Plaintiffs v Defendant

1 One morning in October 2013 Ronald Boxell experienced chest pain while he was getting ready for work. He was taken by ambulance to the emergency department at the Frankston Hospital ('the Hospital'), where he remained for over eight hours for examination, observation and investigation. No cause was found for Mr Boxell's pain, and he was discharged without a diagnosis. The following day Mr Boxell died at home as a result of acute aortic dissection ('AD') causing haemopericardium and cardiac tamponade.

2 The defendant, Peninsula Health, conducted and managed the Hospital.

3 AD is an uncommon condition, which requires urgent surgery. It has a very high mortality rate if untreated. The characteristics of AD make diagnosis difficult. CT aortogram ('CTA'), which is a definitive investigation for AD, was not routinely performed on chest pain patients in hospital emergency departments in 2013.

4 The defendant conceded that, had a CTA been performed during Mr Boxell's Hospital attendance, it would have shown evidence of acute AD, and it is likely he would have had urgent surgery and survived.

5 The plaintiffs are Mr Boxell's wife, Vicki Boxell, and his children. They allege the defendant was negligent because it failed to consider and exclude AD as a cause of Mr Boxell's presentation, and failed to perform a CTA. The defendant argues that it considered the possibility of AD, but on the presenting history, physical examination and investigation results, there was no clinical basis for performing a CTA. Further, the defendant alleges that it acted in a manner widely accepted as competent professional practice and therefore was not negligent by reason of s 59 of the Wrongs Act 1958 (Vic) ('the Act').

6 By agreement, liability was the only issue run at trial. If they succeed, the quantum of each plaintiff's claim remains to be assessed. The key issues to be determined are:

(a) Did Peninsula Health consider AD as a cause of Mr Boxell's chest pain?

(b) Was Peninsula Health negligent because it failed to perform a CTA to exclude or confirm AD?

(c) Was Peninsula Health not negligent because it acted in a manner widely accepted by a significant number of respected practitioners in the field of emergency medicine as competent professional practice in the circumstances?

8 The defendant conceded causation, though the question of damages remains in dispute.

9 Breach is governed by s 48 of the Act. The risk was that a person who presented in the circumstances of Mr Boxell, might suffer harm as a result of failure by the Hospital to consider, and confirm or exclude, a diagnosis of AD. In issue is whether a reasonable person in the position of the Hospital would have taken the precaution of performing a CTA on Mr Boxell in response to the risk of harm. In relation to that question, s 48 provides:

(1) A person is not negligent 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.

(3) For the purposes of subsection (1)(b) -

• (a) insignificant risks include, but are not limited to, risks that are far-fetched or fanciful; and
• (b) risks that are not insignificant are all risks other than insignificant risks and include, but are not limited to, significant risks.

10 Other principles relevant to breach are set out in s 49:

In a proceeding relating to liability for negligence -

(a) the burden of taking precautions to avoid a risk of harm includes the burden of taking precautions to avoid similar risks of harm for which the person may be responsible; and

(b) the fact that a risk of harm could have been avoided by doing something in a different way does not of itself give rise to or affect liability for the way in which the thing was done; and

(c) the subsequent taking of action that would (had the action been taken earlier) have avoided a risk of harm does not of itself give rise to or affect liability in respect of the risk and does not of itself constitute an admission of liability in connection with the risk.

11 The standard of care which applies is modified by s 58 of the Act, which is the statutory expression of the common law:[1]

Standard of care to be expected of persons holding out as possessing a particular skill

In a case involving an allegation of negligence against a person (the defendant) who holds himself or herself out as possessing a particular skill, the standard to be applied by a court in determining whether the defendant acted with due care is, subject to this Division, to be determined by reference to -

(a) what could reasonably be expected of a person possessing that skill; and

(b) the relevant circumstances as at the date of the alleged negligence and not a later date.

12 The defendant relies on s 59 of the Act:

Standard of care for professionals

(1) A professional is not negligent in providing a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by a significant number of respected practitioners in the field (peer professional opinion) as competent professional practice in the circumstances.

(2) However, peer professional opinion cannot be relied on for the purposes of this section if the court determines that the opinion is unreasonable.

(3) The fact that there are differing peer professional opinions widely accepted in Australia by a significant number of respected practitioners in the field concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section.

(4) Peer professional opinion does not have to be universally accepted to be considered widely accepted.

(5) If, under this section, a court determines peer professional opinion to be unreasonable, it must specify in writing the reasons for that determination.

(6) Subsection (5) does not apply if a jury determines the matter.

The operation of s 59

13 The operation of s 59 of the Act has been considered in the Trial Division of this Court by Macaulay J in Brakoulias v Karunaharan ('Brakoulias')[2] and J Forrest J in Grinham v Tabro Meats Pty Ltd ('Grinham').[3]

14 The comparable New South Wales provision is s 5O of the Civil Liability Act 2002 (NSW):

(1) A person practising a profession (a professional) does not incur a liability in negligence arising from the provision of a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice.

(2) However, peer professional opinion cannot be relied on for the purposes of this section if the court considers that the opinion is irrational.

(3) The fact that there are differing peer professional opinions widely accepted in Australia concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section.

(4) Peer professional opinion does not have to be universally accepted to be considered widely accepted

Section 5O has been considered by the New South Wales Court of Appeal in Dobler v Halverson ('Dobler'),[4] Sparks v Hobson ('Sparks')[5] and South Western Sydney Local Health District v Gould ('Gould').[6]

15 In Dobler, Giles JA, with whom Ipp and Basten JJA agreed, identified the question to be determined on appeal in that case:

As I have indicated, the judge held that s 5O operated as a defence. The appellant submitted that the judge was in error in holding that s 5O operated as a defence, and that "the plaintiff bears the onus of proving that the provision of the professional services by a defendant was not widely accepted in Australia by peer professional opinion as competent professional practice"; he submitted that it "define[d] the content of the duty of care owed by [the appellant] to Kurt".[7]

It follows that I do not accept the appellant's submission that s 5O did not provide a defence but defined the content of the duty of care owed by the appellant to Kurt, with the onus on the respondents to prove that the manner in which he acted was not widely accepted by peer professional opinion as competent professional practice. Section 5O may end up operating so as to determine the defendant's standard of care, but the standard of care will be that determined by the court with guidance from evidence of acceptable professional practice unless it is established (in practice, by the defendant) that the defendant acted according to professional practice widely accepted by (rational) peer professional opinion. To require the plaintiff to establish the negative would significantly distort the language of s 5O(1), and would not be consistent with the reference in s 5O(2) to reliance on peer professional opinion for the purposes of the section - the plaintiff does not rely on it in order to negate a liability in negligence.[8]

Giles JA then described, with approval, the approach taken by the trial judge to determination of negligence and the operation of s 5O:

The judge approached breach of duty in accordance with the operation of s 5O which I have described. He held that the appellant "fell short of the requisite standard of care". He then considered whether the appellant nonetheless was not liable because it was established that when he failed to obtain an ECG he acted in a manner widely accepted by peer professional opinion as competent professional practice, and found that it was not.[9]

16 In Brakoulias, Macaulay J decided, in conformity with Dobler, that s 59 of the Act assumes the continued existence of the common law standard in Rogers v Whitaker,[10] and does not exclusively express the content of the standard of care applicable to claims of negligence against professionals. His Honour said:

The only remaining question is whether it truly operates as a defence, as has been found in New South Wales, or merely provides the defendant an opportunity to meet an evidentiary burden by adducing evidence of peer professional opinion, with the legal burden remaining on the plaintiff to negative it.

In my view, there is no support for the evidentiary burden approach either in the text of the legislation or in any of the extrinsic materials. ...[11]

17 In Grinham, J Forrest J referred with approval to the judgment of Gibbs JA in Dobler, and said the common law standard of care replicated by s 58 of the Act was not to be determined by whether the conduct of the defendant accorded with the practice of medical practitioners in its position, though such evidence may be relevant, and in some cases decisive.[12] His Honour agreed with Macaulay J's conclusion in Brakoulias that s 59 of the Act must operate as a defence, which he considered was 'inescapable given the wording of that section'.[13]

18 In Gould, Leeming JA, with whom Basten and Meagher JJA agreed, set out the following propositions in relation to s 5O, which he regarded as uncontroversial:

(1) it is settled that the defendant bears the onus of establishing the elements of s 5O(1) (namely, he or she was a "professional" and acted in a manner which, at the time, was widely accepted in Australia by peer professional opinion as competent professional practice): Dobler v Halverson (2007) 70 NSWLR 151; [2007] NSWCA 335 at [60]-[61] and Sydney South West Area Health Services v MD [2009] NSWCA 343 at [20]-[21], [51] and [58];

(2) it is clear from s 5O(3) that there may be inconsistent bodies of peer professional opinion each of which is widely accepted;

(3) it is clear from s 5O(4) that peer professional opinion may be widely accepted without being universally accepted;

(4) subject to s 5O(2), when the elements of s 5O(1) are made out, the defendant does not incur a liability in negligence;

(5) if the court considers that the opinion is irrational, then the section does not to that extent apply; and

(6) the test of "irrational" in s 5O(2) is not otherwise defined, but in light of s 5O(3) and (4) it cannot be sufficient for peer professional opinion to be irrational merely because one peer, or a body of peers, does not share that opinion.[14]

19 The defendant submitted that s 59 of the Act operates to define the applicable standard of care and that to succeed the plaintiffs must prove the Hospital did not act in a manner that was widely accepted in Australia by a significant number of respected practitioners in the field as competent professional practice in the circumstances.

20 I reject the defendant's submissions. The standard of care against which the conduct of a defendant possessing a particular skill is assessed is to be determined in accordance with ss 48 and 58 of the Act. The plaintiff bears the onus of establishing the standard of reasonable care which applies in the circumstances, and that the defendant's conduct fell below that standard.

21 The effect of s 59(1) is to substitute a standard of competent professional practice for the standard of reasonable care which otherwise applies. The statutory text, 'A professional is not negligent ... if it is established ...' places the onus of proving the elements of the provision on the defendant. That conclusion is consistent with the authorities, and is further confirmed by statutory context.[15]

22 A remaining question is whether, consistent with the decisions in Brakoulias, Grinham and Dobler, s 59(1) is considered once breach is established in accordance with ss 48 and 58, or whether the starting point for analysis of breach is s 59(1) where there is evidence of competent professional practice. In Gould, Leeming JA said:

Read in proper context, it may be seen that Dobler was a very precise statement of the operation of s 5O. Only if the preconditions of the section - namely, that the defendant was "practising a profession" and was doing so "in a manner that ... was widely accepted in Australia by peer professional opinion as competent professional practice" - are established does the section apply. The defendant bears the onus of establishing those preconditions, and if they are not established, then ss 5B and 5C are to be applied. However, if the preconditions are established, then the standard of care against which the defendant's conduct is assessed is that which was widely accepted by peer professional opinion as competent professional practice, unless the court considers that opinion is irrational.

In a case (such as the present) where the defendant establishes the preconditions to s 5O, then there is a single standard against which the defendant is assessed, namely, s 5O, subject always to s 5O(2). That is what Giles JA said at [59]: "then subject to rationality that professional practice sets the standard of care". That is also what his Honour said at [61]: "Section 5O may end up operating so as to determine the defendant's standard of care".

That is what Basten JA and Simpson JA separately suggested in Sparks v Hobson. After reviewing the background to s 5O, Basten JA concluded at [24]:

"[24] ... It is true that s 5O will not be engaged unless there is evidence of a widely accepted professional practice supporting the defendant's conduct, but where there is such evidence, unless it can be rejected by the trial judge, it will fix the relevant standard; there cannot be two legally supportable standards operating in the one case."

"[329] [Section] 5O, like s 5I, provides a complete answer to a claim under Pt 1 A of the CLA... It is in that sense that the section operates as a defence. For that reason, when it is pleaded, it is convenient to deal with it first."

...

It is true that on occasion there has been separate treatment of breach in accordance first with s 5B and s 5C and then with s 5O (see for example Howe v Fischer [2014] NSWCA 286 at [73]- [78] and Melchior v Sydney Adventist Hospital Ltd [2008] NSWSC 1282 at [139]- [145], both cases where breach was not found to have been established under s 5B). But the weight of authority proceeds on the basis as stated in the Ipp Report, assimilating the standard of care by s 5O once the preconditions of the section have been satisfied. That is the gravamen of the empirical research presented by C Mah, A critical evaluation of the professional practice defence in the Civil Liability Acts (2014) 37(2) University of Western Australia Law Review 74.[16]

While I accept the plaintiffs' submission that in this case the result will be the same whichever approach is taken, given that it has been raised by evidence and argument, I will consider first whether Peninsula Health has established the preconditions for the operation of s 59(1).

23 In Sparks, McFarlan JA, referring to his earlier decision in McKenna v Hunter and New England Health District ('McKenna'),[17] said:

I then referred to the wide variety of circumstances that were relevant to the reasonableness of the defendant's conduct in that case, and continued:

165 In summary, the section is directed to something, namely a practice, that was in existence at the relevant time, here July 2004. Whilst at that time there were no doubt many practices in the medical profession concerning the manner in which operations were performed, the types of treatments that were administered, the circumstances in which tests were ordered, the circumstances in which warnings were given and other matters, the evidence here did not identify any such practice that was relevant in the present case. In light of the wide variety of circumstances bearing upon the decision to discharge Mr Pettigrove, it would have been surprising if it had done so. It is unlikely, to say the least, that there would have occurred in or before 2004 a number of situations in which there were sufficient features in common with the present case to enable it to be said that there was a practice concerning how such a situation was to be dealt with by a competent medical practitioner.

These observations are applicable to the present case, which does not relate (at least so far as the issues of negligence on appeal are concerned) to any particular point of medical practice, such as the use of a particular drug, surgical technique or item of surgical equipment. Rather, as in McKenna, determination of the issue of negligence requires reference to a variety of factual considerations including:

• The significance of an elevated blood carbon dioxide level when oxygen and blood pressure readings were normal to high;
• The urgency of the operation, bearing in mind Mr Hobson's pre-existing condition;
• The exhaustion of possibilities, short of termination of the operation, for remedying the carbon dioxide problem and its underlying cause, being the compression of blood vessels preventing blood fully perfusing the lungs.

Evidence from a number of witnesses highlighted the unusual nature of the operation. For example, Dr Barratt had never seen this type of surgery performed on a patient with Noonan Syndrome and Dr Forrest described the operation as involving "a very unusual and difficult anaesthetic challenge". It can be assumed that the particular events that occurred in the course of the operation rendered the situation even more unusual.[18]

24 Relying on what was said by McFarlan JA, the plaintiffs submitted that whether a course of professional conduct is a practice or not lies in whether the 'determination of the issue of negligence requires reference to a variety of factual considerations' or 'to any particular point of medical practice'. It was submitted the former does not constitute a practice, but the latter does. Because determination of the issue of negligence in relation to the treatment of Mr Boxell required reference to a variety of factual circumstances, the course of professional conduct which was involved was not a practice, and s 59(1) was not engaged.

25 In Sparks, Simpson JA did not agree with the approach adopted by McFarlan JA, but concluded he was bound to accept what was said in McKenna:

I consider that I am obliged to accept McKenna (in this Court) as stating the prevailing construction of s 5O: Gett v Tabet (2009) 254 ALR 504; [2009] NSWCA 76 at [277]-[279]. But for that constraint, I would have considered that the language of s 5O makes it plain that "competent professional [here, medical] practice" is intended to denote "the practice of a profession [here, medicine]", and not a specific practice or method of providing the professional services in question. That construction is supported by the absence of the indefinite article in conjunction with "professional practice", and the use instead of the adjective "competent", which to my mind signifies professional practice in a general sense, rather than an identifiable, specific, and discrete aspect of the profession or method of providing the professional service.[19]

Basten JA agreed with Simpson JA as to the construction of s 5O, but concluded the Court was not bound by what was said in McKenna:

Although it is uncertain how this reasoning in McKenna will operate in particular cases, there is a risk in reformulating the statutory language. To speak of "a practice" adopted by a group of professional persons suggests a regular course of conduct adopted in particular circumstances. By contrast, the phrase "competent professional practice" is apt to cover the whole gamut of professional services provided by the practitioner, whether or not the particular circumstances have arisen sufficiently often to result in an established practice.

...

There are other reasons for thinking that the reference to "competent professional practice" does not require evidence of "a practice". First, it is the "manner" in which the defendant acted which must be the focus of the opinion. Secondly, if it were necessary to establish a practice, one might expect subs (3) to refer to "opinions ... concerning that practice", rather than "opinions ... concerning a matter".[20]

26 Peninsula Health relied on the judgment of Basten JA in Sparks and submitted 'competent professional practice' contemplates not just a specific method of performing an activity but is broad enough to capture the response of a professional to a situation which calls for their expertise.

27 This question was not considered in Brakoulias or Grinham, and was considered, but not resolved, in Gould.[21]

28 Whether a defendant is negligent involves consideration of the standard of care required in response to the risk of harm. Usually the standard which applies is fixed by what a reasonable person would do in the circumstances.[22] Where a defendant holds themselves out as possessing a particular skill, the standard is modified to what could reasonably be expected of a person possessing that skill.[23] In both cases the content of the standard is resolved by the finder of fact considering all of the evidence and exercising their common sense.[24]

29 It is then necessary to consider whether the conduct of the defendant satisfied the standard of reasonable care.

30 Section 59 of the Act was intended to introduce a modification of the Bolam principle,[25] which was stated by Lord Scarman in Sidaway v Governors of Bethlehem Royal Hospital[26] as follows:

The Bolam principle may be formulated as a rule that a doctor is not negligent if he acts in accordance with a practice accepted at the time as proper by a responsible body of medical opinion even though other doctors adopt a different practice. In short, the law imposes the duty of care: but the standard of care is a matter of medical judgment.[27]

31 There are three elements which a defendant must establish to rely on s 59(1). First, that the defendant is a professional. Usually this will not be contentious.

32 Second, a standard of care, namely competent professional practice in the circumstances. Usually a defendant will call one or more professionals who practice in the field to establish a standard of competent professional practice. It is unlikely to be sufficient that the experts who give evidence themselves subscribe to the standard. The evidence must establish peer professional opinion, that a standard of care is widely accepted by a significant number of respected professionals in the field in Australia as competent professional practice in the circumstances. If established, peer professional opinion determines the standard of care which applies for the purposes of s 59(1) of the Act.

33 Third, that the defendant acted in a manner which satisfied the standard of competent professional practice. This is a question of fact determined on all of the evidence.

34 The text of s 59(1) does not speak of 'a practice'. A standard of competent professional practice in the circumstances is not limited to a specific practice, and may cover professional practice in a more general sense.[28] However, it remains necessary for a defendant to establish a standard of care which was widely accepted in Australia at the time as competent professional practice responding to the particular circumstances in which the service was provided.[29] In Grinham, J Forrest J referred to the problems of proof inherent in the application of s 59(1).[30] Where a defendant has responded to circumstances which involve a variety of factual considerations, or call for a series of subjective judgments, it may be difficult to prove a standard of response which was widely accepted at the time as competent professional practice by a significant number of respected professionals across Australia who do not themselves give evidence.

Unreasonable peer professional opinion: s 59(2)

35 The plaintiffs submitted that if it was found the Hospital acted in a manner accepted as competent professional practice, then the peer professional opinion which set that standard of care was unreasonable, and could not be relied on.

36 Section 59 was part of a suite of changes responding to the Ipp Report[31] introduced to the Act by the Wrongs and Other Acts (Law of Negligence) Act 2003 (Vic). The qualification in s 59(2), expressed in the Ipp Report as 'irrational' rather than 'unreasonable', was intended to follow the principles settled by the English House of Lords in Bolitho v City and Hackney Health Authority ('Bolitho'),[32] and to give a court power to intervene in the very exceptional instance of treatment that is both irrational and in accordance with an opinion widely held by a significant number of respected practitioners in the field.[33]

37 In Bolitho, Lord Browne-Wilkinson described the qualification in the following way:

The use of these adjectives - responsible, reasonable and respectable - all show that the court has to be satisfied that the exponents of the body of opinion relied upon can demonstrate that such opinion has a logical basis. In particular in cases involving, as they so often do, the weighing of risks against benefits, the judge before accepting a body of opinion as being responsible, reasonable or respectable, will need to be satisfied that, in forming their views, the experts have directed their minds to the question of comparative risks and benefits and have reached a defensible conclusion on the matter.

...

These decisions demonstrate that in cases of diagnosis and treatment there are cases where, despite a body of professional opinion sanctioning the defendant's conduct, the defendant can properly be held liable for negligence (I am not here considering questions of disclosure of risk). In my judgment that is because, in some cases, it cannot be demonstrated to the judge's satisfaction that the body of opinion relied upon is reasonable or responsible. In the vast majority of cases the fact that distinguished experts in the field are of a particular opinion will demonstrate the reasonableness of that opinion. In particular, where there are questions of assessment of the relative risks and benefits of adopting a particular medical practice, a reasonable view necessarily presupposes that the relative risks and benefits have been weighed by the experts in forming their opinions. But if, in a rare case, it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of opinion is not reasonable or responsible.[34]

38 Commenting on the application of the test of irrationality used in the New South Wales provision, Leeming JA said in Gould:

Text, context and purpose all support the conclusion that it is a seriously pejorative and exceptional thing to find that a professional person has expressed an opinion that is "irrational", and even more exceptional if the opinion be widely held. To consider a body of opinion to be "irrational" is a stronger conclusion than merely disagreeing with it, or preferring a competing body or peer professional opinion.[35]

39 To rely on s 59(2) a plaintiff must establish that the peer professional opinion which determines a standard of competent professional practice cannot withstand logical analysis. It will be a rare case in which it is demonstrated that an opinion held by a significant number of respected practitioners in the field is unreasonable, in the sense that those practitioners have not directed their minds to the comparative risks and benefits of a particular response to the circumstances under consideration, or because the opinion has no logical basis.

