COLIN STRAUGHEN and MILITARY REHABILITATION AND COMPENSATION COMMISSION

[2009] AATA 862

Administrative Appeals Tribunal

DECISION AND REASONS FOR DECISION [2009] AATA 862

ADMINISTRATIVE APPEALS TRIBUNAL      )

)          No 2009/1802

VETERANS' APPEALS DIVISION		)
Re		COLIN STRAUGHEN

Applicant

And MILITARY REHABILITATION AND COMPENSATION COMMISSION

Respondent

DECISION

Tribunal M J Carstairs, Senior Member, and Dr M Denovan, Member

Date10 November 2009

PlaceBrisbane

Decision The Tribunal affirms the decision under review. 

..................[Sgd]......................

Senior Member

CATCHWORDS

MILITARY COMPENSATION – acute idiopathic thrombocytopenic purpura with resultant cerebral haematoma and splenectomy in 1984 – medical treatment during service for tinea and malaria – whether this treatment connected with the development of the claimed condition – whether earlier detection a factor had recommended blood tests to monitor Griseofulvin therapy been carried out – employment not a contributing factor to the contraction or aggravation of disease – decision affirmed.

Compensation (Commonwealth Government Employees) Act 1971 (Cth)

Safety, Rehabilitation and Compensation Act 1988 (Cth), s 124

Johnston v Commonwealth (1982) 150 CLR 331

Re Crathern and Military Rehabilitation and Compensation Commission [2006] AATA 1089

REASONS FOR DECISION

10 November 2009  M J Carstairs, Senior Member, and Dr M Denovan, Member  

INTRODUCTION

1.      Colin Straughen, the applicant, was an enlisted member of the Australian Regular Army when in March 1982, at the age of 22, he developed thrombocytopenia purpure.  This is a condition that involves a lower than normal platelet count, often associated with spontaneous bleeding and bruising.  Within days Mr Straughen suffered a cerebral haemorrhage.  Mr Straughen claims the condition is related to his service and that he is therefore entitled to compensation. 

2.      The basis of Mr Straughen’s claim is that his thrombocytopenia was related to his treatment with the drug Griseofulvin as a treatment for tinea, or perhaps his treatment with Chloroquine, for malaria, both drugs being prescribed by treating doctors while he was on service.  An alternative basis to his claim is that his condition was aggravated by his service on the grounds of inability to obtain appropriate clinical management of his medical condition.  In that regard Mr Straughen says that doctors failed to perform regular blood testing to monitor any side effects of Griseofulvin and that such regular blood testing is recommended when the drug is prescribed.  Mr Straughen asserts that such blood tests would have lead to the earlier detection and treatment of his condition, and, as a result, he would not have suffered a cerebral haematoma.

3.      Mr Straughen lodged a claim for compensation and rehabilitation for a “thrombocytopenic purpura condition” under the Safety, Rehabilitation and Compensation Act 1988 (“the SRC Act”). The respondent denied liability.

4.      In order to resolve this dispute, we must determine:

·whether Mr Straughen’s employment contributed to the cause of his thrombocytopenic condition; and, if not,

·whether Mr Straughen’s employment aggravated that condition.

5.      After having careful regard to the medical evidence, we have decided that Mr Straughen’s employment did not contribute to the cause or the aggravation of his thrombocytopenic purpura condition.  We have therefore decided to affirm the decision under review.  We explain our reasons below.

THE FACTUAL BACKGROUND

6.      Mr Straughen was deployed to Butterworth, Malaysia, from June to September 1981.  Prior to, during and after that deployment, he was prescribed Chloroquine, an anti-malaria prophylaxis drug.

7.      On 11 January 1982, Mr Straughen was prescribed Griseofulvin to treat a fungal infection in his toe.  He presented for review of that condition on four occasions, the last being 2 March 1982.  On each occasion the treatment with Griseofulvin was continued.

