Halverson v Dobler - [2006] NSWSC 1307

No judgment structure available for this case.

CITATION: HALVERSON & ORS v DOBLER HALVERSON by his tutor v DOBLER [2006] NSWSC 1307

HEARING DATE(S): 7 August 2006 - 4 September 2006

JUDGMENT DATE :
1 December 2006

JURISDICTION: Civil

JUDGMENT OF: McClellan CJatCL at 1

DECISION: Verdicts for the plaintiffs

CATCHWORDS: PROFESSIONAL NEGLIGENCE - LIABILITY - MEDICAL NEGLIGENCE - general practitioner - rural practice - DAMAGE - brain injury - cardiac arrest - BREACH - diagnosis of recurrent syncope - cardiac cause of syncope - apprpriate diagnostic investigation - facilities readily available - long QT syndrome - causation - chance of investigation revealing long QT interval - EXPERT EVIDENCE - general practitioners - cardiologists - scientif proof and legal standard of proof - role of hindsight - effect of s 5O of the Civil Liability Act 2002 (NSW) - LOSS OF A CHANCE in medical negligence

LEGISLATION CITED: Civil Liability Act 2002 (NSW)
Interpretation Act 1987

CASES CITED: Ambulance Service of NSW v Worley [2006] NSWCA 102
Bennett v Minister of Community Welfare (1992) 176 CLR 408
Capital Brake Service Pty Ltd v Nicholas Kevin Meagher & 8 Ors t/as Sparke Helmore [2003] NSWCA 225
Chaplin v Hicks [1911] 2 KB 786
Chappel v Hart (1998) 195 CLR 232
Elbourne v Gibbs [2006] NSWCA 127
EMI (Australia) Ltd v BES [1970] 2 NSWLR 238
Faferrière v Lawson [1991] 1 SCR 541
Graham v Baker (1961) 106 CLR 340
Gregg v Scott [2002] EWCA Civ 1471
Gregg v Scott [2005] 2 AC 176
Jones v Dunkel (1958) 101 CLR 298
MacArthur Districts MotorCycle Sportsman Inc v Ardizzone [2004] NSWCA 145
Malec v J C Hutton Pty Ltd (1990) 169 CLR 638
Mallett v McMonagle [1970] AC 166
March v E & M H Stramare Pty Ltd (1990) 171 CLR 506
Naxakis v Western General Hospital & Anor (1999) 197 CLR 269
Neindorf v Junkovic (2005) 222 ALR 631
Penrith City Council v Parks [2004] NSWCA 201
Ramsay v Watson (1961) 108 CLR 642
Rogers v Whitaker (1992) 175 CLR 479
Rufo v Hosking [2004] NSWCA 391
Sellars v Adelaide Petroleum NL (1992) 179 CLR 332
Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262
State of New South Wales v Burton [2006] NSWCA 12
State of NSW t/a NSW Department of Agriculture v Allen [2000] NSWCA 141
T C (by his tutor Sabatino) v The State of NSW & Ors [2001] NSWCA 380
Vairy v Wyong Shire Council (2005) 223 CLR 422
Watts v Rake (1960) 108 CLR 158
Wynn v NSW Insurance Ministerial Corporation (1995) 184 CLR 485

PARTIES: 20182/03
Kenneth Halverson (1P)
Janet Halverson (2P)
Annika Halverson (3P)
Kenneth Dobler (Def)
20183/03
Kurt Halverson bht Kenneth Halverson (Pltf)
Kenneth Dobler (Def)

FILE NUMBER(S): SC 20182/03; 20183/03

COUNSEL: M B Williams SC/L Grey (Pltfs)
D Higgs SC/K C Morgan (Def)

SOLICITORS: Maurice Blackburn Cashman (Pltfs)
Blake Dawson Waldron (Def)

IN THE SUPREME COURT
OF NEW SOUTH WALES
COMMON LAW DIVISION
PROFESSIONAL NEGLIGENCE LIST

McCLELLAN CJ at CL

FRIDAY 1 DECEMBER 2006

20182/03 HALVERSON, Kenneth & ORS v DOBLER
20183/03 HALVERSON Kurt by his tutor, Kenneth Halverson v DOBLER
JUDGMENT

1 HIS HONOUR: There are four proceedings before the court. The plaintiff, Kurt Halverson, by his tutor (his father, Ken Halverson), sues his general practitioner, Dr Kenneth Dobler, claiming damages for negligence. Kurt alleges that the defendant failed to exercise due care in the treatment of him from 1995 until 10 February 2001. On 11 February 2001 Kurt suffered a cardiac arrest and hypoxic brain damage leaving him with catastrophic injuries. The other proceedings are brought by Kurt’s father, Ken, Kurt’s mother, Janet, and sister, Annika, who each claim damages for nervous shock. (Throughout these reasons I have referred to the submissions made on behalf of Kurt. Those submissions are, of course, also made on behalf of the other plaintiffs).

2 The essence of the plaintiff’s case was that Dr Dobler should have identified Kurt as having a cardiac problem before he suffered the catastrophic event of 11 February. It was submitted that there were a number of occasions (and I will discuss each of them) when Kurt’s symptoms could have and, it was submitted, should have caused Dr Dobler to refer him to a cardiologist for assessment. It was also submitted that Dr Dobler should have carried out, or ordered to be carried out, an electrocardiogram (ECG) following the various events but most significantly after the detection of a heart murmur followed by a further syncopal event on 4 February 2001. The failure to take either of these steps was identified as a breach of Dr Dobler’s duty of care to Kurt. It was contended that if either of these steps had been taken Kurt’s cardiac irregularity identified as long QT interval (which has since been verified) would probably have been identified and appropriate responses put in place which would have avoided the catastrophe. Alternatively, it was submitted that if an ECG had been performed there was a real chance that a long QT interval would have been found and Kurt should be compensated for having lost that chance.

3 If liability in the full amount is found the parties have agreed damages for Kurt in the sum of $8,086,000. On the same basis, damages for Ken have been agreed at $550,000, for Janet at $150,000 and for Annika at $11,500.

4 The plaintiff was born on 25 September 1982. He is now unable to walk or talk. He came to court on the first day of the hearing so that I could gain an understanding of the surgery he required to his arms and legs following his catastrophic injuries and the general extent of his disabilities. Evidence of previous events in his life, his medical history and relevant incidents was given by his father and grandfather.

5 The plaintiff’s father gave evidence that Kurt was a relatively healthy young man until the time of his injury. There was an incident, when he was thirteen months of age, when, with a high temperature, he started shaking. This was diagnosed as “febrile convulsions.” Kurt suffered from common childhood illnesses such as bronchitis, chicken pox and sometimes had asthma in the winter. He progressed well at school and did well in his School Certificate. He took some time out from school after the School Certificate and embarked upon his Higher School Certificate year in October 2000. During that year he formed a close relationship with his girlfriend Megan McKay.

6 In his adolescent years Kurt played sport, including basketball, tennis, touch football and cross-country running. Although he had a history of migraine headaches, he was described by his father as having a high level of aerobic fitness prior to his cardiac arrest.

7 There are a number of events in Kurt’s medical history which are significant in resolving the present claim. It is necessary to both separately describe them and make findings as to their significance having regard to the response made by the defendant to each of them. However before doing so I have included a lexicon of relevant medical terms with a view to making my reasons intelligible to both medical practitioners and lay readers.

Lexicon of medical terms

Arrhythmia: An abnormal heart rhythm.

Auscultation: The process of listening to the heart, usually with a stethoscope.

Bradycardia: A slow pulse. This is generally accepted to occur when the pulse rate is below sixty beats per minute.

EBV (Epstein-Barr Virus): Causes infectious mononucleosis (glandular fever).

ECG (electrocardiogram; Also known as an EKG): The standard ECG is a 12-lead ECG, which involves attaching electrodes to the limbs of a patient, as well as on pre-determined places across the chest wall. This gives a tracing of the electrical conduction system of the patient’s heart. A Holter monitor ECG is used when a patient is to be monitored continuously. This typically involves the use of only one lead.

Echocardiogram: An echocardiogram is basically an ultrasound of the heart. It looks at the structure of the heart, the dimensions of the various chambers, the configuration and action of the valves and it assesses flow across valves. It gives an indication of cardiac function by measuring the degree to which the various chambers contract at various stages of the cardiac cycle. An echocardiogram usually involves a contemporaneous single-lead ECG.

EEG (electroencephalogram): A neurological investigation that is used, inter alia, to test for epilepsy.

Endocarditis: Endocarditis is a condition where there is a bacterial infection on the inside of the heart, typically affecting the valves of the heart. There are two general manifestations. One is the growth of what are called vegetations, or small wart-like projections, usually on the valve, but it may also proceed to the formation of an abscess on the valve.

Febrile: Affected by a fever; having a high temperature.

Long QT Syndrome (LQTS): Every time a heart beats, an electrical current passes through it. In recording the heart’s electrical conduction, an ECG records a series of peaks and troughs or “waves”. The QT interval is the space between the Q wave and the T wave. Once a current has passed through the heart, it needs to “repolarise.” The QT interval represents the amount of time it takes for ventricular repolarisation to occur. During repolarisation, no current can be conducted. The longer this takes (ie the longer the QT interval), the greater the likelihood that the current will seek an abnormal pathway for conduction, which may cause life-threatening ventricular arrhythmias. The QT interval is measured in milliseconds. A corrected QT measurement (known as the QTc) is used by cardiologists to assess the length of a person’s QT interval. A normal QTc for a male is less than 440 milliseconds and less than 450 milliseconds for a female. A higher QTc is considered to be prolonged. Not all people with LQTS will produce a long QT interval on an ECG all of the time. Professor Saul gave evidence that “in this syndrome we know that 25 to 30 per cent of patients actually have a normal EKG at various times.” The four cardiologists who gave evidence before me concurrently adopted the following definition of LQTS in their joint report: “Long QT syndrome is a complex range of conditions. It is not a single disease with a single outcome. It can be caused by genetic factors, environmental factors or a combination of the two. Environmental factors include drugs, electrolyte abnormalities, myocardial ischaemia, brain injury, bradycardia, hypothermia and stressors which activate the sympathetic nervous system. Regardless of the cause there is a risk of death due to abnormal heart rhythms. The prevalence of the genetic condition is probably in the order of 1 in 3000 of the population. A precise diagnosis of Long QT Syndrome can be difficult to make.”