40 Mr Boxell was 47 years old when he died. He was a qualified electrician, and during the 11 years before his death he worked a rotating four day on, four day off, 12-hour shift.

41 Mr Boxell suffered from hypertension. He smoked about 20-30 cigarettes daily, and consumed alcohol. He had a history of depression and in 2010, following marital disharmony, was an inpatient for a few days in a psychiatric unit, and was treated by a psychologist for a period after discharge. At times he was prescribed medication for depression and hypertension. The last scripts for those medications were issued in October 2011.

42 Mr Boxell had a family history of his mother having suffered an abdominal aortic aneurysm in her fifties, and an uncle a cerebral aneurysm.

43 On 19 February 2012 Mr Boxell experienced chest pain. He was taken by ambulance to the Hospital where he was assessed, before being discharged without diagnosis.

44 Early on the morning of 6 October 2013, Mr Boxell again experienced chest pain. He called an ambulance and was transported to the Hospital, where he was assessed and treated in the emergency department, before being discharged in the early afternoon. Mr Boxell died at home on 7 October 2013.

45 Before setting out the history of Mr Boxell's attendances and treatment I will say something about the witnesses who gave evidence, the Hospital, chest pain presentations and AD.

46 Mrs Boxell described her husband's health generally, and her observations of him on 19 February 2012, and 6 and 7 October 2013.

47 Emergency Registrar Dr Belchi Chiezey gave evidence about Mr Boxell's first attendance at the Hospital on 19 February 2012.

48 The three doctors who attended with Mr Boxell on 6 October 2013, Dr Steven Lindley, Dr Benjamin Harkin and Dr Martin Jackson, each gave evidence.

50 Dr David Eddey qualified in 1983, has worked in emergency medicine since 1988, and has been Director of Emergency Medicine at Geelong Hospital since 2005. In 2013, when asked by the Victorian Coroner to write an expert report on an AD case, Dr Eddey prepared comprehensive explanatory notes, which are evidence of the state of knowledge and clinical practice in relation to AD at the time.

51 Mr Alexander Rosalion qualified in 1975, and has practised as a cardiothoracic surgeon since 1987 at Melbourne hospitals including the Austin, St Vincent's and Epworth Private. He said cardiothoracic surgery involves the chest cavity, including the heart and the aorta. He operates on AD regularly.

52 A/Prof John Raftos qualified in 1976, and has worked in emergency medicine since 1980. He is currently the Senior Specialist in Emergency Medicine at a number of hospitals including St Vincent's Hospital, Darlinghurst, and is Co-joint Associate Professor of the Faculty of Medicine at the University of New South Wales.

53 Dr John Vinen qualified in 1978, worked in emergency medicine from 1981, from 1987 as Head of Emergency Medicine at Royal North Shore Hospital, and from 1999 as Director of Emergency Support Services responsible for cardiac arrest management and training.

54 Prof Peter Cameron qualified in 1981, and has worked in emergency medicine both in Australia and overseas since the 1980s. Since 2003 he has been Professor of Emergency Medicine at Monash University and Academic Director of the Emergency and Trauma Centre at The Alfred Hospital. Prof Cameron has researched, taught and published extensively on emergency medicine, and has held numerous relevant appointments.

55 Dr Anthony Kam qualified in 1995, and has worked as a radiologist since 2004. He is currently Head of Neuroradiology and Director of MRI at The Alfred Hospital.

56 Prof Richard Harper qualified in 1969, and has worked as a cardiologist since 1973. He is currently Emeritus Director of Cardiology, Monash Heart at Monash Medical Centre, and Adjunct Professor of Medicine at Monash University.

57 Prof Biswadev Mitra qualified in 2000, and has worked in emergency medicine since 2004, currently as a Consultant Emergency Physician at Alfred Health. He is a Professor and examiner at Monash University, and has researched and published extensively in the field of emergency medicine.

58 Dr Peter Habersberger qualified in 1965, and has worked as a cardiologist since 1972. He currently works as a Consultant Cardiologist at Cabrini Private Hospital and The Alfred Hospital.

59 Prof Anne-Maree Kelly qualified in 1983, has worked as an emergency physician since 1993, and is currently a Senior Emergency Physician and Academic Head of Emergency Medicine at Western Health, Professorial Fellow at the University of Melbourne, and Adjunct Professor at the Queensland University of Technology. Prof Kelly has lectured and published extensively in the field of emergency medicine.

60 A number of experts referred to and relied on excerpts from text books, journal articles and epidemiological studies, including:

(a) The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease ('IRAD'),[36] a study of 464 patients diagnosed with AD who presented to 12 international referral centres in the years 1996 to 1998 to assess presentation, management and outcomes;

(b) Clinical recognition of acute aortic dissections: insights from a large single-centre cohort study ('Klomp'),[37] a study of 200 AD patients to identify characteristics associated with a lower level of suspicion of the diagnosis;

(c) Epidemiology and Clinicopathology of Aortic Dissection: A population-based longitudinal study over 27 years ('Meszaros'),[38] a study of 84 AD patients to determine the incidence and mortality and analyse the clinical and pathological changes, of AD;

(d) Screening Evaluation and Early Management of Acute Aortic Dissection in the ED ('Strayer');[39]

(e) Clinical Prediction of Acute Aortic Dissection ('von Kodolitsch'),[40] a study of 250 patients with acute chest pain, back pain or both to identify independent predictors of acute AD;

(f) Textbook of Adult Emergency Medicine;[41]

(g) Rosen's Emergency Medicine: Concepts and Clinical Practice ('Rosen's');[42] and

(h) The Emergency Medicine Manual ('Dunn').[43]

61 Dr Jackson said the Hospital's emergency department is now one of the biggest in Melbourne, and sees 250 to 300 patients per day, or approximately 100,000 patients per year. No estimate was given of the number of emergency patients seen by the Hospital in 2013, but I infer it was already large.

62 Chest pain is a common complaint, accounting for approximately 5% of emergency presentations.

63 The causes of chest pain in patients presenting at emergency departments are varied.

64 The most common serious cause is acute coronary syndrome, which includes myocardial infarction (heart attack) and unstable angina. A recent Australian study of 926 adult emergency chest pain presentations found 11% of patients presented with acute coronary syndrome.[44]

65 When a coronary cause is suspected, patients are often placed on a 'cardiac pathway', which involves a period of observation, repeat ECGs and serial troponin blood tests in emergency, and recommendation for further outpatient investigation after discharge. Mr Rosalion explained that troponin is a very sensitive measure for heart ischaemia problems, and if serial troponin tests are performed and are normal, the likelihood of there being an acute cardiac event becomes extremely low. Prof Mitra said normal ECGs and troponins do not exclude acute coronary syndrome, and a small percentage of patients who are discharged will have a positive outpatient scan and will re-present for urgent angiography and stenting, or suffer a heart attack.

66 Other serious causes of chest pain include pulmonary embolism, pneumothorax, oesophageal perforation, pneumonia and AD.

67 AD is a rare condition. A case of acute AD would be expected in about one in 10,000 emergency presentations, or about one in 500 chest pain presentations.

68 Other common causes of chest pain include stable coronary artery disease (ischemic heart disease), pericarditis, other cardiac issues, gastrointestinal disorders and musculoskeletal pain.

69 Dr Eddey said that the number of AD presentations is so small that some emergency providers may only see several cases in their career. He added that among senior emergency doctors, there is group learning from everyone's shared experience which enhances their own medical practice, so that although one doctor may not see an AD for years, the group as a whole would see a number of cases, and a hospital would be expected to run an academic program that allows that experience to be shared.

70 The aorta is the largest blood vessel in the body. It takes the whole of the cardiac output and distributes it via its branches to the head and neck, upper limbs, thorax, abdomen and abdominal organs, pelvis and the lower limbs. It commences at the aortic root and aortic valve at the outflow of the left ventricle of the heart, ascends through the pericardial sac to the aortic arch, then descends through the chest to the lower abdomen where it divides into the iliac arteries which serve the pelvis and the lower limbs.

71 The wall of the aorta is made up of three layers, the inner being the intima, then the media and the adventitia. The passageway for blood flow within the aorta is called the lumen.

72 Dissection occurs when a tear or defect in the intima allows blood to enter and dissect or split the media creating a false lumen. A dissection may progress either proximally toward the heart, or distally from the point of the intimal tear. The two AD classification systems are pictorially represented below:

Mr Boxell suffered a Stanford classification type A, or DeBakey Type II, dissection, which originated in, and was limited to, the ascending aorta.

73 Most ADs are acute. A minority are caused traumatically, either by high speed deceleration injury or as a consequence of catheter procedures. However, most dissections are the end result of a pathological process causing weakening of, and/or increased stress to, the aortic wall.

74 Acute type A dissections are highly lethal with a mortality rate of 1 to 2% per hour after the onset of symptoms. In his notes, Dr Eddey stated, 'Acute aortic dissection is relatively rare, but failure to consider the diagnosis may have catastrophic consequences with untreated mortality rates of 90% or more'.

75 In IRAD, 62% of patients had a type A dissection. The mean age of patients was 63 years (61 years for type A dissection). In von Kodolitsch the mean age of the 78 patients with a type A dissection was 50 years.

76 In relation to the age of patients, Dr Eddey said in his notes:

In general patients with acute aortic dissection fall into two main groups: younger patients with underlying inherited disease predisposing to aortic dissection (eg Marfan Syndrome), or older patients with cardiovascular disease, particularly hypertension and atherosclerosis. However dissection may occur across a range of age groups and in table one below, 30% of aortic dissection occurred in patients 75 years.

77 Hypertension, particularly if untreated, is a significant risk factor for AD. In IRAD 72% of patients had a history of hypertension (69% for type A dissection). Smoking is also a relevant risk factor. The incidence of AD for men is approximately double that for women.

78 It was known in 2013 that a number of genetic connective tissue disorders, such as Marfan syndrome, Ehlers-Danlos syndromes and Loeys-Dietz syndrome were significant risk factors for AD in younger patients.

79 It is now known that a family history of aortic aneurysm is a relevant risk factor for AD. Whether emergency physicians were aware of this connection in 2013 is contentious.

80 In his 2013 notes Dr Eddey sets out the descriptions of the presenting symptoms of acute AD found in a number of medical and emergency medicine texts and papers, including:

Pain is by far the most common presenting complaint, affecting more than 90% of patients. Most patients of painless aortic dissection are chronic in nature. The pain is usually excruciating, occurs abruptly, is most severe at onset and is typically described as 'sharp' more often than 'tearing' or 'ripping'.

The location of the pain may help localise the dissection. Anterior chest pain is associated with the ascending aorta, neck and jaw pain with the aortic arch, pain in the interscapular area with the descending thoracic aorta and pain in the lumbar area of abdomen with involvement below the diaphragm.[45]

(b) Harrison's Principles of Internal Medicine ('Harrison's'):[46]

Almost all patients with acute dissections present with severe chest pain, although some patients with chronic dissections are identified without associated symptoms. Unlike the pain of ischemic heart disease symptoms of aortic dissection tend to reach peak severity immediately, often causing the patient to collapse from its intensity. The classic teaching is that the adjectives used to describe the pain reflect the process occurring within the wall of the aorta - 'ripping' and 'tearing' but more recent data suggest that the most common presenting complaint is sudden inset [sic] of severe sharp pain. The location often correlates with the site and extent of the dissection. Thus dissections that begin in the ascending aorta and extend to the descending aorta tend to cause pain in front of the chest that extends into the back, between the shoulder blades.

(c) Textbook of Adult Emergency Medicine:[47]

Pain is the most common presenting symptom, occurring in 74-95% of patients. Pain is classically described as severe, unremitting, tearing or ripping in nature and maximal at onset. It may be migratory, reflecting proximal or distal extension of the tear. The site of the pain may reflect the site of the dissection with involvement of the ascending aorta typically producing anterior chest pain, whereas neck and jaw pain may suggest aortic arch dissection. Interscapular pain can occur with involvement of the descending aorta, and as distal dissection continues pain may migrate to the lower back or abdomen.[48]

(d) Guidelines for the diagnosis and management of patients with thoracic aortic disease ('American Heart Foundation Guidelines'):[49]

Patients with acute aortic syndromes often present in a similar fashion, regardless of whether the underlying condition is AoD (aortic dissection), IMH (intramural hematoma), PAU (penetrating atherosclerotic ulcer), or contained aortic rupture. Pain is the most commonly reported presenting symptom of acute AoD regardless of patient age, sex or other associated clinical complaint. Pooled data from over 1000 patients in 8 studies found that the pain of acute dissection is perceived as abrupt in onset in 84% of cases (95% CI 80% to 89%) and of severe intensity in 90% of cases (95% CI 88% to 92%). Although classically described as having a tearing or ripping quality, registry data suggest patients are more likely to describe the pain of acute dissection as sharp or stabbing (51% to 64%, respectively) and that report of a migrating quality to pain is highly variable (12% to 55%). Pain may subsequently ease or abate, leading to a false reassurance on the part of the patients and physicians.[50]

Severe pain was the most common presenting symptom and 84.8% of patients recalled abrupt onset. The majority of patients complained of chest pain (72.7%). Anterior chest pain was typical in patients with type A dissection, whereas patients with type B dissection more often experienced pain in the back or the abdomen, although there was substantial overlap. Of note pain was described as sharp (64.4%) more often than tearing or ripping (50.6%). Hypertension at initial presentation was more common in patients with type B dissection (70.1% vs 35.7%) 90% or more of the patients described the pain as "severe or the worst ever".[51]

81 There are differences between the experts as to whether these extracts reflect the state of knowledge of emergency physicians in 2013, and the degree to which the history of pain given by Mr Boxell raised AD as a differential diagnosis which needed to be confirmed or excluded.

82 AD pain is sometimes classically described as unremitting. However, as the American Heart Foundation Guidelines state, pain may ease or abate. Meszaros, a longitudinal population study, includes the following finding:

The initial pain was followed by a painless interval, a "window to in the spectrum of pain" lasting from 1 to 2 h to 4 to 5 days duration, ending with a return of pain or sudden death in 27 of our 66 hospitalized patients (41.0%).[52]

Pain from aortic dissection may completely resolve and should not lead clinicians to discount the diagnosis, particularly if risk factors and high-risk features exist. Dissection may occur in stages, with recurrence of the pain when dissection recommences.

83 Though they frequently present with high blood pressure, and sometimes low blood pressure, patients will often present with normal blood pressure. Other signs on clinical examination are dependent on the location and extent of the dissection.

84 A dissection which progresses toward the heart and involves the aortic valve may cause a heart murmur to be evident on physical examination. A dissection which extends to or beyond the aortic arch may cause restriction of blood flow to organs or limbs resulting in clinical signs such as neurological symptoms, differential blood pressures in the upper limbs, pulse deficit or end organ damage. Because Mr Boxell's dissection was confined to the ascending aorta and did not extend to the aortic valve or the aortic arch, no such clinical signs or symptoms were evident.

85 There are a range of findings on chest x-rays associated with or indicative of AD, the most common of which are widening of the mediastinum (the central compartment of the chest cavity) and abnormal aortic contour. In IRAD 62% had a widened mediastinum, 50% had abnormal aortic contour, 21% had neither and 12% had no abnormality.[53] In his notes Dr Eddey stated:

The radiographic findings classically associated with thoracic aortic dissection are not reliably present and their absence is not sufficiently sensitive to rule out aortic dissection.

The absence of suggestive findings on chest xray makes aortic dissection less likely, however, 10-20% of patients with aortic dissection have a normal chest x-ray; therefore a negative study cannot exclude the disease and should not play a decisive role in the decision to pursue advanced imaging.[54]

86 CTA is the definitive investigation and reliably confirms or excludes the diagnosis.

The clinical assessment of acute severe thoracic pain includes history, physical examination and investigations. A careful history can give important clues as to the cause of the pain, help establish risk factors etc for the condition and formulate differential diagnoses.

Clinical diagnosis of aortic dissection has been known to be difficult with clinicians correctly suspecting the diagnosis in as few as 15-45% of presentations on initial assessment and a diagnostic delay of more than 24 hours after hospitalisation occurs in up to 39% of cases. When the diagnosis is made it may be an incidental discovery made during an advanced imaging procedure (eg coronary angiography) intended to assess for other diagnoses or the patient may die whilst awaiting such an investigation.

Acute aortic dissection may be uncommon, but complications occur often and early, and the outcome is frequently fatal. Since dissection is a dynamic process that may occur anywhere within the aorta, the clinical spectrum of presentation is broad. Symptoms may mimic more common disorders such as myocardial ischemia or stroke, and physical findings may be absent or suggestive of a diverse range of other conditions. Therefore, dissection is often difficult to diagnose, and a high clinical index of suspicion is mandatory. As recently as a decade ago, a large referral center reported on a series of patients in whom the diagnosis was frequently missed on initial evaluation (38%) and first established in 28% of patients at postmortem examination. Although clinicians today are better equipped to deal with the complex threat posed by aortic dissection, mortality rates remain high.[55]

Approximately one in 10,000 ED patients will have aortic dissection, a number so small that emergency providers may only see several cases in their career. Only one quarter of patients with aortic dissection present with a combination of classic features (pain of sudden onset or ripping/tearing quality, blood pressure differential, and widened mediastinum on chest radiograph); 1 in 25 patients diagnosed with aortic dissection has none of the classic features. Furthermore, aortic dissection can cause myriad symptoms localising to any organ system or body part, and each of these symptoms can be explained by more common conditions - often by more common dangerous conditions that quite reasonably establish the focus of care but ultimately turn out to be distractors.

Emergency clinicians are thus confronted with innumerable patients whose symptoms could be caused by aortic dissection but almost certainly are not; aortic dissection could therefore be said to represent not just a needle in a haystack, but a needle disguised as a blade of hay in a haystack. Physicians evaluating patients whose symptoms may be caused by aortic dissection must therefore understand the clinically relevant risk factors and clinical manifestations of this condition and develop a risk stratification strategy that catches as many patients with the disease as possible without overusing advanced imaging studies.[56]

The poetic language used in Strayer to describe the difficulty of the diagnostic task might be explained by the main purpose of the article being to recommend an evaluation pathway tool presented by the authors.

90 Prof Mitra explained the diagnosis of AD is often missed due to insufficient recognition of variable, non-specific symptoms.

91 Prof Cameron said many cases of AD will present with clear-cut reasons for further investigation, but those that fall into the category of undifferentiated chest pain are rare and difficult to diagnose against the backdrop of many cases per week of undifferentiated chest pain of benign origin.

92 Prof Kelly described AD as a well-known chameleon which can be hard to diagnose.

93 During the afternoon of 19 February 2012, Mr Boxell developed chest pain, and called an ambulance. Mrs Boxell said her husband complained he was suffering really bad chest pain and that his arm was hurting. She said he was sweaty, with beads of sweat coming off his face.

94 The ambulance case description records that Mr Boxell developed sudden onset central chest pain that radiated into his left shoulder which had resolved by the time the ambulance arrived, and a slight headache that was increasing in intensity. An ECG showed no material abnormality.

95 Mr Boxell was transported by ambulance to the Hospital, where he was recorded as reporting his chest pain had resolved, that he was lethargic and had a headache, for which he was given Panadol. A CT scan of his brain was reported as normal. A chest x-ray was reported as demonstrating mild unfolding of the aorta, but no other abnormality.

96 Mr Boxell was discharged early the following morning with a letter to his GP recording the diagnosis as chest pain. Treatment given was simple analgesia. The Hospital requested the GP organise a stress test.

97 When he attended his GP on 24 February 2012, Mr Boxell reported no pain. He was referred for a stress echocardiograph, which was subsequently performed on 24 March 2012, and was reported as negative for inducible myocardial ischaemia.

98 Mr Boxell remained well until 6 October 2013. He was due to commence work that day at 6:30am. Mrs Boxell said her husband woke her and said he had called an ambulance, and that he felt like he was having a heart attack. She said he did not look well, his face was all red, he was sweating profusely and his forehead was hot to touch. She said Mr Boxell was agitated, holding his left shoulder and complaining, 'It's killing me, it's just like somebody's got knives just stuck right in here', indicating the hollow below his left shoulder. Mrs Boxell said her husband seemed to be getting worse, his breathing was shallow and raspy, and every time he breathed she could see pain in his face. She said the episode seemed similar to February 2012, but more severe.

99 An ambulance arrived at 6:01am, and Mr Boxell was given 0.15 mg of GTN (nitroglycerin) sublingually and a patch administering 0.4 mg per hour, and 10 mg of morphine by IV. The ambulance case description reads:

47 YO male PT who explains this AM whilst sitting on the computer, states having the onset of tight chest pain radiating down into the L) shoulder with an associated headache and hyperventilation. PT explains previous episode of similar being investigated, which was associated to the PT's anxiety. PT explains recent stressors, however not feeling anxious at the current time. PT explains nil dizziness, nil palpitations and nil N&V, however is a smoker and has a strong cardiac family history. AV called.