8.      On 9 March 1982, Mr Straughen presented with a one day history of a blood blister on his tongue and the inside of his cheek, and multiple petechiae over his arms, legs and back.  Pathology tests indicated thrombocytopenia.[1]  At the time, Mr Straughen’s platelet count was 75,000/L (normal being ≥150,000/L).  He was admitted to hospital for investigation and commenced on 60 mg of prednisone that same night.  Regular pathology tests to monitor Mr Straughen’s platelet count were ordered.

[1] T5 at 70.

9.      Mr Straughen was reviewed in hospital on 11 March 1982 by haematologist Dr J Duggan, who noted a virtual absence of platelets.[2]  Dr Duggan indicated that Mr Straughen had been a drinker of bitter lemon, the last time being three days before the onset of his symptoms.  Bitter lemon drinks contain quinine, a drug known to cause thrombocytopenia.  Dr Duggan opined that quinine was an unlikely cause of Mr Straughen’s thrombocytopenia, because his platelet count did not recover after he stopped drinking bitter lemon.  Dr Duggan further stated that the likely cause of Mr Straughen’s thrombocytopenia was ITP (idiopathic thrombocytopenia purpura).  He recommended the continuation of the prednisone treatment and, if the platelet count did “not recover in the next couple of days”, a bone marrow aspirate.

[2] T5 at 71.

10.     A bone marrow biopsy was performed on 12 March 1982, along with a platelet radioactive coombs test (a special type of pathology test) around the same time. 

11.     Mr Straughen remained in hospital and on 12 March 1982 suffered a cerebral haematoma.  He was treated by urgent platelet transfusion and emergency splenectomy.  Mr Straughen was discharged from hospital on 8 April 1982 and from the Army on 20 August 1984.  The opinion of the doctors treating Mr Straughen was that the results of the above mentioned tests, in combination with the spleen histology, indicated that the likely cause of Mr Straughen’s thrombocytopenia was ITP.

Evidence of Dr P Davidson

12.      Dr Davidson, haematologist, provided a report dated 12 July 2009[3] and gave evidence in person at the hearing.  Dr Davidson explained to us that platelets play an integral role in blood clotting.  He stated that thrombocytopenia is a condition characterised by a shortage of platelets, caused by the liver breaking down platelets faster than they are being produced in the bone marrow.

[3] Exhibit R1.

13.     Dr Davidson told us that the average number of platelets is normally 150,000/L to 400,000/L.  He said that a platelet count greater than 50,000/L is well tolerated and not usually associated with symptoms.  However: a count of less than 50,000/L is associated with an increased risk of bleeding; a count of less than 20,000/L is associated with a dramatic increase in the risk of bleeding; and a count of less than 10,000/L is associated with a very high risk of bleeding.

14.     Dr Davidson explained that when a person is noted to have a platelet count less than normal, the common causes are either ITP or viral.  ITP is a constitutional condition, the result of the body’s immune system working against itself.  There are two types of ITP: chronic and acute.  The first type is present for a very long period, six months or more, and the resultant thrombocytopenia is mild or moderate.  The second type results in a drop of platelets from normal to very low levels in only three days, and patients usually present with bleeding or bruising.  Dr Davidson opined that the rapid decline in Mr Straughen’s platelet count in combination with his clinical presentation made it far more likely he suffered acute, not chronic, ITP.

15.     Dr Davidson said that it was usual to perform a Full Blood Count (“FBC”) every one to two weeks when first commencing a patient on Griseofulvin, and every two to four weeks thereafter.  Whilst Griseofulvin does not affect the platelet count, an FBC test is ordered to monitor the white blood cells for leukaemia.  A consequence of such monitoring is that the platelet count is usually included in the pathology reports.

16.     If Mr Straughen’s platelet count was below normal levels before the relevant tests were first conducted, Dr Davidson told us it could have been discovered. However, the only serendipitous window of opportunity to have done so was, at most, three days prior to Mr Straughen’s clinical presentation on 9 March 1982.  It was only a three day “window” because Mr Straughen was likely suffering from acute ITP (see above).  In 1982, routine blood tests were not reported for 24 to 48 hours.  Thus, even if a blood test had been ordered within the three day “window”, it is unlikely Mr Straughen’s low platelet count would have come to the attention of a doctor prior to 9 March 1982.