Heart murmur: Normally, the heart makes two regular sounds. The first sound is the closing of the mitral and tricuspid valves, and the second sound is the closure of the aortic and pulmonary valves. A heart murmur is an extra sound that can indicate problems with the heart.

Murtagh’s General Practice : A medical text commonly available to and used by Australian general practitioners at the time of Kurt Halverson’s injuries. The 1998 edition was referred to throughout the trial, particularly the chapter titled “Fits, faints and funny turns.”

Myocarditis: An inflammatory process of the heart muscle itself. In contrast, endocarditis involves inflammation of the lining membrane of the heart. In rare cases, myocarditis can be secondary to an EBV infection.

Prodromal events: These are premonitory signs that typically precede benign syncopal events (i.e. vasovagal events and episodes of postural hypotension). Dr Silberberg, a cardiologist, described them as “the cornerstone of diagnosis” in terms of distinguishing between benign syncopes and syncopes with a cardiological cause. He said: “…sudden cardiac events tend to be like switching a light off…[T]here is no chance – no warning of any type, whereas with vasovagal attacks…[t]here is a considerable period of time, always long enough to have a conversation, to say something – it might just be, ‘I’m not feeling well, I’m going to black out.’ But that is the key. When you get that, you are almost never dealing with a ventricular arrhythmia in that situation, because there has been time for some adjustment.”

Syncope: A brief loss of consciousness. Broadly speaking there are three causes of syncope. Dr Dobler stated that “syncope could be broken down into vasovagal events and episodes of postural hypotension, neurological events or cardiac events.” Vasovagal events and episodes of postural hypotension are typically treated as a single category, and were sometimes referred to in evidence as “simple faints.” These syncopes are benign and are usually associated with changes in posture (eg suddenly standing up) or common triggers such as pain, the sight of blood or standing upright for long periods of time. They are usually preceded by premonitory or “prodromal” signs, which enable a person to avoid falling in an awkward or dangerous manner when they lose consciousness. Syncopal events due to neurological or cardiological causes are not benign. Technically, a loss of consciousness with a neurological cause is classified as a seizure rather than as a syncopal event, but for ease of reference they were spoken of in the trial as though they were a type of syncope. An epileptic fit is an example of a loss of consciousness with a neurological cause. Cardiogenic syncope can be caused by a cardiac arrhythmia. Cardiogenic syncope is usually sudden and involves no premonitory signs, or, at most, premonitory signs that are very brief. Consequently it is often accompanied by physical injury suffered when the patient unexpectedly collapses. Professor Saul, a cardiologist, said that recurrent cardiogenic syncope “is the primary symptom of the long QT Syndrome that precedes any sort of malignant events,” but the fact that syncope is recurrent does not of itself indicate that the syncope has a cardiogenic cause.

Tachycardia: A fast pulse. LQTS predisposes a person to arrhythmias, particularly ventricular tachycardia. In his report of 24 March 2006, Dr Raftos states that “ventricular tachycardia is a regular contraction of the ventricles at abnormally high rates. The heart does not fill adequately after each contraction and so the cardiac output drops, the supply of blood to the brain drops, and the patient may collapse unconscious, recovering promptly when the cardiac rhythm spontaneously reverts to normal. If the cardiac output is not reduced to the level at which unconsciousness occurs, the patient may present with palpitations, shortness of breath, anxiety, sweating, nausea, or a feeling of general malaise. Episodes of ventricular tachycardia may last from seconds to days. Most episodes of ventricular tachycardia revert spontaneously.”

Torsades de pointes: a distinctive type of tachyarrhythmia which can be indicative of LQTS.

4 September 1995 – and medical investigation

8 The first medical event of significance to this litigation occurred on the night of 4 September 1995 when Kurt collapsed at home. His father had come home from work early that day. He described the events in the following exchange with counsel:

…

9 The relevant medical records show that Kurt was taken into Cessnock Hospital that night and was seen by the defendant. Dr Dobler’s notes record a “possible fit tonight” and flag the possibility of a viral illness. The notes show that Dr Dobler auscultated Kurt’s heart and that it was making the normal sounds. There was no murmur detected. Dr Dobler ordered some tests to be carried out. The results indicated a reduction in white blood cells consistent with a viral illness. Prolactin levels are known to increase after an epileptic seizure, and Kurt’s levels were high. This suggested to Dr Dobler that the possibility that the incident was the result of a seizure should be further investigated.

10 Mr and Mrs Halverson later consulted Dr Dobler in relation to this incident. According to Mr Halverson, they were told by the defendant that he was of the opinion that Kurt had suffered a petit mal but not an epileptic fit. Mrs Halverson had previously been diagnosed with epilepsy and they were concerned that Kurt had the same condition. Mr Halverson said that:

“What he described was a petit mal was like a short sleep and he said that it was not uncommon for young children to experience that and that it was – school teachers of young children saw it happen; once again, it was not uncommon for school teachers of young children to see that within their class. He also went on to tell us that, despite that, he would like to investigate it further, and he suggested two things. He suggested that Kurt go to the John Hunter Hospital for an EEG and he suggested that that be backed up, or once that EEG happened, that Kurt was to see a paediatric neurologist, Dr Ian Wilkinson, whose rooms were in Lambton.”

11 Dr Dobler referred Kurt for an EEG, which was performed in the Clinical Neurophysiology Unit at John Hunter Hospital on 24 October 1995. The report for that EEG contains a brief history which records, inter alia: “Epileptic fit. ? complex partial seizure. Serum prolactin increased + afterwards. Mother has TLE [temporal lobe epilepsy].” The report ends: “Clinical interpretation: This is a normal report.”

12 Dr Dobler also referred Kurt to Dr Wilkinson, a specialist neurologist. In his referral letter, Dr Dobler described Kurt’s “turn” as an “episode which was not typical of a grand mal seizure but which I thought may have been a complex partial seizure.” In his evidence Dr Dobler described a complex partial seizure as one that does not involve generalised jerking, but which may involve some abnormal movement. Dr Dobler described the event itself as involving Kurt “sitting at the dining table when he became non communicative and then started with some unusual movements which were not violent.” Mr Halverson did not agree that Dr Dobler had been told that Kurt became non communicative, nor did he accept that Kurt had displayed any “unusual movements” other than falling face-first into his food. The differences may be explained by the fact that Dr Dobler wrote the referral letter from memory almost four months after the incident.

13 Dr Wilkinson sent Dr Dobler a letter in respect of his consultation with Kurt in which he states:

“The presenting problem is of an event that took place recently, when he had been generally unwell through the day. It sounds as though it might have been a viral illness, and he was off his food. His father made him some lasagne, which he normally liked very much, and he was sitting down to eat it about 7:30 pm, when he felt that it tasted unpleasant, and at that stage he looked very pale, and his head slumped forward, and he fell out of his chair. He was on the ground briefly for about 30 seconds or so, and there was no stiffness or jerking. He woke a bit confused, and he had a bit of a headache.

He had been vomiting through the day.

…

His had [sic] never had a past history of fainting or seizures, and there is no family history of fainting. His mother has a history of temporal lobe epilepsy since 32 years of age.

There is really nothing in the past history that appears to constitute a hazard to his neurological development.

…

In the presence of the normal EEG, with an event that really sounded as though it could have been a faint, I would be inclined to think of this as a faint and not a fit. I think that elevated prolactin levels can occur in other events that can lead to unconsciousness, but do not have to be actually convulsions….

The family history of temporal lobe epilepsy in his mother is also not a terribly strong point, as temporal lobe epilepsy is usually not inherited.

I think we should regard this as being a faint, not a fit, and consider it a one-off. If he does have further events that are not related to situations that might produce a faint, then it would be worthwhile repeating his EEG, but I think we should get it done with him asleep, and that would probably require sleep deprivation.”

14 At this time it was noted that Kurt’s blood pressure was about 120/60 when lying down, and that it fell to about 80 systolic when he stood suddenly. Dr Dobler said in his evidence that this “suggested that Kurt may be predisposed to episodes of postural hypotension.” Dr Wilkinson also noted that Kurt had a hand tremor and referred him to the Paediatric Occupational Therapy Unit at John Hunter Hospital.

15 With respect to the differing recollections of Mr Halverson and the defendant I am completely satisfied that Mr Halverson’s recollection is accurate. His account of Kurt falling into his food is consistent with Dr Wilkinson’s note that “his head slumped forward” before he collapsed to the floor. Although the matter was the subject of some discussion by various of the doctors who gave evidence I do not believe anything turns on the report that his food tasted unpleasant. Whatever else was occurring, Kurt was ill and had lost his appetite. In these circumstances his food was not likely to taste as pleasant as it normally would.

16 In cross-examination, Dr Dobler stated that he regarded Dr Wilkinson’s use of the word “faint” in his letter as a specific diagnosis of vasovagal syncope. The following exchange occurred:

“Q. Do you say, doctor, that you relied in any way on the wording in Dr Wilkinson’s report where he said words to the effect that it should be regarded as a faint, not a fit –
A. Yes.

Q. – which still left you with a syncopal event, didn’t it?
A. A single syncopal event, yes.

Q. Undiagnosed.
A. Diagnosed as a faint.

Q. But that’s a syncope, isn’t it?
A. A faint is a syncope, but a faint is a specific diagnosis.

Q. Well, doctor, that, I suggest to you, is a very highly contentious proposition in the context of what is being reported on here.
A. Sorry, is that a question?

