Lazarevski v North Metropolitan Health Service

[2019] WADC 84

JURISDICTION     :   DISTRICT COURT OF WESTERN AUSTRALIA

IN CIVIL

LOCATION:   PERTH

CITATION:   LAZAREVSKI -v- NORTH METROPOLITAN HEALTH SERVICE [2019] WADC 84

CORAM:   TROY DCJ

HEARD:   23, 24 & 26 APRIL & 1, 2 & 22 MAY 2019

DELIVERED          :   27 JUNE 2019

FILE NO/S:   CIV 2260 of 2016

BETWEEN:   SANDY LAZAREVSKI

Plaintiff

AND

NORTH METROPOLITAN HEALTH SERVICE

Defendant

Catchwords:

Medical negligence - Failure to apply serial troponin testing - Breach of duty - Causation - Damages - Turns on own facts

Legislation:

Civil Liability Act 2002, s 5B, s 5C, s 5PB

Result:

Judgment for plaintiff

Representation:

Counsel:

Plaintiff	:	Mr J R Johnson
Defendant	:	Mr D R Clyne

Solicitors:

Plaintiff	:	Julian Johnson Lawyers
Defendant	:	Sparke Helmore Lawyers

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

Adeels Palace Pty Ltd v Moubarak [2009] HCA 48; (2009) 239 CLR 420

Ellis (by his Next Friend Christopher Graham Ellis) -v- East Metropolitan Health Service [2018] WADC 36

Jones v Dunkel (1959) 101 CLR 298; (1959) HCA 8

Panagoulias (by His Next Friend Fiona Averil Panagoulias) v East Metropolitan Health Service [No 4] [2017] WADC 118

Rogers v Whitaker [1992] HCA 58; (1992) 175 CLR 479

Strong v Woolworths Ltd t/as Big W [2012] HCA 5; (2012) 246 CLR 182

Wallace v Kam (2013) HCA 13; (2013) 250 CLR 375

Wright v Minister for Health [2016] WADC 93

Wyong Shire Council v Shirt (1980) 146 CLR 40

Table of Contents

Statement of issues

Initial presentation on 6 January 2014

Chest X-ray

Discharge

Events of 9 January 2014

The plaintiff's primary and secondary case

The duty of care imposed on Dr Winton

The defendant's case

The plaintiff's expert witnesses

Why are serial troponin tests performed?

Task of emergency physicians when a patient presents as Ms Lazarevski did

Limitations on clinical assessment alone in accurately classifying patients at acceptably low risk

Importance of Biomarker Tests

Did Ms Lazarevski have typical symptoms of ACS?

Significance or otherwise of the ECG results

Relevance of Ms Lazarevski's level of pain and its duration

The background of anxiety

The relevance of the recent death of Ms Lazarevski's brother

Symptoms of feeling sweaty and clammy

The conflicting approaches

Did the 'Pathway' apply?

Was there a discretion to disregard the Pathway?

Dr Winton's justification for not applying the Pathway

Associate Professor Allan and Dr Lamberth's support for Dr Winton's decision not to apply the Pathway

The Framingham Study

Dr Lamberth's additional reasons for supporting Dr Winton's decision not to apply the Pathway

Risk of false positives

The Than survey

Conclusions on the issues that arise on liability

Section 5B CLA

Reasonable foreseeability

Conclusions on s 5B(1)(c)

Conclusions on s 5B(1)(b)

Conclusions on s 5B(1)(c) and s 5B(1)(d)

Conclusions on Dr Winton's s 5B duty of care

Section 5PB

The relevant practice

The burden of proof in s 5PB

Conclusion on liability

Causation

The relevance of the extent and duration of Ms Lazarevski's pain on 6 January 2014

The relevance of Ms Lazarevski's first troponin reading on 9 January 2014

How quickly does the troponin level in the bloodstream increase?

At what rate does troponin subside?

Third reason for supposing there was an event significant enough to raise troponin on 6 January 2014

Inferential reasoning in considering causation

General principles

Conclusions

Would carrying out troponin tests have made any difference?

Alternative s 5C(2) position - in the event that factual causation is not made out

Orders

TROY DCJ:

Statement of issues

1. At about 4.00 pm on 6 January 2014 the plaintiff, Ms Sandy Lazarevski, then aged 28, suffered a sudden onset of excruciating pain to her chest radiating into her left arm.  It subsequently transpired that she had suffered a spontaneous coronary artery dissection (SCAD).  This occurs when a split or separation suddenly develops between the layers of the wall of one of the arteries providing blood flow to the heart.  She was taken to the Sir Charles Gairdner Hospital where she remained for approximately three hours.  Although Ms Lazarevski's treatment had a number of aspects, it did not include the administration of a series of blood tests designed to measure the level of a particular protein complex called troponin in the blood.  Troponin is released into the bloodstream if there is damage to the heart.  Ms Lazarevski was discharged at 8.10 pm.  Three days later, on 9 January 2014 she suffered a serious heart attack, described as an ST elevation myocardial infarction(STEMI).

2. Three fundamental questions arise:

   •Given Ms Lazarevski's presentation, was it unreasonable not to administer troponin blood tests on 6 January 2014? (Liability).

   •If troponin sensitive tests had been administered on that date, would they have yielded abnormal results?  (Causation).

   •If they had been administered, and if the results were abnormal, would the critical events of 9 January 2014, the STEMI, have been averted? (Causation).

Initial presentation on 6 January 2014

1. Dr James Winton was the emergency physician with the primary responsibility for Ms Lazarevski's care and treatment at the hospital on 6 January 2014.  Dr Winton first observed Ms Lazarevski at 5.10 pm and he subsequently authorised her discharge.

2. Dr Winton has been a fellow of the Australasian College of Emergency Medicine since 2009.  He has worked fulltime in emergency medicine since 2004.  Since early 2012 he has been a co‑director of emergency medicine training at the hospital.  This role is essentially supervisor of training so that he and one of his colleagues are responsible for the training needs of some 25 junior doctors in the department.[1]

   [1] His curriculum vitae was tendered as exhibit 8.

3. Initially, Dr Winton reviewed Ms Lazarevski for some 10 ‑ 15 minutes. On examination her pulse and blood pressure were normal.  A chest and abdominal examination also revealed no cause for concern.  If there is a SCAD that causes a complete blockage of the artery, it results in a characteristic abnormal electrical signal as the heart contracts as it tries to pump.  That abnormal signal is identifiable using an electrocardiogram (ECG) - a graphic record produced by an electrocardiograph, a device for recording electrical conduction through the heart.  Ms Lazarevski underwent two ECGs at 5.22 pm and 5.57 pm.  The results were normal.

4. As Ms Lazarevski's counsel explained uncontroversially, a SCAD occurs when there is a tear in the lining or the wall of a coronary artery, in this case the circumflex artery.  Whilst it is possible for a SCAD to occur without it compromising blood supply to the heart muscle that it supplies, it can cause a reduction in the blood supply to that muscle in a number of ways.

5. A reduction in blood and oxygen supply is a condition called ischaemia.  Where a patient suffers myocardial (the muscle of the heart) ischaemia they will experience chest pain.  If there is an ongoing reduction in the amount of oxygen being supplied to the muscle, the muscle tissue will eventually die or infarct, hence a myocardial infarction.  This is the process by which a SCAD can cause a heart attack.  If the SCAD causes a complete blockage of the artery, then because there is no blood supply or oxygen supplied to the myocardium, infarction occurs more quickly than if there is only a narrowing or a partial blockage.

Chest X-ray

1. Dr Winton arranged for blood tests and a chest X-ray.  The chest X‑ray conducted at 6.53 pm showed that Ms Lazarevski's lungs and pleura were clear and her heart size and mediastinal contours were unremarkable.[2]  The X-ray ruled out the possibility of a pneumothorax (a punctured lung).

   [2] Page 8/92 of exhibit 1 (medical records).

2. One of the experts called by the defendant, Dr Lamberth, considered that one of the four important and urgent diagnoses for Dr Winton to consider was a punctured lung.[3]  Dr Winton's examination and the chest X-ray eliminated that as a possibility.  A second possibility, thoracic aortic dissection (another way of describing a SCAD), is extremely uncommon and the chest X-ray and examination made it acceptably unlikely.[4]

   [3] Page 7 par 62 'p 7 [62]' of first Lamberth report.  

   [4] Page 7 [65] of first report.

3. One of the experts called by the plaintiff, Professor Kelly considered that the chances of Ms Lazarevski having suffered a punctured lung was tiny.  Her clinical presentation and description of pain was not consistent with that disease.  The risk that she had a pneumothorax compared to the risk that she had acute coronary syndrome (ACS) was considerably lower, but Dr Winton should not be criticised for ordering the chest X‑ray to exclude that possibility.[5]

   [5] ts 67.

Discharge

1. The blood tests that were ordered were a Full Blood picture and Urea and Electrolytes[6] but Dr Winton did not order a blood test to measure the level of troponin.  Ms Lazarevski was discharged at 8.14 pm, some three hours after her original admission, with 10 diazepam tablets[7] and a referral to her general practitioner.[8]

   [6] Page 8/92 of exhibit 1. 

   [7] Page 9/92 of exhibit 1.

   [8] Page 15/92 of exhibit 1.

2. Dr Winton wrote, either at the time of discharge or just after,

   Feels improved, bloods normal, chest X-ray normal, discharge home.[9]

   [9] Page 6/92 of exhibit 1.

Events of 9 January 2014

1. On 9 January 2014 Ms Lazarevski was re‑admitted to the hospital as an emergency patient.  Whilst at home at about 2.40 pm she suffered a STEMI with a completely blocked circumflex coronary artery.[10]  This artery branches off the left coronary artery and supplies most of the left atrium, the posterior and lateral free walls of the left ventricle and part of the anterior papillary muscle.

   [10] Professor Kelly's first report of 26 March 2018 (part of exhibit 2), page 5 [2]. In his first report of 10 December 2015 Professor Harper states at page 2 [4] 'there is absolutely no doubt that Ms Lazarevski suffered an STEMI on 9 January 2014'.

2. A STEMI refers to a particular type of heart attack characterised by ST segment elevation on the 12 lead ECG.  It occurs when there is a sudden, complete obstruction of a major coronary artery which completely interrupts blood flow to the heart muscles that are supplied by that artery.[11]

   [11] Harper first report of 10 December 2015 answer 1 at page 1 [A1, p 1].

3. Infarction is a term applied to the death of tissue resulting from a failure of blood supply, commonly due to obstruction of a blood vessel by a blood clot or narrowing of the blood-vessel channel.  Typically, it follows a period of ischaemia, that is where there is a decreased supply of oxygenated blood to a body part with resultant pain.

4. On arrival at the Hospital on 9 January 2014, Ms Lazarevski's condition was correctly identified and she was treated appropriately including urgent coronary artery bypass graft surgery.  Medical staff identified a coronary artery dissection.

The plaintiff's primary and secondary case

1. The plaintiff's primary case on liability is that reasonable care by Dr Winton and the hospital required that they apply the hospital's 'ACS Pathway' (the Pathway) given Ms Lazarevski's presentation.  If they had done so, Ms Lazarevski would have undergone serial troponin testing.  The plaintiff's secondary case is that even if one was to put to one side the Pathway, reasonable care required the performance of serial troponin testing.

The duty of care imposed on Dr Winton

1. Dr Winton bore the responsibility of determining the nature of the treatment provided to Ms Lazarevski at the hospital.  There is no dispute that on 6 January 2014 the defendant and its medical staff, including Dr Winton, owed Ms Lazarevski a duty of care to take reasonable care in their assessment, advice and treatment, such as to avoid a reasonably foreseeable risk of harm occurring to her.  The defendant assumed the Minister for Health's responsibilities upon its incorporation by statute in July 2016.

2. The general principles applicable where a person is said to have breached a duty of care are set out at s 5B of the Civil Liability Act 2002 (CLA):

   5B.General principles

   (1)A person is not liable for harm caused by that person's fault in failing to take precautions against a risk of harm unless -

   (a)the risk was foreseeable (that is, it is a risk of which the person knew or ought to have known); and

   (b)the risk was not insignificant; and

   (c)in the circumstances, a reasonable person in the person's position would have taken those precautions.

   (2)In determining whether a reasonable person would have taken precautions against a risk of harm, the court is to consider the following (amongst other relevant things) -

   (a)the probability that the harm would occur if care were not taken;

   (b)the likely seriousness of the harm;

   (c)the burden of taking precautions to avoid the risk of harm;

   (d)the social utility of the activity that creates the risk of harm.

