Coote v Dr Kelly - [2012] NSWSC 219

Supreme Court

New South Wales

Medium Neutral Citation: Coote v Dr Kelly [2012] NSWSC 219
Hearing dates: 27 February 2012, 28 February 2012, 29 February 2012, 1 March 2012, 2 March 2012, 5 March 2012
Decision date: 14 March 2012
Jurisdiction: Common Law
Before: Schmidt J
Decision:
1. Judgment for the defendant.
2. The usual order would be that costs follow the event. The parties should approach if they wish to be heard on costs.

Catchwords:
TORTS - negligence - medical negligence - whether general practitioner made a wrong diagnosis - a lesion on the foot diagnosed as a plantar wart - whether there was a misdiagnosis of the lesion - whether it was an acral lentiginous melanoma (ALM) - whether there was failure to consider ALM as a differential diagnosis - whether there was failure to refer the plaintiff for specialist investigation - whether there was a failure to perform a punch biopsy of the lesion - plaintiff suffered a plantar wart and also had an ALM - duty of care owed - negligence established - whether there would have been a different outcome if ALM had been earlier treated - causation not established - section 50 of the Civil Liability Act - judgment for defendant - costs

EVIDENCE - admissibility and relevance - opinion evidence - medical evidence - objections to expert evidence
EVIDENCE - witnesses - credit - credibility of evidence - reliability of evidence
Legislation Cited: Civil Liability Act 2002
Evidence Act 1995
Uniform Civil Procedure Rules 2005
Cases Cited: Adeels Palace Pty Ltd v Moubarak (2009) 239 CLR 420; [2009] HCA 48
Amaca Pty Ltd v Booth [2011] HCA 53; (2011) 86 ALJR 172
Dasreef Pty Ltd v Hawchar [2011] HCA 21; (2011) 243 CLR 588
Onassis and Calerropolous v Vergiottis [1968] 21 Lloyds LR 403
Seltsam Pty Ltd v McGuiness [2000] NSWCA 29 (2000) 49 NSWLR 262
Sherry v Australasian Conference Association (trading as Sydney Adventist Hospital) [2006] NSWSC 75
Strong v Woolworths Ltd [2012] HCA 5
Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153
Tabet v Gett [2010] HCA 12; (2010) 240 CLR 537
Category: Principal judgment
Parties: Malcolm Coote (Plaintiff)
Dr Steven Kelly (Defendant
Representation: Counsel:
Mr M Williams SC with Mr O'Keefe
Mr J Morris with Mr T French
Solicitors:
Stacks Goudkamp (Plaintiff)
Norton Rose Australia (Defendant)

File Number(s): 2011/339988
Publication restriction: None

Judgment

Mr Malcolm Coote has brought proceedings in negligence against his former general practitioner, Dr Steven Kelly. Mr Coote claims that in September 2009, Dr Kelly wrongly diagnosed and treated a lesion on his foot as a plantar wart, when it was, in fact, an acral lentiginous melanoma ('ALM'). Mr Coote's case is that despite repeated treatments in September and October 2009 and again in May 2010, the lesion was not correctly diagnosed, with the result that it was not until March 2011 that the ALM was diagnosed and treated. By that time it had metastasised, with what will shortly be fatal consequences.

The negligence alleged in Mr Coote's amended statement of claim includes failure to:

- obtain any history of symptoms;

- examine the lesion with magnification;

- record the features of the lesion, including asymmetry, border, irregularity, colour variation, diameter and evolution;

- consider ALM as a differential diagnosis of the lesion;

- refer the plaintiff for specialist investigation including biopsy and pathological analysis to aid diagnosis of the lesion;

- perform a punch biopsy of the lesion;

- take any steps to exclude the potentially lethal diagnosis of ALM before assigning the diagnosis of plantar wart; and

- misdiagnosing the lesion as a plantar wart when it did not bear any resemblance to that condition.

There was no issue between the parties that Dr Kelly treated Mr Coote; that he owed him a duty of care; and that he diagnosed and treated the lesion as a plantar wart by administering cryotherapy in 2009 and 2010. Nor is it in issue that the lesion grew in size over time, or that it was correctly diagnosed and treated as an ALM in 2011. What is in dispute is whether Mr Coote had a plantar wart in 2009; the state of the lesion when Dr Kelly treated it in September 2009 and to the time that Dr Kelly last treated Mr Coote in March 2010; whether Mr Coote had an ALM in September 2009; and whether or not the alleged negligence occurred.

Causation is also in issue. Dr Kelly also relies on the provisions of Part 1A and Part 2 of the Civil Liability Act 2002, claiming in accordance with s 5O that the services he provided were provided in a manner widely accepted in Australia as competent professional practice.

The evidence

Mr Coote and his wife both gave evidence, as did the three treating doctors, Dr Kelly, Dr Anthony Wall and Dr Rosalind Hiddins. Expert evidence was also called. Professor Levi, an oncologist, gave his evidence on commission. Concurrent evidence was given by Dr James Lynch and Dr Walid Jammal, as to the usual practice of general practitioners. Other concurrent evidence was given by Professor William McCarthy, also an oncologist; Professor Stan McCarthy, a histopathologist; Dr Greg Crosland, a specialist dermatologist; and Dr Ian Katz, also a histopathologist.

Plantar Warts and ALMs

In evidence was various medical literature and articles which discuss the nature, diagnosis and treatment of warts and ALM.

In short summary, plantar warts are a commonly suffered condition which occurs on the sole of the feet and are frequently treated by general practitioners. They are hyperkeratotic, that is, the upper layers of the skin are abnormally thickened and usually skin coloured, although they can become discoloured as the result of contact with the ground, or as the result of treatment. Plantar warts often grow inwards, resulting in pain and discomfort. They are not normally black, but in an article published in Australian Family Physician , December 2010, "Treating common warts" (by L Leung), it was explained that they can 'appear black due to thrombosed capillaries which are used to feed the wart.' As to diagnosis of warts it was said at p 934:

"When several warts with different morphologies cluster together, a mosaic wart is formed. Due to the myriad of morphologies and wide area of possible distribution, cutaneous warts have to be differentiated from other skin conditions such as seborrhoeic keratosis, callous, lichen planus, molluscum contagiosum, mole, melanoma, keratoacanthoma and cutaneous horn."

Most warts are self limiting, resolving in two years. Diagnosis is often conducted with the naked eye, although examination under light and with magnification is recommended, especially in the case of smaller warts. Treatment options for plantar warts are varied, including the types of treatment Mr Coote received. Because of their location on the foot, excision and some other forms of removal are used with caution. This is because of the risk of scarring and resulting permanent pain at the site.

ALM is an uncommon type of melanoma, which can occur on the sole of the foot, a condition, which general practitioners, including Dr Kelly, are aware of, even if they have not treated one themselves. In the 2008 National Health and Medical Research Council Clinical Practice Guidelines ("2008 NHMRC Guidelines") for the management of melanoma in Australia and New Zealand, ALMs are described as accounting for only 1-3% of melanomas in Australia. They are described as 'more often light coloured or pink'. It is noted that melanomas that appear relatively flat on the soles of the feet may have significant depth histologically (see at p 28). It is also noted that patients with early stage melanoma have an excellent prognosis in general, but even in these patients there is no certainty of cure and that some studies suggest that tumours sited on the soles have a worse prognosis (see at p 157).

In an article published in the Australian Family Physician in July 2009, "Cutaneous Melanoma Atypical variants and presentations " (by A Chamberlain and J Ng), a journal to which Dr Kelly subscribed, dermascopical examination of lesions suspected of being an ALM is recommended, in order to examine ridge patterns which are highly specific for melanoma. Their presentation was described as:

"Acral lentiginous melanoma usually presents as a sizeable pigmented macule; there is typically some delay in diagnosis. The presence of invasion can be deceptive and may be present in entirely flat lesions. Occasionally ALM masquerades as a wart, and is verrucous and nonpigmented. In large, warty lesions where there is a poor response to treatment, or where paring does not produce the typical pinpoint bleeding of a verruca, a biopsy should be taken."

Suspected ALM lesions are subjected to bioscopic examination. ALMs must be excised. The question of metastases must also be dealt with and treated, if identified.

There must be judgment for Dr Kelly

For reasons which I will explain, I have concluded that there must be judgment for Dr Kelly.