Q. Yes, it was a question, but it’s probably argumentative and I shall not pursue it. What I do put to you is this, that clearly what the neurologist is saying is that it’s a loss of consciousness which is not epileptiform in origin.
A. He’s saying that, yes.

…

Q. There is no diagnosis as to what caused the loss of consciousness.
A. I don’t believe that is true. Diagnosed “faint.”

HIS HONOUR: Q. What I’m not sure about is whether, in the ordinary course, having diagnosed, as you say, faint, you would go further and look for the cause of the faint?
A. My understanding, from the description that Dr Wilkinson is giving, is that he’s using the word “faint” to signify a vasovagal event.

Q. Where does that come from?
A. They’re commonly interchangeable terms, although – and the fact that he suggests that should further episodes occur, further neurological investigation occur, rather than anything else.

Q. So, in my layman’s language, the faint has been caused by vasovagal indicia?
A. That’s correct.

…

Q. You accepted from what he told you, did you, that he has diagnosed a vasovagal turn?
A. That was my understanding from the letter.

Q. Did you call him up and ask for clarification of this?
A. No, I did not.

Q. This terminology – if you look at the article in Murtagh, it’s specifically called “Faints, fits and funny turns,” isn’t it?
A. That’s the heading of the article.

Q. And it’s all about how you get to a diagnosis for anything that comes under those headings?
A. Yes, it is.

Q. And Dr Wilkinson hasn’t told you what was the cause of this faint in his letter, has he?
A. No.

Q. Did you take comfort at the time in his observation that you could regard it as a one-off – as non-epileptiform, as a faint and a one-off?
A. Yes.

Q. Did you take comfort from that?
A. Yes.

…

Q. Dr Dobler, I don’t mean to be aggressive, but I’m obliged to put to you that your protestation that “faint” is a diagnosis is a nonsense.
A. Sir, if you could read further in Dr Wilkinson’s letter, “if he does have further events that are not related to situations that might produce a faint” – this is highly suggestive to me that Dr Wilkinson believes this is vasovagal, such that there is a precipitating event that caused the faint.

Q. Doctor, I don’t want to argue with you, but where does he use the word “vasovagal”?
A. He does not use that word.

17 Five cardiologists were called in the trial, although one of them – Dr Silberberg – was called as a witness of fact. He gave evidence separately. The four other cardiologists, Professors Harris and Saul and Associate Professors McGuire and Richards, gave evidence concurrently. I have provided a description of the qualifications and expertise of the cardiologists later in these reasons. In this judgment, a reference to “the cardiologists” is a reference to the four cardiologists who gave concurrent evidence, but not to Dr Silberberg, unless the context indicates otherwise. The cardiologists gave consideration to whether Dr Wilkinson had diagnosed a vasovagal faint. When giving their evidence the following exchange occurred:

“PROF HARRIS: It is the third paragraph on Page 54, your Honour, the end of the first sentence:

I would be inclined to think of this as a faint, not a fit.

To me often, in these circumstances, it is as good a diagnosis as you get.

HIS HONOUR: Does that mean that, as you understand it, he is saying, by referring to it as a faint, that it does not have a cardiac connection?

PROF HARRIS: Yes, that he considers this to be either vasovagal or hypotension. That would be my interpretation if I were to receive that letter.

HIS HONOUR: Can I ask each of the other Professors – would you interpret the letter in that way or differently?…

PROF MCGUIRE: I accept that Dr Wilkinson intended to convey the diagnosis of a faint or hypotensive episode, not an arrhythmia. If he’d thought it was an arrhythmia, he would have referred the patient for investigation.

HIS HONOUR: Professor Richards?

PROF RICHARDS: Dr Wilkinson writes:

I think we should regard this as being a faint not a fit and consider it a one-off. If he does have further events that are not related to situations that might produce a faint, then it would be worthwhile repeating his EEG, but I think we should get that done with him asleep.

At that stage, Dr Wilkinson does not address the possibility that it could be anything other than a faint or neurological problem. Because fainting is diagnosed by exclusion of other diagnoses, it is my view that this is simply the view of a neurologist that it was not a fit and he thought it was probably a faint based on the description that he gave of the event. But I don’t really think it establishes a diagnosis of vasovagal syncope or hypotension against a cardiac diagnosis of an arrhythmia.

…

HIS HONOUR: What would you [Professor Saul] tell me?

PROF SAUL: Again, I think being a paediatrician is an advantage in interpreting such a letter. To a paediatric neurologist every syncopal event is a fit or a faint and exactly as Professor Richards said, all he is saying here is that it wasn’t a fit. In every other kind of faint, we have used the word “faint” to mean benign and non-cardiac. A neurologist just means it’s not a fit and there is a great book by John Stephenson from Glasgow who is a quite famous paediatric neurologist who is an expert on fits and faints, and that’s the name of his book, and many of the faints in his book are arrhythmia based, bradyarrhythmias and tachyarrhythmias and other things, and they are all considered faints, whereas the fits are the seizure disorders. So a paediatric neurologist by saying this simply means that, “It’s not me, it’s not my area, and everything else is a faint.”

Then the question came up, should he or could he have referred them to a paediatric cardiologist? That really depends on the neurologist how they deal with it. He didn’t recommend it back to the doctor, but he also is dealing with a GP who he assumes has his own evaluation of what was going on and would carry on the evaluation possibly in some other way. I don’t think in any way we can interpret this as saying that the neurologist has cleared him and he certainly doesn’t say anywhere in the letter that he thinks this is vasovagal syncope.

PROF MCGUIRE: Phil, the training system in Australia is a little bit different from the training system in the United States. All specialist physicians in Australia train in internal medicine before they specialise. We don’t go straight from being an intern or a resident to a specialty. We all train in internal medicine. So this doctor is trained in special medicine. Don’t you think if he’d thought an arrhythmia was a likely possibility, he would have referred the patient on?

PROF SAUL: Except he sees paediatric patients, so he doesn’t think about arrhythmias very much. The whole problem here in the entire case is that nobody thought of arrhythmia. Even when this boy was admitted to the hospital for two days because of a syncopal event, nobody got an EKG and put him on monitoring…I don’t know how to explain what the neurologist says other than that I can’t identify this as being that he is saying that it is not an arrhythmia.

HIS HONOUR: Professor Harris, I think you started this discussion – I will ask Mr Higgs in a moment – but do you want to respond.

18 The plaintiff submitted that because the defendant failed to offer an explanation for not calling Dr Wilkinson as a witness, I should infer that nothing he would have said on this issue would have assisted the defendant’s case: Jones v Dunkel (1958) 101 CLR 298. At the end of the exchange between the cardiologists I am left in doubt as to whether Dr Wilkinson’s words can be taken as far as Dr Dobler contended. It seems clear that Dr Wilkinson was excluding neurological causes (such as epilepsy) as being responsible for Kurt’s syncopal event when he says “we should regard this as being a faint, not a fit,” but whether he was also excluding the possibility that Kurt’s faint had a cardiological cause is uncertain. Without hearing from Dr Wilkinson a certain finding is not possible. However, I have ultimately concluded that the resolution of this issue is not material to my ultimate conclusions in the proceedings.

19 Kurt turned fifteen on 25 September 1997. Shortly before this date he had begun to complain of unusual symptoms, including feelings of déjà vu. His father recounted that Kurt had said “that he felt like he was being there but not there.” Kurt first told Dr Dobler about these symptoms at a consultation on 29 August 1997. Dr Dobler’s notes for that day record, inter alia, “Episodes of light-headedness followed by nausea. Dream like state at beginning.” Dr Dobler organised a sleep-deprived EEG on 23 September 1997 which was normal and revealed no epileptiform activity. Like the first EEG, this indicated that Kurt’s previous syncopal episode was unlikely to have a neurological origin.

20 Although his neurological tests were normal, Kurt continued to suffer from severe headaches. The defendant diagnosed migraine headaches and he prescribed Imigran. Originally this was taken orally but later it was delivered through a nasal spray, which proved to be much more effective treatment.

29 June 1998 – collapse outside Dr Dobler’s surgery

21 On the morning of 29 June 1998 Kurt was quite unwell. He stayed home from school and was cared for by his grandmother at his grandparents’ home until his grandfather (Mr Ron Halverson) had returned from attending to his horses. Mr Ron Halverson gave the following evidence of the events which followed:

…

Q. What happened then? What do you recall?
A. Well, Dr Dobler went to Kurt. I can’t remember what he did or anything else, but he was talking to Kurt and then he questioned me thoroughly as to what happened.

…

Q. Did you stay on for some time at the surgery?
A. Yes, quite some time.

22 Both Dr Dobler and Mrs Dobler (who worked in her husband’s surgery and who is a qualified nursing sister) gave evidence. Neither of them recall being told that Kurt had collapsed and Dr Dober’s clinical note is confined to one word “migraine.” Mrs Dobler stated that if she had been told of the collapse of a patient she would have instituted particular procedures to care for the patient and seek competent advice. She does not remember initiating these procedures in relation to Kurt.

23 I accept Mr Ron Halverson’s evidence. His account of the relevant events was completely convincing. I intend no criticism of Dr Dobler or Mrs Dobler but I am satisfied that with the exigencies of a busy practice (the surgery was full at the time), the particular events were not marked in their memories. I have no doubt that Mr Halverson told the defendant that Kurt had collapsed and that he was very unwell. However, whether the doctor appreciated the full extent of the information he was given seems unlikely. Given the symptoms which I am satisfied were reported to him, a one word note of “migraine” was an inadequate clinical record. Having been told, as in my view he was, that Kurt had collapsed, this should have been recorded and consideration given to the contribution this knowledge could make to a possible diagnosis. I appreciate that to this point Kurt had presented with significant problems with migraine headaches and a headache was reported on this occasion. Understandably, having regard to his history, Dr Dobler would be likely to have assumed that the latest event was confined to being another migraine. Notwithstanding this conclusion, the notes should have made some reference to the circumstances of Kurt’s presentation. The failure to do so indicates that – at least at this point in time – Dr Dobler gave very little, if any, consideration to the potentially sinister nature of recurrent syncope.