17.     When a person is noted to have a low platelet count but no clinical symptoms, the usual course of action is to order a follow up blood test in one to two weeks, unless symptoms develop.  Thus, had Mr Straughen’s platelet count of 75,000/L been noted earlier than 9 March 1982, it is likely that no treatment would have been commenced because of the absence of clinical symptoms (in this case petechiae and blood blisters).

18.     Dr Davidson opined that the earliest time treatment could have commenced in this case would have been 8 May 1982 - when Mr Straughen first noticed his petechiae and blood blisters and one day before treatment was, in fact, commenced.  He said that prednisone therapy usually starts to have a beneficial effect in three days and therefore that it was unlikely commencing treatment one day earlier (on 8 May 1982) would have prevented Mr Straughen suffering a cerebral haematoma (on 12 May 1982).

19.     Dr Davidson told us that in 1982 the only treatment available for ITP was that which Mr Straughen received, that is, prednisone therapy and splenectomy.

CONSIDERATION

20. In accordance with s 124 of the SRC Act, Mr Straughen is only entitled to compensation if it would have been payable in relation to his condition under the previous Act, the Compensation (Commonwealth Government Employees) Act 1971 (“the 1971 Act”).  Compensation under that Act is payable for a disease if a person’s employment contributes to the contraction or aggravation of that disease.

21.     We first considered whether Mr Straughen’s employment contributed to the contraction of his thrombocytopenic purpura condition.  Mr Straughen told us that whilst he believed that Griseofulvin contributed to the cause of his condition, he could not prove it.  Mr Hawker, for the respondent, contended there was no evidence to support a finding that Mr Straughen’s former military employment contributed to the contraction of his claimed condition.  Mr Hawker relied on the medical opinions of Dr Davidson and Dr P Eliadis.

22.     In order to assist with previous claims for compensation lodged by Mr Straughen in 1984,[4] his general practitioner, Dr R Thomas, provided a report in which he stated that Chloroquine and Griseofulvin could not be excluded totally as possible causes of his thrombocytopenia.  Mr Straughen was subsequently reviewed by specialist Dr I Ferguson and clinical haematologists Dr C Stewart and Dr Eliadis.  The consensus of all three doctors was that Mr Straughen’s thrombocytopenia was due to ITP.  In his report dated 18 January 1991, clinical haematologist Dr Eliadis opined that there is very little evidence to link Griseofulvin with the development of thrombocytopenia.  Dr Eliadis ruled out Chloroquine as a possible cause, as Mr Straughen was not taking that drug when he developed thrombocytopenia.  Dr Davidson opined that Mr Straughen suffered from constitutional ITP, and that Griseofulvin and Chloroquine likely did not contribute to the contraction of that condition.

[4] Mr Straughen has sought compensation for his condition previously.  On 16 August 1984, he lodged a claim for “focal right abnormalities”, “loss of spleen”, “continued headaches, insomnia and floating spots right eye”—all of which he noted after suffering the cerebral haematoma.  He also lodged a Claim by Employee for Compensation for Injury or Disease, dated 16 August 1984, under the 1971 Act for cerebral haemorrhage.  In a decision dated 14 October 1985, the respondent denied liability for incapacity resulting from idiopathic thrombocytopenia purpura with resultant cerebral haemorrhage.  The Veteran’s Review Board affirmed that decision on 9 April 1991.  In two separate decisions, both dated 6 March 1987, liability was denied under the 1971 Act for “blood disorder” and “cerebral haemorrhage”.

23.     The only evidence supportive of the claim that Mr Straughen’s thrombocytopenic purpura condition was contracted as a result of either of the two drugs prescribed to him during service is that of his general practitioner, Dr Thomas.  We prefer the opinion of the specialists, which is consistent with the view taken by the treating doctors when Mr Straughen was hospitalised.  We find that Mr Straughen’s thrombocytopenic purpura condition was caused by ITP, and that his employment did not contribute to the contraction of that condition.