Chest pain described as sharp & tightness denies radiation & aggravated by movement; Left Shoulder pain described as sharp & tightness denies radiation & aggravated by movement; anxiety >> +++; headache ; hyperventilation >> +++; light headed >> POST MORPHINE; no facial droop; grips strong bilaterally; speech normal

No altered conscious state ; cough ; cyanosis ; Diaphoretic ; dizzy ; fever ; nausea ; palpitations ; photosensitivity ; rash ; short of breath ; unsteady gait ; vomiting

The ambulance notes record a blood pressure reading of 160/110 at 6:05am, pain as 5 (moderate), reducing to no pain at 6:35am.

100 Mr Boxell arrived at the Hospital at 6:40am and was seen in triage at 6:45am. He was discharged from the Hospital at about 3:40pm. During the period of his admission he was seen by Junior Registrar Dr Lindley, first year Resident Dr Harkin, and Senior Emergency Consultant Dr Jackson.

101 Dr Jackson's treatment was the main focus of the plaintiffs' case. It was alleged he did not consider a diagnosis of AD, and that he should have ordered a CTA to confirm or exclude the diagnosis.

102 Dr Lindley completed his qualifying degree in medicine in 2011, and has since practised as a doctor. He said he worked at the Hospital for just over a month before 6 October 2013, and had previously worked in an emergency department in a UK hospital for about four months. Dr Lindley worked night shift at the Hospital on 5/6 October 2013. He reviewed Mr Boxell at about 7:15am, and made notes at the end of his consultation at 7:40am.

103 Dr Lindley recorded, under 'system review', that Mr Boxell's risk factors for ischaemic heart disease were smoker, 30-40 pack years, normal cholesterol, no diabetes mellitus, hypertension for which he had not been taking medication for the last year, and a blood pressure reading of 180 systolic in the previous week at work. Dr Lindley explained that a pack year was calculated as 20 cigarettes per day for a year. He recorded a family history of Mr Boxell's mother having suffered an abdominal aortic aneurysm in her fifties, and an uncle a cerebral aneurysm.

104 Under 'presenting complaint', Dr Lindley recorded that Mr Boxell was a 47-year-old male who experienced sudden onset central chest pain, left shoulder pain and headache, frontal and occipital, at 5:30am while getting ready for work. Chest pain was described as 8 out of 10 after 30 seconds, sharp, no radiation, associated sweating, no nausea or vomiting, no shortness of breath, no palpitations, no change with GTN. The headache was described as worse on movement, and after GTN. Dr Lindley recorded that Mr Boxell was well prior to 6 October, had no fever or cough, and that the chest pain and headache were ongoing.

105 Dr Lindley recorded 'past medical history' as no exercise intolerance, no angina, anxiety and depression, an episode of chest pain with anxiety about a year previously for which there was no angiogram and no stress test, and hypertension. Against the history of anxiety and depression Dr Lindley recorded that Mr Boxell's wife had phoned to say he was very anxious.

106 Under 'family history', Dr Lindley recorded that there was no family history of ischaemic heart disease.

107 On physical examination Dr Lindley found normal pulse, temperature, respiratory rate and saturation of oxygen, and a blood pressure reading of 161/116. Cardiovascular examination was normal, with normal heart sounds and no murmurs, no heave, no peripheral oedema, and warm, dry skin. Dr Lindley said the ECG was not suggestive of acute ischaemia. On chest examination Mr Boxell was wheezy in the right mid zone, but had no chest tenderness or left shoulder tenderness. Abdominal examination and a thorough neurological examination were both normal. Dr Lindley noted Mr Boxell was 'acting very - chaotic'. He said he remembered Mr Boxell being very anxious.

108 Dr Lindley made the following 'provisional' diagnosis:

Chest pain with cardiac risk features.

Likely large component of this related to anxiety, but needs investigating for [ischaemic heart disease].

Headache? Initial, worse after GTN.

Bloods inc. troponin

CXR [chest x-ray]

Remove GTN patch as BP ↓ [blood pressure decreased] + headache bothering him much more than CP [chest pain] 8/10 vs 4/10.

Panadol/ibuprofen

12° [12-hour] troponin - admit to ESSU

Diazepam PRN

DW [discuss with] senior ? CT.

Dr Lindley said GTN can often relieve chest pain due to angina, and act as a helpful diagnostic informant, but can also leave the patient with a very unpleasant headache. He said his note comments on the fact that the headache preceded placement of the GTN patch, but became worse after the patch was placed.

109 Dr Lindley said he could recall the case because he became aware of Mr Boxell's death several days after seeing him. However, he had little memory of his review of Mr Boxell and was dependent on his notes and what he said his practice would have been.

110 Dr Lindley said chest pain and headache were both common presentations. He said from the tenor of his notes he wanted to exclude common serious causes for chest pain, and his focus was ischaemic heart disease risk factors. He said his thought process would have included that Mr Boxell was not taking medication for hypertension, and was a smoker, which led to his comment 'chest pain with cardiac risk features'. Dr Lindley said he would have thought about the cause of the chest pain in order to balance an argument for investigations, and he was looking at angina, heart attack, musculoskeletal chest pain, chest infection, and post-viral inflammation of the chest wall. He said other pathologies inside the chest included pulmonary embolism and AD. He felt anxiety was playing a large part to Mr Boxell's presentation. Dr Lindley said he wanted to discuss the case with a senior doctor because he wanted support in relation to his plan, particularly whether CT imaging was required, though he could not recall whether that related to the head or the chest. After his shift finished at 8:00am he went to find Dr Jackson, but he could not recall the details of their discussion.

111 Dr Lindley agreed his interpretation of Mr Boxell's history was that there was a sudden onset of chest pain. He said it was likely Mr Boxell used the word 'sharp' to describe the pain. By the time he saw Mr Boxell his physical symptoms had settled down, he did not appear to be severely unwell in the sense of cardiovascular instability, and his consistent feature was that of anxiety. He said Mr Boxell was oriented, not confused, had a normal heart rate, relatively normal blood pressure and was perfused peripherally, which indicated his cardiovascular system was working without signs of compromise.

Pt appeared very anxious and restless - asking "where I am now?", teary, stating the headache and pain on feet, arms and chest.

At 8:00am the GTN patch was removed. Mr Boxell's blood pressure was 127/79.

113 At 9:00am Mr Boxell was reviewed by Dr Jackson with Dr Harkin. A note of Dr Jackson's consultation was made by Dr Harkin.

114 Dr Harkin qualified in 2011, worked as an intern at Freemantle Hospital, then as a first year resident at the Hospital from February 2013. He commenced in the Hospital emergency department in early August 2013.

115 In 2013, Dr Jackson was an Emergency Consultant at the Hospital.

116 Dr Harkin recorded that Mr Boxell was a 47-year-old male who presented with chest pain, with a previous episode of chest pain caused by anxiety. Mr Boxell reported stress secondary to marriage breakdown over the last three to four years, but that the last couple of weeks had been okay. He had a recent medical check-up at which blood pressure 188 systolic was recorded, cholesterol was normal, he was not type 2 diabetic and his blood-sugar levels were good. Mr Boxell is noted to currently smoke 25 to 30 cigarettes per day, occasionally use marijuana, and have a moderate alcohol intake. He reported having three small Jim Beam and Cokes and one joint of marijuana the previous night. That morning he had two cups of coffee and a cigarette. At 5:30am he experienced central chest pain radiating to the left shoulder, was clammy, diaphoretic '+ + +' (Dr Harkin said when he used '+' in notes he was recording a scale where one '+' was mild and '++++' was extreme). He felt short of breath, initially had pleuritic pain (made worse by breathing), and had no nausea. He reported headache '+ + +' over one minute. Mr Boxell had been given GTN, aspirin and morphine by the ambulance officers, and a GTN patch and diazepam in emergency. He wrote, 'chest pain is now mild 1/10, can increase to 6-7/10, but comes and goes quickly'. Mr Boxell reported increase in headache, that pain lasted longer, was exacerbated by movement, and was currently 4/10.

117 Dr Harkin recorded that on examination there was no chest wall tenderness, no chest pain on movement, no shoulder pain on movement, but increased headache on movement. Mr Boxell was not short of breath, and the pain was not pleuritic. Mr Boxell was afebrile, his blood pressure was 149/105, he had a heart rate of 80, a respiratory rate of 12 and oxygen saturation was 97% in room air. Examination of the chest and abdomen were normal, and the calves were not swollen or tender.

118 Dr Harkin recorded Mr Boxell had a previous stress test two to three years previously which he could not complete because of increased blood pressure, but had no chest pain at the time. He reported increased alcohol use in the past, with a history of drinking at least a six pack of light beer every day. There was a previous episode of chest pain and headache in February 2012 for which no significant cause was found.

119 Dr Harkin said he recalled Mr Boxell's case because a couple of days after 6 October 2013 Dr Jackson told him Mr Boxell died of AD. However he relied heavily on his notes when giving evidence.

120 He said he would have recorded examination findings that were significant, either from what Dr Jackson told him or from what he saw. He said Dr Jackson would have listened to Mr Boxell's heart, but he did not make a note of heart sounds because nothing significant was found. He said there would have been other findings made by Dr Jackson as he examined Mr Boxell and in his own mind went through a differential diagnosis of what was significant and what was not. He would not have documented every single one of those unless Dr Jackson told him something was significant to document. He recalled having a discussion with Dr Jackson at the end of the consultation about the next step in Mr Boxell's care, though he could not recall the details of the discussion other than a plan was made for Mr Boxell to go to the short stay unit, he was to have repeat blood tests and an ECG to look for signs of heart ischaemia, and if those tests were normal, Mr Boxell was well and his pain had subsided, he would be discharged with a recommendation that his GP arrange for a stress test. Dr Harkin said he could not recall any discussion about whether Mr Boxell had another condition such as AD.

121 Dr Harkin agreed he wrote down the substance of what Mr Boxell had to say to Dr Jackson. He agreed this was important for the function he and Dr Jackson were performing, and for other doctors down the track, to sort out the cause of Mr Boxell's chest pain. He agreed it is particularly important to know what sort of chest pain a patient has.

122 Dr Harkin agreed the history of blood pressure 188 systolic was very high, and was relevant to assessing the risk of coronary artery disease and other cardiovascular problems. He said the history of pain 'over one minute' referred to the headache, not to the chest pain. He said he made no note of the particular characteristics of the pain, and if Dr Jackson had asked Mr Boxell what the pain felt like he would have recorded Mr Boxell's response. In relation to the pain scores he said it was difficult to know how bad the pain was because people report pain differently. He agreed he was present from the time Dr Jackson started taking a history from Mr Boxell to when the examination finished.

123 Dr Harkin said he emphasised the pain was not pleuritic because of the previous positive finding of pleuritic chest pain, in order to rule out that pathway or potential cause for the chest pain. He recorded that the calves were not swollen or tender on examination as evidence inconsistent with deep vein thrombosis and pulmonary embolus.

124 He agreed he made no note of neurological examination and said he could not recall Dr Jackson undertaking a neurological examination. He said if a full neurological examination had been undertaken he would have recorded it, but if Dr Jackson was just noting that Mr Boxell was moving his arms and legs freely with no obvious deficit he might not have recorded it. He said if Dr Jackson specifically said 'Let's test the blood pressure in both arms and note it down', he would have recorded that. He was asked:

If you are looking to compare the blood pressure in one arm with blood pressure in another arm - - -?---Yes.

• • • the high likelihood is that you will record the blood pressure obtained in the first arm; correct?---Sure. Yes. The first arm, you mean, not the blood pressure I have here but an additional blood pressure.

Correct?---Ah, yes. Yes.

125 Dr Harkin said no plan was recorded by him, but there was a plan throughout the notes, which was a typical plan for someone who presented with chest pain to have repeat troponins and ECG, and monitoring. He said he could remember a general conversation to the effect that Mr Boxell had risk factors for ischaemic heart disease and required further monitoring and repeat testing. He said this was a normal plan for a patient on the cardiac pathway who was being worked up for consideration of ischaemic heart disease or myocardial infarction.

126 Dr Harkin said the consultation he and Dr Jackson had with Mr Boxell may have taken 15 minutes to half an hour. If there had been an additional examination of Mr Boxell by Dr Jackson at which he was present, he would have made some additional notes.

Admit ESSU [Emergency Short Stay Unit]

Maureen Koo aware

Currently pain free

Plan Rpt Trop [Troponin] @ 1500 1330 (a 6/24 trop)

If normal + ECG unchanged + still pain free then discharge with O/P sestamibi

I feel likely anxiety or reflex rather than cardiac however but really quite unsure.

GP follow-up res ↓ smoking

Manage anxiety

128 A chest x-ray taken at 8:38am showed no abnormality. ECGs performed by Ambulance Victoria and at intervals during Mr Boxell's admission were all normal. Troponin tests at 7:24am and 1:45pm showed no evidence of myocardial damage.

129 According to the Hospital notes Mr Boxell remained pain free after 11:20am. His blood pressure was normal, or a little above normal, apart from a final reading of 176/116 at either 2:00pm or 2:30pm. Other recorded observations were within the normal range.

130 The discharge summary signed at 3:22pm records a principal diagnosis of chest pain. Mr Boxell was advised to follow up with his GP for management of hypertension. The recorded discharge plan was:

GP to follow up in next 2-3 days

• Please consider outpatient MIBI scan

• Please review hypertension and re-start anti-hypertensives

131 Mrs Boxell said when she picked her husband up from the Hospital his breathing was not normal, he was still sweaty and complaining of a very bad headache and chest pain that was not as bad as it had been in the morning. She said when they arrived home at about 5:15pm Mr Boxell got himself some water, took some Panadol and went to bed. She said he was restless that night. In the morning, he did not look well and was still complaining of headache. Mr Boxell took his children to school, then returned home to rest. He was found at home deceased later that day.

132 At autopsy the pathologist found an intimal tear approximately 6 cm above the aortic valve in the posterior wall of the ascending aorta. The cause of death was recorded:

(a) Haemopericardium

(b) Aortic dissection

Hypertension was recorded as a contributing factor. The pathologist concluded a prominent mixed inflammatory reaction suggested the dissection was at least one day old, and was a likely cause of the chest pain Mr Boxell experienced when he presented to the Hospital on 6 October.

133 Dr Jackson obtained his qualifying degree in medicine in 1987. He worked at the Hospital initially as an Emergency Registrar from 1998 to 2000, then as an Emergency Consultant from 2001. Dr Jackson is a fellow of the Royal Australian College of General Practitioners, and a member of the Hospital in the Home Society of Australia, but does not have a fellowship of the Australasian College of Emergency Medicine ('FACEM'). He said after he returned to the Hospital as an Emergency Registrar in 1998 he started doing some of the same training activities as other emergency registrars, but it was a long and difficult journey through the training program and, with his family commitments, he decided to return to general practice. However, he was then offered a position as an Emergency Consultant at the Hospital and, after doing some upskilling, he became a fully-fledged Emergency Consultant with the same responsibilities as the other consultants who had the FACEM. He remained in that role in 2013.

134 Dr Jackson said chest pain presentations were very common in emergency departments. He said with every single chest pain presentation you are always thinking 'could there be something serious going on here?'. He said there is a long list of possible causes of chest pain, and the ones that are front and centre are those that are potentially dangerous in the short term, which include acute coronary syndrome, pulmonary embolism, AD, pneumothorax, pneumonia, oesophageal perforation and pericardial tamponade. He said common causes which are not immediately dangerous include gastroesophageal reflux disease, musculoskeletal pain, abdominal causes like biliary colic or peptic ulcer, and anxiety. His process was to take a detailed history of the chest pain, and work through a systematic examination to rule certain things in or out, using investigations such as ECG, blood tests and chest x-rays, and more sophisticated modalities, such as CT scans, to make some things more likely and others less likely, and to exclude immediately dangerous conditions. He said you then work down a pathway to rule out the conditions which still need to be excluded.

135 Dr Jackson said he understood in 2013 that AD was a rare condition, more prevalent in older age and more common in men than women. He did not believe a family history of abdominal aortic aneurysm or cerebral aneurysm to be a risk factor. His understanding of the pain commonly associated with and characteristic of AD was very severe or excruciating pain of a ripping, tearing, shearing, shredding quality, which could be exclusively in the back between the shoulder blades. The onset of pain was typically extremely sudden, perhaps instantaneous or explosive, rather than building up over a period of time. Pain tended to be constant once it started, and intermittent or variable pain goes against the diagnosis without excluding it. He said whilst AD can result just in anterior chest pain, it would usually or more often be associated with pain radiating to the back between the shoulder blades, or just in the back.

136 Dr Jackson said his personal protocol in relation to AD was to consider the specific nature of the pain and whether the patient had a relevant genetic disorder or a history of hypertension. When he examined the patient he considered whether blood pressure was super low; the person was in shock requiring immediate attention and intervention; there were neurological features like speech disturbance, visual disturbance or facial weakness; there was evidence of limb weakness or coldness; there was a difference in blood pressure between the limbs; or there were reduced pulses in the limbs. He would then check the ECG and chest x-ray to look for abnormalities, such as a widened mediastinum, abnormal shape to the aorta, double calcium sign or left basal pleural effusion.

137 Dr Jackson said a history of pain radiating to the shoulder pushes you toward a diagnosis of myocardial ischaemia or acute coronary syndrome, rather than AD. The absence of signs on radiology is reassuring and makes AD unlikely. A difference in blood pressure or pulse between the limbs is found in a minority of cases but would strongly alert to the possibility of AD. Stroke-like neurological symptoms or limb weakness, but not headache, have been described as indicating AD. Shortness of breath was not a common symptom of AD. New heart murmurs were a clinical feature alerting to the likelihood of AD. Hypertension was a risk factor, but was incredibly common, occurring in 30 or 35% of middle-aged Australian men and was also a well-known risk factor for acute coronary syndrome.

138 Dr Jackson said in 2013 the criteria he considered before ordering a CTA were past history; the nature of the pain, in particular looking for ripping, tearing, shredding pain, pain to the back, of instantaneous or explosive onset; stroke-like neurological symptoms; pulse differentials and blood flow differentials into the limbs; aortic murmur; and abnormality on chest x-ray. He said he would weigh those things up and take into account whether there was a really good plausible alternative diagnosis because that might make him a little less likely to 'pull the trigger'. He said the downside of a CTA included the small incidence of allergic reaction to the contrast material, the incidence of acute injury from the dyes that are injected and the increased cancer risk from a high dose of radiation. He said he thought the figure was that about one in every thousand CT scans performed is going to result in cancer down the track. There was a cost to the public health system of CTAs, and a work flow burden on the Hospital because ordering non-evidence-based CT scans takes up a lot of time moving and monitoring patients, and interferes with other patients with more significant requirements for CT scans. He said there was also the problem of finding incidental abnormalities, such as a pulmonary nodule which in most people are innocent but would require ongoing surveillance with repeat CT scans, exposure to more radiation, and the patient experiencing anxiety and distress wondering whether they had cancer. A biopsy might even be required. He said the point was you had to think carefully before ordering a CT scan.

139 There was no evidence the notes of the February 2012 presentation were reviewed by Dr Jackson, Dr Lindley or Dr Harkin at the time of Mr Boxell's presentation on 6 October 2013.

140 Dr Jackson said it was his practice to look at an ambulance report because it contained useful information, and he was pretty sure he looked at the report at the time of Mr Boxell's attendance on 6 October 2013. He said pain described as 'tight' or 'sharp', and other presenting symptoms recorded in the ambulance report, including radiation of pain to the left shoulder, fitted with a diagnosis of myocardial ischaemia. Hyperventilation is non-specific, and can be experienced with any type of pain, but would make him think of pulmonary embolism, myocardial ischaemia, anxiety or panic. Headache was non-specific, but sudden onset of headache would make him entertain the possibility of subarachnoid haemorrhage or intracerebral haemorrhage, and could also fit with anxiety, tension or panic, but would not make him think of AD. The history of the previous episode would make him think anxiety was a possible cause of the earlier episode and the current episode. The history of smoking and strong cardiac family history were risk factors for myocardial ischaemia. The note 'anxiety + + +' indicated the ambulance officers thought Mr Boxell was highly anxious. He said the only things in the ambulance notes that would be associated with AD were chest pain and hypertension, though they were not indicators of dissection and did not make him think it was highly likely to be a cause of the presentation, but would make him want to exclude AD. The ambulance note that Mr Boxell was not diaphoretic or short of breath were both reassuring against AD.

141 Dr Jackson said he could not recall reading Dr Lindley's notes, but thinks he probably would have. He interpreted the word 'chaotic' used by Dr Lindley as meaning Mr Boxell was highly anxious and difficult to get a history from. Dr Jackson said he recalled Dr Lindley telling him Mr Boxell had just come in by ambulance with chest pain and headache and was highly anxious. He said Dr Lindley was concerned Mr Boxell had an acute coronary syndrome presentation but the ECG showed no sign of acute myocardial infarct, he had organised the usual blood tests and a chest x-ray, and said to Dr Jackson 'I think you should have a look at him'.

142 He said he could not really recall who Dr Harkin was, but was pretty sure they saw Mr Boxell together. Dr Jackson said the blood pressure of 149/105 recorded by Dr Harkin was elevated, but nothing dramatic. The examination findings 'calves NOT swollen/tender' was a test looking for deep vein thrombosis, which was a risk factor for pulmonary embolism.

143 Dr Jackson was asked about the history 'diaphoretic + + +' in Dr Harkin's note, and he said sweating could be caused by anxiety. He said he remembered Mr Boxell saying he had been going through a difficult time with his marriage, drinking heavily, feeling anxious, using a bit of marijuana, that he had chest pain about a year and a half before, which had been put down to anxiety, and that he thought this was an anxiety attack or panic attack. He agreed that there was no note made by Dr Harkin of Mr Boxell presenting with or giving a history of emotion or anxiety. It was put to him that if Mr Boxell was presenting with a very high level of anxiety that was memorable he would expect that to be noted, and he said not necessarily, that there were a lot of things that were not noted. He said he considered the possibility that Mr Boxell was feeling anxious about being very unwell, but Mr Boxell did not look like he was in a lot of pain.