24 Kurt spent some time in the treatment room at the surgery. This was unusual. He was visited there by his uncle and aunt who took time from their work to come to the surgery. They confirmed that Kurt was seriously unwell on this day. However, he was allowed to return to his grandparents’ home. This surprised his grandmother. He had appeared so ill that she thought he would end up in hospital.

25 Later that day, Kurt was taken to Cessnock Hospital by his parents. He was seen there by Dr Dobler, who was a Visiting Medical Officer at the hospital. The hospital notes made by Dr Dobler were not much more detailed than the records kept in respect of Kurt’s visit to the surgery earlier that day. The presenting symptoms were listed simply as “Migraine, vomiting, afebrile.” Other information, such as blood pressure and drugs administered, is also recorded. Dr Dobler gave evidence that – in respect of both the notes from his surgery and the hospital notes – it would have been his usual practice to record that the patient had lost consciousness earlier that day if the patient had in fact told him that this was the case. For the reasons given above, I do not accept that this was the case in this instance. In notes taken by nursing staff, it is recorded that Kurt is allergic to MSG and that the headache and vomiting had started after he had eaten a sausage roll the day before. There is no mention of Kurt having lost consciousness earlier that day in these notes. Kurt was discharged from hospital the following day.

26 Kurt’s migraines continued. After a consultation on 25 January 1999, Dr Dobler referred him to Dr Katekar (a neurologist) in relation to his migraines, and to Dr Loblay in relation to possible food allergies. Most of the correspondence from Dr Katekar relates to the use of the medication Sandomigran, which Kurt had been taking since January. It is repeatedly noted that the medication was effective at controlling Kurt’s migraines to some extent, but that there were concerns about side-effects such as drowsiness and lethargy. Correspondence from Dr Loblay to Dr Dobler indicates that Kurt’s migraines might have been triggered by ingestion of biogenic amines and MSG, and that avoidance of these foods had resulted in Kurt’s headaches diminishing in intensity.

27 I consider the significance, if any, of the 29 June 1998 syncopal event later in these reasons.

The events of February 2001

1 February 2001 – a heart murmur is found

28 Kurt continued to suffer from migraines. One night towards the end of January 2001 his symptoms were particularly acute. He complained to his father of headache and nausea and was vomiting. Kurt’s nasal Imigran was not effective. Even after waiting two hours and taking a second dose, his symptoms only seemed to get worse. Reluctant to move Kurt when his symptoms were so severe, Mr Halverson contacted Dr Dobler and asked him to make a house call. Dr Dobler was on duty at Cessnock Hospital at the time and could not get away, but he asked Mr Halverson to come and see him. He gave Mr Halverson some Imigran to administer by injection. Mr Halverson returned home and gave Kurt the injection. His symptoms cleared within 30 minutes. However, Kurt did not recover well from this incident, and the next day he was tired and lethargic. Kurt was concerned about the severity of the incident and an appointment was arranged with Dr Dobler on 1 February 2001.

29 At the appointment Dr Dobler conducted a physical examination of Kurt which included auscultation of his heart. He reported a murmur. Dr Dobler’s notes state “noted to have a mitral type murmur – arrange for CXR [chest x-ray].” The murmur is described as “2/6 Pansystolic murmur radiating to axilla.” Dr Dobler gave evidence of this consultation. The following exchange occurred when he gave evidence-in-chief:

Q. And the "heart sounds times 2", what does that mean?
A. It means that there was a first and second heart sound and no other heart sounds.

Q. How do you give it that score? What's the softest, what's the loudest?
A. The softest is 1 on 6, which would be barely audible, through to 6 on 6, which could be palpated by having just a hand on the chest.

Q. In respect of the normal two sounds that you hear, is the murmur the extra sound in addition to those two normal sounds that you referred to earlier on?
A. That is correct.

…

Q. The murmur being described as "pansystolic", what did you mean to convey by that?
A. It meant that I could hear it from the very start of the - directly from the first heart sound throughout, ceasing with the second heart sound.

Q. Is there another type of murmur?
A. There's an ejection systolic, which tends to start slightly after the first heart sound and finish slightly before the second heart sound. There are also diastolic murmurs, which occur in the interval between the second heart sound and the following first heart sound.

Q. With a murmur that attracts a score of 2 out of 6 in the way that you've been over, is there difficulty in differentiating between, say, for example, whether it truly is pansystolic as opposed to, is it, systolic ejection?
A. Yes. At 2 on 6, it's a relatively soft murmur, so it would be quite difficult to ascertain with absolute certainty.

Q. At the time, what was your understanding as to the implications of this finding, this murmur, in the context of this examination?
A. Having ascertained that I couldn't see any evidence of acute infection within the heart, so-called endocarditis, and that I could detect no evidence of cardiac failure, I believe that the most likely was that this was an innocent murmur, possibly associated with a viral illness.

…

Q. And, as you understand it - I don't think it's controversial - with illness, sometimes you can hear a murmur that simply is a reflection of the blood going through the heart at a different speed, and the murmur is a reflection of simply a turbulence or agitation of the blood within the chamber of the heart; is that a fair layman's description?
A. Yes, that's correct.

30 A chest x-ray was arranged so as to exclude the possibility that the murmur was caused by endocarditis or myocarditis. Kurt had the chest x-ray the following day (2 February 2001). In a report written on the same day the radiologist, Dr Mackley, stated that: “The lungs are clear. The heart, hila regions and pleural surfaces appear normal. The history of heart murmur noted.”

31 Kurt continued to remain unwell.

4 February 2001 – Kurt collapses again

32 The events of 4 February 2001 are an important part of Kurt’s medical history. Kurt collapsed at home. His father’s account of those events was given in the following exchange:

Q. Just stop there, please. When you say you remember him being in the kitchen and he came out – came out from where?
A. Came out from his bedroom. I had been in the lounge room and I went to check on Kurt, and as I got in to the dining room, which was between the kitchen and the lounge room, he walked out of the doorway which would have led to his room and said he was just coming to get a glass of milk.

…

Q. For how long did he appear to remain unconscious?
A. He would have been unconscious over 20 seconds. But to define the upper limit, he would have been unconscious for quite a bit shorter than a minute.

…

33 Kurt arrived at the hospital at 9:25pm. At that time, a triage nurse wrote down Kurt’s presenting symptoms. The record reads as follows:

“Walked into ED [Emergency Department] with parents with H/O [history of] ?? [possible] seizure this pm lasting approximately 20 seconds. Parents state patient has a P/H [prior history] of migraine headache 1/52 [one week] ago. F/B. Lethargy +++ [i.e. extreme lethargy]; has seen m.o. [medical officer] re same ?? viral illness; also has [high] temps. Tonight stiffening of limbs and ? loss of colour for approximately 20 seconds at home. GCS [Glasgow coma score] 15/15 O/A [i.e. fully conscious on arrival]. Pupils = reacting briskly. Patient alert, looks unwell, ? pale.”

34 Dr Wakatama attended Kurt at 10:00pm. She noted the following history:

“Has been unwell with lethargy and fevers. Saw GP 2/7 [2 days] ago – provisional diagnosis viral illness. Has remained unwell. Tonight got up to get a drink of milk and felt dizzy and ? fainted. Father caught him and he had some stiffening of limbs and then went limp. LOC [loss of consciousness] 30 seconds. OE [on examination]: alert and orientated, not post ictal [i.e. not drowsy and combative if roused], no neck stiffness, sweaty, chest clear, ENT NAD [ear, nose and throat – no abnormality detected]. PD [provisional diagnosis]: viral illness with faints, but need to observe for seizures.”

35 Dr Wakatama also ordered blood tests. She has no independent recollection of her consultation with Kurt. She gave evidence that when she wrote “chest clear” in the hospital notes, it would have been her usual practice to “auscultate his chest, to listen to his breath sounds and I would listen to his heart, to check for his heart sounds and to check if there were any added sounds there.” Her notes implied to her that she could not hear a murmur, although usually she would make a note of whether there was or was not a murmur.

36 Kurt was admitted at 10:50pm. The admission sheet was filled out by a registered nurse. Under the heading “Past medical history,” the nurse has recorded “Temp Sweats [for] 3 days with lethargy. Migraines – last one last Saturday. Headaches, swollen gland back of head. [Left] and [right] side.” Under “Current medical conditions,” it says “Temp – sweats lethargy. Dizzy past 3 days tonight fainted ? Fitted at home [indecipherable] approx 20 seconds. Eyes open. Back and neck stiffened then slumped.” At around the same time the same nurse recorded the history of Kurt’s illness in more detail in his “History, Examination and Progress Report.” It relevantly states: “Nursing. New admission B Ward 2250. Wheeled into ward on chair by wardsman, accompanied by mother. Mother (Jan) staying in overnight. P/H migraines. On Sandomigran. Has been unwell last 2-3 days with temps, sweats, lethargy and dizziness. Got up tonight (not quick) to get drink of milk. Whilst drinking milk felt dizzy has no further memory until woke up. Father told mother that when Kurt was drinking milk his eyes were open his neck and back stiffened then he slumped. LOC approx 20 seconds. Kurt stated he has been having déjà vu lately. Mother has history of epilepsy. Kurt has allergy to amines in food [which lead to] migraines.” Kurt stayed in Hospital overnight.

