Amanda Maria Pass as Executor of the Estate of Adam Jefferson Pass (deceased) v Gerling Australia Insurance Company Pty Limited - [2009] WADC 173

JURISDICTION : DISTRICT COURT OF WESTERN AUSTRALIA
IN CIVIL

LOCATION: PERTH

CITATION: AMANDA MARIA PASS as Executor of the Estate of ADAM JEFFERSON PASS (DECEASED) -v- GERLING AUSTRALIA INSURANCE COMPANY PTY LIMITED [2009] WADC 173

CORAM: MARTINO DCJ

HEARD: 9 & 10 NOVEMBER 2009

DELIVERED : 18 NOVEMBER 2009

FILE NO/S: CIV 848 of 2003

BETWEEN: AMANDA MARIA PASS as Executor of the Estate of ADAM JEFFERSON PASS (DECEASED)
Plaintiff
AND
GERLING AUSTRALIA INSURANCE COMPANY PTY LIMITED (ABN 16 069 085 196)
Defendant

Catchwords:

Insurance - Personal accident - Whether death caused by thrombosis of a coronary artery was a death caused by bodily injury resulting from an accident

Legislation:

Nil

Result:

Plaintiff's claim dismissed

Representation:

Counsel:

Plaintiff: Mr S Millman
Defendant: Mr P Jarman

Solicitors:

Plaintiff: Slater & Gordon
Defendant: Jarman McKenna

Case(s) referred to in judgment(s):

Accident Compensation Commission v McIntosh [1991] 2 VR 253
Australian Casualty Co Ltd v Federico (1986) 160 CLR 513
Commonwealth v Hornsby (1960) 103 CLR 588
Dennis v City Mutual LifeAssurance Society Ltd [1979] VR 75
Fenton v J Thorley & Co Ltd [1903] AC 443
Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286
Povey v Qantas Airways Ltd (2005) 223 CLR 189
Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310

MARTINO DCJ: On 17 April 2000, at 8.15 in the morning, Mr Adam Jefferson Pass was at Singapore Airport. He collapsed suddenly. At the time of his collapse Mr Pass was walking and talking normally and no external event happened to him. Mr Pass was taken to the Accident and Emergency Department of Changi General Hospital. On the way to the hospital Mr Pass received cardiopulmonary resuscitation. Mr Pass arrived at Changi Hospital at 8.51 am. He was in a collapsed state with no recordable blood pressure. Attempts to resuscitate Mr Pass were unsuccessful and he was pronounced dead at 9.35 am.
Mr Pass was an insured person under a Group Personal Accident and Corporate Travel Plan underwritten by the defendant, Gerling. The policy was issued to Coflexip Stena Offshore Asia Pacific Pty Ltd. Mr Pass was an insured person under that policy because he had been nominated for cover under the policy by Coflexip Stena or one of its subsidiaries.
In this action the executor of Mr Pass' estate claims the sum of $250,000 under that policy. By its defence Gerling raises a number of issues, but most of those issues have now been resolved.
There is one outstanding issue. It is whether Mr Pass' death was the result of an injury as defined in the personal accident section of the policy. That definition is:
"INJURY means bodily injury resulting from an accident that occurs fortuitously to the Insured Person during the Period of Insurance and results in any of the Insured Events specified in the Table of Benefits within twelve (12) calendar months from the date thereof. Injury does not include:
a.any consequences of an Injury which are ordinarily described as being a disease;
b.an aggravation of a pre – existing injury unless caused by a separate and distinct accident."