For Mr Coote this case was submitted to have some commonality with the conclusions reached by Simpson J in Sherry v Australasian Conference Association (trading as Sydney Adventist Hospital) [2006] NSWSC 75, where her Honour observed:

"553 There are many reasons why this judgment has been exceptionally difficult. Quite apart from the detail of the medical material there has been a consciousness of the high stakes involved for each of the parties. I have striven to exclude those from my mind, and, indeed, this has been made easier by the circumstance that the considerations on each side are evenly balanced. What I have found is that SAH, Dr Walsh and Dr Marshman in their own ways did not, on this occasion, achieve the level of service our high standards of medical practice demand. This involves no judgment of moral culpability, and no judgment as to the general competence or attention to detail of any of the participants. This was a singular occurrence and should not be taken as typical of the standard of work of any of them. In each case the finding of breach of duty is at what may be termed a relatively low level. The degree of breach of duty is not quantitatively related to its consequences. Just as a momentary lapse of attention by the driver of a motor vehicle might have disastrous consequences, so also might - and has - a short term lapse of attention by doctors and nurses. In this case the consequences are tragically disproportionate to the level of breaches of duty I have found. Compensation is, however, not measured by the degree of the breach of duty, but by consequences. The tragic outcome should not overshadow an appreciation of what it was that went wrong."

The submission may be accepted, to a certain extent. This, too, was an exceptionally difficult case. It is unquestionable that all of those who have been connected with these proceedings have the utmost sympathy for Mr Coote and his wife. It is understandable in the circumstances revealed on the evidence, that they fervently wish that the ALM from which he suffers had been diagnosed and treated in 2009. They believe that he might then have had a considerably better outcome. All of these views must be put to one side, however, in determining the issues which have arisen in this case.

As I will explain, the evidence established that in treating Mr Coote, there was a lapse by a busy general practitioner, who did not observe a small black mark, which ought to have drawn Dr Kelly's attention to the need for the unusual lesion Mr Coote had on his foot, to be referred for a biopsy. That would undoubtedly have uncovered the ALM which Mr Coote then suffered. What the evidence did not establish, however, is that this would have made the difference on which Mr Coote's case rests.

Mr Coote has suffered the worst result which the awful disease which he has contracted can lead to. This has not been shown to have been the result of Dr Kelly's failures. Having heard the evidence, I have been unable to conclude that had the lesion been treated in 2009, there would have been a different outcome for Mr Coote, given not only the size of the lesion when he first consulted Dr Kelly, but also the treatment he would then have had to undertake and the risks which it exposed him to. On the evidence it is likely that in September 2009 the ALM had already metastasised. The treatment risks he would then have faced were similar to those which confronted him in 2011. In the result, Mr Coote's case must fail.

Objections to the expert evidence

At the hearing I indicated that I would give reasons for my rulings on objections to certain reports of Dr Lynch and Professor Levi.

Dr Lynch

Dr Lynch is a general practitioner who uses certain statistical information in advising patients as to their prognosis. The tender of his entire February 2012 report was objected to. There he expressed opinions about Mr Coote's prognosis. It was complained that Dr Lynch had not adequately explained his reasoning and that there had been no response to a request for information about a staging and prognosis calculator produced by medical practitioners at the Massachusetts General Hospital and Harvard Law School, which is housed on an American database, which Dr Lynch had used in reaching his opinions.

I took the view that several paragraphs of Dr Lynch's short report did not clearly identify the assumptions on which his opinions rested. I permitted evidence to be called from Dr Lynch, to explain what those assumptions were. He confirmed that in each case, the assumptions were those which he had identified in earlier paragraphs of his report. They included opinions which Professor Levi had reached as to the size of the tumour in September 2009.

The opportunity was then taken, without objection, to clarify a number of other aspects of Dr Lynch's report. There was then quite extensive cross-examination of Dr Lynch which established, amongst other things, that the American database to which he had referred in his report, contained the terms and conditions of use of the calculator Dr Lynch had used. They revealed that users were entitled only to use the calculator for personal non-commercial use, for research purposes and not for the purpose of medical decision-making or providing medical advice. Those conditions also indicated that no representations were made as to the accuracy, reliability, completeness or timeliness of the software.

Dr Lynch was asked whether he had himself taken any steps to understand the assumptions on which the calculator rested. He had not. He accepted that in the circumstances his use of the calculator for the purpose of expressing the opinions expressed in his report had not been appropriate. While he denied that he had wrongly used that calculator to bolster his opinions, he adhered to the other opinions expressed in the balance of the report.

I then declined to receive a technical document downloaded from the American website, which was tendered to support Dr Lynch's use of the calculator, despite what the terms and conditions provided and the concessions which Dr Lynch had made. Dr Lynch's evidence was that he had never seen this document. It was entitled ' A new mathematics, and new comparative effectiveness calculators (CancerMath.net), for predicting melanoma death'. I refused to receive the document, taking the view that it was not relevant to the determination of the objections to the tender of Dr Lynch's report, having in mind the evidence which Dr Lynch had already given.

It was apparent that Dr Lynch's use of the calculator was for purposes for which it had not been designed and contrary to his acceptance of the terms and conditions of his access to the site. Its reliability could not be established by the tender of this technical document. The unreliability of the calculator for the purpose for which it had been used, was explained in an article which was annexed to Dr Lynch's report. In Acral Lentiginous Melanoma, Incidence and Survival Patterns in the United States 1986-2005 there is an explanation given of the study on which the calculator is based. The article explains that care needs to be taken with its use, because it lumps together all patients with tumour thickness ranging from 3.01 - 6mm, thus including patients whose chance of death, before other factors are taken into account, range from 25% to 45%.

In the result I did not receive the paragraph of Dr Lynch's February report, where he expressed an opinion having regard to the American calculator. Even if it had been admissible, which had not been established, it was not persuasive. Indeed, Dr Lynch accepted so much in cross-examination, when he accepted that he should not have made use of the calculator as he did.

The test of admissibility of an expert's report was discussed by the High Court in Dasreef Pty Ltd v Hawchar [2011] HCA 21; (2011) 243 CLR 588. Provisions of the Evidence Act 1995, as well as provisions of the Uniform Civil Procedure Rules 2005 must be considered. The nature of Dr Lynch's expertise was not in issue. Earlier, without objection other of his reports had been received and he had given concurrent evidence with the general practitioner called in the defendant's case, Dr Jammal. They gave evidence about various matters, including what standard practice of a competent general practitioner required in Mr Coote's circumstances The February report did not again specify Dr Lynch's expertise. That information was already in evidence.

What was in issue was whether Dr Lynch had the necessary expertise to express opinions as to Mr Coote's prognosis and life expectancy. Section 79(1) of the Evidence Act provides:

"(1) If a person has specialised knowledge based on the person's training, study or experience, the opinion rule does not apply to evidence of an opinion of that person that is wholly or substantially based on that knowledge."

Given the use which Dr Lynch explained he made of the databases to which he referred in his report in his daily practice as a GP, when advising his patients as to their probable prognosis, I was of the view that it was established both that he had specialised knowledge based on his training, study or experience, to express an opinion as to how the statistics contained in those databases could be used to assess Mr Coote's possible prognosis and that the opinions which he expressed were wholly or substantially based on that knowledge.

It followed that the balance of his report was admissible. Dr Lynch's oral evidence, particularly in cross-examination, revealed matters which were relevant to take into account in later considering whether the opinions he expressed were persuasive and what weight, if any, his opinions should be given. In part, that depends on whether or not the assumptions on which his opinions rest are found to have been established, a matter about which there is a controversy between the parties. In Dasreef , Heydon J observed at [85]:

"When a party tendering the opinion of an expert contends that all the evidence of the primary facts that could be tendered has already been admitted, the court's task in deciding the admissibility of the opinion is relatively simple. It is to assess whether, assuming the evidence of the primary facts is accepted, it will lead to findings sufficiently similar to the factual assumptions on which the expert opinion was stated to be based to render it of value. That task is easier when carried out in the light of actual evidence as distinct from a perhaps imperfect prediction of what the evidence may turn out to be. If, on the other hand, the evidence of the primary facts already admitted, even if accepted, would not lead to the necessary findings, the admissibility of the expert evidence may depend on the giving of an undertaking by the tendering party to call another witness. It is good practice for counsel opposing tender of the opinion evidence to draw attention, at the time of tender, to any significant gap between the primary facts assumed by the expert and the evidence so far received in an attempt to establish those facts, and to seek rejection of the expert evidence unless an appropriate undertaking to fill the gap is offered."