The events of 5 February 2001 and subsequent days – Kurt has glandular fever

37 Dr Dobler saw Kurt in Hospital on 5 February 2001 when he was doing his scheduled rounds. He performed an examination of him. His notes read: “Syncopal episode with seizure on the background of viraemic symptoms. Pulse 80, afebrile.” A symbol then appears which Dr Dobler interpreted as meaning that a chest examination was clear. He notes that Kurt’s abdomen was soft and non-tender and that there was “no neck stiffness.” Dr Dobler cannot specifically recall the chest examination, but his usual practice would involve sounding the patient’s heart with a stethoscope. If nothing (such as a heart murmur) was detected Dr Dobler said that he may not record this in his notes, although it would be unusual for this to occur. Kurt’s prolactin levels were checked but the results (which were available on 6 February) were in the normal range, indicating that Kurt’s syncopal episode was not an epileptic seizure.

38 Dr Dobler saw Kurt again on the same day after having had access to the results of the blood tests ordered by Dr Wakatama the night before. Those results led Dr Dobler to positively diagnose Kurt as suffering from glandular fever. Dr Dobler’s notes state “Glandular fever. May go home. Repeat bloods at the end of the week.” He was discharged that day.

39 Ms Megan McKay, Kurt’s girlfriend at the time, was present when Dr Dobler saw Kurt at the hospital. Although she had some difficulty identifying the time Kurt was discharged, Ms McKay recalls being with Kurt at the time. She gave the following account of her observations that afternoon:

40 I accept her evidence.

41 On Tuesday (6 February) Kurt’s condition was stable. He was not getting any better but his condition was not deteriorating.

42 When Mr Halverson got home from work on Wednesday Kurt had been vomiting. He looked dehydrated. Mr Halverson again took him to hospital. The triage nurse reported Kurt’s symptoms as follows: “Presented to A&E [accident and emergency] in c/o [company of] father who states patient was discharged from BW [B Ward] Sunday [sic – Monday?] and has had nausea today and father is concerned patient is becoming dehydrated.” On the same form Dr David Outridge made the following notes in relation to Kurt: “Readmitted with glandular fever. Concentrated urine. Allergies – nil. On examination, red throat, tongue coated. Examination of the abdomen indicating tenderness of the upper abdomen. Treatment – intravenous fluid, nil stat, oral Phenergan.” Dr Dobler referred to these notes when he saw Kurt in hospital the next day.

43 Dr Dobler’s clinical notes for 8 February 2001 state: “Somewhat unwell. Possible jaundice. Fever overnight. Proteinuria for repeat bloods, 24-hour urine, urinary red blood cell morphology. Mid-stream urine examination. Note: one positive blood culture. Start IV, Keflin.” “Proteinuria” refers to the presence of protein being detected in Kurt’s urine following a dipstick test. The result was consistent with Kurt’s continued viral illness. Other tests gave results consistent with glandular fever. Kurt also returned a positive blood culture, which indicates that he had bacteria growing in his bloodstream. Dr Dobler said of his treatment of Kurt that day:

…

44 After his examination of Kurt, Dr Dobler recalls contacting the infectious diseases department at John Hunter Hospital for advice in relation to Kurt’s positive blood culture. According to Dr Dobler,

“The advice was that this type of germ would be very unlikely to be a pathogenic bacteria in a patient who was not severely immuno-compromised or did not have an artificial valve in place, and their advice was that if there were no signs of endocarditis then it would be prudent to repeat the blood culture after a short course of antibiotic, but they felt reassured by the nature of the bacteria and the other illness that was going on and the white cell – the neutrophil count being relatively normal.”

45 Mr Halverson saw Kurt both before and after going to work that day. When he returned to the hospital after work Kurt was suffering from a pain in the abdomen. Mr Halverson had brought Kurt some magazines and had started to read them out to him. Kurt was in a lot of pain and, with his back to his father, asked if he would “please shut up for a while.” Mr Halverson had now become very concerned about Kurt’s health and was troubled by the report of a heart murmur. He asked Kurt if Dr Dobler had sounded his heart again and whether it was OK. Mr Halverson remembers that Kurt replied in the affirmative, although he could not recall his exact words. Records show that Dr Dobler saw Kurt again that night.

46 Dr Dobler’s notes for the next day (9 February 2001) state: “Much improved. Reduce intravenous fluids. Cervical nodes ? discharge this evening.” Dr Dobler was questioned about this note:

47 That night Dr Dobler saw Kurt again when he was doing unscheduled rounds of the Hospital. His notes record that Kurt had had a dystonic reaction to Stemetil/Promethazine. Dr Dobler described a dystonic reaction as “a reaction that occurs to certain medications which can impact on the ability to control the muscles of the face and the eyes, and so a common presentation would be that the eyes are deviated to one side or that the head is deviated to one side or that the tongue is deviated to one side. This is a severe sort of spastic-type reaction in terms of the muscle goes into quite significant spasm – quite frightening for the person who is undergoing it and certainly for those able to observe it.” Dr Dobler recalls that by about 7:30 this reaction had “resolved” after Kurt was given Cogentin. Kurt remained in hospital that night.

48 Dr Dobler saw Kurt again the next morning (10 February 2001). Mr Halverson was present. Kurt appeared much better and he very much wanted to go home. Dr Dobler’s notes state: “Doing well. Still febrile. May go home. Continue conservative management. Repeat bloods on Monday.” There is no record of a physical examination.

49 Dr Dobler said that he recalls that he performed an examination on Kurt that morning, although he did not record it. He gave the following evidence:

50 In a letter which he wrote on 11 February 2001 after Kurt had suffered his cardiac arrest, Dr Dobler wrote “On 10/2 he had a low grade fever but felt well (the murmur was not now audible).” In the same letter he described the murmur that he had originally detected as being 1/6, when in his earlier records it is shown as 2/6.

51 Mr Halverson’s evidence with respect to Dr Dobler’s examination of Kurt on 10 February was as follows:

52 I am satisfied that Mr Halverson gave an accurate account of what he saw. This does not preclude Dr Dobler from having examined Kurt when his father was not present although the fact that there is no record suggests that Dr Dobler’s recollection may be faulty.

53 As it happens I do not believe it is necessary to resolve this conflict between the recollection of Mr Halverson and Dr Dobler. However, if it had been necessary I would have preferred the evidence of Mr Halverson. At this point the progress of Kurt was not unusual and there would be little, without a note, to mark these events in Dr Dobler’s memory. Mr Halverson’s situation was quite different. His heightened concerns would have made it likely that events would be remembered with clarity and in detail.

The night of 10 February and the morning of 11 February 2001 – Kurt has a cardiac arrest

54 When Kurt arrived home his parents were sufficiently concerned that they tried not to leave him on his own at any point. Mr Halverson required Kurt to shower in the ensuite to the master bedroom so that if anything went wrong Mr Halverson (who was sitting on the bed within earshot) could respond promptly. Kurt’s sister Annika’s room was situated next to Kurt’s. That night Mr Halverson changed beds with her so that he could be near Kurt in the event of anything happening. As it happens this was a prudent step although ultimately he could not prevent the catastrophe which was to occur in the early hours of the morning of 11 February. Mr Halverson described the sequence of events in the following terms:

…

55 The ambulance took Kurt to Cessnock Hospital and from there he was flown by helicopter to John Hunter Hospital. Notwithstanding the care he received the cardiac arrest had already done irreparable damage to his brain.

56 Mr Halverson gave evidence that a few days later Dr Dobler explained to the Halversons that he believed that Kurt’s viral illness had had an impact on his heart which caused a heart attack. He told them that Kurt’s prognosis was not good but that he might be able to recover to some extent. He said that the Halversons were lucky that Kurt had suffered the attack at home because if it had occurred in hospital it would not have been noticed and Kurt would have died.

Dr Dobler’s evidence with respect to an ECG and other matters

57 Dr Dobler gave evidence that ECG facilities were in use at Cessnock Hospital in 2001. A self interpreting machine was available which automatically measured the patient’s QT interval. Dr Dobler was asked why he did not, at any stage, order an ECG. The following exchange occurred:

58 Dr Dobler accepted as a fundamental principle of diagnosis that where a patient presents with symptoms that are susceptible to more than one diagnosis, any diagnosis with lethal potential or a serious morbidity risk should be established and treated or an attempt made to rule it out by establishing a valid alternative diagnosis. He also accepted that a cardiogenically determined syncope has a lethal and/or serious morbidity potential.

59 Much of the cross-examination of Dr Dobler was concerned with whether he accepted propositions from a well known text – Murtagh’s General Practice. Dr Dobler accepted that Murtagh was respected by Australian GP’s and commonly used by them. Dr Dobler accepted that the key to an accurate diagnosis in the context of syncopal episodes is the taking of a very careful history. The patient must be taken second by second through the incident and as many eyewitnesses as possible must be spoken to. He also accepted that the details of the history should be carefully and thoroughly recorded, especially when the syncopal event is undiagnosed. Dr Dobler agreed that the history he had recorded in relation to Kurt’s faint of 4 September 1995 was nothing like the sort of detailed history envisaged by Murtagh. He accepted that if he had been given an oral history of the events of 29 June 1998 consistent with Mr Ron Halverson’s (i.e. Kurt’s grandfather’s) evidence then his notes in relation to that incident would represent a “gross breach” of the principles in Murtagh. However, he did not accept that even with knowledge of the 1998 collapse cardiological investigations would have been appropriate.

60 Dr Dobler was questioned about the effectiveness of his diagnosis and the response to Kurt’s symptoms which he would make today:

The evidence of five general practitioners

61 The plaintiff called two expert general practitioners, Drs Chambers and Mackey. The defendant called three expert general practitioners, Drs Bunker, Ford and Walsh. They are all highly qualified and experienced.

62 Dr Chambers received her MB BS (Hons) from UNSW in 1975. She has been a full time GP in Sydney since 1988 and a Fellow of the Royal Australian College of General Practitioners (FRACGP) since 1993. She has been an examiner for the RACGP since 1994 and a Clinical Supervisor for the RACGP training program since 1995. She is a Clinical Lecturer in the Department of General Practice at the University of Sydney.