The defendant's case

1. The defendant denies that the decision on 6 January 2014 not to call for serial troponin tests was negligent and/or breached a duty of care. The defendant further pleads that this decision was in accordance with a practice that was, at the time, widely accepted by emergency physicians as competent professional practice: s 5PB(1). The defendant contends that conducting troponin blood tests on every patient presenting as Ms Lazarevski did on 6 January 2014 would be unjustifiably intrusive and burdensome.

The plaintiff's expert witnesses

1. The plaintiff called three expert witnesses, Professor Ann-Maree Kelly, Professor Richard Harper and Associate Professor Neil Strathmore.  Professor Kelly has been an accident and emergency specialist for some 28 years.  Professor Harper is an interventional and consultant cardiologist.  He is a Fellow of the Royal Australian College of Physicians, the Cardiac Society of Australia and New Zealand and the American College of Cardiology.  He is an adjunct professor of medicine at the Department of Medicine, Monash University and the Emeritus Director of Cardiology at Monash Heart, Monash Health.

2. Associate Professor Strathmore has been a cardiologist at the Royal Melbourne Hospital and in private practice since 1991.  He holds fellowships of, amongst others, the Royal Australasian College of Physicians and the Cardiac Society of Australia and New Zealand.  He is an Associate Professor in the Department of Medicine of the University of Melbourne.

3. The defendant submits that I should give no weight to the opinions of Professor Harper or Associate Professor Strathmore on the issue of whether serial troponin tests should have been administered, because neither witness has any experience in working in an Emergency Department.  There was no cross‑examination of either witness to that effect nor was any objection raised during their evidence.  Having considered their respective curriculum vitae,[12] I am quite satisfied that each witness had the expertise, through their qualifications and experience, to provide every expert opinion that I set out in this judgment.

   [12] Pages 89 ‑ 118 of exhibit 3.

Why are serial troponin tests performed?

1. If the heart's muscle tissue, the myocardium, experiences ischaemia, then troponin, a protein in the myocardium, is released into the blood stream.  Troponin is a chemical only produced by the heart.  An ECG will not reveal if a patient has suffered an NSTEMI or not, whereas troponin testing will.  A myocardial infarction without this characteristic elevation in the ST segment is termed a non-ST segment elevation myocardial infarction, (NSTEMI) or non-STEMI.

2. Serial troponin tests, rather than just one, are conducted because in addition to evaluating whether the troponin level is elevated, a treating physician would wish to ascertain whether the troponin level is going up, going down or remaining flat.  That has significance in clinically assessing the cause of the symptoms.

3. Each of the plaintiff's three expert witnesses reported and/or testified that if serial testing was employed and the second reading was both abnormally high and higher than the first reading, this would strongly suggest ACS.[13]

   [13] Professor Kelly: page 6 [3] of her first report, Professor Harper page 4 [1] of his first report of 10 December 2015 and Associate Professor Strathmore in evidence at ts 109.

4. A patient's troponin level is regarded as being abnormal if it registers above the 99^th percentile of the general population.[14]

   [14] Professor Kelly at ts 69.

Task of emergency physicians when a patient presents as Ms Lazarevski did

1. Professor Kelly testified[15] that assessment of chest pain in Emergency Departments is essentially a risk stratification exercise.  When a patient comes into an Emergency Department with chest pain, the treating physicians have two tasks.  Firstly they must identify the very highest risk group, those with a particularly dangerous pattern on their ECG associated with the highest mortality.  This group require urgent treatment in a cardiac catheter laboratory, usually within 90 minutes, to have an angiogram.  Not all of them turn out to have a blockage of their major artery, but most of them do, which justifies that approach.

   [15] ts 65.

2. For those patients who do not have those features on their ECG, the second task is to work out which are in a group of sufficient risk that they need further investigation in hospital and which are of such low risk that they are safe to be discharged home, potentially for follow up by their GP.  It is rare for the treating physician to actually make a definitive diagnosis of the non ECG typical ACS in the Emergency Department.  Rather, they identify a group of patients who have features that are of sufficiently high risk for the cardiologists to then deal with.  This risk assessment process involves clinical assessment and an ECG.

3. The scores obtained through one of the tests described by Professor Kelly, as set out at [39] ‑ [40] below, identify higher risk patients. If their score is high, that automatically moves them into that group and the troponin reading just adds to that information. For patients who have lower scores, if the troponin is negative it helps take the risk so low that it is essentially negligible. But without the troponin test it is not possible to get the risk to that level.

4. Professor Kelly reported[16] that it is not the role of an emergency physician to reach a definitive diagnosis.  Rather their role is to investigate and stratify the level of risk.

   [16] Second report page 5 [19] and page 7 [2].

Limitations on clinical assessment alone in accurately classifying patients at acceptably low risk

1. The defendant submits that it was competent professional practice, relevant to my consideration of s 5PB as discussed at length at [196] and onwards, for Dr Winton to exclude a diagnosis of ACS based solely on clinical assessment and Ms Lazarevski's presenting history. In my view Professor Kelly was the best qualified expert witness to give expert opinion evidence on the topic of appropriate practice and standards of care by accident emergency medical staff. I regarded her as a particularly impressive witness.

2. Professor Kelly noted that clinical assessment simply means history and examination.  Some clinicians would regard an ECG as part of the process of clinical assessment.  Clinical assessment refers to things that can be done at the bedside but does not include X‑rays or blood tests.[17] She reported that there is no validated process for ruling out ACS based on clinical assessment alone.  There is no process that accurately classifies patients at such low risk that there is clinical equipoise (equality or evenness) between the risks and benefits, so that further investigation, specifically troponin testing, can be omitted.[18]

   [17] ts 63.

   [18] Page 3 [8] of second report of 15 April 2019 and ts 62.

3. All risk stratification processes in common use in Australia in 2014 included troponin testing in the risk stratification because, as described in a study by Goodacre and others,[19] clinical features do not have sufficient discriminatory value.

   [19] Acad Emerg Med 2002, 9: 202 - 203 as cited at page 3 [8] of second report.

1. Professor Kelly explained that for pulmonary embolism, for example, there is a validated approach using simply clinical assessment that can identify a group of such low risk that further testing is of no particular benefit.  That is not the case with chest pain.  There have been many attempts to find such an answer, none of which have been successful.  That is partly due to the variation in the symptoms with which people present and how they describe those symptoms.  The severity of pain can vary; the description of pain can vary from sharp to pressure, to severe to tight, the associated features such as vomiting and shortness of breath can vary or not be present.  Some patients, particularly the very elderly, might present with no chest pain and just fatigue.[20]

   [20] ts 63.

2. Professor Kelly explained that the limitations of clinical assessment for chest pain were widely understood and accepted in January 2014.  The problem with the clinical assessment of chest pain has been known for at least the last 30 years.

3. During cross‑examination, Professor Kelly testified that the most dangerous and most common diagnosis that should be considered when a patient presents in this way is ACS.  There are a very large number of potential diagnoses and the emergency physician's role is to try and work out whether any of the serious diagnoses are present.  He or she does so by a combined process of clinical assessment and the use of ancillary tests.  They take a history, conduct an examination and look at other materials that are available, such as an ambulance record or a triage record.  Observation is part of the clinical assessment.  Its weight depends on the particular circumstances.  The accuracy of the history can be very helpful.  But when a patient complains of chest pain, there has been no validated collection of features that accurately rule out ACS.[21]

   [21] ts 75.

4. Dr Lamberth accepted that there is no way to completely exclude ACS based on clinical assessment and ECG.[22]  I am quite satisfied that this is so.

   [22] ts 189.

Importance of Biomarker Tests

1. It is because of those limitations that biomarker tests and other tests have been developed to more accurately risk stratify and identify patients.  One such test is the TIMI score where one point is allotted for each item that is positive.  It includes age, presence of risk factors, whether the patient is known to have coronary artery disease or not, whether they have had aspirin in the last seven days, whether they have had more than one episode of pain, whether there are changes on their ECG, but importantly whether there is a positive biomarker.  It is not possible, therefore, to calculate the aggregate score without a biomarker test, these days a troponin test.[23]

   [23] ts 63 - 64.

2. Professor Kelly also referred to a test called the HEART score.  H stands for history, whether it's suspicious, highly suspicious, moderately suspicious or only very slightly suspicious; E: whether there are ECG changes; A is for age; R is for risk factors; and T is for troponin.  A third test, the EDACS score, involves age, gender, risk factors, known coronary artery disease.  It involves clinical features which attract plus or minus scores depending on whether they are present or not.  But even EDACS' lowest risk category requires serial troponin tests.[24]

   [24] ts 64.

3. An approach based on one of these scoring processes, most commonly the TIMI score, in risk-stratifying emergency patients was widely used in Australian Emergency Departments in 2014.  In each of these tests, to get the patient to the level of score where they could be discharged, biomarker testing including troponin tests is required.[25]  Dr Winton accepted in cross-examination that serial troponin tests were required for all the common risk assessment tools used in practice.[26]

   [25] ts 64.

   [26] ts 228.

Did Ms Lazarevski have typical symptoms of ACS?

1. Professor Kelly considered that the group of patients with chest pains who look unwell are usually those with the very high risk ECG pattern.  Most patients who turn out to have ACS, but are not that ECG pattern type, tend to look well on initial examination.[27]  Ms Lazarevski's presentation was suggestive of ACS.[28]  As Professor Kelly explained in evidence, only a couple of features are required to reach a conclusion that a patient who presents with chest pain has possible ACS. In Professor Kelly's view the central chest pain pressure, pain going down her left arm, vomiting and shortness of breath were all factors that would undoubtedly have caused Professor Kelly to order troponin testing.[29]  Professor Kelly regarded the chest and left arm pain as, 'an almost classical presentation.'[30]

   [27] ts 78.

   [28] A1 page 6 [6] of first report.

   [29] ts 77.

   [30] ts 62.

2. Whilst the ECG did not show a pattern of particularly high risk (it seems to me by itself it did not reveal any risk), Professor Kelly considered that there were enough typical features that would make a treating physician concerned.  Ms Lazarevski was at least in the 'possible ACS' category.[31]  Ms Lazarevski did not have any sharpness to her pain, although the absence of such sharp chest pain could not be used to rule ACS out.[32]

   [31] In the Pathway document – see [87] below.

   [32] ts 68.

3. By contrast, Dr Winton had considered that there were a number of factors that made her presentation unlikely to be ischaemic.  The most prominent fact being that Ms Lazarevski was a female in her 20s.  Ischaemic heart disease is a condition that becomes increasingly more common with age and it is extremely unlikely in people in their 20s especially in females.  He felt ischaemic pain was unlikely because of the nature of her symptoms.  She had never had any pains like this before, there were some atypical features of the pain, namely that it was sharp and it was related to breathing, and the ECG showed no ischaemic features.[33]  The pain was not associated with exertion and there was a sudden onset.[34]

   [33] ts 212 - 213.

   [34] ts 235 - 236.

4. Dr Winton noted at the time that Ms Lazarevski looked well shortly before her discharge.  Essentially his evidence was that even though he appreciated at the time that it was theoretically possible that Ms Lazarevski had sustained ACS, his clinical judgment was that for a variety of reasons, it was so unlikely that it would be inappropriate to follow the Pathway.  He concluded that her presentation was more atypical than typical of ACS.[35]

   [35] ts 235 - 236.

5. The defendant called Associate Professor Roger Allan to give evidence.  Associate Professor Allan is the Clinical Executive Director of the Northern Network South Eastern Sydney Local Health District, Senior Staff Specialist, Interventionist Cardiologist, Prince of Wales Hospital, and Associate Professor School of Medicine University of New South Wales.  He is a Fellow of the American College of Cardiology and the Cardiac Society of Australia and New Zealand. Associate Professor Allan has taught at every level since graduating in medicine, including training cardiology advanced trainees and cardiologists.

6. Associate Professor Allan gave supportive evidence as to how unusual it would be for a female of 28 to appear with ACS.  Associate Professor Allan had practised cardiology for 45 years and never seen that, nor had any of the emergency physicians of a similar longevity that he practices with. He noted that in medicine doctors do not look for rarities first.[36]

   [36] ts 130 - 131.

7. Professor Harper acknowledged that a doctor in an Emergency Department assessing a patient such as Ms Lazarevski would have a low index of suspicion that the patient was suffering a heart attack.  That is particularly so if there were no changes on the ECG suggestive of a heart attack which is the case here.[37]  Professor Harper also noted, however, that one of the rare causes of heart attacks is a SCAD. A SCAD is a rare but important cause of heart attack that particularly occurs in young women who often, but not always, have a generalised underlying abnormality of their arteries known as fibro‑muscular dysplasia.[38]

   [37] Page 4 [1] of first report.

   [38] Page 2 [5] of Harper report.