144 Dr Jackson described as absurd the proposition that he did not ask Mr Boxell about the quality and onset of his pain, because he said it was an absolute key to a senior emergency physician's assessment of what could be going on. He said at 9:00am Mr Boxell described his chest pain as tight and sharp and going into his left shoulder, and that he was a bit sweaty and had a headache in the front and back of his head. Dr Jackson accepted he may have been swayed into thinking Mr Boxell used the word 'sharp' by having read the other notes, but said he 'absolutely remembered' Mr Boxell describing the pain as tight, which was a key part of a history taking which he remembered well. He said he asked how long it took for the pain to develop, and Mr Boxell's response was written by Dr Harkin as one minute. When it was put to him that Dr Harkin said that note pertained to the headache, he responded:

---So I can remember asking him about the onset of the pain, about the onset of the chest pain, and he described that pain as building up over a minute.

All right. You claim a recollection of him saying so; is that right?---I do.

It's not a situation where you've read this note and concluded that the reference to "over one minute" refers to the chest pain?---No, I remember him saying that the - I remember exactly him saying that the pain was tight and it was in the centre of his chest, ah, and that it went up to his shoulder, and I remember him describing the pain, on - on questioning from me, as building up over a minute.

145 Dr Jackson agreed he asked Mr Boxell to breathe deeply in and out, and Mr Boxell told him it did not hurt, which went against a diagnosis of pulmonary embolus and, to a degree, pneumothorax. He said Dr Harkin's note 'chest clear' referred to Mr Boxell's lungs. He said he checked heart sounds and listened for a murmur, but agreed there was no note by Dr Harkin, and said he did not say to Dr Harkin 'heart sounds are normal'. He was asked:

You remember that?---Um, pretty much. I don't think I would have said that to him.

146 Dr Jackson said that he could recall checking Mr Boxell's blood pressure in both arms, and checking pulses in the limbs. He said this involved looking at the preceding blood pressure reading, then removing the cuff and placing it on the other arm to take a reading. He said he did not record, or tell Dr Harkin to record, the blood pressure readings. He described the process:

---I mean, I clearly - clearly remember doing that and that is just - that really is stock standard practice for me. And it's not a - a big deal. It's a sort of pretty quick thing that is just sort of slipped in while you're doing all sorts of other things. It's not a massive sort of procedure or anything like that. Um, sometimes I might put it back on the other side, sometimes I might leave it where it is. Sometimes I might do, if I'm - sometimes I might do sort of - pressure for one side and pressure for the other side. Um, I - I definitely did that and I'm not 100 per cent certain that it was done on my first assessment of him but I think that is likely because, I mean, aortic dissection was still, ah, you know - that was - that was still something that was being thought about at the start, ah, as I went and saw him. So yeah, I think I would have done it but it is - it's possible I did it later but I - I believe that I did it in the first sort of, ah, more thorough sort of examination that I did of him.

Dr Jackson said he was '100 per cent certain' that he did the blood pressure test and was 'pretty damn confident' it was during the first assessment, but it was possible he did it later at 11:20am. He said the examination at 11:20am was sort of superficial, looking at Mr Boxell's neurology, making sure he was functioning well, checking his vital signs were still normal, checking skin colour, and looking to see whether Mr Boxell was restless and agitated.

147 Dr Jackson said he reviewed Mr Boxell's chest x-ray on 6 October and was very confident it was normal. He said there would be a chest x-ray abnormality in 60 to 90% of cases of AD, with a widened mediastinum, abnormal diameter and shape of the aorta, or less common features such as the trachea being pushed to one side by an expanding aorta, or blood causing pleural effusion. He said nothing on the x-ray gave rise to a suspicion of AD.

148 Dr Jackson said his own note at 11:20am was to make it clear to everyone involved what the plan was for Mr Boxell, and what he had arrived at as being the likely remaining differential diagnosis after excluding the other things he had considered. He said he used the word 'unsure' to indicate he was uncertain whether the cause of the presentation was anxiety on its own, or anxiety triggered by gastroesophageal reflux, musculoskeletal pain or a mild bronchitis with related pleurisy, or whether myocardial ischaemia was the cause. He said he was not intending to convey that he was unsure whether there might be a different serious cause for Mr Boxell's presentation.

149 Dr Jackson agreed there was no history or hard evidence of gastroesophageal reflux disease, but said it was a common condition which can cause spasms and produce quite intense central chest pain, and Mr Boxell was at risk because he was a heavy smoker, heavy drinker and pretty heavy coffee drinker. When Dr Jackson was challenged on the basis that the notes did not indicate Mr Boxell was a heavy drinker, he said:

---No, I think he told me that he was drinking. He told me he was drinking a lot. He told me that - that he was smoking a lot. And stress and anxiety, they're - they're other risk factors for gastroesophageal reflux disease.

He was challenged about his evidence that Mr Boxell was a heavy coffee drinker:

You refer to him as a heavy - or drinking a lot of coffee. He told you and Dr Harkin he'd had two coffees and a cigarette that morning?---Yep.

Is that the basis for you saying he was drinking a lot of coffee?---Maybe. I mean, I definitely remember him talking about coffee.

You remember him talking about coffee?---I do, because I was asking some specific questions, you know, trying to sort of clarify whether it was possible that it could be something innocent on the go. I mean, I was hoping that there would be an innocent explanation.

He said anxiety and reflux were reasonable things to think about having used 'standard medical algorithmic approaches' to exclude serious causes for the chest pain.

150 Dr Jackson said, in terms of dangerous causes, with a history of sudden onset, sharp, central chest pain reported as 8 out of 10 severity, he would be thinking acute myocardial infarction, pulmonary embolism, AD, pneumothorax, oesophageal perforation and perhaps pericardial tamponade or pericarditis. He agreed that by 11:20am pericardial tamponade, pneumothorax, pneumonia and pulmonary embolus had been confidently excluded. He said the possibility of a dangerous, but not immediately lethal, acute coronary syndrome remained, and for that reason Mr Boxell was sent down the coronary syndrome pathway. He said serial troponins and repeat ECGs rule out myocardial infarct and very unstable angina, but there remains the possibility the presentation is caused by myocardial ischaemia. The sestamibi scan recommended on discharge was intended to increase the level of certainty that there was no coronary artery disease. He said even after normal troponins and ECGs, something like 0.5% of people who were pain free on discharge still had some sort of major adverse cardiac event within 30 days. However, discharging patients in those circumstances was normal practice and considered acceptable.

151 Dr Jackson said he had confidently excluded AD, and that the key things he relied on were the history and the absence of differential blood pressures, heart murmur, neurological features, high blood pressure and abnormalities on the chest x-ray. He agreed no cause had been positively established for Mr Boxell's pain. He did not agree that the history of pain and risk factors meant reasonable practice required that he go further and arrange a CTA to exclude AD. He did not agree the downside of performing a CTA was immaterial and was far outweighed by the potential to diagnose an otherwise lethal condition. He did not agree that he could not confidently exclude AD without a CTA. He said there was no indication to do a CTA.

152 Dr Jackson said the care provided at the Hospital was thorough, well considered and consistent with standard emergency medical practice. Mr Boxell becoming pain free supported the decision to rule out AD. His blood pressure readings were reasonably normal. An elevated first reading coming into emergency was commonly found and might be associated with anxiety, and a final elevated reading was not uncommon, and might relate to being fearful about going home. He said overall the observation chart readings were reasonably reassuring.

153 Dr Jackson said Mr Boxell's presentation was moderately complex, with some notable elements that would have stuck in his mind even had Mr Boxell not died, in particular his level of anxiety, unhappiness and emotion. After he was told Mr Boxell had died, he initially thought of a myocardial infarction, or possibly a subarachnoid haemorrhage or intracerebral bleed, but he also wondered whether they could have missed a pulmonary embolus or AD. He said none of these possible causes was expected, and Mr Boxell's death was a big surprise. Immediately after he became aware of the post-mortem he realised the cause of death was AD. He agreed it was likely the dissection would have been found had a CTA been performed when Mr Boxell was at the Hospital, and that he would probably have survived with surgery. He agreed this cast a heavy burden on him. He was asked:

And then the horror of learning that - as - learning what happened to Mr Boxell has led you to believe that you in fact considered it?---That's just not true. Every single - as I've said - every single significant chest pain presentation that comes into the emergency department - so anything that's sort of moderately severe - stuff that comes in by ambulance; stuff that's triage category 2 - you always think about aortic dissection, along with the other, ah, life-threatening causes of chest pain.

154 Dr Jackson agreed there was nothing specific to AD in the notes. He was asked:

You did not exclude the possibility of aortic dissection as the cause for this presentation on the 6th, did you?---I - as I've said before - I went through the - my stock standard - I went through my usual process of assessing any significant chest pain, and that included all of the history features, the analysis of risk factors, all of the examination findings that we did. There - I agree that there isn't a reference in the notes to equal pulses and blood pressures. But I didn't write those notes; they were written by other doctors. And I didn't tell them what to write or control what they wrote. I assessed him myself, and I didn't list - I didn't write anything down about how I went about excluding pulmonary embolus. I didn't write about how I went about excluding or ruling out (indistinct) I didn't write down the way I went about ruling out aortic dissection. And the reason I didn't write that stuff down, is because it wasn't going to help the patient in any way, shape or form. It was just - it's just - it's kind of a medical, legal, sort of thing, to write that down. It doesn't actually help the patient. What's going to help the patient is going through the process in your head, and with history and exam, which I definitely did, and then writing down what your remaining differential diagnosis is, and conveying to the doctors that are going to be - that are going to continue to be involved with his care, what it is you think is going on and what you believe needs to occur to safely rule out or deal with those remaining diagnoses. Just because I haven't written anything about aortic dissection, it doesn't mean that I didn't think about aortic dissection. And just like I didn't write anything about pulmonary embolus and I didn't write anything about pneumothorax and I didn't write - I just wrote down, in the end, what I thought were leftover - what I thought was likely to be going on, so that the other doctors would understand what was happening, and would know what remained - what still needed to be done with him.

155 At the request of the Coroner, Dr Jackson made a statement in January 2015 in relation to Mr Boxell's presentation to and treatment at the Hospital on 6 October 2013. Dr Jackson said he had access to the medical records when he wrote his statement, understood it was an important document and took the time needed to prepare it and to make sure that it was accurate. Dr Jackson's statement reads:

1. Mr Boxell presented to Frankston Hospital's Emergency Department by ambulance at 0700 on October 6th 2013 with chest pain and headache.
2. He gave a history of an abrupt onset of tight central chest pain radiating into his right shoulder and frontal headache at 0530 while working at his desk. The attending ambulance crew documented anxiety and mild tachypnoea with a heartrate of 80, a blood pressure of 160/110, no fever, a clear chest and no pallor or sweating. Myocardial ischaemia was suspected and he was administered sublingual and topical nitrate, oral aspirin plus 10mg of intravenous morphine then transported to Frankston ED by AV with paramedics in attendance.

Dr Jackson accepted reference to the right shoulder was incorrect. He said the history of developing pain at 5:30am while working at his desk was something remembered by him, not from the notes. The statement continued:

1. On arrival in the emergency department at 0700, Mr Boxell was more comfortable but still had some chest pain and headache. The initial attending physician's assessment revealed a very emotional man who was crying and who believed he was suffering from anxiety. His BP was 130/80, heartrate 70, RR 20, SaO2 96% on room air and temperature was normal. His GCS was 15 without focal neurological signs in limbs or cranial nerves. His chest was clear, his abdomen non-tender and his peripheries warm and dry.

Dr Jackson denied he was trying to downplay the dramatic nature of Mr Boxell's physical complaints, and overstate the emotional aspect at the presentation. Asked whether the blood pressure 130/80 was a misstatement of the recording by Dr Lindley, Dr Jackson said:

---Look, it feels to me like this is, is something of a compilation of ambulance and Lindley and myself, basically trying to give the Coroner sort of a reasonable understanding of the sort of overall nature of the presentation so that he sort of understands.

He added Mr Boxell's blood pressure was 130/80 very soon after his arrival at the Hospital and that was a very important thing for the Coroner to know. The statement continues:

1. Mr Boxell gave a history of an identical episode in February 2012, culminating in a normal myocardial perfusion study and of recently increasing marital stress with increasing anxiety symptoms and use of cigarettes and alcohol. He admitted to poor compliance with his anti-hypertensive medication.

Dr Jackson said this paragraph reflected a history he obtained from Mr Boxell, and was not from Dr Lindley's note. He agreed he wrote down the wrong test, that Mr Boxell had a stress echocardiograph, not a myocardial profusion study. The statement continues:

1. Our initial emergency department workup was unremarkable. CXR [chest x-ray] and ECG were both completely normal, as was his initial troponin level. FBE and U.E. were also normal. His GTN patch was removed in case contributing to headache and he was given oral diazepam for his emotional distress.
2. At 1120 I assessed him myself to ensure no major conditions including SAH, AMI, oesophageal perforation, arrhythmia, thoracic aortic dissection or PE had been missed. He was completely free of headache or chest pain and his vital signs were normal. I noted his low risk for venous thromboembolism, absence of epigastric tenderness, absence of any neurological signs or heart murmurs and equivalence of limb BP.

Dr Jackson agreed there was no reference in the statement to the review by he and Dr Harkin at 9:00am, which he said was his major involvement with Mr Boxell. He was asked:

Let me go back a step just to Dr Harkin. You told His Honour yesterday that you had an actual memory of that consultation - this is the 9 o'clock consultation - with Dr Harkin as you sat in the witness box there yesterday; is that true? That's what you said?---Sir, I've - I've - I've always maintained throughout this whole trial, um, that while I'm absolutely certain of my examining, um, Mr Boxell and my taking a history from Mr Boxell, I am not one hundred per cent certain about whether my thorough examination was 11.20 or was, um, at 9 o'clock. I believe - I've always thought - I - I believe that it was at 9 o'clock and that it was more superficial at 11.20, but - but that could be wrong.

Asked whether the assessment detailed in paragraph 11 of his statement occurred at 11:20am, Dr Jackson said:

---I still feel like I did that at 9 rather than 11.20, um, and I feel like I'm sort of making a reference there to, um, the last time I saw him. Ah, I'd seen him earlier. I'm seeing again, and I've again gone through the sort of mental - I've completed the mental process of, um - of reassuring myself that, ah - that these serious causes have been excluded. But my strongest memories are of talking to him and of examining him and of the mental process that I went through, and I've always thought that, um - although I don't remember Harkin well, I've always thought that it was 9 o'clock that I saw him at the start, ah, and that I saw him again at 11.20, but it's such a long time ago. But I have distinct memories of him and of the examination.

Dr Jackson agreed the reference to 'free of headache or chest pain' could not be from the attendance at 9:00am. He said he felt he performed the blood pressure test at 9:00am, it may have been 11:20am, but 'it was definitely done'. The statement continues:

1. In my judgement at that time myocardial ischaemia was the most likely serious diagnosis and needed exclusion. I considered the serious causes of PE [pulmonary embolism], SAH [subarachnoid haemorrhage] and Aortic Dissection, but my view was that there was only a very small chance of these and that further investigation with CT Brain, CT Pulmonary Angiogram or CT Aortogram was not justified. My other differentials included GORD [gastro-oesophageal reflux disease]/oesophageal spasm and anxiety. There was at this stage no evidence on the history, examination and investigations which suggested that the likely diagnosis was an aortic dissection.
2. With respect to Mr Boxell's headache the history was inconsistent. It should be understood that he was very upset about his marriage problems and frequently crying. It seemed to me that the headache had begun prior to the administration of GTN but I considered it possible that it was a side-effect of GTN. It is common for patients with IHD [ischemic heart disease] to have headache from the GTN. While there is a clear association between thoracic aortic dissection and abnormal neurological signs it is extremely rare for there to be headache. Again I performed a neurological examination which did not identify any neurological impairment.
3. At 1200 I arranged his admission to the Emergency Short Stay Unit for observation, continuous cardiac ECG monitoring and a repeat ECG and Troponin level at about 1500. It was my plan that if he remained pain free and the repeat Troponin and ECG were normal, that he be discharged with arrangements for an outpatient myocardial perfusion study and follow-up in our outpatient "chest pain clinic". Mr Boxell was advised to return to the ED if he experienced any further pain.
4. Please note that my clinical assessment of a patient with chest pain always considers the important possibilities of IHD, PE, aortic dissection, pneumothorax and oesophageal perforation. My history taking, examination and investigations are aimed at excluding these important conditions.
5. By way of additional comment on this case, Mr Boxell's presentation was an atypical presentation of Thoracic Aortic Dissection. In a man in his mid 40's without pain in the back, with considerable headache but no neurological signs, no brief syncope, no heart murmurs, normal BP in both arms with no difference, a CXR that was normal with no widening of the mediastinum and an unremarkable ECG it seemed highly unlikely to be thoracic aortic dissection.
6. It was my view that the most probable cause to be excluded was myocardial ischaemia.
7. The majority of patients with dissection that I have treated have clinical signs which help assist make the diagnosis in particular:

1. History of central chest pain radiating through to the back. 2. More commonly age over 60

1. Often there is a history of collapse then chest pain and maybe hypo or hypertension.

1. BP difference between the upper limbs. 2. Often a heart murmur 3. Sometimes a widened mediastinum on CXR.
2. None of the above was noted in this patient.

156 In re-examination Dr Jackson was shown a letter from the Coroners Court to the Clinical Risk Management Office at the Hospital and an attached statement request detailing issues to be explored in a statement he was asked to provide. Dr Jackson said he could not recall having seen the letter, and added:

---Maybe - maybe I did. I'm not sure, but it's - it's interesting, though, because it sort of - 'cause it sort of - 'cause when - when I was getting asked about, um, that report that I wrote for the coroner, it - it felt like I was sort of, um - it felt to me like I was providing a summary rather than sort of a, I don't know, timeline of exactly what and when. It felt like - it did - it felt to me, as I was reading it, ah, like a summary rather than sort of a timeline. It felt to me like it was a sort of - a report to help the coroner understand, um, the important sort of elements of his presentation, ah, the main thrust of what was going on with him and, um - and a sort of a - and a description to him of - of, um, sort of process we went through. And, really specifically, it was answering the question of, um - of aortic dissection and other serious diagnoses. So - - -

Yes?---So maybe I did see that as I was just writing the, um - 'cause that's what it feels like. Maybe I did see that and I was following those kind of questions, or maybe the legal people asked me to, um - asked me those specific questions verbally or put - put it in an email and - and I followed - followed that approach. That - that - that would make sense. That would make a lot of - that would make sense.

Is the situation you're not able to say whether you saw it or not or - you don't have to. It's simply a case of me ascertaining whether that was - - - ?---So it's - - -

• • • a guide or was not?---So it's - it looks - it looks familiar. It does look familiar now that I see it. I - I - I - my - my hunch is it - that medical legal - - -

Did the Hospital consider AD as a possible diagnosis?

157 The defendant submitted first that AD is an obvious diagnosis to be considered as part of dealing with chest pain patients in emergency departments. A/Prof Raftos said AD is part of a standard list used by every emergency department in Australia of diagnoses which are likely to cause a patient to come to harm in the short term. Prof Mitra gave similar evidence. Second, Dr Jackson said it was his usual practice to consider AD. Third, Dr Jackson said he did consider AD in Mr Boxell's case, and looked for specific signs on physical examination, being differential blood pressure and absent pulses. Fourth, having been made aware of his death, Dr Jackson had good reason to remember Mr Boxell's case. Fifth, subject to some minor discrepancies, his statement to the Coroner accurately reflected Dr Jackson's evidence. The defendant submitted that a very dim view would need to be taken of him as a doctor and as a witness to conclude that Dr Jackson overlooked something so basic as the possibility of AD. However, Dr Jackson should impress as a methodical, systematic and knowledgeable emergency physician, and should be believed.

158 The plaintiffs submitted that, for the following reasons, Dr Jackson's evidence that he considered and excluded AD as a diagnosis should not be accepted.

159 First, Dr Jackson did not have a good recollection of Mr Boxell's attendance at the Hospital, and was quite dependent on the Hospital notes. No attempt was made to have Dr Jackson give evidence from memory before taking him through the notes. He frequently gave evidence in vague terms, by saying what would have happened, or that he was 'pretty sure', or 'that sounds right'. He was particularly vague about his assessment of Mr Boxell at 9:00am. Second, in contrast, Dr Jackson's claim to definitely recall matters, such as performing the bilateral blood pressure test, and emotion being the overwhelming feature of Mr Boxell's presentation, was implausible. Dr Jackson's claim that he asked Mr Boxell about the quality and onset of chest pain, and was told it was 'tight and sharp', or simply 'tight', and came on over a minute, is inconsistent with the Hospital notes, and not credible. Nor were his claims that Mr Boxell said he was a heavy drinker of alcohol and coffee. It was far more likely the Hospital notes accurately record the history obtained from Mr Boxell, and the clinical examinations performed.