Mr Pass

Mr Pass was born on 19 July 1963. His occupation was pilot technician. He had attended at the Emergency Department of Royal Perth Hospital on 22 February and 27 February 2000. A report by Dr Brian Dare of Royal Perth Hospital dated 24 April 2001 and records from Royal Perth Hospital were tendered in evidence by consent.
On 22 February 2000 Mr Pass described two episodes of sharp chest pain lasting five to ten minutes and resolving spontaneously. Examination and ECG were normal. His blood pressure was 145/70.
On 27 February Mr Pass complained of a localised area of sharp chest pain lateral to his left sternum with no associated symptoms. His vital signs were normal, apart from blood pressure of 160/110. An ECG showed no ischaemic changes and his chest x-ray was normal. Past medical history was recorded as being unremarkable apart from him smoking 15 cigarettes a day. Mr Pass was discharged home on Naprosyn and it was recommended that he see his general practitioner for follow up, including an ECG stress test.
On 8 March 2000 Mr Pass saw Dr F V McKnight, a general medical practitioner. Dr McKnight's report dated 15 May 2001 was tendered in evidence by consent.
Dr McKnight had not seen Mr Pass for two years prior to 8 March 2000. On 8 March 2000 Mr Pass told Dr McKnight of his recent chest pain. Mr Pass' blood pressure was 145/50, his heart sounds were normal and his lungs were clear. He was not complaining of chest pain on the day he saw Dr McKnight. He did not tell Dr McKnight of any history of previous heart problems or family history of heart disease. A barium meal test on the following day revealed slight gastric – oesophageal reflux, for which Dr McKnight prescribed medication. Dr McKnight did not see Mr Pass again.

The autopsy report

Dr Wee Keng Poh performed an autopsy on Mr Pass' body on 18 April 2000. Dr Wee Keng Poh's autopsy report was tendered in evidence by consent. In that report Dr Wee Keng Poh recorded that on examination of Mr Pass' coronaries he found:
"Widely patent coronary ostia. The left anterior descending coronary shows severe atheroma proximally with pinpoint narrowing and a fresh thrombosis totally occluding the lumen. The right main and the left circumflex coronary shows moderate atheroma with scattered narrowing of 75%"
Dr Wee Keng Poh certified that the cause of death was thrombosis of the left anterior descending coronary.
Dr Wee Keng Poh wrote a report dated 8 May 2001 which was also tendered into evidence by consent. In that report Dr Wee Keng Poh expanded upon the autopsy report. Dr Wee Keng Poh wrote:
"In brief, Mr Pass' heart was enlarged due to perhaps long standing high blood pressure as reflected in the thickened left ventricular wall and normal aortic valve. Coupled with this, his coronaries which are blood vessels which supply blood to the heart muscles show severe narrowing of the left anterior descending coronary. There was a blood clot occluding the lumen which was already narrowed by severe atheroma. As a result of the blockage, the heart muscle begins to die or what is known as acute myocardial infarction.
The pre-existing conditions which led to him having the coronary thrombosis were: hypertension and coronary arterial disease which was aggravated, to put it in simple layman's terms, usually by high cholesterol (the 'fatty component') levels in the blood."

The report of Professor Leonard F Arnolda

A report dated 15 August 2001 by Leonard F Arnolda, Professor of Cardiology at Royal Perth Hospital, was tendered in evidence by consent. In Professor Arnolda's opinion the reports of Dr Dare and Dr McKnight did not support Dr Wee Keng Poh's view that Mr Pass may have suffered from arterial hypertension.
In Professor Arnolda's opinion the coronary narrowing identified in Mr Pass' autopsy pre-dated Mr Pass' travel between Australia and India. The left ventricular hypertrophy indentified in the autopsy and the history of cigarette smoking increased the risk of coronary events, although their precise contribution to the development of coronary atherosclerosis is not known. Coronary thrombosis is initiated by rupture or fissure of an atherosclerotic plaque. Epidemiological studies have identified a number of triggers for this process, including physical stress, emotional stress or even anger. Physical or mental stress associated with his trip might have triggered an arrhythmia in Mr Pass.
Professor Arnolda's report contains the following summary and conclusion:
"It is impossible to identify the precise reasons why a particular individual has coronary atherosclerotic disease, has a thrombotic occlusion and dies suddenly. Nevertheless, there is sufficient knowledge about the mechanism and circumstances in which coronary events occur to construct plausible hypotheses linking Mr Pass' employment to his demise. It is not possible to either prove or disprove these hypotheses.
1)The coronary narrowing identified by post mortem in Mr Pass would have been present prior to the employment related travel undertaken by Mr Pass. The causation is likely to be related to his genetic endowment and lifestyle. If his employment contributed to his smoking habit or his cardiac hypertrophy, a causal link might have been postulated.
2)The thrombotic event is susceptible to environmental influence and is not a random event. Any of the potential triggers I listed might have a role.
3)It is plausible that physical or mental stress might have triggered an arrhythmia.
4)It is plausible that the unfamiliar circumstances Mr Pass was in deterred him from seeking potentially life saving medical treatment."