8. The defendant's second expert witness, Dr Lamberth has been a fellow of the Australasian College of Emergency Medicine since 1996 and has practised full-time in critical care medicine since that time.  Since 2003 he has been the Director of Public Hospital Intensive Care at Calvary Health Care in the Australian Capital Territory.  He is a senior lecturer at the Australian National University Medical School.

9. Dr Lamberth considered that the SCAD seemingly suffered by Ms Lazarevski on 6 January 2014 is extremely uncommon.  Most emergency specialists will never encounter it.[39]  The two ECG's conducted on 6 January 2014 did not show any changes diagnostic for cardiac ischaemia.[40]

   [39] Page 7 [58] of first report.

   [40] Page 7 [66] of first report.

10. Dr Lamberth considered that on 6 January 2014 Ms Lazarevski's presentation did not suggest that her chest pains had a cardiac origin. That contrasts with her more typical presentation on 9 January 2014.[41] In his evidence Dr Lamberth stated that there were a variety of features that were atypical, particularly the sharpness of the pain, the fact that the pain was worse on inspiration so that the other constellation of hyperventilation was a better fit for the diagnosis.[42]  In cross‑examination he agreed that he should have recorded nausea as a typical feature in his report.[43]  Pressed further, Dr Lamberth agreed that the reported pain in the left arm is a typical feature that would apply if one was considering her case with reference to the Pathway document which grounds the plaintiff's primary case.[44]

    [41] Page 3 [25] of second report.

    [42] ts 171.

    [43] ts 184.

    [44] ts 184 – 185.

11. As Professor Kelly appropriately pointed out, in analysing Dr Winton's thought processes on 6 January 2014 it is important not to give way to hindsight and/or outcome bias.  Hindsight bias refers to the tendency of those with knowledge of the outcome to exaggerate the extent to which they would have predicted the event beforehand.  The event in this case being the STEMI sustained on 9 January 2014.  Similarly, outcome bias refers to the influence of knowledge of the eventual outcome on retrospective evaluations of clinical care.[45]

    [45] Page 2 of first report.

Significance or otherwise of the ECG results

1. During cross‑examination, Professor Kelly testified that an ECG is not sensitive for ACS.  It only picks up about three to four out of 10.  That is why troponin testing is so important.  Serial troponins and ECGs go together because signs of heart damage can develop on an ECG over time.[46]

   [46] ts 79.

2. For the reasons explained by Professor Harper, the ECG results are not necessarily inconsistent with Ms Lazarevski having suffered ACS, albeit less serious than the ACS experienced on 9 January 2014.[47]

   [47] First report page 2 A1 [2].

3. Neither of the ECGs revealed ST segment elevation and so Ms Lazarevski did not have a complete blockage of her circumflex artery on 6 January 2014.  It is clear that the possibility remained that she had suffered an incomplete or partial blockage of her circumflex artery as a consequence of the dissection.  An incomplete blockage can cause ischaemia which can compromise the myocardium, and could lead to infarction.  Because a partial blockage of an artery does not necessarily result in an abnormality of the electrical signal identifiable on an ECG, the fact that the ECGs on 6 January 2014 were normal does not rule out a partial blockage.  As noted, a myocardial infarction without this characteristic elevation is an NSTEMI or non‑STEMI.

4. Associate Professor Allan considered that the fact that both ECG's were normal, stretched out over that period of time; meant that it was unlikely that at that stage Ms Lazarevski was suffering ACS.[48]  If there was myocardial ischaemia, Associate Professor Allan would have expected a change in the ECGs.  The first ECG was taken within 10 minutes of Ms Lazarevski's arrival, which is the appropriate protocol and may well have been normal.  But the second one was taken some 35 or 40 minutes later, and in Associate Professor Allan's opinion if she had suffered a significant event, such as an occlusion of an artery, some dynamic changes on the ECG would be expected.[49]  I note, however, Professor Kelly's evidence that whilst a second ECG was taken, it was not taken after an interval of 120 minutes as the Pathway document recommends.[50]

   [48] ts 125 ‑ 126.

   [49] ts 126.

   [50] ts 79 ‑ 80.

5. In cross-examination, Associate Professor Allan accepted that the second ECG at 5.57 pm did not exclude the possibility that Ms Lazarevski suffered an NSTEMI on 6 January 2014, but he thought it made it unlikely.  He further accepted that with a chest pain patient, even if there was a normal ECG, the treating physician would still have a concern about ACS.[51]

   [51] ts 140.

Relevance of Ms Lazarevski's level of pain and its duration

1. In the event that the first fundamental question, liability, is resolved in favour of the plaintiff, this aspect is particular germane to the second fundamental question.  Ms Lazarevski testified that at about 4.00 pm on 6 January 2014 she was watching television at home when, without any warning, she experienced a massive pain in her chest, recorded at the time as 10/10.[52]  It felt like her chest was being crushed in a vice. Ms Lazarevski also experienced excruciating pain in her left arm and noted that the sound of voices around her was very muffled and unclear.  She testified that the pain that she experienced, was far worse than she had encountered on the two occasions when she gave birth without the assistance of drugs.[53]  She thought she was dying.  She tried to walk towards her mother in the kitchen, but she collapsed.  She was unable to open her eyes and she vomited.[54]  As soon as the chest pain struck, her breathing was very heavy, so that it was very difficult to get air into her lungs.  Her breathing difficulties then got somewhat worse as she realised there was something wrong.[55]

   [52] Page 2/92 exhibit 1.

   [53] ts 33.

   [54] ts 34.

   [55] ts 34 ‑ 35.

2. Her then husband called an ambulance at 4.02 pm and St John Ambulance officers arrived at 4.10 pm.[56]  By that stage Ms Lazarevski's pain had receded to 5/10, but she was hyperventilating with a recorded respiration rate of 30 breaths per minute.  By 4.36 pm the pain had dropped to 1/10 and her respiration rate was normal.[57]  In her evidence Ms Lazarevski maintained that the pain was excruciating for some 10 or 15 minutes and then receded in intensity to being very painful. It never subsided completely, rather it was constant.[58]  Once the ambulance arrived, the pain was a lot better than when she had the sudden onset of pain.  It started to settle and then came back.[59]

   [56] Page 1/92 exhibit 1.

   [57] Page 3/92 exhibit 1.

   [58] ts 35.

   [59] ts 41.

3. Ms Lazarevski provided a history to Dr Winton when she saw him at 5.10 pm. Dr Winton's notes begin by noting her age and gender and the words 'chest pain'.  Dr Winton referred in the notes to the fact that Ms Lazarevski had experienced sudden pain in her chest and left arm and that she became anxious and felt like she could not breathe. Dr Winton noted that she looked well, although she had been noted to be hyperventilating in triage.[60]

   [60] Page 5/92 of exhibit 1.

4. Ms Lazarevski testified that when she first saw Dr Winton she was quite expressive.  She was endeavouring to stress that she had experienced anxiety in the past, but that was different to her present complaint of excruciating pain in her chest and left arm.[61]  She said that when she first saw Dr Winton the pain was quite bad, although not as bad as it was when she experienced sudden onset of symptoms.  On two occasions when she was at the hospital, she remembered the pain as being excruciating and then settling.[62]

   [61] ts 36.

   [62] ts 36.

5. After speaking for a relatively brief period with Dr Winton, Ms Lazarevski said that she was put into a corridor and at that stage her pain started to get worse.  She recalled Dr Winton telling her to take the medication provided and then later to take it home and if the pain re‑occurred, take the medication and lie down.  Dr Winton advised that the medication would work within about 20 minutes.[63]  The medical notes show that Dr Winton prescribed the anti-anxiety medication Lorazepam, at 5.40 pm, Naproxen at 6.10 pm and Valium at 7.15 pm.[64]

   [63] ts 38.

   [64] Page 7/92 exhibit 1.

6. Ms Lazarevski testified that she explained to Dr Winton exactly how she was feeling, that is that she was in a lot of pain and felt like she was dying.[65] She accepted, however, that she reported her pain as being 2‑3/10 at 5.30 pm and 3/10 at 5.50 pm.  She also accepted in cross‑examination, that the summary of facts provided to her lawyers and contained within the plaintiff's book of documents, reveals that following discharge she felt generally unwell but did not experience serious chest pain until 9 January 2014.[66]

   [65] ts 36.

   [66] ts 49 - 50.

7. Dr Winton did not remember Ms Lazarevski saying that she still had significant ongoing pain when he talked with her about discharging her home.[67]  Often a patient's pain is not completely resolved by the time they are discharged.[68]  Dr Winton's did not get a sense, from talking with Ms Lazarevski, that she was feeling worse.[69]

   [67] ts 241.

   [68] ts 242.

   [69] ts 239.

8. I do not accept that Ms Lazarevski ever told Dr Winton that she was still in a lot of pain. I note that she did not recall one of her two ECG's, nor did she recall her chest X-ray being taken.  She also did not recall hyperventilating when the paramedics from the ambulance arrived.[70]

   [70] ts 39 – 40.

9. In closing submissions the defendant contends that the plaintiff should have called Ms Lazarevski's mother to give evidence concerning events at the hospital on 6 January 2014, asserting that a Jones v Dunkel[71] inference arose because of that failure.  I decline to draw such an inference.  The defendant has not identified any particular factual issue which is firstly, in dispute between Dr Winton and Ms Lazarevski and secondly, is necessary to be resolved in order to reach a conclusion on the fundamental questions that arise in this case.

   [71] Jones v Dunkel (1959) 101 CLR 298; (1959) HCA 8.

10. As Professor Kelly explained, even if Ms Lazarevski was not complaining of pain before she was released, that did not mean that there had not been any heart damage.  It is not uncommon for pain associated with ACS to remit spontaneously.  In those circumstances whatever had caused the ongoing heart damage, the biochemical cause of the pain, had settled to a certain degree.  It is quite common for people to have pain that remits spontaneously but to still have suffered ACS.[72]

    [72] ts 77.

11. I am satisfied that the contemporaneous hospital records are the best source of information about Ms Lazarevski's levels of pain at the hospital on 6 January 2014.  It is not necessary for me to make any particular findings of fact as to the extent of her pain at the time of discharge on 6 January 2014, nor in the period until the sudden onset of pain at about 2:40 pm on 9 January 2014.

The background of anxiety

1. Ms Lazarevski provided to Dr Winton a history of her medication including the fact that she was taking a medication called Lovan. Dr Winton documented a background of anxiety and noted the medication that Ms Lazarevski told him she was prescribed. The St John Ambulance patient care records before Dr Winton referred to Ms Lazarevski having a history of anxiety since a teen, including panic attacks with similar symptoms, but without the chest pain.

2. Professor Kelly gave evidence that it is very common for patients with chest pain presenting to hospital to also have a presentation involving some element of anxiety.[73]  Anxiety should be a diagnosis of exclusion,[74] that is based on clinical features after (Professor Kelly's emphasis) ACS had been excluded.[75]

   [73] ts 61.

   [74] Page 7 [1] of first report.

   [75] Page 5 [22] of second report.

1. Dr Lamberth's approval for Dr Winton's diagnosis rested on a number of erroneous assumptions.  For example, he assumed that Dr Winton discharged Ms Lazarevski with a diagnosis of hyperventilation anxiety syndrome and having reached such diagnosis it was therefore reasonable to discharge her without the troponin testing.[76]  Dr Winton did not, in fact, reach such a diagnosis.[77]  In his report Dr Lamberth considered that Dr Winton's diagnosis of anxiety hyperventilation ventilation syndrome was reasonable and consistent with the fact that the symptoms responded so quickly to reassurance and anti-anxiety medication.  Dr Winton accepted in cross-examination that this would be a difficult diagnosis to make on just one encounter with a patient.[78]

   [76] Page 11 [105] of first report and ts 176.

   [77] ts 226.

   [78] ts 226.

2. Dr Lamberth stated that he made that assumption based on Dr Winton's handwritten note of 'likely related to anxiety' when he reviewed Ms Lazarevski.  When Dr Lamberth used the term 'hyperventilation anxiety syndrome' he meant anxiety.  It seems he merged Dr Winton's reference to anxiety with the fact that the paramedics documented that Ms Lazarevski was hyperventilating.[79]  He accepted that Dr Winton had not suggested that at the time he saw Ms Lazarevski, she was hyperventilating.[80]  Given that Dr Winton's written history makes it clear that the pain happened and then secondarily, Ms Lazarevski became anxious and developed breathing problems, the 'hyperventilation anxiety syndrome' could hardly be causative of her chest pain. Counsel for the plaintiff's assertion in closing, that on this aspect Dr Lamberth's evidence[81] was unconvincing is justified.

   [79] ts 176.

   [80] ts 178.

   [81] ts 177 – 179.