In this case Dr Lynch's assumptions relied on certain conclusions reached by Professor Levi about the size of the lesion. That evidence was also in contest. It follows that whether or not Dr Lynch's evidence will be found persuasive, depended in part on the fate of Professor Levi's evidence. Also to be considered is the evidence Dr Lynch gave in cross-examination, where he acknowledged that he did not have the same level of understanding as an oncologist or other specialists of some of the matters about which he was cross-examined, as to the use which could be made of the databases on which his opinions rested.

That one medical practitioner, a specialist in a particular field, for example, might have a greater level of expertise than another, a general practitioner, for example, is not a basis for refusing to receive the general practitioner's opinions, if they are found to satisfy the requirements of s 79. Ultimately, there might be a good reason for preferring the specialist's opinion over that of the general practitioner, if they disagree on a particular matter, or for concluding that the general practitioner's opinion is not persuasive in a particular regard, but that does not make the general practitioner's opinion inadmissible.

In this case, Dr Lynch explained that in his general practice the variables referred to in one of the databases to which he referred, were not such as to cause him ordinarily to qualify his use of the statistical information there provided, which might have an impact in a particular case. That might, once all of the expert evidence is received, be accepted to involve an erroneous approach to the statistical information in question. It may well be, for example, that a specialist using the same database to advise the same patient, would adopt a different approach, given his greater understanding of the impact of the identified variables in the particular case. In my assessment that was not a basis for concluding that Dr Lynch's evidence was not admissible.

It was for those reasons that I received the report, apart from the paragraph dealing with the American calculator, the use of which Dr Lynch properly disavowed.

Professor Levi

By contested order of the Court, Professor Levi's evidence was taken on commission prior to the hearing. Objections to his reports were notified and were to be dealt with at the hearing. Over objection, oral evidence was called from Professor Levi, in order to address the objections notified. He was also cross-examined on his reports.

There was no issue as to Professor Levi's expertise. An objection to Professor Levi's report of 12 February 2012 was resolved in submissions and it was received.

Objections to other of his reports were pressed on the basis that they were not admissible under s 79 of the Evidence Act , the reports not explaining the reasoning by which Professor Levi had reached certain of his opinions, or the facts he had assumed (see Dasreef at [91] per Heydon J). It was also submitted that they did not adhere to the requirements of the Uniform Civil Procedure Rules, which require by r 31.23 that the expert comply with the Experts Code of Conduct provided in Schedule 7 to the Rules, which requires that the report must include:

"5 Experts' reports

(1) An expert's report must (in the body of the report or in an annexure to it) include the following:

(a) the expert's qualifications as an expert on the issue the subject of the report,

(b) the facts, and assumptions of fact, on which the opinions in the report are based (a letter of instructions may be annexed),

(c) the expert's reasons for each opinion expressed,

(d) if applicable, that a particular issue falls outside the expert's field of expertise,

(e) any literature or other materials utilised in support of the opinions,

(f) any examinations, tests or other investigations on which the expert has relied, including details of the qualifications of the person who carried them out,

(g) in the case of a report that is lengthy or complex, a brief summary of the report (to be located at the beginning of the report).

(2) If an expert witness who prepares an expert's report believes that it may be incomplete or inaccurate without some qualification, the qualification must be stated in the report.

(3) If an expert witness considers that his or her opinion is not a concluded opinion because of insufficient research or insufficient data or for any other reason, this must be stated when the opinion is expressed.

(4) If an expert witness changes his or her opinion on a material matter after providing an expert's report to the party engaging him or her (or that party's legal representative), the expert witness must forthwith provide the engaging party (or that party's legal representative) with a supplementary report to that effect containing such of the information referred to in subclause (1) as is appropriate."

An example of objections taken was to paragraph 4 of the report of 29 September 2011, which provided:

"4. Is it more likely than not that there would have been no lymph node involvement as of September 2009, May 2010 or September 2010?

I consider it more likely than not that there would not have been evidence of lymph node involvement as of September 2009 and perhaps by May 2010. I am unable to indicate whether I consider it more likely than not that there would not have been evidence of lymph node involvement by September 2010."

Consideration of the reports showed that Professor Levi had identified the assumptions which he had been instructed to make. He also identified the notes, clinical records, letters and histopathology reports, he had been provided with. He summarised that;

In September 2009 the lesion was black and freckle like in appearance, approximately 3mm in diameter
It was diagnosed as a plantar wart on 3 September and treated as such. It did not regress and was treated similarly in September and October.
The lesion continued to grow slowly and on reassessment in May was further treated as a plantar wart. It grew further and was again treated as plantar wart in September 2010, then being 10mm in diameter
By January 2011 the lesion was ulcerated and it was managed further as a plantar wart until March 2011 when a biopsy was taken. The histopathology report indicated that features consistent with melanoma were found, with the predominate site intraepidermal, but with features of invasion.

It follows that it could not be accepted that the reports did not identify the factual assumptions and other information on which certain of the opinions Professor Levi expressed rested. What was missing from some other parts of the report was an explanation of why Professor Levi came to certain opinions which he explained he held, in those factual circumstances. This was addressed with him in chief when he gave his oral evidence. He there, for example, explained:

"A. Those statements were made on the basis, one , of my clinical experience, two, my long-term knowledge of the normal evolution of melanoma and my understanding of the literature together with a reference to standard textbooks and current literature.

MR WILLIAMS: Q. Could you identify any particular, literature or statistical material on which you drew informing that particular conclusion?

...

A. The literature referred to is literature which I didn't reference, but can be provided on request at any time.

MR WILLIAMS: Q. Are you able to identify any of the statistical literature that you normally apply?

...

THE EXAMINEE: The literature that I would normally refer to is based on internet searches together with standard textbooks of oncology, which I regularly have, which include the most common textbook. The name has just gone out of my head for the moment - De Vita et al."

For Mr Coote, it was submitted that sufficient explanation for the opinions objected to had been given. They lay in the opinions Professor Levi expressed itself. That submission may be accepted, in part. As discussed in Dasreef by the majority at [37]:

"It should be unnecessary, but it is nonetheless important, to emphasise that what was said by Gleeson CJ in HG (and later by Heydon JA in the Court of Appeal in Makita (Australia) Pty Ltd v Sprowles [(2001) 52 NSWLR 705 ; [2001] NSWCA 305 at [85] ( Makita ).]) is to be read with one basic proposition at the forefront of consideration. The admissibility of opinion evidence is to be determined by application of the requirements of the Evidence Act rather than by any attempt to parse and analyse particular statements in decided cases divorced from the context in which those statements were made. Accepting that to be so, it remains useful to record that it is ordinarily the case, as Heydon JA said in Makita [at [85].], that "the expert's evidence must explain how the field of 'specialised knowledge' in which the witness is expert by reason of 'training, study or experience', and on which the opinion is 'wholly or substantially based', applies to the facts assumed or observed so as to produce the opinion propounded". The way in which s 79(1) is drafted necessarily makes the description of these requirements very long. But that is not to say that the requirements cannot be met in many, perhaps most, cases very quickly and easily. That a specialist medical practitioner expressing a diagnostic opinion in his or her relevant field of specialisation is applying "specialised knowledge" based on his or her "training, study or experience", being an opinion "wholly or substantially based" on that "specialised knowledge", will require little explicit articulation or amplification once the witness has described his or her qualifications and experience, and has identified the subject matter about which the opinion is proffered."

It followed that some of Professor Levi's opinions were admissible, being based as they unquestionably were on his specialised knowledge, given his training, study and 41 years experience in his field of oncology. Given the subject matter, little more amplification was require. That conclusion could not be reached, however, in relation to all opinions expressed in the reports.

For Dr Kelly reliance was placed on Heydon J 's observations at [91] - [94]:

The statement of reasoning rule at common law

91 The authorities . At common law there is no doubt that an expert opinion is inadmissible unless the expert states in chief the reasoning by which the expert conclusion arrived at flows from the facts proved or assumed by the expert so as to reveal that the opinion is based on the expert's expertise. The court does not have to be satisfied that the reasoning is correct: "the giving of correct expert evidence cannot be treated as a qualification necessary for giving expert evidence."[ Commissioner for Government Transport v Adamcik (1961) 106 CLR 292 at 303 per Menzies J.] But the reasoning must be stated. The opposing party is not to be left to find out about the expert's thinking for the first time in cross-examination [ Lewis v R (1987) 88 FLR 104 at 124].

