Plattfuss and Reptriation Commission - [2000] AATA 327

DECISION AND REASONS FOR DECISION [2000] AATA 327

ADMINISTRATIVE APPEALS TRIBUNAL )

) NoV1998/1311

VETERANS APPEALS DIVISION )

Re BESSIE MAY PLATTFUSS
Applicant

And REPATRIATION COMMISSION
Respondent

DECISION

Tribunal Mr J. Handley, Senior Member
Dr C. Re, Member

Date28 April 2000
PlaceMelbourne

Decision The decision under review is affirmed.

…...Sgd. Mr J. Handley…..
Senior Member

Veterans' Affairs: Widows application; death caused by tractor accident; multiple chest and rib injuries; existence of ischaemic heart disease; concession of service®smoking®1HD; whether 1HD contributed to death; decision affirmed.

Bushell v Repatriation Commission 1992 109 ALR 30

Repatriation Commission v Delidio 1998 49 ALD 193 at 206

REASONS FOR DECISION

28 April 2000 Mr J. Handley. Senior Member
Dr C Re, Member

The Applicant applies to review a decision of the Veterans' Review Board made on 16 September 1998, which affirmed a decision previously made by the respondent on 7 April 1998. The respondent decided that the death of Robert Frowd Plattfuss, the husband of the applicant widow, was not war-caused.
The late Mr Plattfuss died on 9 November 1976 when aged 53 years. At that time he and his wife were self-employed as farmers near Waaia in Northern Victoria.
Following a Coronial Inquiry conducted at Shepparton on 17 February 1977 the Coroner certified the cause of death to be:
"effects of injuries received in a tractor accident"
The hearing of this application commenced in Yarrawonga on 18 February 1977 and concluded in Melbourne on 10 April 1977. Mrs Plattfuss gave evidence in Yarrawonga. Dr Pilbeam, a pathologist, gave evidence on behalf of Mrs Plattfuss upon the resumption of the hearing in Melbourne. Professor Cade gave evidence on behalf of the respondent. Mr Moore, of Counsel, appeared on behalf of Mrs Plattfuss and Mr Douglass appeared on behalf of the respondent.
A number of documents were received into evidence and will be referred to in these reasons.
The circumstances of the deceased's overseas service, his commencement of a lifelong smoking habit by reason of service, the applicable Statement of Principle, instrument No. 77 of 1996, and the presence of ischaemic heart disease prior to death were not in dispute.
The issue for determination in these proceedings was whether ischaemic heart disease contributed to the death of the deceased. The respondent disputed any contribution to death by ischaemic heart disease and submitted that death was due to severe (secondary) head injury with brain stem haemorrhage, brain swelling and increased intra-cranial pressure by reason of hypoxia due to severe chest injuries suffered in the tractor accident. The applicant submitted the deceased suffered a cardiac catastrophe at Numurkah Hospital (by reason of the presence of ischaemic heart disease) which contributed to his death.
BESSIE MAY PLATTFUSS
Mrs Plattfuss is the widow of the late Robert Frowd Plattfuss.
Mrs Plattfuss said that her husband was first diagnosed with ischaemic heart disease in 1966 following an admission to the Numurkah Hospital. He thereafter suffered from chest pain at night and was prescribed Anginine. He also suffered from lower back pain and was frequently exhausted.
On 8 November 1976 Mrs Plattfuss said that her husband was crushed between a tractor and a steel post on their farm at Waaia. Mrs Plattfuss said that it appears that her husband had started the tractor whilst standing beside it or in front of it and whilst it was in gear. Apparently, when the engine started the tractor lurched forward and trapped Mr Plattfuss against the post. He suffered severe chest injuries but did not suffer head or neck injuries. He was admitted to Numurkah Hospital, however his health deteriorated and he was admitted to Mooroopna Hospital. His condition, unfortunately, continued to deteriorate and arrangements were made to transfer Mr Plattfuss to St Vincent's Hospital in Melbourne.
Despite intensive investigations and treatment Mr Plattfuss died on 9 November 1976. An autopsy was not performed.
Mrs Plattfuss said that her husband smoked cigarettes, cigars and a pipe. She said he was a heavy smoker. She recalled that he was frequently short of breath and had a persistent productive cough.
Following her husband's admission to Numurkah Hospital in 1966, when ischaemic heart disease was first diagnosed, she said Mr Plattfuss would frequently have chest and left arm pain.