160 Third, there were significant discrepancies in his statement to the Coroner that further undermined Dr Jackson's evidence. The emotion of Mr Boxell's presentation was again overstated. There was no reference in the statement to the 9:00am attendance, and the 11:20am attendance was overstated. There was significant inconsistency between the note made by Dr Jackson at 11:20am, and the Coroner's statement in which he said the most serious cause for Mr Boxell's presentation which needed to be excluded was myocardial ischaemia. There is no evidence to support Dr Jackson's statement to the Coroner that he gave active consideration to further investigations, including a CTA. The mantra which Dr Jackson repeated often in court, that the absence of a history of ripping, tearing, shredding, shearing pain of immediate or explosive onset was a significant reason to exclude AD, was completely absent from his statement to the Coroner.

161 I conclude, consistent with the evidence of Dr Harkin, Dr Jackson and the Hospital notes, that Dr Jackson's longer and more detailed attendance with and examination of Mr Boxell took place with Dr Harkin at 9:00am. It is likely the 11:20am attendance involved brief observation, consideration of what Dr Jackson believed were the remaining differential diagnoses, confirmation of the decision to transfer Mr Boxell to the emergency short stay unit and for him to remain on the cardiac pathway to discharge, and recommendations for GP follow up.

162 In evidence in chief, Dr Jackson was taken step by step through the records of the February 2012 hospital attendance, the subsequent GP attendance and stress echocardiograph, and all the notes of the 2013 attendance. Particularly in cross-examination, his answers to questions were frequently discursive, unresponsive or expressed in terms of what would have happened, or what his usual practice was, rather than what did happen. I conclude that Dr Jackson did not have a good memory of the events of 6 October 2013 and that there was an element of reconstruction to his evidence. His evidence may reflect his limited memory and an unconscious reaction to the trauma he experienced in relation to Mr Boxell's death, reinforced by the Coroner's inquiry and this litigation. He appeared to be doing his best when giving evidence. However, given my impression of him as a witness, and for reasons which follow, I do not accept his evidence when it differs from the Hospital notes.

163 Dr Jackson's evidence is inconsistent with the Hospital notes in a number of respects. First, he said Mr Boxell was frequently crying during the consultation with Dr Lindley, and presented to him with a very high level of anxiety in the consultation which was emotionally charged, complained of feeling anxious, and attributed his problems that day to a panic or anxiety attack. The only reference in the notes to Mr Boxell crying is the nursing note of 7:45am, which records 'teary'. Dr Harkin's notes record a history of stress secondary to marriage breakdown over the last three to four years, but the last couple of weeks have been okay. Dr Harkin did not make a note that Mr Boxell appeared anxious, complained he was anxious at the time of the consultation at 9:00am, said he believed his pain was caused by an anxiety attack, or that his marital stress had recently increased and was the cause of his symptoms. There is no doubt Mr Boxell was anxious when he presented to the Hospital and was seen by Dr Lindley. However, Dr Harkin impressed as a careful observer and note taker who would have recorded at least some details had Mr Boxell presented at the 9:00am assessment as Dr Jackson said.

164 Second, Dr Jackson maintained that Mr Boxell told him he was a heavy smoker, heavy drinker of alcohol and pretty heavy coffee drinker, which he said were risk factors for reflux. Dr Jackson used this evidence to justify reflux as a differential diagnosis. The only reference to coffee in Dr Harkin's note is that Mr Boxell had two cups of coffee that morning. Dr Harkin recorded current alcohol intake as moderate, with a past history of increased alcohol use. In the note he made at 11:20am, Dr Jackson recommended that Mr Boxell decrease smoking, but made no recommendation in relation to alcohol or coffee intake. The lack of any recommendation is inconsistent with Mr Boxell having given a history of heavy alcohol and coffee intake, and with such a history being the basis for reflux being listed as a differential diagnosis.

165 Third, Dr Jackson's evidence that he asked Mr Boxell to describe the quality of his pain, and was told it was 'tight and sharp', or 'tight', is inconsistent with Dr Harkin's evidence and his note.

166 Fourth, Dr Jackson's evidence that he asked Mr Boxell about the onset of his chest pain, and was told that it built up over a minute, is inconsistent with the notes made and the evidence given by Dr Harkin and Dr Lindley. In his statement to the Coroner, Dr Jackson said Mr Boxell gave a history of abrupt onset of central chest pain.

167 Fifth, there is nothing in Dr Harkin's note to indicate Dr Jackson checked Mr Boxell's blood pressure in both arms, and pulses in the limbs. Dr Harkin agreed that had the bilateral blood pressure test been performed, it was highly likely that he would have recorded it.

168 Sixth, Dr Jackson said he performed a neurological examination. Dr Harkin did not make a note of a neurological examination, and said if a full neurological examination had been undertaken he would have recorded it.

169 It is likely that had things occurred as Dr Jackson said, this would have been reflected in Dr Harkin's notes.

170 My conclusions are reinforced by the errors and inconsistencies in Dr Jackson's statement to the Coroner. Errors include reference to pain in the right shoulder and to a myocardial perfusion study. The only blood pressure reading in the statement is close to the lowest recorded during Mr Boxell's time at the Hospital, and is significantly lower than the reading taken by Dr Lindley, who was the initial treating physician. There is no mention in the statement of the 9:00am review. References to recently increasing marital stress and anxiety, alcohol and Mr Boxell frequently crying over-emphasises the presentation of anxiety. The history that Mr Boxell was 'working at his desk' when pain commenced is inaccurate. It is inaccurate to say that the episode in February 2012 was identical, and the notes do not suggest Mr Boxell said it was. In the statement, Dr Jackson said he turned his mind to further investigations, being CT brain, CT pulmonary angiogram and CTA, and concluded they were not justified, yet there is nothing in the notes to indicate this was done. Dr Harkin said only that he could remember a general conversation with Dr Jackson to the effect that Mr Boxell had risk factors for ischaemic heart disease and required further monitoring and repeat testing.

171 The Hospital notes are detailed and of good quality. Apart from Dr Jackson's evidence, there is nothing to indicate that the notes are, in important respects, an incomplete record of Mr Boxell's presentation and treatment.

172 I accept the evidence of A/Prof Raftos and Prof Mitra that, in the case of chest pain presentations at emergency departments, AD is included on a standard list of diagnoses to be considered because they are likely to cause a patient harm in the short term. Balanced against this is evidence that often AD is not given the attention it requires as a potential diagnosis. A number of the experts said that AD is overrepresented in hospital deaths, and requires emergency physicians to have a high index of suspicion for the diagnosis. Similar themes run through the literature relied on by the experts. Dr Eddey's involvement with the Coroner in 2013 followed a number of patient deaths from undiagnosed AD.

173 When he presented at the Hospital, statistically the most probable serious cause of Mr Boxell's chest pain was acute coronary syndrome. Mr Boxell did not present with symptoms or signs which Dr Jackson understood to be characteristic of AD. It is unlikely that, prior to or at the 9:00am consultation, the possibility Mr Boxell was suffering AD was considered seriously or treated with a high index of suspicion. Following the consultation, Mr Boxell remained on the cardiac pathway until discharge. Dr Jackson said that at 11:20am he was unsure whether Mr Boxell's presentation was caused by anxiety alone, anxiety triggered by a benign cause like reflux, or myocardial ischaemia. It is unlikely there was any consideration of AD after the 9:00am consultation.

174 I conclude the history obtained from Mr Boxell, observations, clinical examinations performed and investigations undertaken, were as recorded in the Hospital clinical notes.

175 Dr Eddey emphasised Mr Boxell's history of relatively acute onset of severe chest pain radiating to the left shoulder, with associated shortness of breath and profuse sweating. Mr Boxell was a smoker, had untreated and quite high blood pressure and severe pain, onset at rest, that could be associated with AD. He said profuse sweating was an important sign and indicated that a patient was potentially ill. On the basis of Mr Boxell's history, AD should have been considered amongst the differential diagnoses, and ought to have been excluded by performing a CTA. He would have expected when a patient presented with severe chest pain that clinicians would look for the cause and make a diagnosis. The most serious causes of severe chest pain are acute coronary syndrome followed by a pulmonary embolus and AD, which is rare. Nevertheless emergency doctors are taught that you shouldn't miss AD. In 2013 emergency physicians should have undertaken a process to diagnose the cause of pain and at least exclude serious causes.

176 Dr Eddey agreed it was absolutely legitimate to investigate Mr Boxell for acute coronary syndrome, with ECGs and troponin levels. He said Mr Boxell was placed on a cardiac pathway, which only addressed coronary causes and risks. While it was appropriate to put Mr Boxell on that pathway, if you have excluded acute coronary syndrome, which is the most common cause of severe chest pain, you should still look for the other causes of the pain.

177 He had not seen anyone present with severe chest pain as a result of an anxiety disorder. He said people can be anxious and sweaty because they feel terrible.

178 Dr Eddey said the fact that Mr Boxell had severe chest pain which went away did not mean he didn't have a serious problem. Dissection is a dynamic process. While it is ongoing there will be pain. When it stops, the pain generally goes away. In relation to the history of left shoulder pain he said radiating pain anywhere is a feature of aortic pain, and almost 30% of patients will have pain that radiates somewhere. The absence of heart murmurs did not rule out AD. A chest x-ray is frequently normal with AD and cannot be used to exclude the diagnosis.

179 Dr Eddey was asked about von Kodolitsch. He said for patients on that study with aortic pain alone the probability of dissection was 30%.

180 He said it was not reasonable to send someone home with a history of severe undiagnosed chest pain. There was no ongoing clinical curiosity as to why Mr Boxell had such terrible pain to start with. Before he was discharged, nobody thought what other serious causes there could be for his chest pain. He said it was a question of diagnosing a lethal disorder. The problem with cardiac pathways is that people assume the presentation is dealt with by going through the pathway, and turn off their minds or clinical curiosity to alternative causes. Reasonable practice in an emergency department required a physician to consider other causes of the severe pain. If the pathway doesn't answer the diagnostic question, reasonable professional practice requires that you ask the question and answer it, especially in someone who is ill.

181 Dr Eddey said a CTA is an extraordinarily common test done multiple times every day in every hospital. He said it is not done lightly, but is done to diagnose a serious condition. A CTA would not be done with a bit of chest pain that went away with Panadol. It should be evidence based, and used to exclude a serious concern. He said there was a small risk of severe allergic reaction, the test does involve administration of radio contrast medium, and there was a minimal risk of affecting kidney function.

182 He said Prof Harper and Dr Habersberger would see a more select group of patients and would not be dealing every day with undifferentiated chest pain.

183 A/Prof Raftos said in an emergency department where the presenting complaint is central chest pain, the differential diagnoses that should be considered are those which are likely to cause the patient to come to harm in the short term. A standard list, which every emergency department in Australia should use, is coronary artery disease, pulmonary embolism, AD, pneumonia, and pneumothorax. Whenever a patient presents with chest pain, those conditions need to be considered and excluded before the patient is discharged. Australian institutions that practise standard emergency medicine should miss very few ADs. It is necessary to be cautious and thorough in every assessment, because the role as an emergency physician is to prevent people from coming to harm and be assiduous in gathering information and interpreting it. Rather than focusing on a particular diagnosis, it is necessary to step back and force yourself to think what else might be the cause of the presentation. He said the problem with AD is it doesn't present in a typical way, which means you have to go hunting for it. While a complaint of severe central chest pain radiating to the left shoulder was suggestive of a cardiac problem, AD is known to masquerade as cardiac disease. In Mr Boxell's case there was no consideration of causes of chest pain other than of a cardiac nature.

184 He disagreed that Dr Jackson's treatment of Mr Boxell conformed with accepted professional practice. He said that amounted to a suggestion that it was acceptable to misdiagnose Mr Boxell's AD, which he did not accept. He said working through the list of serious causes of chest pain, Mr Boxell's chest x-ray excluded pneumonia and pneumothorax, the normal ECG and normal troponin almost excluded coronary artery disease, which left pulmonary embolism and AD, and there were aspects of history which pointed toward AD.

185 A/Prof Raftos said CTAs involve a small degree of risk, take time and cost money, so clearly cannot be done as a routine part of investigation of any patient with chest pain. The downside is a small chance of an allergic reaction to the contrast, a small, small chance you might get cancer when you're 80, and on the other side there is a chance, if the CTA is not performed, that you might die tomorrow from dissection. He said in Mr Boxell's case the three good reasons to perform a CTA were the abnormalities shown on chest x-ray, his mother's history of aneurysm, and untreated hypertension. A/Prof Raftos said there was a clear obligation to exclude AD, and the only way that could effectively be done was to perform CTA. He said if the doctor was unsure about the diagnosis, potentially life-threatening conditions needed to be excluded.

186 Dr Vinen was told of Mr Boxell's death after he prepared his report. He said the explanation for the presentation could have been an acute myocardial infarction, but the second most likely possibility, given the history of sudden onset of chest pain and risk factors, was AD.

187 Dr Vinen said Mr Boxell's presentation was sufficiently atypical for a cardiovascular cause to indicate the possibility of something else, most likely AD or possibly thromboembolic disease. He said cardiovascular pain is usually described as tight and heavy, and rarely as sharp. While a history of left arm pain was usual for a cardiovascular cause, left shoulder pain was not. Patients with acute myocardial infarction can have headache, but usually don't.

188 Dr Vinen said the timing of onset of chest pain can help narrow the differential diagnosis, and pain that starts suddenly and is severe at onset is associated with acute AD.

189 Dr Vinen said with chest pain presentations you must assume the worst, that the patient has a potentially life-threatening condition. He agreed that there was a high index of suspicion of a cardiac problem, but said you must consider other possibilities and do a parallel workup process, because you couldn't say with any degree of confidence that this was going to be an acute myocardial infarction. Once acute coronary syndrome was excluded by the normal ECG and negative troponin results, it was necessary to go on to do further investigations to find out what the cause of Mr Boxell's symptoms, signs and history was. If the possibility of AD has not been excluded, you cannot just send the patient home, but have to do a CTA. The Hospital had gone down the wrong track and essentially ignored other possible causes for Mr Boxell's presentation. AD was not considered, therefore not investigated, and therefore not excluded, which doesn't fit with the approach required to diagnose patients presenting to emergency with undifferentiated symptoms. The clinician must work through the most serious and life-threatening conditions first, and sequentially confirm or exclude them until a diagnosis is reached. The end result may be that there was nothing wrong, apart from the fact that Mr Boxell had anxiety, but that conclusion can only be reached after the diagnostic workup has been done.

190 Dr Vinen said AD is one of a number of medical conditions which you can't eliminate without doing the appropriate investigation. That's why for every CTA done in emergency on the basis the patient might have AD, you only find 5 or 10 or 15% do. Similarly, the vast majority of CT scans done after head injuries are normal.

191 Dr Vinen said risk factors should not be looked at individually, but should be considered collectively where they are much more powerful. He said the entirety of the patient's context needs to be looked at before deciding what needs to be done about investigating and managing it.

192 Dr Vinen used an AD risk assessment tool, which he said reflected clinical practice well before 2013. He said Mr Boxell scored in two categories, first for the family history of aortic disease, and second for the abrupt onset of severe chest pain, and therefore should have had a CTA.

193 Mr Rosalion said it was not reasonable to discharge Mr Boxell because there was no diagnosis of the cause of severe pain requiring IV morphine at a high dose, in a patient who was clammy, diaphoretic and unwell. He said he would have looked at other possibilities for Mr Boxell's presentation, namely pulmonary embolism or AD.

194 Mr Rosalion said he was taught as a medical student that AD can mimic all sorts of conditions, so what might be thought classical symptoms probably occur in only about a third of patients. The common theme was a history of severe pain, which is typically very sudden. Pain occurs as the dissection is occurring and so needn't be unremitting. Back pain is associated with dissection involving the descending aorta, not the ascending aorta. Absent pulse or a differential blood pressure in the arms are usually very late findings, so if you're waiting for that you will lose a lot of patients.

195 Mr Rosalion said the risks with CTA are minimal. There is a slight risk of anaphylaxis with intravenous injection, which is usually very easily treated, and there is a small radiation dose, and a very low risk of kidney damage, particularly with normal renal function.

196 Mr Rosalion said he did not agree that there was no clinical basis to order a CTA. All you need is a significant suspicion, because the risk of not doing the test is you will miss a heart condition like AD or pulmonary embolism, and the patient is likely to come back the next day dead, which is what happened with Mr Boxell.

197 Mr Rosalion said people who come in with AD will be very anxious because they feel they're about to die, which is probably correct.

198 Prof Cameron said the diagnostic challenge that AD presents for emergency physicians should be understood in context, which includes a busy emergency department seeing 10 to 15 cases of chest pain presentations per day, 1 in 10 of which will have ischaemic chest pain, and the majority of which will have nothing to do with the heart and may have a musculoskeletal or gastrointestinal cause. He said red flags for AD include tearing pain that comes on suddenly and radiates through to the back, syncopal attack, differential pulses, a heart murmur, widened mediastinum on x-ray or an ECG which shows ischaemia or pericardial effusion. Where there are no red flags the risk of the presentation being AD goes down very, very low, which is where we get to in Mr Boxell's case. If there is a red flag, then you go back and look at the presentation more broadly. If there are no red flags, then you proceed through a standard protocol.

199 Prof Cameron said many of the small number of cases of AD which present at emergency will have clear-cut reasons for further investigation and admission. Those that do not, which may be as few as 1 to 2 per year from 50,000 emergency presentations, fall into the category of undifferentiated chest pain. For an individual emergency doctor this may represent only a couple of cases during a career. This is against a backdrop of many cases per week with undifferentiated chest pain of benign origin. The main risk mitigation for a clinician is to think of the diagnosis and look for obvious signs that are not typical of other causes, and for risk factors such as family history. A significant percentage of all dissections that reach hospital alive are misdiagnosed initially.

200 He said it is not possible to diagnose everyone in emergency on the first presentation, so what emergency doctors try to do is make it safe enough for the patient to be discharged home. The lower you make the risk of being discharged, the higher the cost, for the individual and the hospital. The decision to discharge Mr Boxell on 6 October 2013 would be standard practice across virtually every short-stay unit in the country.

201 Most patients who present to emergency will have slightly elevated blood pressure because of anxiety caused by being there, and moderately elevated blood pressure is very common. Hypertension is a noted risk factor for AD, but it is also a noted risk factor for ischaemia and many other illnesses, and a moderately elevated blood pressure in itself would not be a red flag.

202 Mr Boxell presented with pain that was atypical for AD and there were very important and well documented anxiety, depression, alcohol and social issues. The pain was sufficient to warrant entry onto a standard emergency pathway for exclusion of ischaemic heart disease, and was more typical of ischaemia than any other differential diagnosis. He said the x-ray excluded pneumonia and pneumothorax, there was no indication of pulmonary embolism, and there were no features consistent with AD. An acute ischaemic event was excluded by serial troponin and ECGs. There was no indication for subjecting Mr Boxell to a CTA, as opposed to the other hundreds of patients with possible ischaemic chest pain. He said the Australia-wide practice would be not to order a CTA. Things seemed to have settled during Mr Boxell's stay in emergency, which is not saying he did not have anything wrong, but is saying there was less urgency.

203 Prof Cameron said a patient has to have symptoms consistent with AD to justify ordering a CTA, because it is a test with side effects which you cannot do every time someone has a twinge of chest pain. In an emergency department there is an opportunity cost to every major test that is done, because it pushes other requests for tests down the list. There are multiple demands and you have to risk balance when you order certain tests, and question whether the patient has a clinical syndrome which mandates the test. By itself, a family history of a mother who had an abdominal aneurysm does not meet that threshold.

204 In cross-examination Prof Cameron agreed that he based his opinion, at least in part, on Dr Jackson's statement to the Coroner. He said the description of pain that he got was a little bit vague. He had the impression Mr Boxell's pain was not sudden onset. He understood it was central chest pain, did not have an impression about the quality of the pain. I note this evidence is inconsistent given the presenting history recorded by Dr Lindley, and the reference in Dr Jackson's statement to the abrupt onset chest pain.

205 He agreed Mr Boxell's death is one of those deaths which is overrepresented in terms of emergency presentations which result in preventable deaths. The first thing to do is think about AD, because that makes it more likely you will diagnose it. He assumed Dr Jackson thought about it in this case.

206 He agreed that by definition the red flags he referred to are obvious signs, some of which are distinctive of AD. He agreed the problem is that AD may not present with obvious signs, and if you relied on red flags such as radiation of pain to the back, syncope, interruption to vascular supply distal to the dissection, differential blood pressures, heart murmur, then a significant percentage of dissections of the ascending aorta will be missed. He was asked:

And what I put to you before was if you're looking for those signs you will never detect a dissection such as Mr Boxell's, will you?---That's correct.

That cannot be reasonable medical practice. Do you agree with that?---No.

Prof Cameron said a CTA would only be ordered if there were red flags present. He agreed that meant that for many dissections localised to the ascending aorta a CTA would never be ordered, and said:

Every doctor struggles with this in emergency medicine and if we go the other way and as a result of this court case people say anyone with chest pain has to have an aortogram the craziness of that will - I mean, we'll kill more people than we save.

207 Prof Cameron said if he had a patient with history of tearing pain that came on suddenly, a radiologist would do a CTA. If the patient history was sudden onset sharp stabbing pain, he would inquire about the pain in minute detail. He agreed that on a history of sudden onset sharp central chest pain, severity 8 out of 10, AD was definitely a possibility to consider. He was asked:

So what I'm suggesting is that that is a history which is getting very close indeed to your red flag-type history, isn't it?---Um, what I'm - I - I think - yeah, I agree. I mean, I think the fact that he said "sudden", um - we'd have to explore that a little bit. Um, ah, but this - what I'm - the character that he's describing, um, is all over the shop, ah, when you actually look at, you know, this versus this versus this. Um, we're not getting a very consistent story. It's not like every time they say, "Sharp, tearing chest pain" or something like that. It seems to be varying over time.