92 Sir Owen Dixon, speaking extrajudicially, said: "courts cannot be expected to act upon opinions the basis of which is unexplained."["Science and Judicial Proceedings", in Jesting Pilate, (1965) 11 at 18, approved in Samuels v Flavel [1970] SASR 256 at 260. Just before that statement, Sir Owen said that one duty of the expert witness was "to give his own inferences and opinions and the grounds upon which they proceed" (emphasis added). Immediately after the statement quoted in the text, Sir Owen said:

However valuable intuitive judgment founded upon experience may be in diagnosis and treatment, it requires the justification of reasoned explanation when its conclusions are controverted. Reasoned explanation requires care and forethought - qualities the presence of which is not always transparently visible in expert evidence. (emphasis added)]

It was certainly not visible in the challenged evidence in this case, whether given on the voir dire or as part of the trial - full as it was of obscurities, contradictions, and denials of matters necessary to its admissibility.

In R v Jenkins; Ex parte Morrison [[1949] VLR 277 at 303] Fullagar J quoted that statement with approval, and added that expert scientific witnesses should be asked to "explain the basis of theory or experience" on which their conclusions rest [Applied in Samuels v Flavel [1970] SASR 256 at 259-260; R v Haidley [1984] VR 229 at 234-235; R v J (1994) 75 A Crim R 522 at 531; R v Juric (2002) 4 VR 411 at 426 [19]; Police v Barber (2010) 108 SASR 520 at 539 [81].]. On appeal Rich and Dixon JJ approved what Fullagar J had said [ Morrison v Jenkins (1949) 80 CLR 626 at 637 and 641 respectively; [1949] HCA 69]. The witness must explain the basis of theory or experience because the court is not limited to examining the conclusion or the expertise of the expert witness: it must look to the "substance of the opinion expressed." [ Holtman v Sampson [1985] 2 Qd R 472 at 474.] Since choosing between conflicting experts depends in part on "impressiveness and cogency of reasoning"[ Monroe Australia Pty Ltd v Campbell (1995) 65 SASR 16 at 27, quoting Sotiroulis v Kosac (1978) 80 LSJS 112 at 115] their "processes of reasoning" must be identified [ Arnotts Ltd v Trade Practices Commission (1990) 24 FCR 313 at 349.]. In short, as the Victorian Court of Appeal (Winneke P, Charles and Chernov JJA) said in R v Juric [(2002) 4 VR 411 at 426 [18].]:

"[T]he jury must be able to evaluate the strength of [expert opinion] evidence by reference to its factual or scientific basis. Whether it can properly do so is a matter initially for the judge in determining whether that evidence is admissible.

... [T]he admissibility of [expert opinion] evidence must depend upon the judge's satisfaction that the jury can, on the basis of material put before them, properly and reasonably evaluate the differing opinions expressed and make a responsible determination as to which of them is to be preferred."

93 Function of the statement of reasoning rule . The rule protects cross-examiners by enabling them to go straight to the heart of any difference between the parties without the delay of preliminary reconnoitring. It also aids the court in a non-jury trial, because at the end of the trial it is the duty of the court to give reasons for its conclusions. And it aids jurors, because at the end of the trial they have the duty of assessing the rational force of expert evidence. If there is not some exposition of the expert's reasoning it will be impossible for the court to compose a judgment stating, and for the jurors to assemble, reasons for accepting or rejecting or qualifying the expert's conclusion.

"The process of inference that leads to the [expert's] conclusions must be stated or revealed in a way that enables the conclusions to be tested and a judgment made about the reliability of them."[ Pownall v Conlan Management Pty Ltd (1995) 12 WAR 370 at 390 per Anderson J.]

As Lord Cooper, the Lord President, said in Davie v Magistrates of Edinburgh [1953 SC 34 at 39-40 (emphasis added). These passages have been much cited: for example Lysaght v Police [1965] NZLR 405 at 409; R v Robb (1991) 93 Cr App R 161 at 166; O'Kelly Holdings Pty Ltd v Dalrymple Holdings Pty Ltd (1993) 45 FCR 145 at 155; R v Gilfoyle [2001] 2 Cr App R 57 at 67 [24]; R v Luttrell [2004] 2 Cr App R 520 at 539 [36]]:

"The value of [expert opinion] evidence depends ... above all upon the extent to which [the expert's] evidence carries conviction ...

[T]he defenders went so far as to maintain that we were bound to accept the conclusions of [an expert witness]. This view I must firmly reject as contrary to the principles in accordance with which expert opinion evidence is admitted.

... [The] duty [of expert witnesses] is to furnish the Judge or jury with the necessary scientific criteria for testing the accuracy of their conclusions, so as to enable the Judge or jury to form their own independent judgment by the application of these criteria to the facts proved in evidence.

... [T]he bare ipse dixit of a scientist, however eminent, upon the issue in controversy, will normally carry little weight, for it cannot be tested by cross-examination nor independently appraised, and the parties have invoked the decision of a judicial tribunal and not an oracular pronouncement by an expert."

94 It is sometimes said that these words deal with weight only, not admissibility. But this is contradicted by the Lord President's use of the word "admitted"."

It is in this respect that some parts of the Professor Levi's reports were deficient. The submission that all parts of the reports in question were admissible because the Professor Levi's reasoning could have been explored in cross-examination, is contrary to authority. It had to be accepted that Professor Levi did not provide any reasons or explanation for some of his conclusions, for example, that it was more likely than not that Mr Coote would have had an expected subsequent five year survival rate of 60 - 70% as at September 2009 based on a 2.1-4mm acral lentiginous melanoma. The explanation that this opinion rested on unidentified literature, for example, did not reveal the reasoning, based on that literature, which underpinned the opinion expressed.

In the result I concluded in general terms that in so far as the opinions which Professor Levi expressed were diagnostic opinions in his field of specialisation resting on the application of his specialised knowledge, training, study and experience, then his reports should be received because they were admissible. In so far as they were prognostic and relied on conclusions which Professor Levi had reached on the basis of unidentified and unexplained medical literature or epidemiological studies, they were not admissible. It was on this basis that certain aspects of Professor Levi's reports were not received.

Mr Coote suffered a plantar wart

In 2009, 2010 and 2011 the lesion on Mr Coote's foot was diagnosed by three treating GPs as a plantar wart and was treated as such. Warts are described in Murtagh's "General Practice" , 4 th Edition, the publication described as the 'GP's bible' as a skin tumour caused by the Human Papilloma Virus ('HPV'), (see at p 67). On the expert evidence they are able to be quickly recognised by general practitioners who frequently treat them. The diagnosis is simply made, given the presentation of the warts typical hyperkeratotic skin. They often cause pain, while on the evidence that is not the case for ALMs. The experts described a 'small' plantar wart to be 3 to 4mm in diameter.

Dr Lynch and Dr Jammal were not in agreement that the site of Mr Coote's lesion, described by Mrs Coote to have been at the juncture of the heel, the instep and the arch of the foot, was atypical for a plantar wart. Dr Lynch was of the view that it was and Dr Jammal that it was not. The other experts did not deal with this issue. The fact that the lesion was causing pain when Mr Coote first sought treatment was in Dr Jammal's opinion consistent with it being located on a weight bearing part of the foot, where such warts are typically found.

The specialists who gave concurrent evidence did not produce a joint report, but a measure of agreement emerged during the concurrent evidence. They agreed that the image in evidence of the lesion in March 2011 was not adequate to permit a clinical diagnosis of plantar wart to be made. That image showed what was variously described as a very advanced 4.4 mm melanoma, an obvious melanoma, with two different colours, together with the surrounding tissue. With the history of treatment that the lesion had been given in 2011, before the image was taken, it was the experts' view that there was a melanoma present, both when that treatment had commenced in January 2011 and beforehand. A melanoma of that size, with two positive lymph nodes, suggested that it had developed for a considerable time, a period of year or more, Professor William McCarthy assessed.

Professor Levi described the lesion in his report as a 'typical advanced stage melanoma with modularity and some degree of ulceration', as well as marked pigmentation. He thought it was the later stage of the melanoma which Mr Coote had suffered in 2009.