NUMURKAH HOSPITAL

Mr Plattfuss was admitted to the Numurkah Hospital at approximately 5:00 p.m. on 8 November 1976. He was admitted under the care of Dr Hudson. By reason of the relatively unusual, yet complex medical evidence in this application, the notes, excluding clinical data (which will be referred to later) of the Numurkah Hospital are recorded as follows:
"New patient admitted to out-patient department at 5:00 p.m.
Patient has fractured ribs with punctured lung.
Surgical emphysema.
S/B Dr. half hourly obs.
Morphine 15 mgms starting at 5:00 p.m. four hourly
Unable to move right arm
Small amount movement in left arm – tingling sensation
?dislocated clavicle.
Same strapped
S/B Dr at 8:30 p.m.
Mysteclin V 250 mgm QID
Hourly pulse
Two hourly B/P
Now has fluid on base of right side, ? for chest xrays to be arranged later
U/T trace ketones NOAD
Patient sleeping at 11:00 p.m. coughing at 11:30 p.m.
Patient speaking vaguely. Collapsed. Pulse weak and thready. Colour grey.
Intra nasal oxygen administered. Airway in situ
Colour improved. Pulse improved.
11:40 p.m. xray chest by Dr Hudson.
Patient transferred to Mooroopna.
Relatives notified."
The clinical data referred to in the previous paragraph and reproduced below is taken from a "special observation chart". It is reproduced as follows because of the significance of it, having regard to the evidence we heard from Dr Pilbeam and Professor Cade.

Time     T          P         R         B.P  Remarks & Treatment     Initial
  STATE OF CONSCIOUSNESS
O/A                  90        24        140/70  c/o left chest pain and ® shoulder pain
5pm                 90        24        115/60  Morphine 15 mg 1.M1 at 5p.m.
5:30 pm            84        20        115/70  Pain eased resting
6 pm                 100      20        115/45
6:30     37        104      20        125/70
7 pm                 96        20        125/80
7:30 pm            96        20        130/80
8 pm                 96  145/80
8:30 pm            96  140/80
9 pm                 96
9:30 pm            96
10 pm              100                  126/80
11 pm              104  Sleeping
11:35 pm           ?          100  Pt sat up C/O pain very vague collapse
  Colour grey INO2 commenced
11:45 pm  72        32        105/65  Chest Xray. Breathing improved
12:15 am
12:30 pm  92  150/80