208 Prof Cameron said the suddenness of onset needed to be explored, because if it was sudden, as in seconds, that is one thing, but if it is sudden over minutes that is another. A history of sudden onset pain goes toward a diagnosis of AD, as opposed to a cardiac diagnosis. If he considered the onset of pain was abrupt, he would definitely order a CTA. If there was some 'wishy-washiness' about it, then he said you need to start using your clinical judgment. He said:

These guys clearly didn't get that picture of, you know, a sudden onset like that.

Again I note the inconsistency to the history recorded by Dr Lindley, and to Dr Jackson's statement which records abrupt onset of pain.

209 He agreed pain commencing from rest was more consistent with AD than cardiac pain. Profuse sweating meant Mr Boxell was sick, but did not differentiate between causes. He said:

Now, at the end of the day, it's a subjective - which is the reason we're here, I guess - is a subjective decision and you have to bump that risk up to high enough to order the scan.

He said what is required is not a single history or single observation, but taking history and making observations over the period of the patient's stay. Mr Boxell was relatively young, his history was not straightforward, his blood pressure came down during the admission, his pain was not ongoing, which, combined, meant Mr Boxell did not look like he was at high risk. He said patients with similar histories present at emergency departments across Victoria in significant numbers every day, and if they all have a CTA they will be exposed to radiation and the risk of cancer, and incidental findings will emerge which require investigation and follow up, and may cause complications.

210 Prof Cameron agreed Mr Boxell had risk factors for AD, including the familial history, hypertension, smoking history and being male, but said those risk factors did not differentiate him from many patients that were seen every day, and the same factors gave him an increased risk of coronary artery disease and many other conditions. He said generally with a dissection there will be constant severe pain which may even escalate if it keeps tearing, but there are exceptions and you can get a little bit of a tear and it settles down, which happened in this case. He agreed aortic pain is caused by the process of dissection, and that when the process stops, pain will generally settle down.

211 He was taken through IRAD, and it was put to him that a history of sharp pain was a more significant red flag than tearing or ripping pain, and he said:

What it's saying is that a lot of people described their pain as sharp, but it didn't say how many people who didn't have aortic dissection described it as sharp. So I can tell you now that half the people I see in the emergency department, when you ask them to describe their pain, they will say "sharp", and, as I said to you before, that can mean anything, so you've then got to explore it further.

212 Prof Cameron said the evaluation pathway in Strayer was not used in Australian emergency departments, and was a theoretical approach which would lead to hundreds more unnecessary CTAs.

213 Prof Mitra said the Hospital's investigation, treatment and management of Mr Boxell was in accordance with widely accepted Australian peer professional practice. Mr Boxell was promptly assessed and treated, documentation of clinical findings was to a high standard, he was admitted for observation and regularly assessed, all reasonable investigations were undertaken and he was discharged with advice for reasonable follow-up.

214 He said chest pain is a serious complaint which is considered life threatening. After a history is taken and the patient is examined, risk stratification is performed to make sure that immediate life-threatening causes can be excluded. The patient is then placed on a pathway for further investigation. The most common life-threatening cause is ischemic heart disease, followed by less common causes such as pulmonary embolism, AD, aortic aneurysm and lesions of the lung, such as pneumothorax. The role of the emergency medicine clinician is to exclude the immediate life-threatening causes as far as practicable, then move on to the causes that could be life threatening in the short term and then to causes that are unlikely to be life threatening.

215 Prof Mitra said AD presentation can be very varied, and there are no definitive diagnostic criteria on history or examination. The most common description of pain is sudden onset severe central chest pain that radiates through to the back and is of a tearing quality, usually persistent, with the patient looking unwell. If the dissection extends higher up in the aorta, it can cause blood pressure differences in both arms. If it extends to the blood vessels going to the heart it can present as ECG abnormalities. Other distinguishing features include heart failure, atrial fibrillation, neurological deficits, transient loss of consciousness, abnormality on chest x-ray, and a history of previous vascular disease, connective tissue disorder or diabetes.

216 Prof Mitra said Mr Boxell's risk factors for AD were being male, sudden onset of chest pain which was sharp in nature, uncontrolled hypertension and smoking history. These risk factors overlap with the presentation of chest pain due to coronary artery disease, and there were other risk factors for AD which were not reported to be present. He said sudden onset of chest pain is a common complaint that is very poorly described by patients, and sharp pain is hard to characterise, and may mean different things to different people. The history of fluctuating pain is very unusual even with ischaemic chest pain, and does not point toward AD being the cause. Once the pain disappeared, it pointed toward a less serious condition rather than an immediately life-threatening condition. Mr Boxell's blood pressure readings were at a level commonly observed in emergency departments, and had no clinical significance. Prof Mitra said based on that medical record, even knowing the outcome, he could not convince himself that he would have definitely done a CTA. He said whether or not to order a CTA was a matter of clinical judgment after engaging in the process of carefully teasing out history. Whenever AD is suspected as a reasonable differential diagnosis CTA is the investigation of choice. It is an investigation which is properly used to rule out the disorder, and most that he requests are normal.

217 Prof Mitra agreed it is necessary to have a high clinical index of suspicion for AD. A normal x-ray does not allow the clinician to exclude AD, and clinical examination is unreliable, refocusing attention on the need to tease out every slightly atypical bit of history. A proportion of patients with AD which is confined to the ascending aorta will not present with differentiating features, and there will be a greater risk of missing the diagnosis. There is not a lot the emergency medicine community can do to diagnose every case of AD. Thankfully this will be a very small number of patients. You need to weigh performing a CTA against submitting a large number of patients to that investigation. Untreated, proximal AD will invariably result in the death of the patient.

218 Prof Mitra said IRAD dealt with patients that were already diagnosed with AD, whereas emergency departments are dealing with all the patients who present with chest pain. Some symptoms and history which IRAD identified as common in AD patients, such as hypertension, and sharp pain of sudden onset, occur with other disorders, so they do not help you discriminate.

219 Prof Mitra said the cardiac pathway remains very safe, even if patients with atypical signs end up on it, because they get a decent period of observation, assessment by a doctor and nurses over a period, they are on a cardiac monitor, and it is expected if some adverse signs show up that will change the clinician's mind. However, once a patient has gone down the pathway, unless there is something that changes, the alternate diagnosis does not come about during that presentation, and if the troponin, x-ray and ECG are normal, the patient goes home to have outpatient tests. His strong view was that the sestamibi scan should be done in the emergency department before discharge, but that is not the practice in Australian public hospitals. He agreed that if you get to the end of the pathway without a diagnosis, it would be a good point to rethink, before discharge, whether the patient has a high risk of death from some other condition. Given Mr Boxell had some risk factors for AD, it may have been a time to think about another differential diagnosis, but those three features are commonly observed in a lot of other patients on cardiac pathway, so the question is how do you pick a single patient or a small group of patients out of a wide range of other patients.

220 Prof Mitra said there are no protocols or objective clinical criteria that dictate when a CTA has to be done. It is a matter of assessing the patient and making a clinical judgment, weighing up the benefits against the risks. While it is not completely clear, there appears to be an association between a large dose of radiation and blood-borne cancers later in life, there is the immediate risk of damage to the kidneys, allergic reactions and discomfort. Current epidemiological studies suggest the risk of causing cancer is not zero, but is small. There are also the far less important issues of time and cost.

221 Prof Mitra agreed it was unsatisfactory that there was no diagnosis for Mr Boxell, but that it is a very common occurrence in emergency departments around Australia when patients present with chest pain. The risk of discharge of patients such as Mr Boxell is not zero, there is a possibility of death from both ischaemic causes and other causes. Prof Mitra said, in his opinion, when there was a serious presenting complaint such as chest pain, emergency departments owe the patient a duty of care to provide a definitive diagnosis during the presentation before discharge. He said they are slowly trying to change practice and to impress on health services that complete assessment and achieving a diagnosis for the patient's presentation would be a better practice.

222 Prof Kelly, like Dr Vinen, was not aware of Mr Boxell's death when she wrote her first report.

223 Prof Kelly said there were a large number of causes of chest pain, so what the doctor is trying to do is collect information as to the characteristics of the pain from the history given by the patient, and from clinical examination, to test hypotheses. At the start you have different likelihoods, for instance, heart-related problems are around 10% of presentations, whereas pulmonary embolism is around 2 to 4%. Those probabilities are recalibrated based on the information that is collected. She said the description of chest pain is really important, including how it started, whether onset was sudden or gradual, in response to activity or not, what its characteristics are, where it is located, if it goes anywhere else, if anything makes it better or worse, and whether there are any associated features. Clinical assessment and diagnosis is a continuing process. The time in emergency allows for symptoms to progress or change, and the opportunity for review by a fresh clinician, to re-evaluate the story and double-check it, having the advantage of test results.

224 She said chest pain with AD can be quite diverse, but the most common recognised pattern is one of tearing or ripping pain that reaches its maximal intensity very, very quickly, almost instantaneously, and is usually continuous rather than intermittent.

225 Prof Kelly said her initial differential diagnosis in Mr Boxell's case would most likely have included acute coronary syndrome, gastrointestinal causes, musculoskeletal causes and anxiety. She would have discounted AD as a potential diagnosis based on the atypical description of pain (tight, squeezing, worse on movement and fluctuating rather than tearing or ripping and unremitting) and the absence of neurological symptoms or signs, or a new cardiac murmur. She said tight and squeezing is a quite common description of heart pain, that people talk about bricks sitting on their chest or tight bands around their chest. Pain that is worse on movement is usually musculoskeletal. The aorta is an internal organ and there is no plausible logical connection between physical moving of the upper torso and AD. Left shoulder pain is a very common complaint with heart-related pain. Hypertension has a recognised association with AD, but a stronger association with heart disease. At the end of his stay at the Hospital Mr Boxell was well and pain free, no abnormality was shown by any of the investigations, and she would most likely have discharged him with a diagnosis of unspecified chest pain and headache. She would have regarded the likelihood of the diagnosis of AD in Mr Boxell's case as so, so low that subjecting him to a CTA would have carried more risk than the risk of missing the diagnosis.

226 In cross-examination Prof Kelly said she had checked all four of the Australian emergency medicine textbooks and two of the international ones, and tearing and ripping was definitely the most common description of pain for AD. She agreed the learning in IRAD is that features such as sharp pain can be consistent with AD, but said that doesn't tell us about the prevalence of those features in other patients with chest pain who do not have AD. IRAD does state that AD symptoms mimic much more common disorders, for example, myocardial infarction. She agreed it was a message of IRAD that it is a mistake to look for tearing or ripping pain because you will miss cases of AD, but said the article needs further exploration and validation. She agreed IRAD was the best study of its type.

227 Prof Kelly agreed the greatest factor in her decision-making is the presentation of pain. She agreed there was a difference between tight pain as noted in the ambulance record, and Dr Lindley's note of sharp pain, and said she would have clarified that with the patient to get a clearer picture. She agreed that nowhere in the ambulance and Hospital notes was the quality of pain referred to as squeezing. She wasn't sure where she got a history of squeezing pain from. Prof Kelly was unable to say why she assumed a history that chest pain was worse on movement. She agreed the description of pain recorded by Dr Lindley was potentially consistent with AD, but radiation of pain to the left shoulder is not a typical feature. She agreed IRAD referred to radiating pain as a common presenting symptom. She agreed sweating is associated with a number of serious diagnoses. She agreed AD was a potential diagnosis that had to be considered.

228 Prof Kelly said when she wrote her report she guessed something probably quite bad had happened to Mr Boxell, otherwise she would not have been asked for her opinion. She thought the most likely thing to have happened was that Mr Boxell had died, and the cause of his death was AD. She said:

---I considered that of the potentially lethal conditions, the others had been - had been reliably ruled out, which left that as the - the most likely one given it was sort of the last man standing, 'cause the - the troponin analysis ruled out a, ah, heart attack. The - the other features and low PERC score and the chest X-ray ruled out the pulmonary embolism. There was no pneumonia. There was no pneumothorax. We're sort of only really left with one on that list that you generated, so I don't think it was unreasonable of me to think that that was the most likely of that list.

229 Prof Kelly said a lot of patients get assessed in emergency departments for chest pain, probably in the order of 30,000 in Victoria every year. She said the vast majority go home, the incidence of anything like this happening are tiny, and the proposition they should all be tested further raises a whole lot of risks around complications for those patients, but also issues for the system and inconvenience for the patient. She said there will always be cases where the diagnosis of AD is missed, and it's about how our antennae work, and how we balance the risks of advanced imaging and the number of patients involved - which are thousands - against the small risk of an adverse outcome. She agreed when Mr Boxell was discharged there was no diagnosis for his pain, and said that was the case in about 70% of chest pain patients who come to emergency.

230 Prof Kelly said the risk assessment tool on which Dr Vinen relied has not been shown to be valid or useful in the broad population of patients who attend emergency departments with undifferentiated chest pain. It was derived from a registry of patients with known AD, and had not been prospectively validated in an emergency chest pain population. The specificity of the tool in this population is likely to be so low as to subject a very large number of patients to CTA.

231 Prof Kelly said the risks for every one thousand CTAs was perhaps one induced cancer, three or four patients who suffer a significant allergic reaction, a couple who suffer tissue damage pain, and about 2% of patients will get some form of kidney impairment, which for many is transient, but for a very small proportion is permanent.

232 Relying on von Kodolitsch, Prof Harper said from a diagnostic point of view the three main clinical features of AD are:

(a) an abrupt onset of a severe ripping-type chest pain radiating through to the back;

(b) a widened mediastinum or widened aortic contour on the chest x-ray; and

(c) differential pulse strength and blood pressures in the arms.

Only one in 25 cases of AD had none of these three features. Typically pain is unremitting and does not fade, or come and go. The absence of the three features in Mr Boxell's case made the probability of AD extremely low, and a CTA was not justified. He said an atypical presentation of a rare disease is very difficult to diagnose. Given the rarity of AD, and the fact that Mr Boxell had no features pointing to that diagnosis, an emergency department would have to do many hundreds, perhaps thousands, of CTAs to pick up one dissection. It is just not feasible to do a CTA with every patient who presents with chest pain.

233 He said acute coronary syndrome is a far more common disease. Usually patients present with an oppressive feeling in the front of the chest, often with radiation to the left shoulder or arm, associated with diaphoresis and sometimes a feeling of impending doom. The symptoms Mr Boxell presented with were more suggestive of that diagnosis.

234 Hypertension is a risk factor for AD, but is very common in the community, and is a very strong risk factor for acute coronary syndromes.

235 Patients who come into emergency can be anxious and have higher blood pressure which then settles down, but with a dissection that does not usually happen unless blood pressure drops to a catastrophic level.

236 It was very common with chest pain presentations that if the pain settles down, troponins are negative, observations are normal, then the patient is discharged. It was reasonable to discharge Mr Boxell to be further assessed by his GP or in an outpatient appointment. The Hospital's management of Mr Boxell was in accordance with widely accepted Australian peer professional practice in October 2013.

237 In cross-examination Prof Harper agreed Dr Lindley's note indicated sudden onset pain. However he said radiation of pain to the left shoulder is not typical, sharp is not a word usually used to describe AD pain, and is more typical for pleuritic pain. He did not agree pain caused by AD starts and stops when the dissection starts and stops. Prof Harper was then taken to the descriptions of pain in von Kodolitsch, Strayer and IRAD, and he agreed on the basis of those articles that Mr Boxell's presenting symptoms and signs fitted quite well with AD, but added most commonly those symptoms would be due to an acute coronary syndrome.

238 He said a CTA is very safe, but not completely safe; there are allergic reactions which can be life threatening; and they can cause impairment of renal function. In Mr Boxell's case it was reasonable not to perform a CTA.

239 Dr Habersberger said there was nothing in Mr Boxell's case to indicate the possibility of AD. Usually patients will have pain radiating to the back, and there were no physical findings such as unequal pulses. In Mr Boxell's case there was no indication to do a CTA. Sudden onset pain is no guide at all, because if you have an acute event of whatever cause, pain usually occurs suddenly. A history of sharp pain does not mean much either. Pain going into the back would have set off alarm bells. Ongoing pain is of some concern because obviously there is some pathological process going on. In Mr Boxell's case the pain seemed to settle down, which would tend to favour the possibility of it being a cardiac rather than aortic in origin. If no evidence of an acute coronary syndrome was found, you might come back to the possibility of AD. However, it is very easy to work backwards once you know the diagnosis and say a CTA should have been performed. In real life doctors follow a protocol, assess risk and follow the most likely diagnosis.

240 He said Mr Boxell's risk factors for AD were untreated hypertension, heavy cigarette smoking and a family history of abdominal aortic aneurysm. In view of the family history, and the fact that this was the second episode of similar chest pain, it would have been reasonable to consider AD. Perhaps in retrospect further investigation with a CTA would have been appropriate, but it is very easy to say this when the result is clearly known.

241 The Hospital's investigation, treatment and management of Mr Boxell was in accordance with widely accepted Australian peer professional practice. Mr Boxell's pain settled and his function was normal, and the observations at the Hospital were quite consistent with a patient who is ready to go home.

242 Dr Habersberger agreed it is likely Mr Boxell's dissection started at around 5:30am on 6 October. The process of dissection is what causes the pain. The dissection went on for some time then stopped.

243 He said anxiety can magnify pain, but does not produce it. There has to be a pathological cause for the pain.

244 When the second troponin was performed, there was no evidence of acute coronary syndrome. The standard practice throughout Australia would then be to do further investigations looking for myocardial ischaemia. He agreed by the time of the second troponin the only potentially dangerous diagnosis left was AD, but said that was the case for hundreds if not thousands of cases in emergency departments around Australia every day. It was put to Dr Habersberger that in Mr Boxell's case there were features which were quite suggestive of AD, and he said that was an interpretation taken at this point in time when you know the diagnosis.

245 Each emergency physician who appeared as an expert is well-qualified.

246 Dr Eddey's evidence was clear and well-reasoned. The note he prepared in 2013 was very useful evidence of the state of knowledge and clinical practice at the time. The defendant submitted Dr Eddey's thinking was dominated by the need to record differential diagnoses, which lead him to wrongly conclude that the failure to do so in this case meant AD was not considered by the Hospital. I have concluded Dr Eddey was correct to assume AD was not seriously considered by the Hospital in Mr Boxell's case (see [161] to [174] above). Central to Dr Eddey's thinking was the need to diagnose the cause for a presentation of severe chest pain, the lack of ongoing clinical curiosity in Mr Boxell's case, and the need to exclude AD before he was discharged.

247 The plaintiffs attempted at trial to make a case on the basis of A/Prof Raftos' evidence that the chest x-rays taken on 19 February 2012 and 6 October 2013 both showed changes consistent with AD. However radiologist, Dr Kam, said the x-ray films showed no abnormality of the aorta or mediastinum. In closing, counsel for the plaintiffs accepted Dr Kam's evidence should prevail. A/Prof Raftos' willingness to argue so strongly that the x-rays demonstrated relevant abnormalities, together with some unconvincing answers he gave as to the diagnostic relevance of the history of headache, robbed his evidence of some weight.

248 Both A/Prof Raftos and Dr Vinen recommended the d-Dimer blood test as a useful investigation when considering the risk of AD. Other witnesses disparaged the usefulness of the test for this purpose. Given that d-Dimer is inconclusive, and there can be false negative results, the logic of using the test is difficult to follow. Further, Dr Vinen was the only witness to use an AD risk assessment tool, similar to the evaluation pathway proposed in Strayer. I accept the evidence of Prof Cameron and Prof Kelly that the assessment tool is a theoretical approach which has not been validated in emergency practice. These matters affected the weight of evidence given by A/Prof Raftos and Dr Vinen.

249 Three matters affect the weight of Prof Cameron's evidence. First, his opinion was based on a pain history that was incomplete, because he did not have an impression about the quality of Mr Boxell's pain, and inaccurate, because he had the impression the pain was not sudden onset. Given that the presenting history is so critical to assessment of the risk of AD, this was a significant matter. Prof Cameron justified the decision of the Hospital not to perform a CTA on the basis they did not get a picture of sudden onset of pain. When the history recorded by Dr Lindley was put to him, he agreed it was getting very close to a red flag for AD. He said he based his opinion in part on Dr Jackson's statement to the Coroner, yet did not take account of the history of abrupt onset of pain. Second, Prof Cameron relied too heavily on a red flag being present to raise suspicion of AD and justify CTA. I accept evidence given by a number of witnesses, consistent with conclusions expressed in a number of the tendered articles, to the effect that AD is characterised by variable presentations, will often mimic another condition or present without a red flag or discriminating symptom or sign which points strongly to the diagnosis, and that the emergency physician must have a high index of suspicion for the disorder. Third, Prof Cameron's evidence that a CTA could not be performed whenever there was a 'twinge of chest pain' did not grapple with the case actually put by the plaintiffs or the evidence of Dr Eddey, which focused on the presenting history of severe, sudden onset sharp central chest pain for which there was no diagnosis in a patient with risk factors for AD.