The other experts considered it possible that treatment given in early 2011 may have removed a verrucous (wartlike) surface present for a considerable period before the lesion was first seen by Dr Hiddins in January 2011; and that this treatment may also have caused the melanoma to grow more rapidly.

Pathological investigation of the tissue excised from Mr Coote's foot in 2011 found the presence of both HPV and ALM cells. HPV cells can be found anywhere in the body, but they are always found in warts. The expert evidence was that melanomas are not routinely tested for HPV cells, but that such cells have been found in small numbers of melanomas on microscopic examination, when they have been looked for.

Professor Levi's evidence was given before this pathological investigation was undertaken. He had earlier expressed the opinion that it was very unlikely that the lesion was a plantar wart in September 2009, which was later replaced by an ALM. He had no experience of treating plantar warts, but his literature review had failed to find such an association between the two conditions.

The tissue sample examined by Professor Stan McCarthy was only a thin slice of the lesion, in two slides representing both halves of the lesion. The HPV cells were not found in the melanoma, but were located at one side of the sample, between the melanoma and normal skin. That was where a papillomatous pattern was found, that being a pattern which is seen in plantar warts. Professor Stan McCarthy explained that ALM spreads sideways in the junctional zone of the epidermis. That HPV cells were present elsewhere in the lesion could not be discounted. That possibility had not been examined, but such cells had not been found in the part of the ALM which was examined.

The possibility that the lesion was a verrucous melanoma, that is a melanoma with elements that look like a plantar wart, was also considered during the concurrent evidence. This was a possibility, in Professor William McCarthy's opinion. The other experts disagreed. Professor William McCarthy agreed, however, that a reactive element in a melanoma would not result in a plantar wart developing. That was an unrelated condition.

Dr Katz' opinion was that it was very likely Mr Coote had suffered a plantar wart. Professor William McCarthy was not of that view. He had observed in his report that studies suggested that HPV infection becomes more prevalent as a melanoma progresses and that the cells found did not necessarily mean that there was a plantar wart. It was statistically unlikely that as well as the rare ALM condition, Mr Coote also had a plantar wart, but Professor William McCarthy accepted that the cells found could have been the residual remnants of a plantar wart.

Professor Stan McCarthy explained that on his examination of the slide the pattern was that of a plantar wart, given how it was indented into the underlying tissue, with the melanoma in the centre. A verrucous melanoma would have had verrucous elements throughout. A verrucous pattern was not found right throughout this lesion. In his opinion, the lesion was not a verrucous melanoma, but two lesions. The photograph of the lesion alone did not permit that conclusion to be drawn, but the pathology suggested it.

It was agreed by the experts that to suffer both an ALM and a plantar wart was an extremely rare condition, but a possible one. Growth of a wart as a reaction to a melanoma had not ever been encountered by the experts, but a lesion with more than one component had. The rate of growth of skin lesions, including warts and ALMs is known to be unpredictable. What the rate of growth of this wart and ALM was, could not be determined by the experts. In his evidence, Professor Levi had explained that the rate of growth could change.

The experts considered it to be relevant that between September 2009 and March 2010, three general practitioners had each examined the lesion, diagnosed it to be a plantar wart and treated it as such. They also noted the evidence of Mr Coote in 2009 having a lesion of about 3mm, raised 1 to 2mm, with the skin being darkened, which was becoming increasingly painful when he walked. Mrs Coote described then seeing a black spot, about the size of a match head, raised about 1mm, which she could not scratch off the skin. She was familiar with plantar warts and it did not look like one to her. Dr Kelly described the lesion in his clinical notes of 3 September 2009 as a large plantar wart, which he explained was a term he used to describe a wart of between 5 and 10mm diameter. In the face of that account the experts considered that that this lesion was very difficult to diagnose.

Conclusion

Mr Coote's case was that Dr Kelly was completely wrong in his diagnosis of plantar wart; Dr Wall was programmed by Dr Kelly's notes to see a plantar wart; and Dr Hiddins was a trainee, who Mr Coote told he had a plantar wart, was surprised at the suggestion that the lesion then on Mr Coote's foot was a plantar wart, but treated it as a wart anyway, without adequate investigation.

It was accepted, however, that one possible scenario which the evidence left open, is that what had stayed in Mrs Coote's memory was the small black mark which she described and which had caused her to urge Mr Coote to seek medical attention. What Dr Kelly had observed and acted on, at the end of a busy day, having already seen 26 patients and observing the lesion with only the naked eye, was also there, but he missed the small black spot which Mrs Coote had observed.

Given that the pathological investigation has established that even after all of the treatment which this lesion received between 2009 and 2011, there were still HPV cells and a papillomatous pattern at one side of the lesion, it seems to me that it cannot rationally be concluded that Mr Coote did not have a plantar wart in 2009 when Dr Kelly first saw him, notwithstanding Mrs Coote's evidence that the lesion did not then look to her as if it were a plantar wart.

The evidence that plantar warts often cause pain of the type which Mr Coote described, while ALMs do not may not be overlooked, nor may the HPV cells and the papillomatous pattern found on pathological examination. Before the lesion was excised, it had received repeated treatment since 2009, including repeated cryotherapy, repeated paring by Mr Coote and later by Dr Hiddins, acid treatment and the use of a pumice. Plantar warts generally resolve even without treatment within 2 years. Three general practitioners thought the lesion was a plantar wart and treated it accordingly. By the time of excision in 2011 the wart appears largely to have resolved, but the ALM had grown to an advanced state.

That there were still HPV cells and a papillomatous pattern present, at the time of excision, despite all of this treatment, suggests that Mr Coote did have a plantar wart when he first sought treatment for his painful lesion in 2009. I am satisfied that it must be concluded that it is probable that Mr Coote did have a plantar wart when Dr Kelly first saw him.

For reasons which I will explain, I am also satisfied that it must be concluded that Mr Coote had both an ALM and a plantar wart in September 2009. That is an extremely rare situation, one not previously encountered by the experts who gave concurrent evidence, but one which they accepted as being possible and which the treating general practitioners had to confront.

Mr Coote also had an ALM in September 2009

In issue between the parties was the state of the lesion in September 2009 and during the time it was being treated by Dr Kelly, up to March 2010.

For his part Dr Kelly accepted that it was possible that he could have erred in his diagnosis. On Dr Kelly's evidence he frequently treats plantar warts, seeing patients with plantar warts about once a month. They are usually easy to diagnose, given their distinctive characteristics. Dr Kelly had no memory of Mr Coote's consultations or of the lesion, but he gave evidence of his usual practice when diagnosing and treating plantar warts. Mr Coote's evidence confirmed that Dr Kelly followed that practice.

The consultation on 3 September was very short, after Dr Kelly had seen 25 other patients. Dr Kelly's diagnosis was made without magnification or additional illumination. He kept no notes of the features of the lesion or its location, apart from the description of the lesion being a 'large plantar wart'.

Dr Kelly's evidence was that this signified to him that the wart was then 5 to 10mm in diameter. On his evidence, if he had observed a discolouration of the type which Mrs Coote described, a small black spot the size of a match head, he would have adopted a different approach and referred Mr Coote for urgent specialist assessment.

That accorded with the evidence of Dr Lynch and Dr Jammal, who were agreed that a match head sized round black spot was atypical for a plantar wart, which more typically are observed to have tiny bloodspots at capillary sites. If such a spot was present, it required investigation.

The image of the lesion taken in March 2011 shows a large, highly pigmented, advanced ALM, which the experts agreed could not be mistaken for a plantar wart. They were of the common view that it was not possible to establish from this photograph alone, whether the lesion was pigmented in 2009 when first seen by Dr Kelly. The lesion could then have been virtually non-pigmented, slightly pigmented, or heavily pigmented. A pigmented melanoma does not typically acquire pigmentation, although the cells can lose that ability. Given the heavy pigmentation in 2011, it was considered that it would be very surprising if there was no pigmentation present in 2009, but whether it was then observable, could not be established from the photograph.

The dispute over the state of the lesion before March 2011 must be resolved in this context. Mrs Coote gave clear, unshaken evidence that she observed a match head sized circular black spot raised about 1mm, when her husband asked her to look at it. She could not scratch it off. That caused her to urge him to see a doctor. Mr Coote's description of what he could see and feel at the time was different. He first noticed the lesion in August 2009. He described feeling a 3mm lesion which was raised 1 to 2 mm above the skin and which he could feel below the skin as well. He could not see it clearly, only that the skin was darkened in that area.