STANLEY THOMAS HUBERT HENRY PILBEAM

Dr Pilbeam, who has recently retired, has an extensive experience as a Pathologist, practising in the United Kingdom, Australia and South Africa. He was the Director of Pathology at the St John of God Hospital in Ballarat from 1990 until his retirement.
In a report of 13 August 1999, Dr Pilbeam acknowledged that the deceased's chest injuries accelerated death, but were not the sole cause. He said, "the effect of a relatively minor chest injury would be amplified by ischaemic changes in the heart".
He concluded:
"the deceased may have had a brief period of circulatory failure associated with trauma to a diseased heart with resultant ischaemic changes in the brain resulting in foci of necrosis followed by haemorrhage and oedema at a later time.
The damage to arterial walls, initiated by smoking, is not confined to coronary arteries, but at its peripheral arteries of similar sizes. Similar changes could be expected to occur in the cerebral vessels. These changes would produce the changes noted at St Vincent's Hospital.
In this sense the deceased's death is clearly associated with generalised atherosclerosis and smoking. The accident was a precipitating factor".
In a later report (undated but attached to a letter from the applicant's solicitors of 20 October 1999) Dr Pilbeam reported
"I note Professor Cade's comments. While admitting that Professor Cade is an acknowledged expert in these cases, I still think it possible that the collapse, six and a half hours after admission could have been an episode of ventricular fibrillation, which subsequently returned to normal rhythm, although one must admit that other causes are perhaps more likely. It was this episode which induced the fatal brain damage".
In a third report (again undated but attached to a letter from the applicant's solicitor of 3 April 2000) Dr Pilbeam reported (apparently having been referred to an additional report from Professor Cade):
"I agree with him (Professor Cade) that generalised ventricular fibrillation is rarely self-correcting. I think that it would have been more appropriate for me to describe the attack as cardiac arrhythmia or an ischaemic cardiac episode.
My reasons for favouring a cardiac rather than a respiratory cause for the episode in the Numurkah District Hospital on 8 November 1976 are as follows -
the patient Mr Plattfuss was stated to be sleeping at 11:00 p.m.
At 11:35 p.m. he sat up and complained of pain. He then collapsed with a pulse that was difficult to record. His blood pressure, recorded 10 minutes later had fallen significantly. His condition responded to oxygen therapy. This response to oxygen would equally support a response to a cardiac or respiratory cause. Administration of oxygen is part of the usual resuscitation measures for ischaemic as well as respiratory collapses and is frequently effective in improving the patient's condition.
The sudden collapse with pain is the picture of an acute ischaemic cardiac episode rather than a progressive cerebral anoxia.
The associated cerebral ischaemia could equally well result in the cerebral anoxic changes referred to by Professor Cade, especially if there was associated cerebrovascular degeneration.
I would therefore contend that although the thoracic trauma which all are agreed was not of a serious or fatal nature may have contributed to his cerebral anoxia, his pre-existing cardiac lesion was a significant factor in his subsequent cerebral complications."
In evidence, Dr Pilbeam said that support for the opinions expressed by him in his reports, were based on the clinical data found in the special observation chart.
He said that the deceased was observed to have sat up, complained of pain, collapsed, was grey in colour, with a pulse difficult to record (as evidenced by the expression "? 100") and with a blood pressure which had fallen 15 systolic points in a period of ten minutes between 11:35 and 11:45. Dr Pilbeam said that this data was evidence of a cardiac episode, either being a small infarct or an arrhythmia i.e. a minor coronary thrombosis, precipitating a failure of blood supply to the brain, resulting in loss of consciousness and eventual death. He said this was more likely to have a cardiac, rather than a respiratory cause.
He said the administration of oxygen is standard treatment when a patients colour is grey, and that improvement would be expected as was evidenced from the observation chart.