3. Dr Lamberth considered that another explanation for Dr Winton's approach was a feeling of uncertainty that had been engendered by the recent introduction of high sensitivity troponin at the hospital.[82] Dr Winton gave no evidence that this was the case or, more particularly, that it influenced his decision.

   [82] ts 192 and page 9 [82] ‑ [83] and page 12 [1] of first report.

4. Dr Lamberth also suggested that prior to reaching a diagnosis, by exclusion, of anxiety, Dr Winton had ruled out ACS.[83]  He refined that somewhat, by testifying that he meant reducing the possibility to a level at which physicians have no useful tools for discriminating further.[84]  Given that in cross‑examination Dr Winton accepted that the possibility of ACS remained at the point of discharge it follows that he could not, in fact, have ruled it out.[85]

   [83] Page 11[106] of first report and ts 174.

   [84] ts 174.

   [85] ts 243.

5. As noted, Dr Lamberth assumed that whilst at the hospital at least Ms Lazarevski's pain resolved completely with reassurance.[86]  In fact the recorded pain scores up to the last such assessment at 5.56 pm showed a slight escalation whilst at hospital.  It was not reasonable for Dr Lamberth to interpret Dr Winton's final note, 'feels improved' as meaning that the pain had completely resolved.

   [86] A1 at page 12 [2] of first report.

The relevance of the recent death of Ms Lazarevski's brother

1. Following her arrival at the hospital at 4.52 pm, Ms Lazarevski advised a nurse in triage that her brother had passed away the previous day from a heart attack.[87]  It turned out that was not his cause of death, but the relevance lies in the fact that this was the information that was provided to hospital staff.  According to Dr Winton's notes, Ms Lazarevski advised Dr Winton that her brother had recently died, having been found home alone deceased, and that there was currently a coronial investigation.[88]  Dr Winton recalled that Ms Lazarevski said that she did not know what caused his death saying, 'my family told me it was a heart attack, but I don't know.'

   [87] Page 4/92 exhibit 1.

   [88] Page 5/92 exhibit 1.

2. Professor Kelly considered that if she had been told that Ms Lazarevski's brother had died of what she thought was a heart attack, that would add another piece to the picture.  But it would not change the fact that the picture, without that piece, reached the threshold requiring investigation.  Although it transpired that Ms Lazarevski's brother had not in fact died from a heart attack it was information given to her clinicians that, if true, was an additional risk factor for ACS.  Decisions should be made on what is known at the time, and so the fact that this information was inaccurate is irrelevant. Its relevance lies in the fact that it was conveyed.[89]

   [89] ts 77 and page 4 [16] of second report.

3. It is not necessary to make any findings as to whether Ms Lazarevski advised Dr Winton that her brother's body was in the morgue in the same hospital and suggested that medical staff should examine her brother's heart.[90]

   [90] ts 36.

Symptoms of feeling sweaty and clammy

1. Ms Lazarevski testified that she felt very sweaty and clammy.[91]  Professor Kelly was advised that Ms Lazarevski became sweaty and clammy, vomited and fainted.[92]  Professor Kelly testified that sweatiness and vomiting are associated with ACS, whereas fainting is neither here nor there.  Given that the contemporaneous clinical records did not record any sweating, it is not possible for me to be satisfied that Ms Lazarevski did present with these symptoms.  Professor Kelly considered, however, that the features that were present were suggestive of ACS.[93]

   [91] ts 33.

   [92] ts 76.

   [93] ts 76 – 77.

The conflicting approaches

1. In essence the experts called by the plaintiff stressed the need to err on the side of caution, whilst the defendant's experts were concerned as to the desirability of avoiding intrusive, burdensome and pointless testing. Professor Harper's view, as I have noted, was that the medical staff treating Ms Lazarevski on 6 January 2014 were entitled to regard the risk of ACS as low.  To that extent his assessment differs from that of Professor Kelly who considered that Ms Lazarevski was at least in the 'possible ACS' category and from Associate Professor Strathmore who thought that the first diagnosis, if dealing with a patient presenting like Ms Lazarevski, should be myocardial infarction.

2. In any event, Professor Harper also stated that given the seriousness of a diagnosis of a heart attack, as a general principle when dealing with someone suffering from a chest pain, such a diagnosis should be eliminated.  Particularly when the description of the chest pain is consistent with a heart attack.  The treating physician should take all practical steps to eliminate such a diagnosis.  A simple and practical way to exclude a heart attack in these circumstances is to take serial troponin blood tests.[94]  As Dr Winton accepted, all that was required would have been to add the letters 'tp' on the pathology request form that he completed to accompany the blood sample that had already been taken from Ms Lazarevski.[95]

   [94] A4 page 4 [2] of first report.

   [95] ts 228.

3. A normal level of highly sensitive troponin taken four hours after the onset of symptoms excludes a heart attack.  Elevated troponin in such a setting confirms the diagnosis of heart attack.[96]  Ms Lazarevski was already having blood tests, so it would be simple to add a troponin test.[97]

   [96] A4 page 4 [2] of first report.

   [97] ts 85.

4. In closing submissions the defendant criticises an approach which would mean that every patient who presented with chest pain would have to be provided with serial troponin testing.  It did not, however, challenge Professor Harper's evidence that where there is chest pain, it is standard procedure to add a troponin test to the standard blood tests that would be performed whenever a patient presents to an Emergency Department.[98]

   [98] ts 85.

5. Associate Professor Strathmore concurs with the approach urged by Professor Harper.[99]  Associate Professor Strathmore gave evidence that in 2014 a condition called Takotsubo cardiomyopathy was a well‑recognised syndrome.  Takotsubo cardiomyopathy mimics a STEMI but the coronary arteries are normal, it often follows severe emotional stress and may recover spontaneously.  The combination of chest pain following major stress (here the recent death of a brother) is part of the syndrome of Takotsubo cardiomyopathy.  Someone with chest pain coming to hospital in this way would be at low risk for standard atherosclerotic coronary disease, but one would have to consider the other diagnoses that could cause coronary pain without atherosclerosis, such as myocardial infarction, Takotsubo cardiomyopathy or unstable angina.[100]

   [99] A3 page 3 [2] of report.

   [100] Page 2 [5] and pages 3 [1] of report and ts 108.

6. As noted, Associate Professor Strathmore expressed the view that the first diagnosis, if dealing with a patient presenting as Ms Lazarevski did, should be myocardial infarction.  Given Ms Lazarevski's age, a SCAD or Takotsubo cardiomyopathy were more probable diagnoses than the more generally common artherosclerotic cause and should have been considered.[101]

   [101] Pages 3 [1] and [3] of report.

7. The defendant submitted that Professor Kelly had not adequately considered the inherent unlikelihood of Ms Lazarevski having sustained ACS on 6 January 2014 given her age and gender.  That is incorrect.  In her first report, Professor Kelly commented that while ACS is uncommon in young people, especially women, she had personal experience of identifying ACS in patients in their early 20s and a common feature is often a history of cardiac events at a young age and in close relatives.[102]  Professor Kelly observed that Ms Lazarevski's presentation was consistent with a possible diagnosis of ACS despite her young age.[103]

   [102] A1 page 6 of first report.

   [103] Page 7 of first report final paragraph.

Did the 'Pathway' apply?

1. As of 6 January 2014 the North Metropolitan Health Service, had a written guideline for its A & E department staff entitled 'ACS Pathway' (the Pathway).[104]  This guideline governed the approach to patients who presented with possible ACS.  A very important issue is whether it applied here so that Dr Winton should have followed it.  The plaintiff's primary case is that if Dr Winton formed the view that Ms Lazarevski did present with possible ACS, then applying the terms of the document he would be required to perform serial troponin blood tests.  Indeed that was so, even if Dr Winton had concluded that Ms Lazarevski fell within the 'probable non-ACS category' depicted in the Pathway document.

   [104] Page 14/92 of exhibit 1.

2. The plaintiff submits that the Pathway document should be applied on its terms, whereas the defendant contends that there is a discretion not to comply with it, if the treating physician's clinical assessment is that it is, at the very least, unlikely that the patient has ACS.

3. As well as her work with the National Heart Foundation, Professor Kelly has had an involvement with the Department of Health Victoria's Safer Care, Victoria Section.  One of the major projects for this group was the updating and standardisation of chest pain pathways across Victoria in Emergency Departments.[105]  Professor Kelly has been involved in a number of studies in chest pain, some of which are in the area of ACS and particularly the validation of pathways and the predictive value of those pathways with respect to future long‑term events.

   [105] ts 60.

4. Guidelines were developed to achieve a consistency of practice so as to reduce error and to enhance standardisation of practice, across both the emergency component and the post admission component of care.[106]

   [106] ts 61.

5. Professor Kelly testified that in January 2014 most Australian hospitals had a pathway document of some type.  This Pathway was generally consistent with those in other Australian hospitals, in that it required an ECG to be performed at an early stage to identify the very high risk group of patients.  It then stipulated a clinical assessment.  For all groups of patients in which ACS was a possibility, biomarker testing is required.[107]

   [107] ts 67.

6. By reference to the Pathway document Professor Kelly would have placed Ms Lazarevski in the second box from the right marked 'possible ACS'.  As a consequence she would undergo serial biomarker (troponin) testing every two to three hours.[108]  If Ms Lazarevski's troponin was positive on the first or the second occasion, she should be admitted under the care of a cardiology service.[109]

   [108] ts 68 ‑ 69.

   [109] ts 69.

7. Professor Kelly was asked to comment on Dr Lamberth's suggestion in his report[110] that the Pathway would only be relevant for a patient with a significant a priori risk of ACS.  According to Dr Lamberth[111] the Pathway is only engaged for a patient with a significant risk of ACS. He went so far as describing the Pathway in the circumstances in this case as obsolete.[112]

   [110] Page 2 [15] of second Lamberth report.

   [111] Page 14 [1] of first report and page 2 [15] and pages 3 ‑ 4 [24] ‑ [29] of second report.

   [112] Page 4 [29] of second report.

8. Professor Kelly's view was that if one applies the Pathway according to its terms, even patients in the 'probably non ACS' category (having very atypical characteristics though they may have cardiac risk factors) should not be discharged without biomarker testing. So where a patient ends up in the category 'Negative test (probable non ACS group) discharge patient further cardiac investigation not required' they will be discharged, but only after they have undergone serial biomarker testing.[113]

   [113] ts 70.

9. Professor Kelly's view was that the pathway should be adhered to save for exceptional circumstances, such as where a patient has an otherwise terminal illness.  If there is a deviation from the Pathway, she stated that it is accepted practice that the detailed reasons for such deviation need to be documented and the patient informed.  That is because it is the patient that bears the risk not the doctor.[114]  In the present case the reasons for not adhering to the Pathway by applying serial troponin testing were not documented nor were they discussed.

   [114] ts 70.

10. Leaving aside exceptional circumstances, Professor Kelly's evidence was that it is only in circumstances where a diagnosis of possible ACS could not be reached, that it would it be permissible to omit troponin tests.  If the emergency physician was convinced that ACS was not a possibility, it would then be permissible to omit these tests.  If the possibility exists, troponin tests are required.  It is almost impossible to exclude such a possibility based on clinical assessment alone.  If there is not something that the physician can definitively see, then ACS remains a possibility and needs to be ruled out.[115]

    [115] ts 80 – 81.

11. I accept Professor Kelly's evidence that Ms Lazarevski's symptoms were typical of ACS.  I further accept Professor Kelly's evidence on the limitations on clinical assessment alone.  I turn to consider the Pathway document in more detail.

Was there a discretion to disregard the Pathway?

1. Dr Winton accepted in cross-examination that even if one was to accept Ms Lazarevski had more atypical than typical features she would fit in the 'possible ACS' box if one applied the Pathway.[116]

   [116] ts 236.

2. Although Dr Winton contended that the Pathway only applied if ischaemic heart disease or ACS was either suspected or likely,[117] he also accepted that the document on its terms did not provide for any exercise of discretion as to whether it was or was not to be followed.[118]

   [117] ts 214 and 233.

   [118] ts 236 ‑ 237.

3. There was no evidence to explain why Dr Winton had any latitude in choosing whether or not he followed the Pathway.  No-one in a senior position at the hospital gave evidence about the role of this Pathway or any discretion given to practitioners to choose whether or not to comply with it.

4. Accordingly, the Pathway and therefore the need to administer serial troponin tests applied, unless one is able to read the word 'possible' in the Pathway document as imposing a higher threshold then 'merely possible', albeit without stating it.  Or, even if the theoretical possibility exists, a treating physician is entitled to disregard the Pathway if in his/her clinical assessment the risk of an ACS is particularly remote. Dr Winton considered that one could divert from applying a pathway like this where the treating doctor did not think that ACS was present.[119]  There is no obvious reason why a decision not to apply the Pathway at all does not have to be documented, whereas a decision, once in the Pathway, to deviate from its stipulated requirements does.[120] 

   [119] ts 237.