The evidence of Dr Richard Byron Collins

Mrs Pass called evidence from Dr R Byron Collins. Dr Collins is a consultant forensic pathologist of many years experience. His evidence is contained in his written reports dated 28 August 2001 and 24 June 2009 and the oral evidence he gave at trial.
Dr Collins agreed with the cause of death stated in Dr Wee Keng Poh's autopsy report. In Dr Collins' opinion the following disease processes could also have been listed:
(i)severe coronary atherosclerosis;
(ii)myocardial infarction (healing).
In Dr Collins' opinion there is no doubt that Mr Pass suffered from extensive and severe atherosclerotic narrowing of all the major coronary arteries. "This pathological condition was long – standing and would have been relentlessly progressing in its severity for a considerable period of time (years)."
Dr Collins had examined microscopic slides prepared as part of the autopsy and in his report of 28 August 2001 he noted:
"3The light microscope slide prepared from a segment of the left anterior descending coronary artery showed three, complete cross – sections with histological abnormalities as listed:
(i)up to approximately 95% luminal narrowing (either central or eccentric) by atherosclerosis in which there was widespread hyalinization, patchy calcification, abundant cholesterol clefts and delicate revascularisation channels.
(ii)extensive haemorrhage within the atherosclerotic plaque (red blood cells intact).
(iii)recent intra – luminal thrombus, not in continuity with intraplaque haemorrhage."
In one of the microscope slides of the left coronary artery the thrombus almost totally occluded the lumen.
In his report of 28 August 2001 Dr Collins expressed the opinion that:
"the most likely explanation in relation to the development of the thrombus … was as consequence of recent haemorrhage into the subjacent atherosclerotic plaque. In other words, the intraplaque haemorrhage was a sudden and separate catastrophic event, which then precipitated thrombus formation and, therefore, this blood clot could not be regarded as having been generated as an inevitable and natural progression of the pre–existing atherosclerotic disease…
In summary, it is my opinion that the death of the late Mr Pass was as a consequence of haemorrhage into the atherosclerotic plaque and subsequent formation of a thrombus in the left anterior descending coronary artery, which was an actual physical injury and not an inevitable progression of the pre‑existing atherosclerosis."
Examination of the two sections of the heart muscle (the myocardium) showed multiple small, patchy areas of predominantly perivascular fibrosis, some of which extended into the surrounding myocardial tissue. These areas were areas of healing and had resulted from death of heart muscle tissue consequent upon coronary atherosclerosis. In Dr Collins' opinion these areas were consistent with Mr Pass having suffered a previous acute myocardial infarction at about the time of his presentation to Royal Perth Hospital in February 2000.
In his oral evidence Dr Collins explained his findings and opinions further. The atherosclerosis in Mr Pass' coronary arteries was consequence of the laying down in those arteries of a variety of substances such as cholesterol and calcium which formed an atherosclerotic plaque in the arteries. Those substances precipitated an inflammatory reaction which resulted in a number of different types of cells entering into the blood vessels. There was also the development of very delicate and tiny blood vessels that infiltrated into the atherosclerotic plaque. Such tiny blood vessels are not always present in the atherosclerotic plaque of a person who has atherosclerotic arteries. They were present in Mr Pass' atherosclerotic plaque.
The haemorrhage into Mr Pass' atherosclerotic plaque was a result of these tiny blood vessels rupturing. That rupture caused the vessels to haemorrhage. This resulted in part of the plaque detaching from its position in the coronary artery which precipitated the development of the thrombus in the artery. The development of the thrombus was not an inevitable result of the presence of atherosclerotic plaque in Mr Pass' coronary arteries. Some people with more atherosclerotic plaque than Mr Pass had do not develop a thrombus. Some people develop a thrombus even though they have less atherosclerotic plaque than Mr Pass had.
The rupturing of the tiny blood vessels in Mr Pass' atherosclerotic plaque may have been caused by an increase in his blood pressure. This increase in blood pressure could have been caused by a number of factors. For example, it could have been caused by stress. It could have been caused by physical activity. It could have been caused by circulating catecholamines such as adrenal or noradrenal.