Dr Pilbeam dismissed a conclusion expressed by Professor Cade in his report, that the limited use of left and right arms was evidence of neurological damage, because in his opinion the potential dislocation of the deceased's right clavicle, with strapping, would explain limited movement with referred pain into the left arm.
Dr Pilbeam dismissed an opinion of Professor Cade that there was evidence of progressive neurological injury shortly after admission and said that in his opinion there was no significant deterioration in the deceased's neurological function before his collapse at 11:35 p.m. In his opinion, there was also no concern expressed by any of the nursing staff as to the neurological function of the deceased, prior to his collapse.
It was the opinion of Dr Pilbeam that whilst the deceased did suffer from cerebral anoxia, it was contributed to by a cardiac infarct suffered by the deceased, while he was an in-patient at the Numurkah Hospital.
Dr Pilbeam concluded that the deceased's prior smoking habit was a major cause of his impaired lung function. He said that smoking impairs a persons airways and the persistent cough of the deceased pointed to impairment of the lungs. He concluded that the deceased, having suffered ischaemic heart disease was likely to have atherosclerotic changes in other arteries and a combination of arterial disease, a history of smoking, and a productive cough all contributed to the cause of death.
In cross-examination Dr Pilbeam said that any infarct suffered by the deceased could spontaneously resolve, however, he acknowledged that there was no evidence of cardiac failure or cardiac shock, which he said he would have expected if the hypoxia had its origin in a cardiac injury or catastrophe.
Dr Pilbeam said that the evidence of a sudden attack of chest pain is found in the observation chart at 11:35 p.m., manifested by the applicant, who is recorded as having "sat up". He acknowledged that at 11:35 p.m. he would have expected a reduction in the effect of morphine which was apparently administered at 5:00 p.m. but would not have expected a sudden onset of pain in the absence of an infarct, which he felt was indicated by the sudden reduction in blood pressure to 105/65 at 11:45 p.m.
Dr Pilbeam said he generally agreed with the opinions expressed by Professor Cade in his reports "as a general proposition" but disagreed that the deceased's blood pressure had been normal in the six hours that he was an in-patient at the Hospital. He acknowledged that Professor Cade had recorded that the deceased's blood pressure had been taken on ten occasions in this period, but disagreed that the readings were normal. He said the deceased had a history of hypertension and the blood pressure readings were "hypotensive for him". He said, further, that the blood pressure of 105/65 would have been sufficient to cause neurological damage and "may have caused a degree of brain damage".
Dr Pilbeam said that he had no specialist qualifications in cardiology or neurology, and did not treat cardiac patients, but said that he had performed many autopsies of persons who had had a cardiac death.
Despite the opinions of Professor Cade and Dr Jensen, Dr Pilbeam remained of the opinion that the injuries, which were sustained in the tractor accident, were not "serious" and were not, of themselves, fatal. It was his opinion, that even 25 years ago in Numurkah, the deceased would have survived the accident with the treatment that he had (at the Numurkah Hospital) were it not for the fact that he had previously smoked cigarettes.
He said the contribution to death by ischaemic heart disease was greater than a possibility but lesser than a probability.
JOHN FRANCIS CADE
Professor Cade is the Director of Intensive Care at the Royal Melbourne Hospital. He has extensive experience as an Intensivist and has specialist qualifications in thoracic medicine.
Professor Cade provided two reports dated 30 September 1999 and 4 February 2000.
In his first report, Professor Cade reported that the chest injury was severe because "it was associated with multiple rib fractures, punctured lung and surgical emphysema". He noted that six and a half hours after the deceased was admitted to hospital he collapsed "due to hypoxia (because his colour and pulse improved rapidly with oxygen) and cerebral damage (because he became unconscious and remained so).