63 Dr Mackey also received his MB BS from UNSW in 1975. He joined the medical practice at Scone in 1977 before moving to the single-doctor town of Lockhart in 1989. He is a Visiting Medical Officer at a small rural hospital. Amongst other things, Dr Mackey is a Fellow of the Australian College of Rural and Remote Medicine (FACRRM), a member of the NSW Rural Doctors Association Management Committee (he was President from 1999 to 2001) and he was President of the Rural Doctors Association of Australia between 2001 and 2003.

64 Dr Bunker received his MB BS (Hons) from UNSW in 1983 and was awarded, inter alia, the University Medal. He became a FRACGP in 1994 and has been a supervisor for the RACGP Training Program since 1992. He worked as a GP in Ultimo between 1986 and 2004. Since 2003 he has been the Director of Training at the Sydney Institute of General Practice Education and Training and he has been a Staff Specialist at the Fairfield Hospital GP Unit since 2004.

211 In no case has any member of the High Court suggested that the decision in either Sellars or Malec displaces the civil standard of proof in relation to causation in negligence. In Sellars itself Mason CJ, Dawson, Toohey and Gaudron JJ expressly said that “the general standard of proof in civil actions will ordinarily govern the issue of causation,” and Brennan J in his separate judgment (at 368) said that:

“A constant standard of proof applies to the finding that a loss has been suffered and to the finding that the loss was caused by the defendant’s conduct, whether those findings depend on evidence of historical facts or on evidence giving rise to competing hypotheses. In any event, the standard is proof on the balance of probabilities.”

Loss of a chance – the concept of vicissitudes

212 The common law faces a difficulty in providing a uniform approach to questions of causation and damage in cases of negligence. Although when a commercial opportunity is said to have been lost, quantification by calculation of the percentage chance of making a profit, acquiring an asset, or avoiding a loss is a familiar task, such concepts are entirely foreign in personal injury matters. A commercial opportunity will have a market value but the value of the percentage chance of a successful medical outcome allegedly lost, although personal to the plaintiff and no doubt of immense value to him or her, does not have the same value to others. It is not a chance which can be expressed to exist in a conventional market, or indeed in any market.

213 The difficulties in utilising the concept of the loss of a chance in personal injury cases arises against a background of a settled approach to causation and damages. Responsibility for a plaintiff’s injury will lie upon a defendant if the plaintiff can prove “that the defendant’s conduct materially contributed to the plaintiff suffering that injury:” Chappel v Hart (1998) 195 CLR 232 at 244 per McHugh J. Although in theory the contribution of the defendant to the plaintiff’s injury may have been less than 50%, if the contribution is nevertheless material the plaintiff will recover against that defendant. Materiality must be proved on the balance of probabilities. The problems encountered with proof were considered by the Court of Appeal in State of New South Wales v Burton [2006] NSWCA 12; and see: Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262; Elbourne v Gibbs [2006] NSWCA 127 esp. at [74]-[75].

214 It is accepted that damages in a personal injury matter should be assessed having regard to the vicissitudes of life and the pre-existing characteristics of the plaintiff. For this purpose assessments are made of the probability of a plaintiff living to a certain age, the prospects of working to an identifiable age, the possibility of independent accidents occurring and so on. Positive vicissitudes, such as the possibility of promotion, may also be taken into account. In a real sense this requires the court to assess the chance of future events occurring.

215 The modern approach to vicissitudes is summarised by Dawson, Toohey, Deane and Gummow JJ in Wynn v NSW Insurance Ministerial Corporation (1995) 184 CLR 485 at 497-498:

Arthur Robinson (Grafton) Pty Ltd v Carter

‘Ill health, unemployment, road or rail accidents, wars, changes in industrial emphasis, so that industries move their location, or are superseded by new and different techniques, the onset and effect of automation and the mere daily vicissitudes of life are not adequately reflected by merely – and blindly – taking some percentage reduction of a sum which ignores them.’

Bresatz v Przibilla

216 Citing Malec and Sellars, amongst other decisions, Dawson, Toohey, Deane and Gummow JJ go on to say (at 498) that in order for a vicissitude to be taken into account, all that needs to be established is “a real possibility” of its occurrence. The relevant standard of proof is not the balance of probabilities. However, a court must not take into account as a “vicissitude” a benefit (such as a pension) that would have accrued to a plaintiff independently of his or her right of action and regardless of whether or not that right is enforced: Graham v Baker (1961) 106 CLR 340 at 343 per Dixon CJ, Kitto and Taylor JJ. And while it is appropriate to assess the possibility that an injury would have occurred regardless of the negligence due to a pre-existing condition and to discount the damages by the percentage arrived at (see, eg, Malec), this does not alter the principle that the defendant must take the plaintiff as he finds him. As Dixon CJ said in Watts v Rake (1960) 108 CLR 158 at 160: “If the injury proves more serious in its incidents and consequences because of the injured man’s condition, that does nothing but increase the damages the defendant must pay. To sever the remaining leg of a one-legged man or put out the eye of a one-eyed man is to do a far more serious injury than it would have been had the injured man possessed two legs or two eyes.”

When is the cause of action complete?

217 In the context of assessing damages for economic loss, Dixon CJ, Kitto and Taylor JJ said in Graham v Barker at 346-347 that:

“A plaintiff’s right of action is complete at the time when his injuries are sustained and if it were possible in the ordinary course of things to obtain an assessment of his damages immediately it would be necessary to make an assessment of the probable economic loss which would result from his injuries. But for at least two obvious reasons it has been found convenient to assess an injured plaintiff’s loss by reference to the actual loss of wages which occurs up to the time of the trial and which can be more or less precisely ascertained and then, having regard to the plaintiff’s proved condition at the time of the trial, to attempt some assessment of his future loss. We mention this matter because it has been suggested that since an injured plaintiff is entitled to recover damages for the impairment of his earning capacity, the fact that a totally incapacitated plaintiff has, during the period of his incapacity, received his ordinary wages is not a matter to be taken into consideration. To be more precise, however, an injured plaintiff recovers not merely because his earning capacity has been diminished but because the diminution of his earning capacity is or may be productive of financial loss.”

218 This passage highlights one of the difficulties associated with the loss of a chance approach in the personal injury context. If the lost chance results in an injury that sounds in damages, then the right of action is complete at the time the injury is sustained. This means that the plaintiff’s right of action accrues some time before the occurrence of the ultimate physical injury upon which the lost chance is contingent. Gaudron J identified this conceptual difficulty. In Naxakis at 278, her Honour said:

where no other loss is involved.

219 In medical negligence cases the lost chance is inseparable from the physical injury. Unless and until the physical injury occurs, it cannot be concluded that the chance has gone. Suppose that a patient has a 40% chance of survival but through his doctor’s negligence this chance is reduced to 20%. Suppose further that, against the odds, the patient survives. Could the patient still recover damages for the lost chance? The lost chance of a better outcome is dependent on the adverse outcome occurring.

220 A lost chance of a better medical outcome is readily distinguished from a lost financial opportunity. Chaplin v Hicks [1911] 2 KB 786 was the first case in which loss of a chance was recognised as a type of compensable damage. It involved a competition for young ladies who wished to be actresses. Over six thousand ladies sent in their photographs, and the best 300 were published in a newspaper. The 50 “most beautiful” were selected by public vote, and each of these ladies was to attend an appointment with the defendant. From these 50 ladies, the defendant would select 12 whom he would engage for three years at various levels of pay. The plaintiff was voted one of the “most beautiful” 50, but through the defendant’s breach of contract she could not attend her appointment. The 12 winners were chosen from those who had had an appointment. The Court of Appeal concluded that the plaintiff had suffered a compensable loss. Vaughan Williams LJ said (at 793):

“The jury came to the conclusion that the taking away from the plaintiff of the opportunity of competition, as one of a body of fifty, when twelve prizes were to be distributed, deprived the plaintiff of something which had a monetary value. I think that they were right and that this appeal fails.”

221 What the plaintiff lost in that case truly was a chance. She lost the chance to impress the defendant at an appointment, which deprived her of the opportunity to be one of the winners of the competition. The damage was complete at the moment she was denied an appointment. It had crystallised. There is no difficulty in finding on the balance of probabilities that the defendant’s breach of contract caused her to lose that chance. The quantum of the lost chance has nothing at all to do with whether or not the defendant’s breach of contract was causative of the loss.

222 The following passage from Laferrière at [89], which refers to the work of Jean Penneau (La Responsabilité Médicale, Paris, Sirey, 1977) illustrates the problem:

“In order to make his argument clearer, Penneau transfers the chance analysis temporarily to the classical example of a student who, due to an accident, is prevented from taking an important career-related exam. According to the classical loss of a chance analysis, the individual who caused the accident will be required to indemnify the student for the loss of a real and serious chance of passing the examination and embarking on a career. The situation is entirely different, in Penneau’s view, where, despite the accident, the student attends the examination and fails: ‘Here, the chance has been tried, and we know that it has been lost; loss made concrete by the final damage – the failure, death or infirmity – with which it is precisely and necessarily confused.’ To speak, nonetheless, of a loss of chance in this situation would be to speak of the same damage in different and now irrelevant terms, according to Penneau.”

223 Baroness Hale of Richmond noted the difference between the two types of damage in Gregg at 232:

“One counter-argument is that, in this as in many other respects, there is a real difference between personal injury and financial loss. As Tony Weir puts it:

‘where the claimant is suing in respect of personal injury or property damage, he must persuade the judge that that injury or damage was probably due to the defendant’s tort, whereas in case of financial harm it is enough to show that the claimant had a chance of gain which the defendant has probably caused him to lose. There is nothing irrational in this, unless one supposes it is sensible to speak of “loss of a chance” without saying what the chance is of. Losing a chance of gain is a loss like the loss of the gain itself, alike in quality, just less in quantity: losing a chance of not losing a leg is not at all the same kind of thing as losing the leg.’