The evidence of Associate Professor Johan Duflou

Gerling called Associate Professor Johan Duflou to give evidence. Associate Professor Duflou is a specialist forensic pathologist of many years experience with a special interest in research into sudden death through cardiac arrest. His evidence was contained in his reports dated 27 December 2005 and 4 November 2009 and his oral evidence at the trial.
In Associate Professor Duflou's opinion Dr Wee Keng Poh correctly attributed the cause of death to thrombosis of the left anterior descending coronary artery. In his report dated 27 December 2005 he expressed the opinion that although a diagnosis of an acute myocardial infarction was not made at the time of Mr Pass' attendances at Royal Perth Hospital in February 2000 it is reasonable to infer that his symptoms at the time were those of an acute myocardial infarction.
In that report Associate Professor Duflou also provided the following opinions:
"In my opinion, there is no evidence of an accident occurring or causing death in this case…there was pre – existing pathology which naturally progressed to a not – unexpected fatal outcome…
The deceased had severe coronary atherosclerosis, a natural disease process. In coronary atherosclerosis, there is accumulation of lipid, fibrous tissue, debris and other substances in the wall of the coronary artery, producing an atherosclerotic plaque, with consequent narrowing of the vessel lumen. This in turn decreases the amount of blood and oxygen supplied to heart muscle. When the narrowing reaches a critical stage, generally thought to be where there is more than 75% cross–sectional area narrowing, or stenosis, of the coronary artery, the plaque itself has a tendency to rupture, causing bleeding into the plaque and release of atherosclerotic debris into the lumen of the coronary artery. This in turn is a potent stimulant for thrombosis of the coronary artery, resulting in a sudden blockage of the vessel …
In my opinion, the deceased had a natural disease process which progressed to death. My concept of an accident relative to this opinion can be outlined as follows: an accident is any external event, including physical force, chemical exposure, radiation and deleterious alterations in a person's immediate environment, and the direct and indirect consequences of such an event, which causes an injury or other damage to the deceased. In the case of Mr Pass, there was pre–existing pathology which naturally progressed to a not–unexpected fatal outcome.
I agree with Dr Collins that the intraplaque haemorrhage was sudden and that this in turn precipitated thrombus formation. I also agree with Dr Collins that such a progression is not inevitable, in that not all patients with severe coronary artery narrowing will progress to plaque rupture. However, I am of the view that the progression of severe atherosclerosis to plaque haemorrhage, rupture and thrombus formation is very well‑described, and is considered to be the primary mechanism whereby patients with severe atherosclerosis suddenly develop an acute myocardial infarction by pathologists and clinicians alike."
I have quoted Associate Professor Duflou's view as to what constitutes an accident because it assists in the understanding of his opinion that Mr Pass did not suffer an accident. What is an accident within the meaning of the policy is to be determined by reference to the policy and relevant authorities. I make that determination without reference to the medical experts' views as to the meaning of the word.
In his report of 27 December 2005 Associate Professor Duflou wrote:
"From the information provided by Mr Power, the deceased was walking and talking normally immediately prior to his collapse, and there was no external event, including physical force, chemical exposure, radiation and deleterious alterations in the patient's immediate environment, which could have caused the thrombosis."
I was informed by counsel that it was agreed that the contents of this sentence as to Mr Pass' activity at the time of his collapse were true.
At the time he wrote his report of 27 December 2005 Associate Professor Duflou did not have available to him the microscopic slides that Dr Collins had examined. The slides were provided to him and he referred to them in his report of 4 November 2009. The coronary artery slide showed advanced atherosclerotic narrowing, complicated by plaque haemorrhage and thrombotic occlusion of the vessel. The thrombus appears to have formed on at least two separate occasions, with both an eccentric layer of non occlusive thrombus and a more recent occluding or near total occluding thrombus.
Associate Professor Duflou did not change his opinion as a result of viewing the slides. He remained of the opinion that the cause of death had been correctly attributed to thrombosis of the left anterior descending coronary artery, that there were significant pre–existing medical conditions, namely coronary artery atherosclerosis and ischaemic heart disease, there was no evidence of bodily injury resulting from an accident, the direct cause of death was the consequence of a disease which had naturally progressed in severity, leading to death and that the cause of death, namely coronary artery thrombosis, is not ordinarily described as an injury.
He agreed with Dr Collins that plaque haemorrhage and rupture is not an invariable progression of coronary artery atherosclerosis. Nevertheless, plaque rupture is more likely as narrowing of the artery increases in severity and at a level of approximately 75 per cent it is generally held that such plaques have a much greater propensity to rupture than those causing lesser narrowing of the coronary arteries. "Plaque haemorrhage and rupture, followed by thrombosis in severely narrowed coronary arteries is, in my opinion, a generally accepted mainstream view of the natural progression of coronary artery disease."
Associate Professor Duflou expanded on his opinions in his oral evidence. Where a person has atherosclerotic plaque in the coronary arteries there is a higher than normal likelihood of that person developing thrombosis, or clotting of that artery, resulting in a myocardial infarction. The development of thrombosis in such a person is very common, but not inevitable.