Professor Cade noted that the deceased did not suffer head injury, however, he noted on admission to hospital that one hour following the accident, the deceased was unable to move his right arm and his left arm only slightly. He said this was indicative of "serious neurological damage". Professor Cade noted that the deceased collapsed six and a half hours after admission, was speaking vaguely (indicating impaired consciousness) and by reason of the deceased being comatose and unresponsive, and having fixed dilated pupils there was evidence then, of severe brain injury. He concluded that these symptoms were the manifestation of "severe neurological injury (progressing) rapidly from shortly after the accident". He said the injury was secondary, was typical of head injuries and would have been caused by hypoxia. He reported that the likely mechanism would have been initial chest compression with raised intrathoracic pressure, punctured lung and generalised hypoxia. He said "secondary brain injury remains one of the most frequent causes of death in patients who survive an initial severe traumatic event, whether or not there is a significant direct head injury at the time".
With respect to the presence of ischaemic heart disease Professor Cade said that this diagnosis was not definite although probably reasonable. He concluded that any contribution to death from heart disease would have required brain damage caused by severe hypotension. He noted that the deceased's blood pressure had been recorded on ten occasions in the first six hours of admission, and "on each occasions it was normal". He said there was no significant tachycardia or arrhythmia and there was, therefore, no evidence of any "cardiac problem" between admission and collapse at Numurkah.
Professor Cade concluded that any hypothesis linking service with death was "not plausible".
In a report of 4 February 2000 (apparently in response to reports of Dr Pilbeam) Professor Cade reported that the "problems" with the "suggestion" of Dr Pilbeam that the hypoxia suffered by the deceased may have been caused by an episode of ventricular fibrillation arising from ischaemic heart disease were that ventricular fibrillation "is a sudden catastrophic event and would not have been overlooked during his admission at Numurkah Hospital". He also said that ventricular fibrillation is "rarely self-terminating and requires cardiopulmonary resuscitation and electrical defibrillation for its reversal". He noted that the deceased continued to have a pulse after his collapse "whereas there can be no pulse during ventricular fibrillation". He also reported that the resuscitation of the deceased was by oxygen, which "restored his weak pulse and grey colour to normal. This indicates that the collapse was due to hypoxia from a respiratory cause. Moreover, ventricular fibrillation due to cardiac disease cannot be reversed so simply". He also noted that throughout the admission to Numurkah Hospital, the deceased's pulse rate and blood pressure were normal, including immediately after collapse at 11:35 p.m. He said that it would have been "quite extraordinary for ventricular fibrillation not only to spontaneously reverse, but then to be followed by a normal blood pressure as if nothing untoward had just happened to the circulation".
He concluded that the clinical data does not accommodate the suggestion of cardiac arrest but it directly describes serious chest injury.
In answer to questions from Mr Douglass, Professor Cade said that the deceased's blood pressure of 105/65 at 11:45 p.m. was not characteristic of an infarct or an arrhythmia. He said it was non-specific. He regarded this blood pressure reading as "moderately impaired", "clinically satisfactory and not possible to cause neurological damage". In his opinion, a systolic reading of 60 or below would have to have been recorded to precipitate brain damage.
Professor Cade said that hypoxia having a cardiac origin would only exist if there was a cardiac arrest, a cardiac shock or pulmonary oedema. He said only these three mechanisms could account for cardiac hypoxia, and none of them was present. Additionally, he said the administration of oxygen, which relieved some of the deceased's symptoms, would have had no effect in the case of a person suffering from cardiac hypoxia.