That Mr and Mrs Coote were later unsure as to when exactly he first saw Dr Kelly, does not cast doubt on the reliability of their memories of what they saw, and what Mr Coote had felt, which caused him to seek treatment.

It was accepted by Dr Kelly that if Mrs Coote's recollection was accurate, he had erred in the treatment which he gave Mr Coote.

Both Mr and Mrs Coote's evidence was that the lesion was always dark, after the first treatment, even in the period between October 2009 and May 2010 when there was no cryotherapy. Their evidence is that the lesion continued to grow during that time. Mr Coote was then repeatedly paring it.

This evidence has to be considered in the face of the fact that Dr Kelly, Dr Wall and Dr Hiddins, who each treated the lesion over the course of some 18 months, diagnosed it as a plantar wart and treated it accordingly. In September 2009, Dr Kelly noted it to be a large plantar wart, which he explained meant a wart of between 5 to 10mm, when he saw it. That evidence must be accepted as reflecting a contemporaneous record of at least part of what Dr Kelly then observed. It is certainly consistent with Mr and Mrs Coote's evidence that the lesion was constantly growing.

Dr Wall also treated it as a plantar wart, but made no record of its features. His memory of it in September 2010 was that it was a hyperkeratotic lesion, thicker at one end and at the other where it was more superficial, it ended in a rim of dry skin. The surface had a yellow discolouration. It was not black.

It was Dr Hiddins' evidence that it was during the time that she treated the lesion, commencing in January 2011, that its appearance changed dramatically. On first presentation it looked like a typical plantar wart. Initially it responded to treatment, which involved paring, cryotherapy, application of acid between treatment, as well as use of a pumice stone. At the third treatment there had been no use of acid in between treatments and the lesion had not responded further. There was further treatment and on the fourth consultation a second lesion had grown and when she attempted paring, it bled profusely, with the result that a biopsy was undertaken.

On the expert evidence it is possible that in January 2011, there was a melanoma which was covered by verrucous tissue and that the treatment then given by Dr Hiddins and Mr Coote, repeated paring, cryotherapy, application of acid and use of a pumice stone, removed that tissue, uncovering the melanoma and affecting its rate of growth. That it looked like a typical plantar wart in January 2011, given its heavily pigmented appearance in March, did not seem likely, but it was accepted as being possible.

Mr and Mrs Coote's evidence that it always appeared black and crusty after it was first treated with cryotherapy, was not consistent with it looking like a typical plantar wart. However, given Mrs Coote's evidence that Mr Coote was initially picking at the lesion and himself later repeatedly paring it back with an army knife, before he saw Dr Hiddins, it does seem possible that there was verrucous tissue covering the lesion, including when it was seen on the one occasion by Dr Wall in September 2010 and when Dr Hiddins first saw it. Mr Coote was repeatedly paring something back to the skin. As Dr Katz put it, it was possible that there was so much keratin and scale and thickening then, that the melanoma was not obvious. That possibility accords with Dr Wall's description.

All of this does not, however, explain how Dr Kelly failed to observe and deal with what Mrs Coote said she observed in September 2009. What has to be resolved is whether or not that evidence can be accepted.

Mrs Coote's credit was not put in issue, but the reliability of her evidence was. The reliability of the three doctors was also put in issue. This was to be assessed, it was argued for Dr Kelly and accepted for Mr Coote, in accordance with the approach discussed in Onassis and Calerropolous v Vergiottis [1968] 21 Lloyds LR 403 at 431:

" "Credibility" involves wider problems than mere "demeanour" which is mostly concerned with whether the witness appears to be telling the truth as he now believes it to be. Credibility covers the following problems. First, is the witness a truthful or untruthful person? Secondly, is he, though a truthful person, telling something less than the truth on this issue, or, though an untruthful person, telling the truth on this issue? Thirdly, though he is a truthful person telling the truth as he sees it, did he register the intentions of the conversation correctly and, if so, has his memory correctly retained them? Also, has his recollection been subsequently altered by unconscious bias or wishful thinking or by overmuch discussion of it with others? Witnesses, especially those who are emotional, who think that they are morally in their right, tend very easily and unconsciously to conjure up a legal right that did not exist. It is a truism, often used in accident cases, that with every day that passes the memory becomes fainter and the imagination becomes more active. For that reason a witness, however honest, rarely persuades a Judge that his present recollection is preferable to that which was taken down in writing immediately after the accident occurred. Therefore, contemporary documents are always of the utmost importance. And lastly, although the honest witness believes he heard or saw this or that, is it so improbably that it is on balance more likely that he was mistaken? On this point it is essential that the balance of probability is put correctly into the scales in weighing the credibility of a witness. And motive is one aspect of probability. All these problems compendiously are entailed when a Judge assesses the creditability of a witness; they are all part of one judicial process. And in the process contemporary documents and admitted or incontrovertible facts and probabilities must play their proper part."

All of those who gave evidence in the proceedings, apart from the experts, have an interest in its outcome. As to motive, it is not relevant to Mrs Coote, whose credit was not put in issue. It is only Dr Kelly against whom Mr Coote has brought proceedings, but prior to the hearing, the other two doctors were put on notice that Dr Kelly reserved his rights to seek contribution from them, in the event that negligence on his part was established. They were both provided with Mr Coote's statement and Dr Wall's legal representative was present while Mr Coote gave his evidence on commission.

Even taking those matters into account, in my assessment, the credibility of all four witnesses may not be doubted, but their reliability has to be assessed.

All three doctors readily made concessions which were warranted, particularly in the case of Dr Kelly, even when they were contrary to their interests. Dr Wall and Dr Hiddins gave evidence that they had a recollection of their consultations with Mr Coote and the state of the lesion, which Dr Kelly said he did not have. This evidence must be considered in the face of Dr Lynch and Dr Jammal's doubts that a general practitioner could have a reliable recall of a particular patient's lesion at a particular time, especially with the lapse of time after treatment. It seems to me that while it is possible that their recall is entirely reliable, it is unlikely, having in mind the lapse of time, the number of patients they have each treated since seeing Mr Coote and the number of lesions which they must have seen over that period.

The reliability of the respective evidence must also be assessed in circumstances where the contemporaneous records prior to March 2011 shed little light on the appearance of the lesion, other than Dr Kelly's description of it as a large plantar wart on 3 September 2009. In each case the treating doctors' notes record a diagnosis of plantar wart and that cryotherapy treatment was administered. That, of itself, is a factor to be considered, given that these records were contemporaneous, even though they shed but little light on the presentation of the lesion after 3 September.

Given the controversy, it is necessary to consider all of this evidence, as well as giving close attention to the evidence which Mr and Mrs Coote gave as to what could be seen on Mr Coote's foot.

Mr Coote

Mr Coote is gravely ill. By consent his evidence was taken on commission. He had provided a witness statement and also gave oral evidence. Mr Coote's evidence was that he enjoyed good health and was physically fit and active before being diagnosed with melanoma in March 2011. He had first experienced pain on a spot on the sole of his left foot in August 2009. It was difficult for him to see, but his wife described it to him as:

" There is a dark circular mark, about the size of a match head, between the heel and arch of your foot which is raised above the adjacent skin."

When he saw Dr Kelly on 3 September, it was diagnosed as a plantar wart and treated with cryotherapy until the treatment became too painful. Dr Kelly advised that multiple treatments would probably be required. He advised that it was viral and of the steps needed to be taken to clean the shower floor to ensure that it did not spread. Neither Mr nor Mrs Coote ever questioned that diagnosis.

Mr Coote's evidence was that his foot was painful for about 10 days and he returned for a review with Dr Kelly on 15 September. He told him it was painful, Dr Kelly examined the lesion without any magnification instrument, used a scalpel and repeated the cryotherapy treatment for about 30 seconds, stopping when Mr Coote asked him to, due to pain. By then it had become asymmetrical crustier and darker in colour. This treatment was repeated on 30 September and 14 October 2009, with Dr Kelly scraping the lesion and applying cryotherapy on both occasions, for as long as Mr Coote could tolerate, about 30 seconds.