   [120] As Dr Winton suggested at ts 237.

Dr Winton's justification for not applying the Pathway

1. Given those possible ways that the Pathway is said to be inapplicable, I now move onto consider the unlikelihood that Ms Lazarevski presented with ACS on 6 January 2014, starting with Dr Winton's assessment.  I have concluded that Ms Lazarevski's symptoms were typical of ACS but have noted Professor Harper's view that Dr Winton was entitled to regard the risk of ACS as low.  In his evidence Dr Winton referred to the inherent unlikelihood of coronary artery disease.  There is no doubt, given Ms Lazarevski's age, that however unlikely ACS might have been, coronary artery disease would have been even more unlikely.  However, the Pathway document does not refer to possible coronary artery disease.  It refers to possible ACS.  It is not clear why Dr Winton referred in his evidence to the inherent unlikelihood of coronary artery disease rather than addressing the real question which is the possibility of ACS. Dr Winton accepted that ACS could arise from other causes than coronary artery disease.[121]

   [121] ts 227.

2. Dr Winton's evidence fluctuated in terms of his assessment on 6 January 2014 of the level of risk.  He stated that he did not think it was possible that Ms Lazarevski had ischaemia but it was not impossible.  He thought it was so unlikely in a female in her 20s that it was below a 'threshold for test and treatment'.  The likelihood was so small that even a positive test is unlikely to represent a true positive.[122]

   [122] ts 229.

3. He then stated that his clinical judgment at the time was that he did not think it was possible that she had ACS.[123]  His final answer in cross‑examination, however, was as follows:

   (do you) agree with me that even though you thought it was very unlikely, the possibility remained at the time she went home that she had ACS?   I - I just - it - it is very unlikely.[124]

   [123] ts 234 ‑ 235.

   [124] ts 243.

4. To state the obvious, if something is very unlikely but not impossible, it is possible.  On his own evidence, not with hindsight bias, Dr Winton should have followed the Pathway.  Dr Winton seeks to insert a provision into the Pathway that is just not there, namely if the patient presents with possible ACS, but at a low or very low level of likelihood, one can disregard this protocol.  Such an approach would render the 'probable non-ACS' box otiose, because although for patients in that category one might say that it is very unlikely that they have ACS, they still must go through the Pathway and receive the troponin tests.

5. In Dr Winton's contemporaneous notes[125] he assessed the risk of ischaemia as being unlikely, by which he meant, 'not likely' or not 'impossible.'[126]  There is no reason to suppose that Dr Winton actually thought that the risk was at a lower level than merely being 'unlikely' but confined his documentation of that level of risk as he did.  In the formal pleadings on behalf of the defendant it is not asserted that the risk was assessed at the time as being even less than unlikely.

   [125] Page 6/92 of exhibit 1.

   [126] ts 227 ‑ 228.

6. In essence Dr Winton seemed to be saying that even if troponin testing had occurred whilst Ms Lazarevski was a patient at the hospital on 6 January 2014, any positive result from such testing would simply just be noted, nothing would change so far as her management was concerned and presumably she would still have been discharged in the same way.  The reasoning behind this assertion was not really exposed. Moreover Dr Winton appears to have conceded the point himself in his answer at one point[127] that an elevated troponin would certainly warrant admission and further investigation.  That final position is inconsistent with his earlier assertion that there was no point in conducting these tests, because even if they yielded a positive result it would be meaningless.

   [127] ts 230.

1. It is not clear whether Dr Winton, in seeking to explain his rationale for his actions on 6 January 2014, was reliant upon Dr Lamberth's argument of the dangers of false positives and the resultant risks of possible angiogram.  If he was, then such reliance is misplaced for the reasons discussed below at [126] and following.

Associate Professor Allan and Dr Lamberth's support for Dr Winton's decision not to apply the Pathway

1. I have considered whether my view that Dr Winton should have followed the Pathway is altered by my consideration of the expert evidence called by the defendant.  Associate Professor Allan and Dr Lamberth support Dr Winton's clinical judgment that ACS was extremely unlikely.  Dr Lamberth considers, uncontroversially it seems to me, that emergency physicians are required to strike a balance between minimising death through a missed diagnosis and on the other hand avoiding the unnecessary and intrusive investigation of patients without disease.[128]

   [128] Page 8 [74] of first report.

2. Associate Professor Allan testified that based on her symptoms Ms Lazarevski would not have been considered to be suffering coronary syndrome and would not have been triaged to the Pathway.[129]  Following the tests that were performed she was simply a person with chest pain of unknown origin.  The majority of presentations to an Emergency Department are non-cardiac chest pains.  The majority of the work that the emergency physician does is to screen out the patients who do not have a chest pain related to their heart.  If they do, then they are referred through to the cardiology team.  Of all those patients that come through Associate Professor Allan's unit at the Prince of Wales Hospital, about 1 in 10 present with a diagnosis of 'chest pain', 'query cardiac' or 'further investigations to exclude or confirm cardiac.'[130]  This hospital sees 52,000 patients a year.[131]

   [129] ts 149.

   [130] ts 127.

   [131] ts 152.

3. Associate Professor Allan thought that the fact that Ms Lazarevski experienced pain into her left arm is not uncharacteristic.  But the fact that it was quite sharp, tends to point more towards a musculoskeletal issue from either the nervous tissue in the neck or muscular abnormalities around the shoulder.  If it was the same sense of pain that she experienced in the middle of her chest, then that would be quite a different interpretation.  The fact that it was sharp tends to move a diagnosis away from the feeling that this is purely cardiac.  The central chest pain by itself could be considered to be cardiac, were it not for the atypical pain into her left arm.[132]

   [132] ts 128.

4. Associate Professor Allan considered that the likelihood of a 28‑year‑old female patient suffering myocardial ischaemia in these circumstances was so low that a troponin test would not be warranted. These circumstances being her presentation with chest pain syndrome with atypical features, no evidence of myocardial ischaemia on two ECG's and a background of requiring anxiety medication.  The most likely diagnosis was gastro-oesophageal reflux against a background of anxiety.[133]

   [133] Page 5 [1] of first report (A3).

5. Associate Professor Allan considered that the Pathway did not apply here because (implicitly) any physician dealing with this presentation would have considered it unlikely that Ms Lazarevski had experienced ACS.[134] Associate Professor Allan reasoned that this unlikelihood, as he saw it, precluded the application of a possible ACS pathway.  The decision on whether to apply the Pathway would be made by the admitting doctor and possibly the triage nurse and would be made on many factors. Associate Professor Allan testified:

   You would probably say, yes, she has a chest pain but it'd be very unlikely that she has an ACS.  So that's why the ACS pathway would not be followed. [135]

   [134] Pages 4 ‑ 5 of first report and page 1 of second report.

   [135] ts 138.

6. Associate Professor Allan re-iterated a belief that there is a threshold question about whether or not the probability reaches the likely/unlikely balance before one applies this Pathway.[136]  He observed that the pre‑test probability of finding an abnormal troponin is important to determine the value of the result that is obtained[137] and that the role of protocols and pathways depends on the likelihood of having an event appropriate to that pathway. [138]

   [136] ts 147.

   [137] Page 4 [3] of first report.

   [138] Page 2 [1] of second report.

The Framingham Study

1. In assessing that pre-test probability Associate Professor Allan reported that the chance of Ms Lazarevski having a cardiac event was less than 1% in the following 10 years.[139]  He based that risk assessment on his use of the United Kingdom Framingham Study, a longitudinal study of a population.

   [139] Page 4 [4] of first report and page 2 [1] of second report.

2. Professor Kelly was asked to comment on Associate Professor Allan's risk assessment based on his use of the Framingham Study.  In that study the researchers followed a group of people, all of whom lived in a particular postcode area, over time to see what happened to their cardiac risk factors and any cardiac events.  It was a population based study, not of people who came to a hospital with chest pain.  Professor Kelly considered that Associate Professor Allan's assessment that Ms Lazarevski's score based on that study would be less than 1% within 10 years is misplaced because something important had changed.  Ms Lazarevski had developed symptoms that were suggestive of ACS which has substantially increased her risk.  For Ms Lazarevski, the Framingham Score is the score she would have had sitting on her couch at 3.00 pm on 6 January 2014, not when she developed acute chest pain at 4.00 pm.[140]

   [140] ts 66.

3. For the same reasons, Professor Harper also firmly stated that the Framingham Score is inapplicable here.  If Ms Lazarevski had consulted him a few weeks before 6 January 2014, when she was well, and asked what her chances of having a heart attack in the next 10 years were, he would have regard to the Framingham risk data.  He would have concluded that the risk was extremely low.  If, however, she presented in an Emergency Department with severe chest pain and asked the same question, the risks would be much, much higher.  The Framingham risk score is applied to patients who are symptomatically well to find out what their risk over the next 10 years or so is of having a heart attack.  It does not apply to people who are acutely unwell.[141]

   [141] ts 84.

4. Associate Professor Strathmore took the same view.  He explained that the Framingham Score relates to specifically looking at asymptomatic people, who are being screened to see what their risk is of a coronary event.  It is not in any way related to people actually having chest pain.  So if one looked at Ms Lazarevski the month before this happened, one could use the Framingham Score to assess the likelihood of her having a coronary event in the next five years.  The Framingham Score is essentially based on looking at atherosclerotic coronary artery disease. It calculates risk factors of cholesterol and hypertension, cigarette smoking and does not include entities which are uncommon, such as coronary artery spasms, spontaneous coronary artery dissection or Takotsubo cardiomyopathy.

5. This study is a good way of looking at someone's long term risk.  It is not a way of assessing the likelihood that a person's chest pain will be coronary pain or cardiac pain when they actually present with chest pain.  It was never designed for that.  That was not the intention.[142]

   [142] ts 107 - 108.

6. When Associate Professor Allan gave evidence, he had plainly abandoned any substantial reliance on what he referred to as, 'the now discredited Framingham data'.[143]

   [143] ts 138.

7. Associate Professor Allan had explained that the Framingham data was generated to predict someone that might develop an event, using many parameters.  It is a very robust way of predicting someone of having an event.  He elaborated,

   The reason I wanted to include it here is to make sure that the person who was seeing this patient, the plaintiff, first up, this would've gone through his or her mind.  And if you have someone coming in that is very, very unlikely to have the event that you think they might be having, then you'll look back onto this and say, well look, she's not got hypertension, she's a female, she's very young, the only risk factor is smoking, which I think was intermittent, as I understood.  She was very anxious, which was a notable thing as well.  So while the application of those tables isn't absolutely appropriate to the situation, it does help put some perspective for the person seeing her as to whether he's going, or she's going, to see someone with an ACS or not.[144]

   [144] ts 129.

8. Associate Professor Allan relied upon the Framingham score in support of his argument that the chances of a 28-year-old patient like Ms Lazaravski having a cardiac event in the next 10 years would be less than 1%.  He asserted that this was a factor that should be taken into account in assessing how unlikely it was that she presented with ACS. That reliance was clearly misplaced, even if I was to ignore the fact that there was no evidence from Dr Winton that he had heard of and had applied this study, when he made the decisions that he did on 6 January 2014.

9. Professor Kelly's unchallenged evidence was that there is no literature to the effect that in January 2014 there was wide acceptance of a practice, in accident and emergency care, of deciding whether or not to arrange troponin testing based on assessing whether the patient's ACS risk was 1% or lower.[145]

   [145] ts 73.

10. Professor Kelly noted that although the literature refers to interpretation issues, none of them even mention the possibility of a level of risk so low that troponin testing can be avoided.  The adjectives 'essential' or 'invaluable' are often applied in the relevant literature to such testing. It is not possible to reach a confident conclusion that a patient was in a 1% or less risk category based solely on clinical assessment.[146]

    [146] ts 74.

Dr Lamberth's additional reasons for supporting Dr Winton's decision not to apply the Pathway 

1. In evidence Dr Lamberth testified that as the likelihood of the disease gets towards zero or negligible, one reaches a situation where virtually any positive test is a false positive test and thus misleading.  The likely result is a whole array of consequences of worry for the patient such as risks from further testing.[147]  It is necessary to explore Dr Lamberth's conclusions in more detail with respect to two issues, the concept of 'false positives' and the relevance of a survey by a Professor Than.

   [147] ts 171.