250 The following matters affect my consideration of Prof Mitra's evidence. Prof Mitra said Mr Boxell had three features which were consistent with AD, being the sudden onset of pain, ongoing chest pain without another cause, and untreated hypertension. He said, however, that the following observations meant AD would have been very low on the list of differential diagnoses, and CTA was not reasonably indicated. First, Mr Boxell did not have other frequently reported symptoms of AD, including back pain, abdominal pain, migration of pain, focal neurological deficits, transient loss of consciousness, pulse deficits or abnormalities in haemoglobin and creatine. In support, Prof Mitra cited Klomp, and said the whole premise of the study was that those are the possible symptoms or signs of AD. Contrary to Prof Mitra's evidence, the purpose of Klomp was to discover why the diagnosis of AD was often initially missed. The authors compared the symptoms and signs in patients where the diagnosis was made to those where it was initially missed, and concluded AD was not initially recognised in 31% of patients, and that this was more likely to occur in the absence of a report of back pain. Among patients not initially diagnosed, 61% reported chest pain, and 68% pain of sudden onset. The study conclusions are inconsistent with the use to which it was put by Prof Mitra.

251 Second, Prof Mitra said ECG is normal in less than 10% of reported cases of AD, and multiple ECGs taken throughout Mr Boxell's admission were normal. In support of this observation, Prof Mitra cited Meszaros, a longitudinal population study which found 84 AD patients. The onset of pain was analysed in 72 patients, 64% of whom reported the site of initial pain as anterior chest, and 9.7% as back. The study found ECG was normal in only 5 of 66 patients. The authors stated ECG may be helpful in differentiating from acute myocardial infarction, however results require careful evaluation, and abnormalities may have a number of causes. In Strayer the authors state:

The electrocardiogram in aortic dissection may demonstrate changes associated with longstanding hypertension, as well as nonspecific ST-T wave changes; however the importance of ECG testing is to evaluate the differential diagnosis.[57]

IRAD states ECG was frequently not helpful, and there were no abnormalities in 31% of AD patients. In Dunn the authors note the ECG most commonly shows non-specific abnormalities, and is normal in 30% of cases. Rosen's notes that ECG is often useful in excluding myocardial infraction. In the tendered articles and text extracts I could not find any reference or recommendation to use normal ECG results, alone or in combination with other symptoms, signs and investigation results, to exclude AD.

252 Third, Prof Mitra said the 2012 presentation with similar symptoms, for which no serious cause was found, further discounted AD as a differential diagnosis. The parties relied on Mr Boxell's 2012 Hospital attendance in different ways. The plaintiffs submitted the lack of a diagnosis for similar but less severe symptoms experienced in 2012 should have resulted in increased clinical curiosity at the time of Mr Boxell's attendance on 6 October 2013, and in combination with other factors meant it was necessary that the Hospital exclude potentially lethal causes, including AD, before Mr Boxell was discharged. The defendant submitted, in line with Prof Mitra's evidence, that Mr Boxell's recovery from the 2012 episode was reassuring, making it more likely that the cause of the 2013 episode was benign, and, taken together with other factors, meant it was reasonable to discharge Mr Boxell on 6 October 2013. There is little to recommend either approach. There was no diagnosis for the earlier presentation. All the Hospital knew on 6 October 2013 was that there had been a previous episode of chest pain with headache and anxiety for which no significant cause was found. It would have been speculating to conclude that the cause of the 2012 presentation was benign, the two episodes had the same cause, and therefore it was more likely the cause of the 2013 presentation was also benign. Equally, suspicion that a related pathological process was the cause of both presentations was speculative. Even knowing Mr Boxell's outcome, the experts struggled to explain how the 2012 presentation was associated to the pathological process which resulted in AD in 2013. Knowledge of the earlier presentation added little, if anything, to reasonable consideration of the 6 October 2013 presentation.

253 I do not accept Prof Mitra's evidence that AD pain is most commonly described as radiating to the back and being of a tearing quality. I accept the findings of IRAD, which are summarised in [80(e)] above.

254 Prof Mitra said that, while it was common practice in 2013 for patients presenting with chest pain to be discharged from emergency without a diagnosis, his own view was that this was unsatisfactory. He said complete assessment and diagnosis during presentation would be a better practice, and emergency departments owe patients a duty to make a definitive diagnosis before discharge.

255 Three matters affected the weight of Prof Kelly's evidence. First, having emphasized the importance of presenting history to the diagnosis of chest pain, she discounted a diagnosis of AD on the basis of a history that pain was tight, squeezing, worse on movement and fluctuating. There was no history of squeezing pain. It was the headache, not the chest pain, which was worse on movement. Pain is described as 'sharp and tightness' in the ambulance notes, and sharp, 8 out of 10 after 30 seconds in Dr Lindley's notes. Prof Kelly was unable to explain the errors she made. Second, she said pain associated with AD was classically severe, unremitting, tearing or ripping and worst at onset. She said a description of sharp pain was not typical of AD, and radiation of pain to the left shoulder was not consistent with the disorder. She said that description was repeated in all other relevant textbooks current in 2013, and that IRAD was new at the time, and had not filtered through to emergency medicine. She described IRAD as a 'one off article' which required 'exploration and validation'. IRAD was published in 2000, and the findings contained in it were referred to with apparent approval in a number of the articles and textbooks tendered in the proceeding, including two of the six textbook extracts provided by Dr Kelly. Both were published in 2010, and are marked as being in the Western Hospital Library. Dunn is a South Australian text which refers to IRAD and sets out in point form most of its findings. Many of the authors to the text hold positions in the Australasian College of Emergency Medicine. Rosen's, which is an American text, states:

Pain is by far the most common presenting complaint, affecting more than 90% of patients. ... The pain is usually excruciating, occurs abruptly, is most severe at onset, and is typically described as "sharp" more often than "tearing" or "ripping".

The location of the pain may help localize the dissection. Anterior chest pain is associated with the ascending aorta, neck and jaw pain with the aortic arch, pain in the interscapular area with the descending thoracic aorta, and pain in the lumbar area or abdomen with involvement below the diaphragm.[58]

256 Third, Prof Kelly, like Prof Cameron, misstated the case put by the plaintiffs by likening it to a proposition that the 30,000 chest pain patients who present to emergency departments in Victoria every year should all have CTAs performed.

257 Dr Kam is a well-qualified radiologist. He reviewed the 2012 and 2013 chest x-rays which he said were normal and showed no sign consistent with AD. He did not agree with the reported finding of mild unfolding on the 2012 x-ray, and said if such a finding were made it would be of no clinical significance. I have no hesitation accepting Dr Kam's evidence.

Objection to the evidence of Professor Harper and Dr Habersberger

258 The plaintiffs objected, on the grounds of relevance, to evidence of cardiologists Prof Harper and Dr Habersberger relating to the reasonableness of the Hospital's conduct, and peer professional opinion. The plaintiffs submitted the case brought by them concerned the management of Mr Boxell in an emergency department by emergency physicians. The cardiologists did not have training, qualifications or experience in emergency medicine, and therefore were not qualified to give evidence as to what is reasonably required of an emergency physician, or what is widely accepted by respected emergency physicians as competent professional practice.

259 The defendant submitted the evidence establishes that the standards of cardiologists mirror the standards of emergency medicine, emergency physicians engage with cardiologists in relation to chest pain patients with suspected cardiac and aortic conditions, and cardiologists attend emergency departments to consult and advise, and were aware of the standard of care which ought to be exhibited by emergency physicians in relation to chest pain patients.

260 Prof Harper said as a cardiologist he deals with diseases affecting the aorta, aortic valve and aortic root. He is an interventional cardiologist, which he explained involved performing catheter-based procedures inside the heart or the surrounds of the heart, and included replacement of aortic valves, but did not extend beyond the valve into the aorta. He was frequently called to the emergency department to assess patients with chest pain when there was a question whether the patient could have AD. This occurred particularly when he was on ward service, which he now does twice a year, but used to do more frequently. Prof Harper said he had worked in the public hospital system the whole of his career, and he was familiar with what goes on in emergency. Many patients discharged from emergency without a definite diagnosis are referred for outpatient review by cardiologists.

261 He said he regularly confers with emergency colleagues. Between 2009 and 2014 he was Clinical Co-Lead of the Victorian Cardiac Clinic Network, which involved visiting many hospitals across Victoria to see how they managed emergency patients. There was a combined symposium held with the emergency clinical network. He read literature, which is distributed Australia-wide, in relation to the science of cardiological diagnosis. He had no reason to believe that emergency standards would differ from cardiological standards in relation to presentations of chest pain. There is a general consensus between cardiologists and emergency physicians in relation to diagnosis and cardiac pathways.

262 Prof Harper said he felt able, in a general sense, to express a view in relation to the standard of care which should be exhibited by emergency physicians. He had not conferred with interstate emergency physicians, and had no experience of emergency departments interstate, but it was hard to imagine that treatment protocols present in Victoria would be much different from other states. He said there were no protocols to determine when to do a CTA. In general, when there is a suspicion of AD, a CTA is ordered.

263 Dr Habersberger said he was regularly called upon by the emergency department seeking advice in relation to patients who presented with chest pain. He said the Cardiac Society of Australia and New Zealand advises the Australasian College of Emergency Medicine as to the most appropriate way to manage patients with chest pain.

264 Evidence is relevant if it could affect (directly or indirectly) the assessment of the probability of the existence of a fact in issue in the proceeding, by making the fact more probable or less probable.[59] The definition of relevance is broad, and the bar for admission of evidence is low. Prof Harper and Dr Habersberger have specialised knowledge in relation to cardiac and aortic conditions and chest pain presentations. Both have some experience in the management of chest pain patients in Victorian emergency departments by emergency physicians. Their specialized knowledge and experience qualified them to give evidence relevant to reasonable care and competent professional practice in the management of chest pain presentations to emergency departments in Victoria. Proving competent professional practice in Victoria is a step toward establishing peer professional opinion for the purposes of s 59(1) of the Act. Whilst their evidence above may not be sufficient to determine the issue of breach, it does satisfy the test for relevance.

265 However, the weight of the evidence of Prof Harper and Dr Habersberger remains to be considered. As a general proposition, the evidence of the emergency physicians, each of whom is well qualified with decades of experience working in emergency departments of major hospitals, will carry greater weight in relation to the central issues of the standard of reasonable care and competent professional practice.

266 For the following further reasons I attribute less weight to the evidence of Prof Harper. First, he misstated the first of three clinical predictors of AD identified in von Kodolitsch, on which he relied to conclude that the probability of AD in Mr Boxell's case was extremely low. In contrast to what is recorded in [232], the first clinical predictor of AD in von Kodolitsch is 'aortic pain of immediate onset, a tearing or ripping character, or [60]th'.60 The study considered onset of pain within less than two minutes as immediate. A table of signs and symptoms in von Kodolitsch recorded a history of immediate onset of pain in 79% of patients in the study, intense severity of pain in 86%, tearing or ripping in 62%, migrating pain in 44%, and anterior chest pain in 76%. On the history taken by Dr Lindley, Mr Boxell's presenting pain satisfied the clinical predictor for aortic pain. A finding of aortic pain alone, not together with other predictors, was associated with a 31% probability of dissection in the study group. Prof Harper did not give a satisfactory explanation for misstating the predictor. Second, I do not accept Prof Harper's evidence that radiation of pain to the left shoulder was not typical of AD, sharp was not a word used to describe AD pain, and AD pain is unremitting and does not stop with the dissection. These matters caused Prof Harper to overstate the atypicality of Mr Boxell's presentation and affected his consideration of whether a CTA was reasonably required in the circumstances.

267 For similar reasons, I do not accept Dr Habersberger's evidence that immediate onset of sharp, central chest pain is not a guide to the probability of AD. While those pain descriptors may not be as distinctive for AD as a history of tearing or ripping pain, or pain radiating to the back, as studies such as IRAD and von Kodolitch show, they are consistent with AD, and may be predictors of the disorder. I do not accept Dr Habersberger's evidence that there was nothing in Mr Boxell's case to indicate the possibility of AD.

Should the Hospital have recognised Mr Boxell's family history as a risk factor for AD?

268 A/Prof Raftos said 10% of patients with thoracic aortic dissection have an identifiable disease such as Marfan syndrome either personally or in their family, and a further 20 to 30% have an identifiable genetic disease which causes abnormalities of the connective tissue. He said it was theorised such genetic abnormalities interfere with the normal formation of connective tissue in the arteries, predisposing to arterial disease, aortic aneurysm, AD and aneurysms elsewhere. He said this issue had been identified since about 2010. Upon being challenged in that regard, A/Prof Raftos produced three articles from the genetics field published in April 2005, June 2008 and July 2011 which examined a family history of aortic aneurysm as a risk factor for AD. It is worth noting that these articles, and other later articles to which Prof Kelly referred, distinguish between thoracic and abdominal aortic aneurysm. The familial link as a risk factor for AD appears to be stronger with the former than the latter.

269 In his 2013 note, under the heading 'High risk conditions and historical features', Dr Eddey quoted from the American Heart Association Guidelines:

Patients presenting with sudden onset of severe chest, back, and/or abdominal pain should be questioned about a history of aortic pathology in immediate family members, as there is a strong familial component to acute thoracic aortic disease.

However, Dr Eddey did not refer to family history as a relevant risk factor which should have been taken into account in respect of Mr Boxell in 2013.

270 Dr Vinen treated Mr Boxell's family history of abdominal aortic aneurysm as a risk factor when he applied the risk score tool.

271 Prof Cameron said there was no doubt there was some familial element to AD, but less than 20% of thoracic ADs were genetic or familial in origin. He said the family history of abdominal aortic aneurysm was relevant, but was a small percentage of the overall risk pattern of these illnesses and would be stronger with a history of dissecting thoracic aneurysm. He said the exact genetics are being mapped out by the experts, but in terms of what's happening on the ground, there was a need to take note of family history.

272 Prof Mitra referred in his report to the possible relevance of connective tissue disease, given the family history of abdominal aortic aneurysm, but did not elaborate.

273 Prof Kelly said that while the relevance of connective tissue disorders such as Marfan syndrome was known by emergency physicians in 2013, the relevance of a family history of aortic disease was not widely known, and was not known by her. She said a family history of abdominal aortic aneurysm would not have made her nervous in 2013, but would do so now. Having searched she said she could not find emergency medicine textbooks or journals current in 2013 which identified a family history of aortic disease as a risk factor for AD. She said in 2013 she would have regarded the family history of abdominal aortic aneurysm as favouring a diagnosis of heart disease, and that most aortic aneurysms were due to atherosclerotic vascular disease, which was more of a coronary artery-type problem than a thoracic wall-type weakness problem. She said she would now regard a family history of aortic aneurysm as significant for AD, and it would push her toward undertaking a CTA.

274 Mr Rosalion said the family history suggested an inherited predisposition to weakness of the aorta, predisposing to developing aortic dilatation or AD. He said there was not a sharp distinction between aneurysm and dissection, and while they were not the same, there was a comparable pathological process related to abnormalities in the collagen of the aortic wall, so that looking at patients with dissection there was a higher incidence of family history, whether it be of aneurysm or dissection. He said the relationship between aortic aneurysms and AD was longstanding, was less strong than with conditions such as Marfan syndrome, but was still there and would have been known in 2012.

275 Prof Harper said he now accepted there may be a relationship between a family history of aneurysm and AD, but that was not widely known in 2013, even though the studies may have been done before then. He said it was something he would now take into account when he saw a patient. In Mr Boxell's case the autopsy finding of medial necrosis suggested there was a connective tissue disorder of the aorta. He said the family history would not have been widely thought of as a risk factor in 2013, and he did not think many emergency physicians would have taken it into account.

276 Dr Habersberger said the family history increased the likelihood of aortic disease being present and if the possibility of acute coronary syndrome was excluded, it might have swayed him to doing a CTA. He agreed the history of the mother's abdominal aortic aneurysm occurring in her fifties would raise the index of suspicion a little higher in relation to AD.

277 Strayer lists family history of aortic disease as a relevant risk factor on the evaluation pathway proposed by the authors, but there is no discussion of the issue in the article. However, a family history of aortic aneurysm is not noted as a risk factor in other tendered literature which was available in 2013.

278 With the exception of Profs Kelly and Harper, all of the experts acknowledged a family history of abdominal aortic aneurysm as a relevant risk factor for AD. However, a number of them, including Dr Eddey and Prof Mitra, did not refer to family history as a relevant risk factor in Mr Boxell's case. This supports a conclusion that in 2013 a family history of aortic aneurysm would be considered a low order risk factor. On this issue I prefer the evidence of Prof Cameron. I conclude that in 2013 a family history of aneurysm was a known risk factor for AD, but the mechanism and degree of association was not well understood, the relationship was stronger with thoracic than abdominal aneurysm, and the understanding was that it was a small percentage of the risk pattern for AD.

Is the defendant not negligent because the Hospital acted in a manner widely accepted as competent professional practice in the circumstances?

279 Peninsula Health is a statutory incorporated entity which operated through its servants and agents. The defendant submitted that the medical practitioners engaged by it were providing a professional service within the meaning of s 59(1) of the Act, which gave it the protection of the provision.

280 The defendant submitted that the field of professional practice is properly defined in this case as that of a medical physician treating a patient presenting to a hospital. The expert evidence leads to the inescapable conclusion that there is a body of professional opinion in respect of the field of practice in issue.

281 Competent professional practice involved the response of doctors called upon to exercise clinical judgment in the specific circumstances of Mr Boxell's presentation. The evidence of Profs Cameron, Mitra, Kelly, Harper and Dr Habersberger establishes that the response to investigate Mr Boxell for a coronary cause of his condition, and not perform a CTA, was in accordance with competent professional practice. Profs Cameron, Mitra and Kelly, having seen all of the evidence relating to Mr Boxell's attendance at the Hospital, were unanimous that the conduct of the Hospital was accordant with competent professional practice, and that it would have been inappropriate, on that clinical picture, to have subjected Mr Boxell to a CTA. The logic of Mr Boxell remaining on the cardiac pathway to discharge is justified by a coronary condition being the most likely serious cause for his presentation, AD being highly improbable, and him asymptomatic and apparently well for some hours.

282 If it is found there was a failure by the Hospital to consider AD, which meant its conduct fell below a standard of competent professional practice, that failure was not a cause of Mr Boxell's death. The relevant cause was not performing a CTA. Because competent professional practice did not require that the Hospital perform a CTA, the plaintiffs' case fails.

283 There is no basis for finding that peer professional opinion proved by the evidence of Profs Cameron, Mitra and Kelly, supported by the cardiologists Prof Harper and Dr Habersberger, is unreasonable.

284 The plaintiffs submitted that determination of the issue of negligence in Mr Boxell's death requires reference to a variety of factual considerations, including:

(a) whether an AD was considered at all;

(b) the significance and clinical evaluation of this particular presentation;

(c) the reasonable response to a patient with such a presentation where there was prior to discharge a high likelihood of the cause not being an acute coronary syndrome;

(d) where no diagnosis was reached, whether it was reasonable to discharge him;

(e) whether further consideration should have been given to the diagnosis of AD as at 11:20am or thereafter; and

(f) whether a CTA was reasonably required in the circumstances (identifying such circumstances).

This case is not about completion of a cardiac pathway. The defendant has not proved a standard of competent professional practice in the circumstances. Because the Hospital did not consider the diagnosis of AD, it did not act in a manner that was accepted in Australia as competent professional practice.

285 The Hospital's failure to consider a diagnosis of AD is inextricably connected to the failure to undertake a CTA. No decision was made in relation to the latter by reason of the former. In the circumstances, it cannot be said that the defendant acted in a manner that was widely accepted as competent professional practice.

286 Further, the plaintiffs maintain that the peer professional opinion relied on by the defendant is not 'widely accepted in Australia'. The plaintiffs rely on the evidence of Dr Eddey, Dr Vinen and A/Prof Raftos.

287 The plaintiffs submitted that, in any event, the opinion sought to be relied on is unreasonable within the meaning of s 59(2) of the Act because:

(a) it is inconsistent with patient safety;

(b) it prioritises cost and convenience over patient safety and clinical care;

(c) it is founded on a misconception as to the true signs and symptoms of most common presentations (type A) of AD;

(d) it relies on overestimates of the risks of CTAs;

(e) it discourages clinical curiosity; and

(f) it promotes an over-reliance on clinical pathways.

288 The plaintiffs did not take issue with the submission that, as a corporate entity, Peninsula Health was entitled to the protection of s 59(1) in respect of professional services provided by doctors it engaged. I accept the defendant's submission.

289 To succeed the defendant must establish a standard of competent professional practice in the field of emergency medicine which, in the circumstances of Mr Boxell's presentation on 6 October 2013, did not involve performing a CTA.

290 The defendant's case relies for its success on the evidence of Profs Cameron, Mitra and Kelly.

291 For the following reasons, I do not accept Prof Cameron's evidence that Australia-wide practice in Mr Boxell's circumstances would be to not order a CTA, and the decision to discharge him would be standard practice across virtually every short stay unit in the country. First, it is inconsistent with the evidence of Dr Eddey, A/Prof Raftos and Dr Vinen, each of whom is very experienced in the field of emergency medicine, with a history of holding senior positions at major public hospitals in Victoria and New South Wales. Dr Eddey considered relevant issues of practice when he prepared his note to the Coroner in 2013. Dr Eddey, A/Prof Raftos and Dr Vinen said that a CTA ought to have been performed before Mr Boxell was discharged, which I infer represents the standard of practice at least at the hospitals which they represent, and probably more broadly. Prof Cameron's evidence that the standard he espoused was practised in every Australian emergency unit was clearly inaccurate, which is a reason to doubt whether it is a standard of care widely accepted by a significant number of respected practitioners in the field. Second, as I have explained at [249], Prof Cameron misunderstood Mr Boxell's circumstances and misstated the plaintiffs' case. When he addressed his attention to the presenting history recorded by Dr Lindley, Prof Cameron agreed AD was definitely a possibility to consider, and it was getting very close to his red flag-type history. He said if chest pain was abrupt, which is the history recorded by Dr Jackson in his statement to the Coroner, he would definitely order a CTA.