He agreed with Dr Collins that Mr Pass suffered from extensive and severe atherosclerotic narrowing of all the major coronary arteries and that this was a long–standing pathological condition which would have been relentlessly progressing in severity for a number of years.
The development of thrombosis is almost expected if a person with severe atherosclerotic narrowing does not obtain appropriate medical treatment for the condition. However, while it is almost expected, it is not inevitable.
Associate Professor Duflou thought that there had been haemorrhages in Mr Pass' coronary arteries on a number of occasions. From his examination of the microscopic slides, Associate Professor Duflou concluded that the bleeding that ultimately resulted in Mr Pass' death occurred approximately eight hours before death.
Associate Professor Duflou agrees with Dr Collins that the intraplaque haemorrhage was from small blood vessels that were in the atherosclerotic plaque. In Associate Professor Duflou's opinion it is not possible to say what caused those blood vessels to rupture and bleed. Medical practitioners know that this happens frequently, but it is not inevitable.

Findings of fact

There is very little, if any, difference between the medical witnesses as to the physical process which led to Mr Pass' death. I find that Mr Pass died as a result of a thrombosis of the left anterior descending coronary artery. The artery was blocked by a thrombus, which caused myocardial infarction.
At the time he developed the thrombus Mr Pass had severe coronary atherosclerosis. The coronary atherosclerosis had existed for many years and had been progressing over those years. The thrombus was formed as a result of small blood vessels in the atherosclerotic plaque haemorrhaging. The presence of the atherosclerotic plaque was a necessary pre–condition for the development of the thrombus but the development of the thrombus was not inevitable. Not all persons with atherosclerotic plaque develop a thrombus. However because he had severe coronary atherosclerosis Mr Pass had a higher than normal likelihood of developing thrombosis and the development of thrombosis in a person with severe coronary atherosclerosis such as that suffered by Mr Pass is very common.
There had been previous bleeding in Mr Pass' coronary arteries. The bleeding that resulted in his death resulted from rupture of the blood vessels approximately eight hours before he died.
It is not possible to determine what caused the blood vessels to rupture. An increase in Mr Pass' blood pressure may have caused them to rupture, but it is not possible to conclude from the evidence that Mr Pass' blood pressure did increase at the time that the blood vessels ruptured and, even if it did, it is not possible to conclude that such an increase caused the blood vessels to rupture and, further, it is not possible to determine what caused any increase in his blood pressure.
In February 2000 Mr Pass suffered a myocardial infarction. There was some death of the heart tissue caused by an obstruction to a coronary artery at that time, although this was not diagnosed at Royal Perth Hospital.
There is some difference in the evidence of the medical practitioners as to whether Mr Pass suffered from long standing high blood pressure prior to his death. Counsel for both parties submitted that the difference of evidence on this issue was not significant in the resolution of the case, but I mention it for completeness.
Dr Wee Keng Poh's view is that Mr Pass' heart was enlarged due to perhaps long standing high blood pressure as reflected in the thickened left ventricular wall and normal aortic valve. Professor Arnolda has expressed the opinion that Dr Wee Keng Poh's view that Mr Pass may have suffered from arterial hypertension is not supported by the contents of the reports of Dr Dare and Dr McKnight. Dr Collins did not express an opinion on the issue. In his report dated 27 December 2005 Associate Professor Duflou recorded that according to information provided in the report by the Office of Health Review Mr Pass had hypertension. The report of the Office of Health Review was not tendered in evidence. I raised the matter with counsel. Counsel informed me that the parties agreed that there was no objection to the information contained in Associate Professor Duflou's report about the content of the Office of Health Review being before me.
The reports of Dr Dare and Dr McKnight show that Mr Pass' blood pressure on 22 February 2000 was 145/70, on 27 February 2000 it was 160/110 and on 8 March 2000 it was 145/50. Associate Professor Duflou's evidence was that the reading on 27 February 2000 was hypertension. The readings on the other two dates showed high systolic blood pressure with low or normal diastolic blood pressure.
I find there was one occasion – 27 February 2000 – when Mr Pass' blood pressure was high before his death. On each occasion that his blood pressure was taken in February and March 2000 Mr Pass had high systolic blood pressure. His diastolic blood pressure was low or normal on 22 February 2000 and 8 March 2000.