Risk of false positives

1. The defendant maintains its position that the risk of a false positive exceeded the risk that Ms Lazarevski had ACS.  On that approach the Pathway document is inherently flawed, mandating, as it does, the use of biomarker and troponin tests, even for patients in the 'probable non ACS' box, without factoring in any risk of false positives.  No witness for the defendant identified a flaw in the Pathway document itself. Rather, the two defence experts agitated for a triage process, that is a decision to be made about whether one enters the Pathway, with the threshold for that triage being something more significant in terms of risk than a mere possibility.

2. Associate Professor Allan had testified that in any test on a patient it is necessary to understand what the chances of it being positive or negative are.  If there is a very low chance of it being positive, then physicians might measure it too often and experience many false positive results which would be no use to anyone. He referred to a concept called 'Bayes' theorem', where the abnormality one might expect on doing a test has to have built into the chance of it being abnormal in the first place.  Otherwise the significance of the test is not very useful.[148]  As I have noted, Associate Professor Allan relied in his reports, although not in his evidence, on the Framingham study.

   [148] ts 127 – 128.

3. The approach suggested by the two experts for the defendant runs counter to the Pathway's apparent underlying rationale, which is that everyone in the designated population is to receive that testing. It comes back to the limitations identified by Professor Kelly in making a sensible assessment of the probability of risk based only on a clinical assessment.  Professor Kelly considered that in this field, one cannot achieve the requisite level of confidence, which justifies discharging the patient without further investigation, which includes troponin testing.

4. Professor Kelly was asked to comment on Dr Lamberth's contention that there was a risk of a false positive if troponin testing is performed.[149]  I note that in his oral evidence the only risk mentioned by Dr Lamberth were risks associated with angiography.  The potential consequence of a false positive here is that a patient might unnecessarily undergo coronary angiography and might be harmed by that further investigation.[150] 

   [149] As set out at page 9 [81] of first report and page 3 [22] ‑ [23] of second report.

   [150] ts 166 and 171.

5. Professor Kelly has published widely on the topic of management of chest pain patients in this type of situation.  She has participated in the work of the peak body, the National Heart Foundation, in settling appropriate guidance to be provided to clinicians in accident emergency departments when confronted with this type of presentation. Dr Lamberth's contrary views appear to be based on his review of literature and an extrapolation from the general principles to the particular clinical situation that arises here.  In his current role Dr Lamberth is not required to make decisions as to whether or not troponin testing should be performed.[151]

   [151] ts 175.

6. As Professor Kelly explained, there is also no support in any of the literature referred to by Dr Lamberth in his reports, for the proposition that emergency physicians should be reticent in resorting to serial troponin testing because of the risk of a false positive with high sensitivity troponin.[152]  Rather, as Professor Kelly explained,[153] the literature discusses the issue of interpretation of troponin testing results after such testing has occurred, the assumption being that testing will occur, but that caution may need to be exercised as to interpretation.

   [152] ts 73 – 74.

   [153] ts 72 ‑ 73.

7. Professor Kelly testified that all of the biomarkers used over the last 20 years have had a rate of false positives that physicians have had to develop processes to deal with.  The importance of a positive test, be it false positive or true positive, lies in the fact that it is an indicator of increased risk of serious illness, be it cardiac or non-cardiac.  It is not up to an emergency physician to decide whether the result is a false or a true positive.  A positive result puts the patient in that high risk category that needs further investigation to identify the cause, so as to give the patient the opportunity to have the problem treated.  The false positive question is moot from the emergency physician's point of view. There are a number of papers dealing with the interpretation of the new high sensitivity troponins.  It is to be expected that every time a new technology is introduced, there would be considerable discussion about how best to apply it.[154]

   [154] ts 73.

8. The defendant continues to rely upon Dr Lamberth's assertion that when any test is applied to a population where the presence of the disease of interest is very low, the test's utility becomes extremely poor.[155]

   [155] Page 9 [81] and page 10 [89] of first report.

9. As noted, Professor Kelly testified that a patient's troponin level is regarded as being abnormal if it registers above the 99th percentile of the general population.  It follows, as Dr Lamberth observed,[156] that 1% of the population would therefore have troponin levels which would be regarded as abnormally elevated.  Clearly Ms Lazarevski could have been in that category.  It is necessary, however, to consider that possibility in the context of the typical features of ACS that she presented with on 6 January 2014.

   [156] ts 166.

10. Moreover, if Ms Lazarevski had a naturally high elevation in her troponin, the requirement to administer serial troponin tests would inform the treating physician that there was no cause for concern, because a second reading would be at the same level.  Conversely, if the second reading showed an increase in troponin levels the need for admission and further assessment would be obvious.  Associate Professor Strathmore could not envisage how one would see that pattern other than because of ACS.[157] 

    [157] ts 109.

11. In cross‑examination Dr Lamberth was asked if he agreed that if Ms Lazarevski had undergone troponin testing and the results had been abnormal, then the only significant risk would be related to angiography.  Dr Lamberth testified that this was the major risk, without specifying what other risks existed.[158]

    [158] ts 189 – 190.

12. Dr Lamberth asserted that, as he put it, the next step in the algorithm involves some very serious complications.  He accepted, however, that the next step in the algorithm is admission and ongoing assessment, before a patient contemplates an angiogram.  He also accepted that the decision to have an angiogram is a decision for the patient, not for the accident and emergency doctor.  He further accepted that the question of whether Ms Lazarevski would or would not agree to undertake the one to two in a thousand risk, that Professor Kelly considered was associated with an angiogram, was her decision.[159]  Dr Lamberth did not dispute Professor Kelly's assessment of the risks arising from an angiogram.

    [159] ts 202.

13. I have evaluated the merit of the contrary arguments to the conservative approach as advanced by Professor Kelly.  By conservative approach I mean always having recourse to serial troponin tests where a patient presents with possible ACS or even probable non-ACS, save for truly exceptional circumstances.  Professor Kelly considered that there were no countervailing arguments.  There are no risks in utilising the serial troponin tests in contrast to the application of the PERC test where there is a possible pulmonary embolism.[160]  It is not possible to embark upon a risk evaluation exercise prior to the administration of these tests. That is because decisions that might be made following any elevated reading would be made with the consent and knowledge of the patient and with the benefit, in those circumstances, of expert cardiology advice.  The risk is borne by the patient and not the doctor.[161]

    [160] Page 2 [8] of second report.

    [161] ts 70.

14. In cross-examination Dr Lamberth acknowledged that if there had been a positive troponin result and Ms Lazarevski was admitted, then an angiography would have been recommended within 48 hours, assuming that the pain had settled.  He accepted that this would be a decision for the cardiology team in consultation with the patient.  In terms, it was Ms Lazarevski's decision whether or not she agreed to an angiogram, not Dr Winton's.[162]

    [162] ts 198.

15. Dr Winton accepted that there was no risk in that regard for Ms Lazarevski unless cardiologists got to a point where they recommended an angiogram.  He considered that the risk lay in having the angiogram, but accepted that Ms Lazarevski would participate in the decision in that regard. She would be guided in that decision by the cardiologists, based on the information which they believed justified that intervention.[163]

    [163] ts 230.

16. In commenting on Dr Lamberth's concerns about a risk of a false positive, Professor Harper began by reminding me that an elevated troponin level means that troponin has leaked from the myocardial cells.  That only occurs if there has been myocardial damage or strain.  In ACS the troponin is elevated because there has been a change in the coronary artery impairing the flow to the myocardium which releases troponin.  Troponin can be released under circumstances that are not due to ACS, such as when the heart is put under a great deal of strain from, for example, a pulmonary embolism, septicaemia, prolonged hypotension or a prolonged arrhythmia.  But a positive troponin indicates that there is a problem within the heart.  Even if it is not due to ACS, it is still a serious condition.  If someone presents with a chest pain, a physician should assume that any troponin elevation is due to ACS until proven otherwise.  If the troponin is elevated, they would need to find out why.[164] 

    [164] ts 85 – 86.

1. There are two relevant scientific questions about troponin.  Firstly, how quickly after damage to the myocardium does the troponin level in the bloodstream increase? Secondly, if there is an elevation in troponin how quickly does it subside?  I now turn to those two questions.

How quickly does the troponin level in the bloodstream increase?

1. Is it possible that the reading of 30ng/L at 4.25 pm on 9 January 2014 only relates to the events of that day, or is the gap of 1 hour 45 minutes between Ms Lazarevski's chest pain that day at 2.40 pm and when the blood sample was taken, 4.25 pm, too short for this to be likely?

2. Professor Harper testified that generally it takes some time after the initial cardiac insult, for troponin to be released from the degraded cells into circulation.  With the highly sensitive troponins, it usually takes from two hours to between two and four hours, so an average of about three hours.  The comparison between an initial troponin reading and a subsequent one is a very important piece of information.  If the first troponin taken, say, within two hours of the onset of pain, is normal but the next one is elevated, that would be very suggestive of ACS.  If a patient comes into Accident and Emergency and the first troponin is elevated, a diagnosis can be made then.  But it is well known that the treating physician must allow at least four hours before it is safe to conclude that the troponin is going to be negative.[209]

   [209] ts 86 – 87.

3. Ms Lazarevski's troponin level went from 30ng/L at 4.25 pm to 535ng/L at 6.00 pm, 3 hours and 20 minutes after the first onset of pain. Professor Harper considered that was attributable to the fact that Ms Lazarevski had a completely obstructed circumflex coronary artery, resulting in a very large heart attack.  Professor Harper did not consider that the rapidity at which troponin gets into the circulation relates to the severity of the particular event.  He was unaware of any references in the relevant literature which say the more severe the original insult the more likely an earlier rise in troponin.[210]

   [210] ts 96.

4. Professor Harper considered that there would be a massive release of troponin because of the amount of myocardium involved.  The artery was completely obstructed and it resulted in a STEMI, which always indicates a big heart attack. At 12.05 am on 10 January 2014 Ms Lazarevski's troponin level was at 76,900. 

5. Professor Harper's view was that if the episode of 6 January 2014 had not occurred, Ms Lazarevski's troponin level as of 4.25 pm could well have been normal, even though she was sustaining a very large heart attack.[211]  In his view there are three possibilities to explain the reading of 30.  One is there was a residue of a troponin elevation that occurred three days earlier. Secondly, this reading could have been related solely to the events of 9 January 2014.  The third possibility is a combination of those two.  Of the three, the first is the most likely.  It was early for troponin to be elevated, relative to the event that occurred on 9 January 2014 although it was still within the bounds of possibility.[212]  Neither Professor Harper nor Associate Professor Strathmore excluded the possibility that Ms Lazarevski's troponin level at 4.25 pm on 9 January 2014 could have been related to the events of that day only.[213]  By contrast, Associate Professor Allan was not prepared to accept that the three suggested alternatives were all possible.[214]

   [211] ts 97.

   [212] ts 89.

   [213] ts 96.

   [214] ts 157.

6. Associate Professor Strathmore agreed that an elevation in troponin will generally arise two to four hours after the particular event.  So from two hours onwards, the treating physicians would expect to see a troponin rise.  He considered that the first reading showing an elevation of troponin was very early, 1 hour 45 minutes and so under two hours.  It is likely that the troponin would not have been elevated at that stage. Whilst it is very difficult to work it out completely, he considered that on balance, the 9 January 2014 STEMI would not have caused troponin to start to escalate at that stage.[215]

   [215] ts 111 and 117.

At what rate does troponin subside?

1. The second issue is if there is an elevation in troponin, how quickly does it subside? As I have noted, Associate Professor Allan considered that the events of 9 January 2014 caused the reading of 30 which would have been higher if there were any residual effects from 6 January 2014.[216]

   [216] A2 page 4 of first report.

2. Associate Professor Allan testified that troponin I starts at the earliest point in time and rises the fastest of all of the troponin measurements he is aware of. If after two hours of pain, the troponin level was only 30, that implies that the initial troponin when she first experienced pain that day was probably normal. He would have expected the troponin, had it been abnormal on the first occasion of 6 January 2014, to still have been abnormal on 9 January 2014 when Ms Lazarevski first presented. So therefore he would have expected a much higher level of troponin I, something like 150, 200 as of 4.25 pm. He considered that even if the troponin level was abnormal on 6 January 2014, it would probably not have been so significantly elevated to warrant any further investigations, given the two normal ECGs. The defendant repeats its reliance on Associate Professor Allan's evidence as to the significance of the ECG results discussed at [55] ‑ [56] above.

3. In my view, Associate Professor Allan did not adequately explain how he arrived at the figure of 150 ‑ 200, particularly given his acceptance that 30 could be extrapolated back to 240 which would, in turn, be consistent with a relatively modest NSTEMI on 6 January 2014.[217]  He partially relied upon a graph entitled 'troponin kinetics in the index cases' from a journal article for his conclusions.[218]

   [217] ts 155 and 157. Although the question at ts 157 referred to the preceding date I am satisfied that Professor Allan understood he was being asked about the events of 6 January 2014.