Dr Kelly gave no advice about the importance of monitoring any changes to the appearance of the lesion, or changes in size, shape, thickness, colour, surface, border, or any bleeding or ulceration. He took no photographs and did not suggest the need for a biopsy.

In November 2009, Mr Coote consulted Dr Jacqui Chirgwin about varicose veins in his left leg. He did not seek further treatment for the lesion until May 2010. By then it had tripled in size. This was after he had received endogenous laser and other treatment on the varicose veins in his left leg. By April, the lesion was so painful that it was causing a limp, to the extent that it was interfering with Mr Coote's work.

On 20 May, Dr Kelly again applied the same treatment, advising that 'there is nothing much else we can do'. Again, he gave no advice as to the need to keep the lesion under observation and did not suggest a biopsy. The lesion continued to grow. Mr Coote was limping and walking on his toes, in order to avoid the lesion making contact with his shoes or the ground. He made jokes that he had given it a postcode, because it had grown so big.

When Mr Coote saw Dr Wall in September he told him he was seeking treatment because he was having difficulty walking because of the lesion. Dr Wall also applied cryotherapy treatment. He began using corn pads to cushion the lesion. He sought further treatment from Dr Hiddins in January. She also initially applied cryotherapy treatment which later ceased and she sent him for biopsy.

In cross-examination, Mr Coote's evidence was that he had a good memory of what had transpired. He denied that he had instructed his solicitors that the first time that he noticed a black spot on his foot was in March 2010. When he saw the surgeon in 2011 and later instructed his solicitors, he did not recollect the precise dates when he first saw Dr Kelly, but he recollected first noting the spot in 2009. He did not then actually examine it himself, because he had difficulty seeing it, but he felt like he had a small pebble in his shoe, he felt the lump and he could see ' a slight colouring of my skin'. His wife then told him it was 'a dark circular mark'. It was very uncomfortable, but he was not sure how long it had been developing for, before he sought treatment.

Between September 2009 and September 2010, he looked at the lesion a number of times. After cryotherapy the skin around the lesion was slightly darker and he used a Swiss army knife to pare the skin because the pressure was causing discomfort, but not to the point of bleeding. He did not notice any small black spots in the centre. It was never flat. In September/October 2009 it was 'maybe a millimetre, a couple of millimetres' and it felt like it had some depth under the skin. There was something pushing into his foot. After the cryotherapy it became considerably darker, grey going onto black, it became crusty and more raised in appearance. Over time it became bigger.

Between May and September 2010, he had not been using any topical treatment, but it had grown even bigger, even though he had been continuing to scrape it off. It was very painful. When he saw Dr Hiddins in January the lesion was black, but it had grown, now being 2, 3 or 4mm high. It was crusty and irregular in shape, asymmetrical . A fortnight later it was basically the same size. There was only ever one lesion. It was bigger than 5mm in size. He was then looking at the lesion every day. It was always black.

Mrs Coote

Mrs Coote is a PDHPE teacher at a high school, a part-time academic at university and a former successful athlete. She herself suffered plantar warts as a teenager, which she treated herself with topical medications such as acid; she has taught about such warts at high school and has frequently seen them on student's feet. When Mr Coote asked her to look at his foot in August 2009 she did not think that he had a plantar wart. She thought he had a small piece of tar stuck to his foot and tried to scrape it off. It was a black lesion about the size of a match head, slightly raised by about a millimetre.

In her statement Mrs Coote's description was that the lesion changed after the cryotherapy treatment. It grew in size, becoming very black in the middle and dark brown on the outsides. It became crusty, asymmetrical and more raised. It looked like it had bled into the skin and was leaching outwards. As it became more raised Mr Coote shaved the top of the lesion with an army knife, because it was uncomfortable. He was then training for entry into the police force. He later had to use a corn pad to cushion the lesion and eventually two.

Mrs Coote's evidence in cross-examination was that when she first saw the lesion it was not 10mm in diameter. It was not then raised 2mm, it was only slightly raised. She regularly saw the lesion, because she had to put a bandaid over it each day after the cryotherapy treatment and later had to help her husband cushion the lesion with corn pads, when it became more painful to walk on. After cryotherapy the skin around the lesion was red, but the centre was black, with the red fading over time. It got bigger over time, but between August and September 2009, Mr Coote was scraping the top off with his fingernail. It continued to grow and at the beginning of 2010 he was paring the lesion with an army knife, sometimes to the point of bleeding. He also used a pumice stone. It was still black and bleeding into the surrounding skin. When he saw Dr Wall in September 2010 it was the size of a one cent piece, (which I understand to be about 17 mm in diameter). It was crusty on top and round and black and had dark brown purply bits at the bottom coming out, where it was leaching. It was more than 2mm high and Mr Coote was continuing to pare it.

By January 2011 when he saw Dr Hiddins, Mrs Coote's evidence was that the lesion looked similar, but it was no longer round and was slightly larger than the size of a 5 cent coin (by which I understand that it was about 20mm in diameter). By 28 January there were not two lesions, but the original lesion had extended. Mrs Coote did not see it after Dr Hiddins' final treatment, because it was dressed.

Conclusion

It does not necessarily follow from the presence of the advanced ALM in March 2011, that in September 2009, Mr Coote already had an ALM. Mrs Coote's evidence was that there was only ever one lesion and that what looks like two lesions in the 2011 photograph, was only the result of the growth of the original lesion. Mr Coote also said there was only one lesion. Dr Hiddins' evidence that a second lesion emerged in February 2011, admits of the possibility that the ALM appeared only then, but that was viewed by the experts to have been most unlikely, given the advanced stage of the ALM on excision. They also doubted that the lesion in the photograph could have looked like a plantar wart in January, although accepting that it was possible. On all of the evidence, it appears that in January there was then an advanced ALM, given its size in March, even if it was covered with verrucous skin.

What points most strongly to the presence of an ALM in 2009 when Dr Kelly first saw Mr Coote, was Mrs Coote's description that when she first saw the lesion in August 2009, there was a slightly raised black spot at the site and Mr Coote's evidence that he could not see the lesion clearly, but he could see that the skin was darkened. That caused Mrs Coote to urge Mr Coote to seek a doctor's advice. Had she thought it was a plantar wart she would have first treated it topically, as she had treated her own warts in the past.

Mrs Coote described the lesion after cryotherapy to have been black. Dr Crosland explained that cryotherapy would have produced red/black/brown pigmentation consistent with Mr and Mrs Coote's description of its appearance after that treatment, but that should have healed prior to the next treatment. The continued presence of such discolouration after October 2009 suggests a different cause, namely the presence of the ALM. Mrs Coote's description of the lesion after cryotherapy, of a black spot in the middle of the lesion, with dark brown around it, is also consistent with the presence of both an ALM and a plantar wart.

Having carefully considered all of the evidence, I am satisfied that it has been shown that it was probable that Mr Coote was suffering an ALM when Dr Kelly first saw him in 2009. I have concluded that Mr and Mrs Coote's evidence cannot be rejected as being unreliable, even though the presence of the small black spot which she described was not noted by Dr Kelly, who candidly admitted that he could not recall the lesion and that there was a possibility that he had made an error.

The acceptance of Mrs Coote's evidence must lead to the conclusion that Dr Kelly did err, even though I am entirely confident that his error was not deliberate and that what he was confronted with was extremely unusual, given that Mr Coote was suffering from both an AML and a plantar wart. On the expert evidence, this lesion was difficult to diagnose. Nevertheless, I am of the view that the black spot which Mrs Coote described was present when Mr Coote saw Dr Kelly and had to be investigated.

The aftermath

Mr Coote was referred by Dr Hiddins to Dr Ralph Gourlay, an oncologist and the lesion was excised on 29 March 2011, when a skin graft was performed. It was then found to be 4.2 - 4.4mm deep, after having been repeatedly pared by Mr Coote, as Mrs Coote described. He used a pumice stone as well and then it was pared further by Dr Hiddins in January. It follows that the unpared thickness of this lesion could have been greater than that measured on excision.

On 6 April, Mr Coote was advised that the melanoma had metastasised to the lymph nodes in his groin and on 13 April he underwent radical groin dissection surgery. The skin graft later failed and he developed a staph infection. After release from further hospitalisation, two satellite melanoma were removed from his left foot. Three further spots later developed and then three more. Mr Coote developed lymphedema and received painful isolated limb infusion treatment, involving injection of chemotherapy.