Interpretation of the policy

The policy provides cover if an "Insured Person" suffers an "Injury". An Insured Person is defined as any person nominated by Coflexip Stena, one of its subsidiaries or another party with an insurable interest. There are seven categories of insured person. The definitions of those categories include the terms "Blue Collar Workers", "Directors", "Executives" and "Declared Expatriates". Mr Pass was a declared expatriate. It was a policy that could provide cover to a wide range of people and, in my view, the approach to its interpretation should be that explained by Wilson, Deane and Dawson JJ in Australian Casualty Co Ltd v Federico (1986) 160 CLR 513 at p 525. The approach to the meaning of injury in the policy should be a consideration of what the words of the policy convey, as a matter of contemporary language read in the context of the whole policy, to a reasonable non‑expert. "If that meaning is plain, it can be of but limited significance if, at other times and in other places, other courts, however eminent, have held that similar words in other policies were to be construed as having had some different meaning."
The definition of injury contains two sentences. The first sentence contains a statement of what the word means. The second sentence specifies two types of matters that are not included in the meaning of the word. I conclude that for an event to be an injury covered by the policy it must be included in the first sentence, that is, it must be a bodily injury resulting from an accident that occurs fortuitously to the insured person during the period of insurance which results in any of the insured events within twelve calendar months of the date of the bodily injury. If the event comes within that definition the second sentence is to be considered.
In Federico (supra) Wilson, Deane and Dawson JJ said at p 527 that in the context of the policy that they were considering the word "injury" would include any physical damage sustained as the identifiable result of a traumatic occurrence such as the external application of force or the internal application of pressure generated by personal exertion. However, that must be read in the context of a policy that consistently showed "injury" and "sickness" as alternatives and in the context of a case where the insured had suffered a central disc prolapse while engaged in heavy work. I do not regard their Honours inclusion of damage so sustained within the meaning of injury in the policy as being intended to limit what they said at p 525; that the approach to the meaning of injury in the policy should be a consideration of what the words of the policy convey, as a matter of contemporary language read in the context of the whole policy, to a reasonable non‑expert.
As Murphy J said in Accident Compensation Commission v McIntosh [1991] 2 VR 253 at p 255 injury means in its normal usage harm or damage. The relevant definitions of the word in the Macquarie Dictionary, fourth edition, are:
"1. harm of any kind done or sustained: to escape without injury. 2. a particular form or instance of harm: severe bodily injuries."
The word "bodily" in the definition expresses what would have been implied – Federico at p 527. It requires that the injury must have been of or to the body or a part of the body.
I interpret the words "bodily injury" in the definition as meaning harm or damage done to the body or a part of the body.