   [218] Vinay S Mahajan and Petr Jarolim Circulation 2011; 124: 2350 - 2354 page 5 - 6 of first report included at pages 34 ‑ 38 of exhibit 3. The graph relied upon is #3 myocardial infarction.

4. In commenting on Associate Professor Allan's view, Professor Harper considered that it all depends on the size of the 6 January 2014 NSTEMI.  If it was a small NSTEMI, than 30 would be entirely consistent.  If the decay characteristics in the Mahajan article quoted by Associate Professor Allan are applied, there is about a seven to eight fold decrease in the troponin level over three days.  On that basis, a troponin elevation corresponding to 30 on 9 January 2014 would have been about 240 on 6 January 2014.[219]

   [219] ts 89 – 90.

5. Associate Professor Strathmore was also asked to comment on Associate Professor Allan's view.  Associate Professor Strathmore considered that allowing for the approximate half life of troponin and the decay of the troponin level, if one was to extrapolate back from the reading of 30, Ms Lazarevski's troponin levels would probably have been somewhere between 120 and several hundred at a peak on 6 January 2014.[220]  That would be consistent with a NSTEMI on 6 January 2014.

   [220] ts 111.

6. Associate Professor Strathmore explained that academic articles suggest that the half life for troponin is around 24 hours.  The gap between the events of 6 January 2014 and 9 January 2014 is 72 hours which constitutes three half lives.  That means that one doubles the level each 24 hours.  So, if one works back from 30 and double it three times the result is 240.  Associate Professor Strathmore considered that the Mahajan article is designed to give a very general picture.  He did not think that that article actually gave a half-life or a kinetic measurement for the troponin. In that article, the graph is a single patient's troponin levels, not a population summation.[221]

   [221] ts 111-112.

7. By contrast, the Laugaudin article[222] that Associate Professor Strathmore referenced considered a large group of patients.[223]  On figure 3[224] the relevant curve is the green coloured curve because the assay used the hospital is the Abbott hs-cTnl assay.  One of the purposes of this study was to compare the decay rates based on different cardiac markers and the different test regimes.  The decay with the Abbott assay, the green line, was very different from the blue line Roche assay for troponin. The Roche line measured troponin T which is a slightly different assay to the troponin I.  It showed a decay and then a rise whereas the Abbott and the Siemens assays, both measuring troponin I, both fell in a similar fashion.  The green line in figure 3 shows a very steep ascent of the troponin level.[225]

   [222] 'Guillaume Laugaudin and others 'Kinetics of High-sensitivity Cardiac Troponin T and I - Different Patients with ST-segment Elevation Myocardial Infarction Treated by Primary Coronary Intervention' tendered as exhibit 5.

   [223] ts 113.

   [224] Page 104 of exhibit 5, see also figure 2(c) at page 103.

   [225] ts 114.

8. Associate Professor Strathmore then tried to discern from this graph what Ms Lazarevski's serial troponin levels would have been, if they had been taken on 6 January 2014, on the basis of a period of 72 hours from her onset of pain that day and the onset on 9 January 2014. He explained that measuring out at about halfway along the X axis, drawing a vertical line up to intersect with the green line and reading across to the Y axis, one gets to a number that's about 25%.  On that basis, 30 is 25% of what it would have been on 6 January 2014, namely a peak of 120.[226]

   [226] ts 114.

9. In cross‑examination, Associate Professor Strathmore accepted that this study dealt with patients who had sustained STEMIs, and that their troponin levels would accordingly be much higher than Ms Lazarevski would have experienced on 6 January 2014.  Nevertheless, he considered that in terms of its description of the kinetics it showed very similar results to other papers that he had studied.[227]

   [227] ts 116.

10. Associate Professor Strathmore agreed that it was difficult to know the exact rate Ms Lazarevski's troponin would have fallen at after 6 January 2014.  He was asked to comment on Associate Professor Allan's observation that the rate at which the troponin levels increased on 9 January 2014 from 30 to 535 within 95 minutes, was a factor that suggested that the reading of 30 was likely to be due to the STEMI on 9 January 2014.  Associate Professor Strathmore found it difficult to be conclusive, given the absence of an earlier troponin result from 6 January 2014.[228] 

    [228] ts 117.

11. Whilst agreeing that Associate Professor Allan's proposition was possible, given that the reading of 30 was only 105 minutes from the onset of pain, Associate Professor Strathmore thought it quite reasonable that at that point the initial troponin would still have been normal, that is less than 16.  The subsequent rise to 535 is a reasonable number for someone three and a half hours into a STEMI.  It is certainly possible that the reading of 30 could have been the precursor, showing the rise of the troponin on 9 January 2014, but it is probable, and therefore more likely, that the troponin from the STEMI would have been still normal.[229]

    [229] ts 118.

12. Associate Professor Allan generally accepted Professor Harper and Associate Professor Strathmore's analysis that the level of 30 was consistent with there having been a small NSTEMI on 6 January 2014.[230]

Third reason for supposing there was an event significant enough to raise troponin on 6 January 2014

[230] ts 155 – 157.

1. Associate Professor Strathmore observed that on 9 January 2014 Ms Lazarevski had a coronary occlusion.  In his view it is hard to see what else, other than a SCAD, she could have had on 6 January 2014, barring the highly unlikely scenario that she had two separate diseases on 6 January 2014 and 9 January 2014.[231]

   [231] ts 119.

2. Associate Professor Strathmore noted from the angiographers' report of 9 January 2014 that it was not certain whether the dissection was related to the guide catheter, the guide wire or propagated spontaneous dissection.[232]  Associate Professor Strathmore noted that the cardiologists were obviously very concerned that they had in avertedly caused the dissection, but for the purposes of the issues in this trial, one needs to consider what was the original cause of the occlusion.  Associate Professor Strathmore's opinion is that the original cause of the occlusion was a spontaneous coronary dissection rather than being an atherosclerotic plaque.[233]

   [232] Report of the cardiologist Dr Latchem at 30/92 of exhibit 1.

   [233] ts 120.

Inferential reasoning in considering causation

1. The defendant submits that unless it can be shown clearly, and not speculatively, that the reading on 6 January 2014 would have been elevated such as to cause Ms Lazarevski to have undergone other tests, then any omission, negligent or otherwise, did not result in her STEMI. Secondly, that it is not possible to say, with any certainty, what the hospital's response would have been in the event that the reading was elevated, given the uncertainty about what the levels were likely to have been on 6 January 2014. 

2. Professor Harper's evidence was that if the troponin levels been normal, the chest pain had settled and she was clinically stable, then and only then, would it have been reasonable to discharge her from hospital. Those circumstances did not occur.[234]  He stated that, 'you always err on the side of safety.'[235]

   [234] A11 page 10 of report.

   [235] ts 99.

3. In Ellis, at [803] ‑ [819] onwards, Gething DCJ set out 16 principles relevant to the application of inferential reasoning to determine causation which I consider and apply. They are as follows (citations omitted):

   803.First, the factual inquiry as to causation has to be decided on the balance of probabilities.  Inferential reasoning takes place within this framework.

   804.Second, if the probable causal connection is established, then the law treats as certain that there is such a connection even though otherwise no certain answer can be given.

   805.Third, I must make a finding on the evidence and not assume the existence of a fact.  The evidence must go beyond guesses and speculation.  I am required to be actually persuaded as to the probability of a fact being true.  The 'facts proved must form a reasonable basis for a definite conclusion affirmatively drawn of the truth of which the tribunal of fact may reasonably be satisfied'.  I must have 'the appropriate degree of confidence in its existence or correctness based on or judged according to reason'.

   806.Fourth, the test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility. …

   807Fifth, causation may be proven by inference.  Inferences 'from actual facts that are proved are just as much part of the evidence as those facts themselves'.

   808.Sixth, in order to draw an inference, I must be satisfied that the circumstances raise a more probable inference in favour of what is alleged: 'where direct proof is not available, it is enough if the circumstances appearing in evidence give rise to a reasonable and definite inference'.  … '[c]haracterisation of a reasoning process between permissible inference and conjecture often occurs on a continuum, in which there may be no bright line division'.

   809.Seventh, the drawing of an inference is an assessment of what is human experience, rather than a mathematical or scientific calculation. …

   810.Eighth, if I am satisfied that there are two conflicting inferences of equal probability, that would not be sufficient to make a finding on the balance of probabilities.  This is because the choice between them would be a matter of conjecture. …

   …

   812.Ninth, mere proof of fault followed by injury does not show that the fault caused the injury.

   813.Tenth, the fact that no alternative cause or hypothesis was established or suggested in the evidence is a significant circumstance in favour of drawing an inference of causation.

   814.Eleventh, the issue of causation involves a question of fact on which expert opinion evidence may be received.

   815.Twelfth, evidence of possibility is admissible as part of the factual basis for an inference. …

   816.Thirteenth, the fact that experts do not infer causation on a balance of probabilities does not mean that a court may not. …

   817.Fourteenth, a finding of causal connection may be made even when the expert evidence does not rise above the possible; the question is always whether the evidence as a whole establishes causation on a balance of probabilities.

   818.Fifteenth, the sequence of events may be called in aid of drawing an inference which, according to the expert evidence, is open.

   819.Sixteenth, causation, may be inferred from a series of primary facts each of which is not of itself sufficient to found the inference, but, when taken together, form the basis for a reasonable and definite inference. …

General principles

1. Section 5C of the CLA provides:

   5C.General principles

   (1)A determination that the fault of a person (the tortfeasor) caused particular harm comprises the following elements -

   (a)that the fault was a necessary condition of the occurrence of the harm (factual causation); and

   (b)that it is appropriate for the scope of the tortfeasor's liability to extend to the harm so caused (scope of liability).

   (2)In determining in an appropriate case, in accordance with established principles, whether a fault that cannot be established as a necessary condition of the occurrence of harm should be taken to establish factual causation, the court is to consider (amongst other relevant things) -

   (a)whether and why responsibility for the harm should, or should not, be imposed on the tortfeasor; and

   (b)whether and why the harm should be left to lie where it fell.

   (3)If it is relevant to the determination of factual causation to determine what the person who suffered harm (the injured person) would have done if the tortfeasor had not been at fault -

   (a) subject to paragraph (b), the matter is to be determined by considering what the injured person would have done if the tortfeasor had not been at fault; and

   (b)evidence of the injured person as to what he or she would have done if the tortfeasor had not been at fault is inadmissible.

   (4)For the purpose of determining the scope of liability, the court is to consider (amongst other relevant things) whether and why responsibility for the harm should, or should not, be imposed on the tortfeasor.

2. As Sweeney DCJ stated in Wright [236] a plaintiff must prove that any negligent act or, failure to act, on the part of the defendant's staff caused him/her harm.  The expression 'necessary condition' in par (1)(a) means a condition that must be present for the occurrence of the harm, so that the defendant's negligent act, or failure to act, must be present for the occurrence of the harm.  Such negligent act/failure to act need not be the sole cause of the harm.  This is a statutory statement of the 'but for' test of causation: that, but for the defendant's negligent act or failure to act, the plaintiff would not have suffered the harm: Strong v Woolworths Ltd t/as Big W [2012] HCA 5; (2012) 246 CLR 182 [18].

   [236] [820] ‑ [822].

3. As Gething DCJ noted in Ellis at [710] ‑ [712] (citations omitted) the CLA guides, but does not displace, the application of common law methodology on the issue of causation. The CLA retains the two stage analysis, requiring the court to first determine factual causation and then determine the appropriate scope of the defendant's liability. Where the breach is by way of a failure to act, the question of causation is to be resolved by determining the difference between the relevant state of affairs as they existed after the negligent act or omission, and the state of affairs that would have existed had the negligent act or omission not occurred. If the issue of factual causation is resolved in favour of the plaintiff, a second issue arises under CLA s 5C, being whether it is appropriate for the scope of the tortfeasor's liability to extend to the harm so caused.

1. As Gething DCJ also observed in Ellis at [714] the High Court pointed out in Wallace v Kam (2013) HCA 13; (2013) 250 CLR 375 at [11] – [12] the distinction between factual causation and scope of liability reflects the common law:

   The common law of negligence requires determination of causation for the purpose of attributing legal responsibility. Such a determination inevitably involves two questions: a question of historical fact as to how particular harm occurred; and a normative question as to whether legal responsibility for that particular harm occurring in that way should be attributed to a particular person. The distinct nature of those two questions has tended, by and large, to be overlooked in the articulation of the common law…. Statute now requires that the two questions be kept distinct.

Conclusions

1. I have concluded that the relevant fault was the failure to administer serial troponin tests on 6 January 2014.  The relevant harm was the STEMI suffered by Ms Lazarevski on 9 January 2014.