Professor Cade agreed that there was a note in the hospital records of a suspected dislocated right clavicle, but he said there was no evidence of this, and it was not demonstrated on chest xray. He remained of the view that the inability of the deceased to move his right arm and the small amount of movement in the deceased's left arm with tingling sensation, was evidence of neurological damage.
In cross-examination, Professor Cade said there was no musculo skeletal explanation for left arm pain or limitation of movement by any dislocation of the right clavicle, even with strapping.
Professor Cade dismissed the suggestion that the deceased had had a small infarct or an arrhythmia with or without infarct between 10:00 p.m. and 11:45 p.m. (by reference to the blood pressure readings and the readings taken of the deceased's pulse) as a cause for his hypoxia because an infarct or arrhythmia was not recorded, nor identified and the deceased's blood pressure had not reduced to a level sufficient to cause damage of this type.
Professor Cade said that even if the deceased had had an infarct, it would not have contributed to the hypoxia, because cardiac hypoxia could only be caused by cardiac arrest, cardiac shock or pulmonary oedema.

CONCLUSIONS AND REASONS FOR DECISION

In the present case, the deceased was crushed by a tractor, and suffered severe chest injuries. He was noted on admission to the Numurkah Hospital, to have multiple rib fractures, a punctured lung, surgical emphysema, inability to move his right arm and small amount of movement of left arm with tingling sensation. The possibility of dislocated clavicle was not supported by chest xray. Administration of morphine on admission eased the deceased's pain and he was able to rest.
Approximately six hours later the deceased "sat up", complaining of pain, was found to be vague, he collapsed and was grey in colour, yet following administration of oxygen his breathing improved, as did his pulse and blood pressure, but he did not regain consciousness.
We thought the evidence of Professor Cade to be compelling and note that the only basis for hypoxia having a cardiac origin would be cardiac arrest, cardiac shock or pulmonary oedema, none of which was reported, or recorded, or apparently existed. We note Dr Pilbeam said that there was no evidence of heart failure or cardiac shock.
We are satisfied on the evidence heard that the restoration of the deceased's pulse and elevation of his blood pressure, after the administration of oxygen, is consistent with the hypoxia being respiratory in origin and not cardiac. We thought the opinions expressed by Dr Pilbeam were not supported by the evidence, indeed, we thought that his opinions, at least expressed in his reports, shifted and varied and were not consistent. We are not satisfied on the balance of probabilities that the blood pressure of 105/65 at 11:45 p.m. with an accompanying pulse rate of 72 was characteristic of an infarct or an arrhythmia and it would not have precipitated neurological damage.
Taken in isolation, we believe that the opinions expressed by Dr Pilbeam are sound, but in the circumstances of the present application, particularly in regard to the catastrophe which caused the admission to the Numurkah Hospital, we are of the opinion that the hypothesis advanced by Dr Pilbeam is not reasonable. Whilst we acknowledge that he is a responsible medical practitioner, he does not have the qualifications of a thoracic physician or an intensivist (being qualifications, of long standing, possessed by Professor Cade.) (refer Bushell v Repatriation Commission 1992 109ALR 30).
We are additionally of the opinion that the hypothesis advanced by Dr Pilbeam is not supported by raised facts. We are not satisfied that the deceased did suffer any cardiac arrest or cardiac shock or pulmonary oedema, sufficient to give rise to hypoxia having a cardiac origin. That the hypoxia had its origin in the respiratory trauma is consistent with the circumstances on admission, namely multiple rib fractures, punctured lung and surgical emphysema. We are not satisfied that the reduced blood pressure at 11:45 p.m. was evidence of an infarct, nor are we satisfied that the deceased "sat up" suddenly, as was the opinion of Dr Pilbeam. There is no evidence that the deceased – when he did sit up – did so suddenly. The nursing notes record that he was sleeping at 11:00 p.m., coughing at 11:30 p.m. and speaking vaguely, and sat up, at 11:35 p.m. He then collapsed, with a weak pulse and grey colour. The sudden chest pain, as manifested by the deceased's sitting up, is not necessarily consistent with infarct. To this extent we note that there is no reference within the hospital notes to any infarct, indeed there is no note or reference to chest pain, as was assumed by Dr Pilbeam.
Additionally, we are not satisfied that the absence of use of the deceased's right arm and the limited use of the deceased's left arm may be connected with the possibility of a dislocated right clavicle. The chest xray did not demonstrate the presence of any right clavicle dislocation and, in our opinion, the complaint of tingling, together with limitation of use of the limbs, is consistent with the neurological damage, reported by Professor Cade. We are also of the opinion, that the left arm limitation being explained by a possible right clavicle dislocation has no musculo skeletal explanation.
Having regard to the factors recorded at the conclusion of the decision in Repatriation Commission v Delidio 1998 49 ALD 193 at 206, we are satisfied that the hypothesis advanced on behalf of Mrs Plattfuss is not, in the circumstances, "reasonable". Whilst, we acknowledge that the deceased did suffer from ischaemic heart disease, we are not satisfied that a reasonable hypothesis exists connecting it with the circumstances of death. We are satisfied that the circumstances of death are more consistent with the opinions expressed by Professor Cade, than the opinions of Dr Pilbeam. In reaching this conclusion, we have not preferred the opinions of Professor Cade over Dr Pilbeam, nor have we chosen his opinions to the exclusion of Dr Pilbeam, however, it is our opinion, that the opinions of Dr Pilbeam are not supported by raised facts or material which point to the hypothesis, as being reasonable.
The decision under review is affirmed.

I certify that the fifty six (56) preceding paragraphs are a true copy of the reasons for the decision herein of
Mr J. Handley. Senior Member.
Dr C. Re, Member
Signed:   Linda Nemeth          ......................................
                Secretary
Date/s of Hearing  10 April 2000
Date of Decision  27 April 2000
Counsel for the Applicant        Dr Moore
Solicitor for the Applicant
Counsel for the Respondent    Mr Douglass
Solicitor for the Respondent