24.     We next considered whether Mr Straughen’s condition of ITP had been aggravated due to his employment.  Mr Straughen relied on the evidence of Dr Eliadis and Dr Davidson to support his contention that he received incompetent treatment from the military staff, in that they failed to organise recommended monitoring of his Griseofulvin therapy.  Mr Straughen said he was injured as a result of that failure and that his injury therefore occurred in compensable circumstances.  However, Mr Hawker contends that the medical evidence only raises a possibility, not a probability, that monitoring of Griseofulvin therapy would have resulted in the earlier detection and treatment of Mr Straughen’s thrombocytopenic purpura condition.  He relied on the decision of the High Court in Johnston v Commonwealth,[5] and the Tribunal decision in Re Crathern and Military Rehabilitation and Compensation Commission.[6]

[5] (1982) 150 CLR 331.

[6] [2006] AATA 1089.

25.     Dr Eliadis raised the possibility of early detection and treatment of thrombocytopenia in his report dated 18 January 1991.  He stated that if Mr Straughen’s Griseofulvin therapy had been properly monitored with blood tests, his thrombocytopenia would have been detected sooner rather than later.  Dr Davidson told us during the hearing that whilst he agreed this was possible, he did not consider it likely.

26.     Dr Davidson’s evidence was that only a very small window of opportunity had existed to detect that Mr Straughen had a lower than normal platelet count before his presentation on 9 March 1982.  Mr Straughen last presented for review of his fungal condition on 2 March 1982.  Had Mr Straughen had the blood test prior to 6 March, the evidence of Dr Davidson is that he would not have been suffering from an abnormal platelet count. For a low platelet count to be detected, Mr Straughen would have had to delay having the test until at least 6 March 1982.  Yet, the evidence of Dr Davidson was that even if a blood test had been taken on 6 March 1982, it was unlikely the results would have been reported before one or two days, that is, before 7 or 8 March 1982.  Had such a blood test been done, according to Dr Davidson, the likely course of action would merely have been to repeat it in one to two weeks - because Mr Straughen had not yet developed symptoms.  That is, had Mr Straughen presented when he immediately noticed his symptoms, the treatment and likely clinical progress of his condition would not have been any different.

27.     Dr Davidson’s evidence was clear, logical and consistent with the other expert evidence before us.  There is no evidence pointing to early detection and treatment being a probability had Mr Straughen’s Griseofulvin therapy been monitored by regular blood tests.  Further, there is no evidence pointing to it being probable that such monitoring would have improved the clinical outcome for Mr Straughen.  We accept Dr Davidson’s evidence that the possibility of early detection preventing the clinical course of Mr Straughen’s ITP and subsequent cerebral haematoma was very unlikely.

28.     This is not a case of medical treatment, which likely would have arrested the natural course of a disease or injury, being delayed.  We find that even if appropriate monitoring of Mr Straughen’s Griseofulvin therapy had been performed, it is unlikely that this would have lessened the severity or altered the treatment and clinical outcome of Mr Straughen’s ITP.  It follows that his employment did not cause any aggravation of his condition.

CONCLUSION

29.     In summary, the Tribunal is not satisfied that Mr Straughen’s condition of ITP is connected with his employment in the sense as required under the 1971 Act.    That is, Mr Straughen’s employment in the Army did not contribute to the contraction of injury or disease; nor did it contribute to the aggravation, acceleration, or recurrence of injury or disease.

DECISION

30.     The Tribunal affirms the decision under review.

I certify that the 30 preceding paragraphs are a true copy of the reasons for the decision herein of M J Carstairs, Senior Member, and Dr M Denovan, Member.

Signed: .............................[Sgd]...........................................
             Mátyás Kochárdy, Research Associate

Date of Hearing  7 October 2009
Date of Decision  10 November 2009
Applicant was self-represented
Solicitor for the Respondent     Mr M Hawker, Sparke Helmore