The injury must be bodily injury "resulting from an accident that occurs fortuitously". To result from an accident the bodily injury must have been caused by an accident. An accident "is something which happens without intention or design. When used with reference to something which causes injury, it means an unexpected and unintended mishap. In that context, the ordinary and natural meaning of the word still corresponds with Lord Macnaghten's definition in Fenton v J Thorley & Co Ltd [1903] AC 443 at 448 which, although propounded in a Workmen's Compensation Act case, has commonly been accepted as applicable to the use of the word in public liability and other insurance policies: 'an unlooked – for mishap or an untoward event which is not expected or designed'" – Federico at p 527.
I have quoted earlier in these reasons Associate Professor Duflou's concept of an accident. There are several cases, of which Dennis v City Mutual Life Assurance Society Ltd [1979] VR 75 is one, where the accident is defined to mean "violent, accidental, external and visible means". Accident is not so limited in this policy. In Povey v Qantas Airways Ltd (2005) 223 CLR 189 the High Court held that in the Warsaw Convention 1929 an injury is caused by an accident only if caused by an unexpected or unusual event or happening external to the passenger. However the history and status of that international convention mean that the interpretation of a term in it does not necessarily apply to an insurance policy. In the absence of a limitation in the policy of an accident to an external event, it is immaterial that the accident is not violent, external or visible. An accident can be internal – Federico per Brennan J at p 535.
I conclude that the word "accident" covers a wider field than understood by Associate Professor Duflou. An accident need not be an external event. It can be an internal event. What is required is that it is an unexpected and unintended mishap.
The word "fortuitously" is an adverb, in this phrase it modifies the verb occurs, of which the subject is an accident. An event is fortuitous if it is an event "happening or produced by chance; accidental" – Macquarie Dictionary, fourth edition. I find it impossible to conceive of how an accident could not occur fortuitously. In my view the word "fortuitously" is otiose and adds nothing to the words "resulting from an accident".
The first exclusion in the second sentence of the definition of injury is "any consequences of an injury which are ordinarily described as being a disease". The plural "are" makes clear that it is the consequences to which the exclusion applies. If an injury has consequences and those consequences are ordinarily described as being a disease then they are not an injury within the definition. The use of the passive tense does not make clear by whom the consequences are described as being a disease. The word "ordinarily" suggests that the exclusion is referring to descriptions in ordinary conversation, not a medical expert. I conclude that this exception means consequences which a reasonable, ordinary member of the public would regard as being a disease are excluded from the definition of injury. A disease is a morbid condition of the body, or of some organ or part; illness; sickness; ailment – Macquarie Dictionary, fourth edition.
The second exclusion means that the aggravation, or making worse, of an injury that already existed is not an injury, unless that aggravation is itself caused by a separate and distinct unexpected and unintended mishap.

Whether Mr Pass' death was the result of an injury as defined in the personal accident section of the policy