It is unfashionable these days to distinguish between financial loss and personal injury. Losing the money one has may not be so different from losing the leg one has. But many claims for financial loss do not relate to the money one has but to the money one expected to have – a prospective financial gain. There is not much difference between the money one expected to have and the money one expected to have a chance of having: it is all money. There is a difference between the leg one ought to have and the chance of keeping a leg which one ought to have. There is perhaps an even greater difference between the disease free state one ought to have and the chance of having a disease free state which one ought to have.”

The impact of the

Civil Liability Act

2002 (NSW)

224 The Civil Liability Act 2002 (NSW) makes specific provision for the assessment of future economic loss, including a mandatory discount rate. It provides:

13 Future economic loss – claimant’s prospects and adjustments

(1) A court cannot make an award of damages for future economic loss unless the claimant first satisfies the court that the assumptions about future earning capacity or other events on which the award is to be based accord with the claimant’s most likely future circumstances but for the injury.

(2) When a court determines the amount of any such award of damages for future economic loss it is required to adjust the amount of damages for future economic loss that would have been sustained on those assumptions by reference to the percentage possibility that the events might have occurred but for the injury.

(3) If the court makes an award of damages for future economic loss, it is required to state the assumptions on which the award was based and the relevant percentage by which damages were adjusted.

14 Damages for future economic loss – discount rate

(1) If an award of damages is to include any component, assessed as a lump sum, for future economic loss of any kind, the present value of that future economic loss is to be determined by adopting the prescribed discount rate.

(2) The ‘prescribed discount rate’ is:

(3) Except as provided by this section, nothing in this section affects any other law relating to the discounting of sums awarded as damages.”

225 Section 13 gives rise to significant issues when the injury alleged is the loss of a chance of a better medical outcome. It would seem that unless the chance of a better outcome is greater than 50%, there can be no award for future economic loss. This is because the plaintiff’s damages are based on what their future earning capacity would have been but for their injury (Penrith City Council v Parks [2004] NSWCA 201 at [51]; cf MacArthur Districts MotorCycle Sportsman Inc v Ardizzone [2004] NSWCA 145 per Hodgson JA). If the relevant injury is the loss of a chance of a better outcome that is less than 50%, then on any view the plaintiff’s “most likely future circumstances but for the injury” will be that he or she would have suffered the physical injury anyway. That is, even if the chance had never been lost, it is still more likely than not that at the time of the trial the plaintiff would be in the same position. In such a case, “a court cannot make an award of damages for future economic loss.” On the other hand, if the lost chance was greater than 50% but less than 100%, any award for future economic loss must be discounted by the percentage chance that the ultimate physical injury would have occurred anyway (s 13(2)).

226 The position is otherwise where the alleged damage is loss of a financial opportunity. This is because in such a case the cause of action is complete at the time that the chance is lost. That is, the damages are not contingent upon the occurrence of some event after the chance is lost. It does not matter whether the opportunity turns out to be good or bad: the loss may be valued when the negligent breach occurs.

The problem of causation

227 In Vairy v Wyong Shire Council (2005) 223 CLR 422 at 461, Hayne J observed that “[t]he inquiry into the causes of an accident is wholly retrospective. It seeks to identify what happened and why.” Causation is a question of what was i.e. did the defendant’s conduct cause the injury. To the extent that this involves any hypothetical questions, the answers to those questions only go to proof of the historical fact on the balance of probabilities (see Bennett v Minister of Community Welfare (1992) 176 CLR 408 at 422-423 per Gaudron J). The hypothetical questions are not themselves the facts in issue, although in a theoretical sense causation will always involve hypothetical questions. As Hayne J pointed out in Chappel at 282:

“The search for causal connection between damage and negligent act or omission requires consideration of the events that have happened and what would have happened if there had been no negligent act or omission. It is only by comparing these two sets of facts (one actual and one hypothetical) that the influence or effect of the negligent act or omission can be judged.”

228 Unlike Sellars, Chappel v Hart was a personal injury case. It involved a failure to warn a patient about a risk of surgery that ultimately eventuated. There were five separate judgments. No member of the High Court decided the case on the basis of a lost chance. It was accepted that the injury in respect of which the plaintiff sought damages was her entire physical injury rather than the loss of a chance of a better medical outcome.

229 Gaudron J did not express an opinion about the role of a theory of loss of a chance in personal injury cases. McHugh J dissented but noted that the case did not fall within the principles defined in Sellars.

230 Gummow J (at 258-263) gave detailed consideration to the issue of loss of a chance. His Honour noted that Dr Chappel sought to avoid liability by arguing that Mrs Hart had lost no real and valuable chance of the risk of injury being diminished or avoided due to the defendant’s negligent failure to warn. His Honour then stated (at 258):

“In this way the submissions of Dr Chappel tended to divert attention from the central issue, namely whether there was adequate reason in logic or policy for refusing to regard the ‘but for’ test as the cause of the injuries sustained by Mrs Hart, by the allurement of further cogitation upon the subject of ‘loss of a chance.’

Sellars

231 Gummow J noted that the traditional standard of proof of causation in negligence (which his Honour appears to accept was not disturbed by Sellars) has led to difficulties in proving causation in some types of case. His Honour acknowledged that there has been some suggestion in other jurisdictions that these difficulties can be avoided by applying the loss of a chance analysis to causation. However, his Honour was concerned to emphasise that in Australia the loss of a chance analysis only affects the standard of proof at the stage of the assessment of damages. Gummow J stated (at 260) that:

Sellars v Adelaide Petroleum NL

232 And at 263:

“In the present case, it would have been for Dr Chappel to show that Mrs Hart’s damages were to be reduced to reflect the possibility, being more than a speculation, that independently of his negligence Mrs Hart would have sustained at some later date the injuries of which she complained. That was not the way in which the case for the appellant [Dr Chappel] was presented. Rather, the attempt was to show a lack of causation and to deny any liability. The submissions by Dr Chappel in a large measure attempt to turn speculative matters, which are relevant, if at all, upon the assessment of damages, to account by disrupting the principles governing causation. In this Court, as in the Court of Appeal, Dr Chappel seeks an order setting aside the verdict for Mrs Hart and its replacement by a judgment in his favour.

Malec

233 Kirby J is the only member of the court who indicated a preference for the loss of a chance approach in the context of causation, although his Honour expressed no concluded view. At 274-275 Kirby J said:

CES v Superclinics (Aust) Pty Ltd

234 In marked contrast, Hayne J (at 289) took the view that the loss of a chance analysis should be rejected outright:

“…how does one assess the value of the chance that has been lost? It was suggested in the course of argument that it is reflected in the assessment of damages by discounting the damages otherwise allowed. But that invites attention to what are those damages that are to be discounted – is it, as the argument appeared to assume, the damages attributable to the physical consequences which the respondent suffered? That could be so only if the physical consequences which the respondent suffered were caused by the appellant’s negligence.

All of these considerations point to the conclusion that the loss of chance analysis is flawed and should not be adopted.”

235 Naxakis concerned a young lad who suffered a burst aneurysm in circumstances where it was alleged that if appropriate medical care had been provided the adverse outcome would have been avoided.

236 Although not necessary for her decision, Gaudron J considered whether the plaintiff could recover for the lost chance of a successful outcome. In doing so her Honour addressed some of the issues surrounding loss of a chance in the personal injury context. Her Honour accepted that in cases involving the failure to diagnose a pre-existing condition “there is no philosophical or logical difficulty in viewing the loss sustained as the loss of a chance” and accepted that this analysis may be “strictly correct.” However, in rejecting the approach that damages should be awarded on that basis her Honour, inter alia, observed that the lost chance approach cannot easily be applied in conjunction with the traditional balance of probabilities approach. Her Honour said at 280:

“As already indicated, the lost chance approach requires proof that a valuable chance has been lost. A chance would have no value if the defendant could establish, on the balance of probabilities, that the pre-existing condition would have resulted in the injury or disability in question in any event. Thus, if proof on the balance of probabilities were also retained, damages for loss of a chance would be awarded only in those cases where the plaintiff cannot establish, on the balance of probabilities, that the risk would not have eventuated and the defendant cannot establish that it would. There is, thus, limited practical significance for an approach which allows for loss of a chance if the traditional approach is also retained.”

237 Gaudron J joined in the majority in Sellars, but in Naxakis her Honour was careful to limit the application of the loss of a chance analysis to cases involving loss of a commercial opportunity. In rejecting loss of a chance in personal injury cases her Honour observed that although it is usually justified in this context on the basis that it is a legitimate type of damage, the reality is that it is used to alleviate problems with uncertainty of causation: Naxakis at 278-279. The problem is expressed by the commentator Jacques Bore quoted by Gonthier J in Laferrière at [64]:

suffered the damage in its entirety;

determined in relation to the probable causal link

238 Gaudron J expressed the view in Naxakis that the difficulties of proving causation in medical negligence cases had been exaggerated (see 278-279) and that the concept of a lost chance was not required to overcome them. Her Honour confirmed (at 279) that where the defendant negligently creates or increases a risk of harm and that risk eventuates, the tribunal of fact is entitled to conclude that causation has been established on the balance of probabilities unless the defendant can establish that their breach had no effect or that the damage the plaintiff suffered was inevitable.

239 Callinan J was the only other member of the court in Naxakis who considered the issue of loss of a chance. His Honour also accepted McHugh J’s “material contribution test” and continued (at 312-313):

“On the evidence here the jury were entitled to hold that the failure, the treating doctor’s omission to either undertake an angiogram or the failure to give any consideration to the undertaking of it, materially contributed to the appellant’s condition. They would be entitled to take an alternative view that the second respondent’s conduct, although it might not be possible to say (on the balance of probabilities) that it definitely materially contributed to the plaintiff’s final condition, at least caused him to lose a valuable chance (the value of which it was for them to assess) of avoiding being in the condition that he now finds himself. There is still, in my opinion, room for the operation of the loss of a chance rule (particularly in cases involving the practice of what is even today said to be an art rather than a scientific skill), enabling a plaintiff to recover damages to be equated with, and reduced to the value of the chance he or she has lost, rather than the damages which would be appropriate if it has been proved on the balance of probabilities that the plaintiff’s condition owes itself to the defendant’s acts or omissions.”

