated by the delay in diagnosing Conn’s Syndrome.  I do not agree.

27.     I have found that the course of Mr Crathern’s ischaemic heart disease would not have been different if Conn’s Syndrome had been diagnosed and treated sooner.  It follows that no aggravation in compensable circumstances is made out.

28.     It remains to address the issue Mr Crathern agitated concerning whether an increase in the risk of myocardial infarction that results from the delay in diagnosing and treating Conn’s Syndrome is an ‘aggravation’ within the meaning of the SRC Act.  As will appear, I am reasonably satisfied that it is not.

29.     Considering the evidence given by Dr Jeffery, Dr Schmidli and Professor O’Rourke, I am satisfied that delay in the diagnosis and specific treatment of Conn’s Syndrome may have increased the risk of Mr Crathern suffering from a myocardial infarction.  However, the concept of risk is imbued with the character of possibility.  It is necessary to distinguish between the risk of something occurring and the factors that materially contributed to cause the occurrence in the particular circumstances.  It is not controversial that age, family history, male gender, high cholesterol and a variety of other factors, including Conn’s Syndrome, are risk factors for heart attack.  Professor O’Rourke’s evidence was that it was more likely than not that Mr Crathern’s high cholesterol, his obesity and other factors including his family history of heart disease would have caused him to suffer a heart attack whether or not he was treated for Conn’s Syndrome sooner.  I accept that evidence. 

30.     What is required is a material contribution by the employment to the aggravation of disease.  While the factors associated with an increase in risk may be related to employment, as in this case, it does not follow that those same factors materially contributed to aggravate the disease in the particular circumstances.  In this case there is insufficient evidence to establish that the delay in diagnosing and treating Conn’s Syndrome materially contributed to aggravate Mr Crathern’s ischaemic heart disease or his Conn’s Syndrome, even though it can be accepted that such delay may have increased his risk of suffering a myocardial infarction.

31.     Thus, I am compelled to conclude that the delay in diagnosing and treating Conn’s Syndrome did not materially contribute to aggravate Mr Crathern’s heart disease or the event of his myocardial infarction, even though the delay may have increased the his risk of suffering a heart attack.

32.     It follows therefore that Mr Crathern’s case is not made out on the evidence.  The delay in diagnosing and treating Conn’s Syndrome did not materially contribute to change the course of his ischaemic heart disease.  It cannot be said, therefore, that his (then) employer is liable for the aggravation of Mr Crathern’s ischaemic heart disease or of his Conn’s Syndrome as a result of that delay.

33.     The decision under review is affirmed.

I certify that the 33 preceding paragraphs are a true copy of the reasons for the decision herein of Mr S. Webb, Member

Signed:       Peter Edwards
  Associate

Date of Hearing  25 & 26 October 2006
Date of Decision   18 December 2006
Counsel for the Applicant  Mr S. Pilkington
Counsel for the Respondent                  Mr D. Ranigah