Mr Pass had severe coronary atherosclerosis. The coronary atherosclerosis had existed for many years and had been progressing over those years. Because he had severe coronary atherosclerosis Mr Pass had a higher than normal likelihood of developing thrombosis. The development of thrombosis in a person with severe coronary atherosclerosis such as that suffered by Mr Pass is very common. The formation of the thrombus was not, however, inevitable.
The thrombus formed because fine blood vessels in the atherosclerotic plaque in Mr Pass' coronary artery ruptured. The plaintiff's case is that the intraplaque haemorrhage was an accident. The rupture of those blood vessels was unexpected and unintended. It could not have occurred unless Mr Pass suffered coronary atherosclerosis. Because he had severe coronary atherosclerosis Mr Pass had a higher than normal likelihood of developing thrombosis and the development of thrombosis in a person with his level of severe coronary atherosclerosis is common. The rupture of the blood vessels was nevertheless unexpected – it was not expected by anyone – and it was unintended.
However it does not follow automatically that because the rupture and bleeding of the blood vessels were both unexpected and unintended the event was an accident. It was certainly an injury. It was damage done to a part of Mr Pass' body. For an injury to be caused by an accident there must be an accident which causes injury, it is not enough that the injury may be described as accidental – Federico per Gibbs CJ at p 521.
In Federico Wilson, Deane and Dawson JJ at pp 527‑528 gave examples of an accident – it may occur independently of any act of the person injured such as an explosion of a boiler, the collapse of a building or the failure of brakes of a motor vehicle. It may involve an involuntary act of the injured person such as slipping and falling or dropping a heavy object on one’s foot. It may represent an unintended and unexpected characteristic or consequence of an intended act such as the application of excessive force by holding a fragile object too tightly so that it is unintentionally broken or creating internal pressure within a person's body by the exertion involved in lifting, pushing or pulling which unintentionally and unexpectedly causes damage to the body, such as straining a muscle or bursting a blood vessel. Of this last example their Honours said:
"If the muscle or blood vessel be already in an unsound condition, there may be room for argument about whether the straining of the muscle or the breaking of the blood vessel is properly to be seen as having been caused by the pre‑existing condition rather than by the unintentional and unexpected excessiveness of the pressure created by the exertion. If it was in a sound condition, however, it will be plain that the damage to muscle or blood vessel was caused by the unintentional and unexpected excessiveness of the pressure. As a matter of ordinary language, the injury in such a case is caused by accident or mishap."
I am unable to conclude what caused the blood vessels to rupture. I am unable to conclude that it was the result of any external or internal event or activity. It would not, as a matter of ordinary language be described as an accident. In my view neither the rupture of the blood vessels nor the haemorrhaging that followed it, alone or in combination, constitute an accident.
Counsel for the plaintiff did not submit that any other event constituted an accident. I can find no other event that constituted an accident. I find that there was no accident. The plaintiff’s case must therefore fail. In case I am wrong in that conclusion I will consider the application of the remaining provisions of the definition of injury in the policy.
Mr Pass died because his left anterior descending coronary artery was blocked by a thrombus. This blockage caused the death of heart tissue. This resulted in Mr Pass dying. The thrombus was formed as a result of the rupture of the blood vessels in the atherosclerotic plaque. The bleeding from those blood vessels resulted in the development of the thrombus. The death of the heart tissue was damage done to a part of Mr Pass' body. It was an injury. That injury resulted from the rupture of the blood vessels. If the rupture of the blood vessels were an accident the death of the heart tissue would have been an injury resulting from an accident.
None of Mr Pass' death, the myocardial infarction, the formation of the thrombus and the blocking of the artery by the thrombus is ordinarily described as being a disease. The first exclusion to the definition of an injury would not apply.
In February 2000 Mr Pass had suffered a myocardial infarction. The myocardial infarction he suffered on 17 April 2000 was a separate myocardial infarction. None of Mr Pass' death, the myocardial infarction, the formation of the thrombus and the blocking of the artery by the thrombus was an aggravation of a pre–existing injury. The second exclusion to the definition of an injury would not apply.
In Commonwealth v Hornsby (1960) 103 CLR 588 the High Court held that a person who had suffered stroke as a result of a thrombus in a blood vessel had not suffered personal injury by accident and so was not entitled to worker's compensation. The stroke was held to be a disease, not a personal injury by accident because no particular incident or activity of the worker accelerated or contributed to the occlusion. However more recent decisions of the High Court such as Zickar v MGH Plastic Industries Pty Ltd (1996) 187 CLR 310 and Kennedy Cleaning Services Pty Ltd v Petkoska (2000) 200 CLR 286 now make clear that internal damage to the cardio‑vascular system can constitute an injury.
I conclude that Mr Pass suffered bodily injury, that the exclusions to the definition of injury in the policy do not apply and that the injury resulted in Mr Pass' death. However the bodily injury did not result from an accident. The plaintiff's claim does not succeed.