240 Callinan J’s analysis would seem to be consistent with subsequent authority in the NSW Court of Appeal.

241 When the conduct of a defendant is shown to have “materially contributed” to the plaintiff’s injuries causation on the balance of probabilities will be satisfied. The defendant, as a matter of legal proof, has caused the plaintiff’s entire injury. Where, however, all that can be shown is that the defendant’s breach of duty made some contribution to the plaintiff’s injury as opposed to a material contribution, then the only way that the plaintiff can succeed is on the basis of a lost chance of a better outcome. In State of New South Wales v Burton [2006] NSWCA 12 at [14], Spigelman CJ stated that:

some

that

material

242 His Honour concluded (at [24]) that “… the end result is that damages were assessed on an inappropriate basis. The matter should be remitted to the District Court for damages to be assessed on a loss of a chance basis” (see also the judgment of Basten JA at [66]). While his Honour agreed with Spigelman CJ’s opinion that the evidence in the case was insufficient to justify a finding of material contribution, Hunt AJA qualified his agreement by stating (at [91]) that:

“…The Chief Justice has found…that the distinction drawn by Dr Wright between cause and contribution/exacerbation should be interpreted as reducing the extent of the contribution made to the respondent’s condition of post-traumatic stress disorder by the appellant’s omissions to something necessarily less than a material contribution…The word ‘exacerbation’ is generally used by the medical profession as meaning only that the original condition is made worse (or more serious), usually involving a greater intensity in the symptoms of that condition. That increase in severity may be minor, medium or extreme. The word exacerbation does not mean to me that the act which led to the exacerbation was necessarily something less than a material contribution to the condition exacerbated.”

243 Spigelman CJ had earlier considered the question of the proof necessary to satisfy the “material contribution” test in Seltsam. In that case, His Honour (at 280) accepted as fundamental the proposition that proof of “a mere possibility is not sufficient to establish causation for legal purposes.” However, evidence of a possibility is circumstantial evidence which, cumulatively, may amount to proof on the balance of probabilities or even beyond reasonable doubt. At [287] the Chief Justice approved the following passage from the judgment of Herron CJ in EMI (Australia) Ltd v BES [1970] 2 NSWLR 238 at 242:

“Medical science may say in individual cases that there is no possible connexion between the events and the death, in which case, of course, if the facts stand outside an area in which common experience can be the touchstone, then the judge cannot act as if there were a connexion. But if medical science is prepared to say that it is a possible view, then, in my opinion, the judge after examining the lay evidence may decide that it is probable. It is only when medical evidence denies that there is any such connexion that the judge is not entitled in such a case to act on his own intuitive reasoning. It may be, and probably is, the case that medical science will find a possibility not good enough on which to base a scientific deduction, but courts are always concerned to reach a decision on probability and it is no answer, it seems to me that no medical witness states with certainty the very issue which the judge himself has to try.”

244 The Chief Justice set out the passage from McHugh J’s judgment in Chappel v Hart that has been quoted above. His Honour said (at 279):

Naxakis…

that

If there was such evidence then, to use the words of both Gaudron J…and Callinan J…the tribunal of fact was ‘entitled’ to find that the conduct which increased the risk, materially contributed to the injury – entitled, but not, of course, required to so find” (emphasis in original).

245 Importantly, his Honour stated (at 280) that:

Chappel v Hart

because

246 The effect is that evidence of a possibility that the relevant conduct caused the plaintiff’s injury is circumstantial evidence that may contribute to proof, on the balance of probabilities, of a material contribution. On the other hand, if the evidence taken as a whole does not establish anything more than a mere possibility that the conduct caused the injury, then causation has not been proved to the requisite standard of proof. Nevertheless, the plaintiff may still be entitled to receive damages on the basis of a lost chance.

Does

Rufo

bind me in this case?

247 It is necessary to return to Rufo.

248 The Court of Appeal’s decision is, of course, binding on me. However, it was concerned with a chance that was assessed to be less than 50%. Santow JA (at 688-690) suggests that the loss of a chance analysis should also apply where the chance is greater than 50%. If this is the correct approach to causation it would displace the presently accepted standard of proof in medical negligence cases. The other judgments in the case are confined to defining a principle where the chance is less than 50%. Hodgson JA expressed (at 681) the view that the loss of a chance analysis should only apply to chances of less than 50%, while in cases where the plaintiff can prove causation on the balance of probabilities (i.e. where the chance is greater than 50%) Malec should continue to apply so that damages are assessed taking into account the percentage chance that the injury would have occurred in any event. Accordingly, insofar as “loss of a chance” presently has a place in personal injury cases on the current state of the law in New South Wales it is in cases where the plaintiff cannot prove causation on the balance of probabilities, and accordingly the lost chance is less than 50%. This is consistent with the view expressed by Callinan J in Naxakis, and with the approach adopted by Spigelman CJ in Burton.

Conclusion in this case

249 I have already determined that on the balance of probabilities an ECG administered after 4 February would have revealed Kurt’s long QT. In my view the chances of that occurring were at least 65% and may have been greater. If his condition had been identified the chance that he would not have been effectively managed and a cardiac arrest avoided was negligible. Accordingly, the various plaintiffs have each made out their case and are entitled to verdicts in the sums agreed.

Orders

250 Although damages have been agreed it may be necessary to consider matters of interest and costs. I direct the parties to bring in short minutes of order on which occasion any necessary submissions can be made.

**********

Actions

Download as PDF Download as Word Document

Citations

Halverson v Dobler [2006] NSWSC 1307

Most Recent Citation

Thirlway v Parnell LP Gas Systems Pty Ltd [2009] WADC 36

Cases Citing This Decision

9

Quach v New South Wales Health Care Complaints Commission [2016] NSWCA 10

Gett v Tabet [2009] NSWCA 76

Dobler v Halverson [2007] NSWCA 335

Cases Cited

28

Statutory Material Cited

2

Romeo v Papalia [2012] NSWCA 221

State of New South Wales v Burton [2006] NSWCA 12

CITATION:	HALVERSON & ORS v DOBLER HALVERSON by his tutor v DOBLER [2006] NSWSC 1307
HEARING DATE(S):	7 August 2006 - 4 September 2006
JUDGMENT DATE :	1 December 2006
JURISDICTION:	Civil
JUDGMENT OF:	McClellan CJatCL at 1
DECISION:	Verdicts for the plaintiffs
CATCHWORDS:	PROFESSIONAL NEGLIGENCE - LIABILITY - MEDICAL NEGLIGENCE - general practitioner - rural practice - DAMAGE - brain injury - cardiac arrest - BREACH - diagnosis of recurrent syncope - cardiac cause of syncope - apprpriate diagnostic investigation - facilities readily available - long QT syndrome - causation - chance of investigation revealing long QT interval - EXPERT EVIDENCE - general practitioners - cardiologists - scientif proof and legal standard of proof - role of hindsight - effect of s 5O of the Civil Liability Act 2002 (NSW) - LOSS OF A CHANCE in medical negligence
LEGISLATION CITED:	Civil Liability Act 2002 (NSW) Interpretation Act 1987
CASES CITED:	Ambulance Service of NSW v Worley [2006] NSWCA 102 Bennett v Minister of Community Welfare (1992) 176 CLR 408 Capital Brake Service Pty Ltd v Nicholas Kevin Meagher & 8 Ors t/as Sparke Helmore [2003] NSWCA 225 Chaplin v Hicks [1911] 2 KB 786 Chappel v Hart (1998) 195 CLR 232 Elbourne v Gibbs [2006] NSWCA 127 EMI (Australia) Ltd v BES [1970] 2 NSWLR 238 Faferrière v Lawson [1991] 1 SCR 541 Graham v Baker (1961) 106 CLR 340 Gregg v Scott [2002] EWCA Civ 1471 Gregg v Scott [2005] 2 AC 176 Jones v Dunkel (1958) 101 CLR 298 MacArthur Districts MotorCycle Sportsman Inc v Ardizzone [2004] NSWCA 145 Malec v J C Hutton Pty Ltd (1990) 169 CLR 638 Mallett v McMonagle [1970] AC 166 March v E & M H Stramare Pty Ltd (1990) 171 CLR 506 Naxakis v Western General Hospital & Anor (1999) 197 CLR 269 Neindorf v Junkovic (2005) 222 ALR 631 Penrith City Council v Parks [2004] NSWCA 201 Ramsay v Watson (1961) 108 CLR 642 Rogers v Whitaker (1992) 175 CLR 479 Rufo v Hosking [2004] NSWCA 391 Sellars v Adelaide Petroleum NL (1992) 179 CLR 332 Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262 State of New South Wales v Burton [2006] NSWCA 12 State of NSW t/a NSW Department of Agriculture v Allen [2000] NSWCA 141 T C (by his tutor Sabatino) v The State of NSW & Ors [2001] NSWCA 380 Vairy v Wyong Shire Council (2005) 223 CLR 422 Watts v Rake (1960) 108 CLR 158 Wynn v NSW Insurance Ministerial Corporation (1995) 184 CLR 485
PARTIES:	20182/03 Kenneth Halverson (1P) Janet Halverson (2P) Annika Halverson (3P) Kenneth Dobler (Def) 20183/03 Kurt Halverson bht Kenneth Halverson (Pltf) Kenneth Dobler (Def)
FILE NUMBER(S):	SC 20182/03; 20183/03
COUNSEL:	M B Williams SC/L Grey (Pltfs) D Higgs SC/K C Morgan (Def)
SOLICITORS:	Maurice Blackburn Cashman (Pltfs) Blake Dawson Waldron (Def)