2. I am satisfied that Ms Lazarevski's pain on 6 January 2014 lasted for at least two hours.  That duration and severity of her pain makes it very likely that she suffered damage to the heart, a non STEMI, rather than an attack of angina.  Accordingly, I draw the inference that on that date troponin would have been present at abnormal levels in her blood. Given that Ms Lazarevski had an occluded circumflex coronary on 9 January 2014, I am inferentially satisfied that she could not have experienced anything other than a non-STEMI on 6 January 2014.

3. I conclude that the proximity of the reading at 4.25 pm to the onset of pain at 2.40 pm on 9 January 2014, is such that it is unlikely that the reading of 30 is attributable to the events of that date.  If that is so, it must be the residue of the events of 6 January 2014.

4. In my view, the level of troponin as of 4.25 pm on 9 January 2014 in combination with the intensity and duration of pain on 6 January 2014 makes it more likely than not that Ms Lazarevski's troponin levels, if measured, would have been abnormally elevated on 6 January 2014. I would have reached the same conclusion even if the only factor to be taken into account was the intensity and duration of her pain on 6 January 2014.

5. Where there is a conflict, I prefer the evidence of Professor Harper and Associate Professor Strathmore to the evidence of Associate Professor Allan.  Each reached essentially the same conclusion independently of each other. There are not the same weaknesses that adversely impact on the intellectual robustness of the reasoning process of Associate Professor Allan and Dr Lamberth.  I note, without repetition, my criticism of some aspects of Dr Lamberth's evidence.

6. The force of Associate Professor Allan's opinions is lessened by his inappropriate recourse to the Framingham tests in reaching his conclusions in his reports.  In his evidence Associate Professor Allan effectively disavowed any such reliance.[237]  I found Associate Professor Allan's continued assertion that the Pathway document did not apply to be untenable.  He was incorrect when he stated in his first report that Ms Lazarevski's symptoms resolved at the hospital so that she felt well on discharge and was discharged pain free.[238]  He seemed to hold the view that it was the triage nurse not Dr Winton who made the decision not to apply the Pathway.[239]  Finally, the references in his first reports to Ms Lazarevski's symptoms being atypical[240] are not accurate, as he effectively accepted.[241]

   [237] ts 138.

   [238] Page 3 [5] of first report.

   [239] ts 130, ts 138.

   [240] Page 4 [5] of first report.

   [241] ts 146 and ts 151.

Would carrying out troponin tests have made any difference?

1. The second issue on causation is whether or not if troponin sensitive tests had been administered on 6 January 2014, and if the results were abnormal, the critical events of 9 January 2014, a STEMI, would have been averted.

2. Professor Harper considered that if the NSTEMI had been diagnosed on 6 January 2014, the resulting treatment would have included blood thinning medication.  The purpose of that would have been to prevent thrombosis occurring on the unstable site in the coronary artery, thus completely occluding the artery and causing a STEMI.  Further, an angiogram would have shown a dissection in the proximal portion of the circumflex coronary artery, but in all likelihood flow down the artery past the dissection would have been satisfactory.[242]  The NSTEMI of 6 January 2014 progressed to a STEMI on 9 January 2014, probably related to the development of thrombus (a blood clot formed in and remaining in a blood vessel) at the site of the initial dissection.[243]

   [242] A10.1 page 7 of report.

   [243] A1 page 3 [1] of report.

3. If Ms Lazarevski's troponin tests had been elevated, the physician in Accident and Emergency would typically notify the cardiologist that they had a patient with chest pain, a positive troponin and a presumptive diagnosis of ACS or non-STEMI.  Ms Lazarevski would have been admitted to a Coronary Care Unit and started on a particular medical regime, as outlined in Professor Harper's report.[244] She would have had an angiogram within 48 hours of admission, applying the guideline recommendations of the Cardiac Society Heart Foundation.[245]

   [244] A10.1.

   [245] ts 88.

4. As Professor Harper explained, on 9 January 2014 there was a new dissection to the left main coronary artery when she had a catheter inserted.[246]  If that technique had been necessary 48 hours earlier, the artery would have been open, it would have looked dissected. The standard treatment of a dissected coronary artery is not to try and do anything about it, not to put in a stent, as long as there is good coronary flow.  The treating physician relies on the medications that are being used to keep the artery open until the dissection heals.  It is inadvisable to put things into the coronary arteries because to do so can cause further dissection, as happened in this case.[247]

   [246] A10.3 pages 8 ‑ 9 of report.

   [247] ts 98.

5. Professor Harper was asked whether if Ms Lazarevski had serial troponin tests, and the second one was lower than the first, it would then have been safe to release her.  He considered that if the first reading had been elevated, a second test would not have been required. She would have been admitted.  That is because, as I have noted, the treating physician should always err on the side of safety.  If there is an elevated troponin level in the setting of someone with pain, and the chest pain is consistent with myocardial ischaemia, the treating physician would admit the patient.  Professor Harper could not conceive of a circumstance where the first troponin was abnormal and the second would be normal, in this scenario.  The course would have been to admit her as an inpatient, start her on treatment, two anti‑platelet agents and Heparin, as well as a beta blocker, and a statin medication to lower cholesterol.  That would be the standard treatment in ACS.[248]

   [248] ts 99.

6. Similarly, Associate Professor Strathmore's view was that it is very likely that if the troponin tests had been performed Ms Lazarevski would have avoided the subsequent STEMI.  Conservative treatment with anticoagulation would likely have avoided the artery's occlusion that caused the STEMI. She would have definitely been admitted.[249]

   [249] A7 page 4 of report.

7. Associate Professor Strathmore testified that there was a very high probability that Ms Lazarevski would have been admitted and observed, with her troponins repeatedly measured every four to six hours, along with repeat ECGs, to identify what was going on.[250]  When people have ST elevation revealing that there is an infarction, it is likely to be a large infarction.  Accordingly, the protocol in use in Australia, then and now, was for the treating physician to go straight to angiography as an emergency procedure, generally within 24 hours.  If there was a troponin rise, but the pain settles and the ECG does not show any acute changes, the next investigation may be coronary angiography. In the present case, that would only be the position if Ms Lazarevski developed ECG changes subsequent to the last ECG at about 6.00 pm. Such an angiogram would not have been performed until the next day or the day after.[251]

   [250] ts 109 – 110.

   [251] ts 110.

8. Associate Professor Strathmore accepted that a coronary angiogram is an invasive test, in that it involves puncturing the radial artery or the femoral artery, and so there is some slight risk.  He explained, however, that CT scan technology has improved significantly in the last few years, so that with a fast CT scanner physicians can get very clear pictures of the coronary arteries with only an intravenous injection.  As of 2014 many treating physicians would have been using CT coronary angiography. They may well have used it in Ms Lazarevski's case where the diagnosis was not clear.[252]

   [252] ts 110.

9. In cross-examination he explained that the duration of Ms Lazarevski's admission would depend on whether the pain recurred or continued, whether her ECGs changed and what her troponin rose and fell to. The length of admission would depend on what investigations were decided upon.  The cardiology service would have been presumably involved in her care and they would be dealing with a young women with chest pain, obviously severe at the start and with, in these suggested circumstances, a troponin rise.

10. The cardiology service would have been concerned about the possibility of a SCAD, coronary artery spasm or Takotsubo cardiomyopathy.  There would have been a level of investigation. Ms Lazarevski probably would have had an echocardiogram, she may have had a stress test and she may have had a CT coronary angiogram. If the troponin reading had been significantly higher or the ECG had changed, she may have gone on to have coronary angiography.  It would be extremely unlikely that she would have been admitted, observed and sent home. Any decision to discharge her would be based on a consideration of ECG results, troponin readings and levels of pain as a whole.[253]

    [253] ts 118.

11. If Ms Lazarevski had been admitted, those treating her would have discussed in detail the appropriate management strategy.  They would have explained to her that as well as her chest pain, her troponin had gone up, and so there was a concern about a coronary artery narrowing.  The need to do further investigations would have been explained and those treating her would discuss the risks of those investigations versus the potential benefits.  If her troponin levels became much higher or she developed more ECG changes, they might have advised that she needed a coronary angiogram, but Ms Lazarevski would have been involved.  Patients are involved in their own care.  Doctors try and explain to them the risks and benefits of a particular investigation.[254]

    [254] ts 120 – 121.

12. The conclusions articulated by Professor Harper and Associate Professor Strathmore on this aspect, both in their reports and in their oral evidence, were not challenged or disputed by Associate Professor Allan in his evidence.  Whilst the defendant submits that Professor Harper did not definitively state that the medications or the angiogram would have prevented the SCAD on 9 January 2014, I am satisfied that the probability is that they would have done.

13. So far as Dr Lamberth's evidence is concerned on this point, he stated that even if a troponin test had been carried out, and even if it met some criteria for positivity, Ms Lazarevski would probably not have been admitted.[255]  Even if she was admitted for observation and specialist cardiology review she would have been discharged a day later with the same advice.  The critical events would still have occurred on 9 January 2014, but simply two days after discharge rather than three.[256] Accordingly, the defendant's case is that the failure to apply the troponin test did not cause Ms Lazarevski's injuries.

    [255] Page 10 [98] of first report and page 4 [34] of second report.

    [256] Page 10 [98] and page 12 [5] of first report and page 4 [36] of second report.

14. There was no support for this suggestion from Associate Professor Allan.  Moreover, Professor Harper could not conceive that it could be correct.  No one would send a young person home who presented with chest pain and had an elevated troponin.  That would not be acceptable medical practice.[257]

    [257] ts 89.

15. The test of factual causation in CLA s 5C(1)(a) is to be determined by the 'but for' test: but for the negligent act or omission, would the harm have occurred.[258]  I am satisfied that had the omission to order troponin testing not occurred, and the results were abnormal, the probable course of events is that Ms Lazarevski would have been admitted to the hospital's coronary care unit.  Further, that it is more likely than not that conservative management would have avoided her STEMI on 9 January 2014.[259]

    [258] Ellis [716] citing Wallace [16]; Adeels Palace Pty Ltd v Moubarak [2009] HCA 48; (2009) 239 CLR 420 [45]; Strong v Woolworths Ltd t/as Big W [20].

    [259] Page 5 of Associate Professor Strathmore's report.

16. The plaintiff has established factual causation on the balance of probabilities for the purposes of s 5C(1)(a) and no normative[260] considerations arise under s 5C(1)(b), bearing in mind s 5C(4).

    [260] As explained in Wallace [14] (substituting the relevant references to the CLA in place of the references to the equivalent provision of the Civil Liability Act 2002 (NSW), being s 5D and 5E), cited in Ellis [741].

Alternative s 5C(2) position - in the event that factual causation is not made out

1. In the event that I had not been satisfied on the balance of probabilities of factual causation, I would have concluded that the uncertainty, that so precluded me, was attributable to the shortcomings of Dr Winton and the hospital in not ordering the troponin testing.  This would be an appropriate case where the defendant's fault and the circumstances established by the evidence should be taken to establish factual causation even if, contrary to my view, the plaintiff had not proved factual causation.

2. The plaintiff placed the defendant on notice of its intention to rely, if required, on s 5C(2).[261]  The defendant should not benefit from any evidentiary gap, namely an inability to scientifically determine from the 9 January 2014 blood tests whether, on 6 January 2014, Ms Lazarevski's unmeasured troponin levels would have been elevated. They should have been measured.  The defendant should not benefit from that failure to measure.  That is particularly so when the unilateral decision not to comply with the Pathway was not disclosed.

   [261] Paragraph 29 of the plaintiff's opening written submissions.

3. Applying the relevant factors that O'Neal DCJ considered persuasive in this regard in Panagoulis,[262] there was no sensible reason to withhold the administration of serial troponin testing. Notwithstanding the 'false positives' argument, I am quite satisfied that there was no harm to Ms Lazarevski by providing troponin testing. Ms Lazarevski played no role, and in no way contributed to the harm that she sustained on 9 January 2014.  The treatment that would have avoided the harm she suffered was known to the hospital staff, it was available, and it was simple to implement.

   [262] Panagoulis [469].

4. The defendant is not a vulnerable tortfeasor who needs some protection against suit.  To the extent that the law of negligence can, by a finding of liability, encourage other potential tortfeasors to take reasonable care, responsibility for this harm should be imposed on the defendant.  There is no sensible reason for leaving Ms Lazarevski to bear the harm that she has suffered.

Orders

1. Judgment for the plaintiff in the sum of $450,000.  I will hear from the parties as to costs.

I certify that the preceding paragraph(s) comprise the reasons for decision of the District Court of Western Australia.

MW
Associate to Judge Troy

27 JUNE 2019