292 Prof Mitra said the cardiac pathway was commonly followed by emergency departments around Australia, and it is standard practice to discharge a patient who presents with chest pain deemed to be of low risk of ischaemic heart disease with advice for outpatient follow-ups. He added:

It is accepted that such management pathways result in high healthcare utilization by patients after discharge, some risk of major adverse cardiovascular effects and a low (not zero) risk of death, but is consistent across Australia.

293 Prof Mitra said, in his opinion, a patient presenting with chest pain is owed a duty of care by the emergency department to provide a definitive diagnosis before discharge. For reasons just stated, the practice described by Prof Mitra is not consistent with that practised in the hospitals represented by Dr Eddey, A/Prof Raftos and Dr Vinen. There is a difference between a standard being commonly practised, and it being widely accepted as competent professional practice by a significant number of respected practitioners in the field. While his evidence supported the former proposition, given that he did not subscribe to the standard he said was commonly practised, it gave little, if any, support to the latter.

294 Like Prof Cameron, Prof Kelly misunderstood Mr Boxell's presenting history and misstated the plaintiffs' case. Prof Kelly's appreciation of aortic pain was inconsistent with at least two of the textbooks she provided and with IRAD. I infer a standard accepted by respected practitioners in the field as competent practice would be based on current learning in relation to the diagnostic characteristics of life-threatening disorders they may encounter, and an accurate history, so as to allow the comparative risks and benefits of proceeding in a certain way to be assessed. The combined effect of these matters was to significantly reduce the weight of Prof Kelly's evidence that the decision to discharge Mr Boxell without first performing a CTA was widely accepted as competent professional practice.

295 Each of Profs Cameron, Mitra and Kelly emphasised the critical importance of the description of the onset and quality of pain in the diagnosis of chest pain. Profs Cameron and Kelly said this was a continuing process throughout the period of the emergency presentation. Prof Kelly described the need to re-calibrate the probability of different diagnoses, re-evaluate, and double-check with the advantage of investigation results and other information obtained throughout the presentation. This contrasted to some degree to the evidence of Prof Mitra, who said the cardiac pathway is exclusive, and once the patient is on the pathway alternate diagnoses are not considered during the presentation unless there is something that changes. However, Prof Mitra said Mr Boxell added it would have been a good idea to reconsider the differential diagnosis before discharge, given the normal ECGs and troponins.

296 The evidence of Prof Harper and Dr Habersberger does not significantly advance the case of the defendant on this issue. Neither can speak to emergency practice in states other than Victoria. Like Prof Kelly, their opinions were not based on the findings of IRAD, von Kodolitsch, and texts such as Rosen's and Dunn.

297 The circumstance requiring a professional response was the whole of Mr Boxell's presentation at the Hospital on 6 October 2013. Factual considerations included:

(a) the presenting history, and the extent to which it was consistent with, or characteristic of, AD;

(b) clinical evaluation and history-taking throughout the presentation;

(c) evaluation of the life-threating diagnoses, most of which were excluded;

(d) ECG, troponin and investigation results, the outcome of the cardiac pathway, and reduced probability of a cardiac cause for the presentation; and

(e) there being no diagnosis for the presentation.

The decision to discharge Mr Boxell, and to not perform a CTA, must take account of these matters. The response of the emergency physician to these factual circumstances may determine the course of events. It is difficult to identify a common standard which Profs Cameron, Mitra and Kelly all accept represents competent professional practice which takes all these matters into account. There were differences between the experts, for example, Prof Cameron's red flags, his acceptance of the family history as a risk factor, and his evidence that he would definitely perform a CTA if the onset of pain was abrupt; Prof Mitra's identification of three risk factors for AD; and Prof Kelly's appreciation of the symptoms, signs and risk factors which are characteristic of AD. Their evidence does not establish a standard widely accepted in Australia by a significant number of respected practitioners in the field as competent professional practice in the circumstances.

298 A standard of care accepted by Profs Cameron, Mitra and Kelly as competent professional practice in the circumstances would have included considering the diagnosis of AD with a high index of suspicion throughout the emergency presentation, teasing out the history of the onset and quality of pain in minute detail, and reconsidering the probability of AD before discharge, when other possible life-threating causes for the presentation had been excluded or rendered less likely. The relative risks and benefits of performing a CTA could only be known and assessed if these steps were taken. The Hospital did not consider the diagnosis of AD with a high level of suspicion at any stage of Mr Boxell's presentation, carefully tease out the pain history, or reconsider the diagnosis before discharge. It is not possible to know what further information would have been obtained had these steps been taken, or what the outcome would have been in terms of whether the standard required that a CTA be performed. Because the Hospital did not take the steps to which I have referred, it cannot be concluded that its conduct satisfied a standard of competent professional practice had such a standard been established by the evidence of Profs Cameron, Mitra and Kelly.

299 Peninsula Health has not satisfied the preconditions of s 59(1), and cannot rely on the provision to establish that it was not negligent in providing the service to Mr Boxell on 6 October 2013. Therefore ss 49, 49 and 58 of the Act are to be applied, and it is necessary to consider the conduct of Peninsula Health against the standard of reasonable care.

Did the defendant breach its duty because the Hospital failed to perform a CTA?

300 The plaintiffs submitted that Mr Boxell's presenting symptoms and signs required that a number of potentially lethal causes of chest pain be identified and excluded. In fact the only potentially lethal cause that was not excluded was AD. Further consideration of that diagnosis was required, particularly once Mr Boxell completed the cardiac pathway and acute coronary syndrome had effectively been excluded.

301 The history of sudden onset severe central chest pain radiating to the left shoulder was consistent with the description of AD pain in IRAD. Mr Boxell had relevant risk factors, including the family history, hypertension, smoking history and age. The sweatiness and clamminess with which he presented indicated a serious physiological cause. The presentation and risk factors justified performing a CTA, particularly after other potentially lethal causes had been excluded.

302 The defendant's experts misunderstood the true nature of Mr Boxell's presentation, perhaps because they relied on Dr Jackson's statement to the Coroner, which was not provided to the plaintiffs' experts, and were over-reliant on the presence of classic signs, most of which will be irrelevant to a type A dissection. Further, the defendant's witnesses showed a different willingness to accept risk, and placed too great a reliance on Mr Boxell's pain settling.

303 It should be concluded the Hospital failed to consider a diagnosis of AD, which infected the whole process of treatment and investigation while Mr Boxell was in hospital. There was a failure to adjust probabilities and to reassess Mr Boxell throughout his stay, particularly when it was established that the cause of his presentation was not an acute coronary syndrome. Anxiety and reflux were not adequate explanations for the presentation. At the end of the cardiac pathway, when all investigation results were negative, if there was justification for undertaking a sestamibi scan, there was no justification for not performing a CTA.

304 Dr Vinen and Prof Kelly were not told of Mr Boxell's outcome when they provided their reports. Both concluded AD was a probable diagnosis. This evidence puts into perspective Prof Mitra's concern about the degree of risk of there being a dangerous coronary condition, even after the negative troponins and ECGs.

305 The outrage expressed by the defendant's experts about the prospect of submitting so many chest pain patients to CTA examination is not justified. As Dr Eddey said, CTA is an extraordinarily common everyday investigation. Further, the requirement for CTA investigation was overstated by the defendant's experts. Prof Cameron's extreme and colourful complaint that every person who suffers 'a twinge of chest pain' cannot be submitted to a CTA does not inform Mr Boxell's case. He did not have a twinge of chest pain. Every other potentially lethal cause of his presentation had been excluded, and his presentation and history taken as a whole more than justified performing a CTA.

306 There was a failure by the Hospital, and by the defendant's experts, to approach the analysis in an open-minded way. The focus on distinctive, but often uncommon, signs of AD in effect placed too much weight on the wrong thing. The Hospital and the defendant's experts should have considered the common things, as described in IRAD, as opposed to looking for the distinctive things. The risk of the approach taken by the defendant's experts is that type A dissections, which most often will not be productive of distinctive signs, will be missed. That cannot be a reasonable approach. There was no evidence that the Hospital had an appropriate index of suspicion for AD. No one thought about the diagnosis. If it is not thought of, one risks relying on the patient having a distinctive sign or symptom. The end result of that approach is that, in a case such as Mr Boxell's, no diagnosis will be made.

307 The defendant submitted that whilst Mr Boxell had severe pain initially, it reduced to nil, and remained that way for some hours, which was encouraging. Mr Boxell's blood pressure and observations were relatively normal. This impacted the reasonableness of Mr Boxell being discharged.

308 When he arrived at the Hospital it was probable Mr Boxell's chest pain had a coronary cause. In his case the history of smoking and alcohol use, family history, hypertension, anxiety, nature and onset of chest pain, and complaint of left shoulder pain moved the probabilities even further in favour of a coronary cause.

309 Comparatively, the risk of AD was very low. Mr Boxell was only 47, which placed him in the demographic where the condition was even rarer. The description of pain had none of the classical features of ripping or tearing, radiating into the back or being unremitting. The chest x-ray was normal. There was no evidence of differential blood pressures, absent pulses or other relevant clinical signs.

310 Even after the negative repeat troponins and ECGs, a coronary cause remained by far the most likely serious cause of Mr Boxell's presentation.

311 There was no proper clinical basis to justify performing a CTA, and there were risks associated with the investigation, which included exposure to radiation causing cancer, an adverse reaction to the dye and kidney impairment. Further, there was a cost to the health system in terms of prioritisation of patients, and a potential cost to the patient in terms of inconvenience and incidental findings requiring monitoring and further investigation.

312 The standard of reasonable emergency care of Mr Boxell did not require that a CTA be performed.

313 For the following reasons I conclude that it was not reasonable emergency practice to discharge Mr Boxell without diagnosis before performing a CTA to confirm or exclude AD.

314 I conclude that the presenting signs and symptoms of AD, and the results of investigations such as chest x-ray, are best described in IRAD, which was published in 2000. The IRAD outcomes appear to have been adopted by other articles and texts published before 2013, including Rosen's, Dunn, Harrison's, the American Heart Foundation Guidelines and Strayer, and are consistent with the analysis of signs and symptoms in von Kodolitsch.

315 I accept the evidence of Dr Eddey. His evidence was based on an accurate understanding of Mr Boxell's presenting history. The opinions he expressed were considered and well-reasoned. His conclusions were supported by A/Prof Raftos, Dr Vinen and Mr Rosalion, and were consistent with the literature. In the final analysis the difference between Dr Eddey's opinion and those expressed by Profs Cameron and Mitra was not as great as appeared at first blush. When he addressed his mind to Dr Lindley's history, Prof Cameron agreed it was close to a red flag justifying investigation of AD. Prof Mitra's opinion was that there should be a definitive diagnosis for chest pain before a patient is discharged from emergency.

316 The role of emergency physicians is to keep patients safe from harm by taking reasonable precautions to exclude or confirm immediately life-threatening causes for their presentation to the emergency department. When the presenting complaint is chest pain, that involves considering a list of diagnoses including AD.

317 The experts agreed that the history of the onset and character of pain is critically important to investigation and diagnosis of chest pain presentations. There is a material difference between the description of pain recorded in the ambulance notes and that recorded by Dr Lindley. Prof Cameron said the description of pain was varied and inconsistent, and what you were looking for, in terms of a red flag, was a consistent history over time. Prof Kelly relied on the history recorded in the ambulance notes to discount AD as a potential cause of Mr Boxell's presentation. The presenting history was not resolved at the 9:00am assessment with Dr Jackson and Dr Harkin. It is not an answer to the plaintiffs' case that the ambulance history was inconsistent with AD, or made the diagnosis so unlikely that a CTA was not clinically justified. Reasonableness required that the Hospital act on what appeared to be a carefully taken history of presenting symptoms recorded by Dr Lindley. That need was reinforced by the fact that Dr Lindley was sufficiently concerned about Mr Boxell's presentation to go out of his way, after the end of his shift, to find the Senior Emergency Consultant Dr Jackson to discuss the presentation and encourage him to review Mr Boxell. It is worth noting Dr Lindley considered the possible need for investigation by CT scan, though he could not recall whether of the chest or the head.

318 There were features of the pain history recorded by Dr Lindley which were consistent with, and to a degree characteristic of, AD. First, severe sudden onset central chest pain at 8 out of 10 after 30 seconds. Second, the character of pain was described as 'sharp'. Third, there was radiation of pain to the left shoulder. Fourth, the reported diaphoresis was consistent with Mr Boxell being unwell. These features fitted well with the presenting symptoms of AD described in IRAD and von Kodolitsch, and by Dr Eddey in his 2013 notes.

319 Mr Boxell presented to the Hospital with a number of risk factors for AD. He was male, suffered hypertension which was untreated, was a heavy smoker and had a family history of his mother having suffered an abdominal aortic aneurysm in her fifties. The same risk factors applied to the more statistically probable diagnosis of acute coronary syndrome. However, it is hardly the point that risk factors meant the Hospital had to seriously consider and investigate other disorders. It would not be reasonable, given the risk factors and the presenting history, for the Hospital to focus attention only on acute coronary syndrome to the exclusion of other serious or potentially lethal causes for the presentation, including AD. Acting reasonably, it was necessary for the Hospital to keep AD under consideration throughout the course of Mr Boxell's attendance, when other possible serious causes for his presentation were eliminated or rendered less likely. I accept Dr Eddey's evidence that there was a need for ongoing clinical curiosity as to the cause for the sudden, severe chest pain suffered by Mr Boxell, and that it was not reasonable to discharge him without a diagnosis before performing a CTA to confirm or exclude AD. I would still reach this conclusion had I found that the family history was not a relevant risk factor.

320 The history of fluctuating pain and headache were atypical for AD. Mr Boxell did not present with classical features of ripping and tearing pain radiating to the back, there were no distinguishing signs identified on clinical examination, and no relevant abnormalities on ECG or chest x-ray. Mr Boxell's symptoms subsided, and from 11:00am his observations were relatively normal. The defendant's experts all relied on the absence of these classical symptoms, clinical signs or abnormalities on investigation to conclude that a CTA was not clinically justified. That approach did not take proper account of two defining characteristics of AD. First, that the symptoms and signs are variable and very dependent on the location and extent of the dissection, and the disorder will often mimic other more common disorders. A type A dissection which is limited to the ascending aorta may present with none of the distinctive signs and symptoms, or red flags, on which Profs Mitra and Cameron relied. Second, acute type A dissections are highly lethal. Further, the approach of the defendant's experts did not take proper account of the degree to which the presenting history and risk factors, considered in combination, pointed to the possibility of a diagnosis of AD.

321 There are downsides to performing CTAs which include a small risk of developing cancer later in life, risks of suffering impaired kidney function or an adverse reaction to the dye, and complications associated with incidental findings. There is a cost to the health system in terms of patient prioritisation and potential delay in access to investigations and management of emergency patients. However, the cost of CTAs should not be overstated. To a greater or lesser degree there will be similar costs which attach to other radiological investigations. Further, account should be taken of the cost of not performing the investigation. In a letter published in Emergency Medicine Australia in 2013, Profs Mitra and Cameron noted costs of discharging chest pain patients with a recommendation for outpatient stress test, rather than performing the test while the patient was in emergency, included the high frequency of health care utilisation by discharged patients, patients re-presenting to emergency before outpatient testing is performed, adverse patient outcomes following discharge, costs and inconvenience from fragmented care, and poor patient compliance with recommended outpatient testing. While the force of these considerations may be somewhat different in the case of CTA for investigation of AD, the analysis by Profs Mitra and Cameron show that there will be benefits from undertaking investigations to confirm or exclude serious diagnoses while the patient is in emergency. I note Klomp found that absence of AD in the differential diagnosis was associated with use of more imaging tests. I accept Dr Eddey's evidence that a CTA is a common investigation performed multiple times daily at busy hospitals. Further, it is a substantial overstatement to propose, as Profs Cameron and Kelly did, that acceptance of the plaintiffs' case would result in CTAs being performed on any patient with a 'twinge of chest pain', or on the 30,000 chest pain patients who present to emergency in Victoria each year.

322 In von Kodolitsch, which involved over 41,000 patients who presented to emergency with acute chest pain, back pain or both, nearly 39,000 patients were excluded because an alternative diagnosis was established by routine evaluation. The remaining patients were jointly considered by two experienced emergency physicians, and those whose symptoms that were not clinically suspicious of AD were excluded. I infer patients presenting with aortic pain were included in the final study group of 250, 128 of whom were diagnosed with AD. As previously stated, Mr Boxell's presenting history met the description for aortic pain used in the study. I accept that most often there will not be an opportunity in emergency for chest pain patients to be screened by two experienced physicians, and that the results in von Kodolitsch may not reproduce the circumstances experienced in Victorian emergency departments in other respects. However, subject to these riders, the study does serve to illustrate the substantial overstatement by Profs Cameron and Kelly of the cost and burden on the health system of investigating patients such as Mr Boxell by CTA. I accept Dr Eddey's evidence that the decision to perform a CTA is evidence based, and that it is done to diagnose a serious condition, not in cases of more minor pain.

323 I have taken account of the matters in s 48(2) of the Act. On the basis of the presenting history and risk factors, AD should have been considered with a high level of suspicion during Mr Boxell's presentation at the Hospital emergency department on 6 October 2013. Reasonable care required that the Hospital confirm or exclude AD by performing a CTA before Mr Boxell was discharged on that day. Because it failed to do so the defendant was negligent.

324 I find in favour of the plaintiffs in relation to the issues to be determined to this stage of the trial. I will hear from the parties as to the appropriate orders.

CAITLIN ROSE (BY HER LITIGATION GUARDIAN VICKI BOXELL)

TIMOTHY BOXELL (BY HIS LITIGATION GUARDIAN VICKI BOXELL)

STEPHANIE BOXELL (BY HER LITIGATION GUARDIAN VICKI BOXELL)

[1] Rogers v Whitaker [1992] HCA 58; (1992) 175 CLR 479, 487.

[2] [2012] VSC 272.

[3] [2012] VSC 491.

[4] [2007] NSWCA 335; (2007) 70 NSWLR 151.

[5] [2018] NSWCA 29; (2018) 361 ALR 115.

[6] [2018] NSWCA 69; (2018) 97 NSWLR 513.

[9] Ibid 168 [64] (citations omitted).

[10] [1992] HCA 58; (1992) 175 CLR 479, 487.

[12] Grinham 34 [131]; Dobler 157 [35].

[15] Dobler [61]; Brakoulias [34]-[35]. Further, contrast the text of s 48(1), 'A person is not negligent ... unless ...', which places the onus on the plaintiff.

[17] [2013] NSWCA 476; [2013] Aust Torts Reports 82-158 (note this decision was overturned by the High Court without considering s 5O: Hunter and New England Local Health District v McKenna [2014] HCA 44; (2014) 253 CLR 270).

[22] Wrongs Act 1958 (Vic) s 48.

[23] Ibid s 58.

[24] Erickson v Bagley [2015] VSCA 220, 13 [37].

[25] Bolam v Friern Hospital Management Committee [1957] 1 WLR 582, 587.

[26] [1985] UKHL 1; [1985] AC 871.

[28] Sparks 187 [332] (Simpson JA).

[31] Law of Negligence Review Panel, Review of the Law of Negligence (Final Report, September 2002) 41 [3.17]-[3.20].

[32] [1997] UKHL 46; [1998] AC 232.

[33] Hucks v Cole [1993] 4 Med. LR 393 was cited as an example.

[36] Peter G Hagan et al, 'The International Registry of Acute Aortic Dissection (IRAD): New insights into an old disease' (2000) 283(7) Journal of the American Medical Association 897.

[37] WW Jansen Klomp et al, 'Clinical recognition of acute aortic dissections: insights from a large single-centre cohort study' (2017) 25(3) Netherlands Heart Journal 200.

[38] Istvan Meszaros et al, 'Epidemiology and Clinicopathology of Aortic Dissection: A population-based longitudinal study over 27 years' (2000) 117(5) Chest 2171.

[39] Reuben J Strayer, Peter L Shearer and Luke K Herman, 'Screening Evaluation and Early Management of Acute Aortic Dissection in the ED' (2012) 8(2) Current Cardiology Reviews 152.

[40] Yskert von Kodolitsch, Ann G Schwartz and Christoph A Nienaber, 'Clinical Prediction of Acute Aortic Dissection' (2000) 160 Arch Intern Med 2977.

[41] Peter Cameron et al (eds), Textbook of Adult Emergency Medicine (Elsevier, 3rd ed, 2009).

[42] John A Marx et al (eds), Rosen's Emergency Medicine: Concepts and Clinical Practice (Elsevier, 7th ed, 2010).

[43] Robert Dunn et al (eds), The Emergency Medicine Manual (Venom Publishing, 5th ed, 2010).

[44] Louise Culten et al, 'Cost and outcomes of assessing patients with chest pain in Australian emergency departments' (2015) 202(8) Medical Journal of Australia 427, 429.

[46] AS Fauci et al (eds), Harrison's Principles of Internal Medicine (McGraw Hill, 17th ed, 2008).

[47] Peter Cameron et al (eds), Textbook of Adult Emergency Medicine (Elsevier, 3rd ed, 2009) 264.

[49] Loren F Hiratzka et al, 'Guidelines for the diagnosis and management of patients with thoracic aortic disease' (2010) 121(13) Circulation 1544.

[52] Meszaros 1273-4 (citations omitted).

[59] Evidence Act 2008 (Vic) s 55.