Mr Coote was unable to exercise, gained weight and was diagnosed with diabetes in September 2011. He gave oral evidence as to the ulcerated state of the lesion and the difficulty of treating it. The melanoma metastasised to his spine and later through many other parts of his body, externally and internally. The quality of Mr Coote's life has been severely affected, as has his emotional condition. He has been unable to work since March 2011 and is unable to pursue his normal activates. He now faces imminent death.

Prognosis for ALM

Murtagh's " General Practice ", 4 th Edition suggests that ALMs have poorer prognosis than other types of melanoma.

In the 1999 National Health and Medical Research Council's Clinical Practice Guidelines ("1999 NHMRC Guidelines") for the management of cutaneous melanomas 10 year survival rates for melanomas 1.5 mm - 3mm thick was estimated to be 75.4%; for those 3.0 mm - 4mm thick, 55%; and for those over 4mm, 40%. These estimates can be affected by the presence of other factors, including ulceration, lymphatic invasion, satellites and high mitotic rate.

The 2002 American Joint Committee on Cancer ("AJCC"), Cancer Staging Manual indicated that in localised melanoma, the most powerful characteristics to consider were thickness, with ulceration second. Increasing nodal involvement also significantly decreased survival. The 10 year survival rates for a T3 melanoma, a melanoma of 2.01 - 4.0mm, without ulceration or metastases, was 63.8%. At greater than 4mm, a T4 without ulceration, was 53.9%. With metastases the rates decline. The same staging criteria are used for ALMs as for other melanomas, even though it was noted that their prognosis may differ somewhat. The range of survival rates varies significantly, depending on the nature of any metastases.

In the 2008 NHMRC Guidelines for the management of melanoma in Australia and New Zealand, a melanoma of 2.01 - 4.0mm, without ulceration or metastases, was also 53.9%.

Dr Lynch based his opinions on an acceptance of Professor Levi's assessment "that as at September 2009 the melanoma would have been somewhere between 2.1 mm and 4 mm thick (say 3mm) and there would not have been any lymph node metastases. There was not any ulceration." I have already referred to Professor Levi's opinions, On the 2009 AJCC ( Melanoma of the Skin Staging ) publication data he considered this to be a IB or IIA melanoma with a 10 year survival indicator of between 63 - 80%. Under the 2008 NHMRC Guidelines, it was at T3a stage, with a 10 year survival indicator of 63.8% and under the 1999 NHMRC Guidelines, a pT3a with a 10 year survival indicator of 75.4%.

Dr Crosland's opinion was that given the size of the tumour in August/September/October 2009, raised above the skin by 1-3mm, it was entirely possible that it was already in an advanced or invasive stage and that metastasis to the lymph nodes or blood vessels had already occurred. At a 2mm elevation, the 5 year survival rate was in the order of 50%, about 10% more if no nodes were involved and 10% less, if they were. That it could be pared back suggested that it was significantly raised.

As well as giving concurrent evidence, Dr Crosland was shortly cross examined, without objection. His evidence was that a patient presenting with a thin melanoma had a high probability of being cured, but that this reduced substantially with the growth and increased thickness of the melanoma. The thickness of this melanoma in 2009 was not known, but on the available information it was not thin. He explained that tumours expand more or less symmetrically, as they go up they go down. If it was only 2 mm thick in September 2009, it had grown significantly to 4.4 mm in March 2011. On the expert evidence the chance of metastases increased with its increasing size.

The case pressed for Mr Coote was that in September 2009 he did not have a lethally advanced melanoma. The thickness of the ALM was then only 2 mm. As I will explain below, that case was not established on the evidence.

Dr Kelly departed from common practice

Concurrent evidence was given by Dr Lynch and Dr Jammal, as to the practice of general practitioners. While they initially disagreed about a range of matters, a joint report emerged, which revealed that their disagreements had been significantly reduced. Those conclusions and the evidence which they gave concurrently, established aspects of the negligence alleged.

The joint report had regard to two scenarios. One in which on presentation to Dr Kelly Mr Coote had the small black lesion on his foot which Mrs Coote described and the other where the lesion was a plantar wart. It was agreed that if the lesion had looked like a plantar wart on initial diagnosis, a differential diagnosis of ALM would not have been considered by a competent general practitioner, but if there was a black spot, it required further investigation.

I have found that Mr Coote suffered from both a plantar wart and an ALM when Dr Kelly first saw him. There was a small black mark to be seen at the site of the lesion, as well as the keratinised lesion Dr Kelly explained his description of the lesion in his notes as a 'plantar wart' encompassed.

In the event that the lesion seen was dark or black in colour, the experts agreed that Dr Kelly did not act in accordance with widely accepted practice, but should have examined the lesion with magnification; obtained a history of the lesion; considered ALM as a differential diagnosis; and referred Mr Coote for biopsy and specialist assessment. A spot of about 2mm, like a match head, was not consistent with blood spots typically seen in plantar warts, which are capillaries. It follows that this spot was atypical and required investigation.

This conclusion is particularly relevant, given the evidence of Mr Coote and Mrs Coote, that the lesion was always black from the time that Dr Kelly first began cryotherapy treatment. A plantar wart treated with cryotherapy can become darkly pigmented, because of the effect of that treatment on the blood vessels. Such damage normally heals. On the evidence that did not occur in the case of this lesion. As Dr Jammal explained, in general practice consideration of a differential diagnosis is called for when something atypical is presented.

Even if on first presentation the lesion had the appearance of a plantar wart, by May 2010, the experts agreed that Dr Kelly ought to have taken a history as to what had occurred to the lesion since he last saw Mr Coote in October 2009. That did not occur. Dr Kelly noted the lesion on initial presentation as a large plantar wart, by which he explained he meant one sized 5 to 10mm. Thereafter the lesion is only ever described as a plantar wart, without any description given, or changes noted.

As explained by the experts, keeping a clinical note of the appearance of the lesion at that time was important, both because it is impossible to retain an accurate memory of what the lesion looked like, for future care and in order to meet legal obligations. As the experts explained, the capacity to remember particular patients and consultations varies, hence the importance of keeping records.

Duty of care and breach

There was no issue between the parties as to the nature of the duty of care which Dr Kelly owed Mr Coote and that in the event that it was concluded that Mrs Coote's description of what she observed on Mr Coote's foot was accepted, namely that the lesion was pigmented when first seen by Dr Kelly, that this duty had been breached. The risk of harm to which Mr Coote was exposed was also not in issue.

Given the conclusions I have reached, it follows that this aspect of the case was established. The lesion was pigmented as Mrs Coote described when Dr Kelly first saw Mr Coote.. There was a risk that Mr Coote was suffering from a melanoma. That risk required the investigations Dr Kelly described should be pursed, in accordance with the National Health and Medical and Research Council's Guidelines, which recommend identification and treatment of melanomas at the earliest stage possible. The failure to refer Mr Coote for that assessment exposed him to a risk of death, with it being noted in the 2008 NHMRC Guidelines that only 34% of those diagnosed with metastatic melanoma are alive 5 years afterwards.

It thus is not necessary to deal with the requirements of s 5B and s 5C of the Civil Liability Act .

Causation

In order for Mr Coote's claim to succeed, causation must also be established. That issue must be approached in light of the provisions of s 5D of the Civil Liability Act , as discussed in Adeels Palace Pty Ltd v Moubarak [2009] HCA 48; (2009) 239 CLR 420. A t [45] it was observed:

"Next it is necessary to observe that the first of the two elements identified in s 5D(1) (factual causation) is determined by the "but for" test: but for the negligent act or omission, would the harm have occurred?"

The High Court's recent decision in Strong v Woolworths Ltd [2012] HCA 5 at [17] to [35] was also relied on. There it was observed, amongst other things at [34] that:

"a plaintiff must prove his or her case on the balance of probabilities and it is no answer to the question whether something has been demonstrated as being more probable than not to say that there is another possibility open [ Kocis v S E Dickens Pty Ltd [1998] 3 VR 408 at 430]. The determination of the question turns on consideration of the probabilities."

The section provides:

"5D General principles

(1) A determination that negligence caused particular harm comprises the following elements:

(a) that the negligence was a necessary condition of the occurrence of the harm (factual causation), and

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

(2) In determining in an exceptional case, in accordance with established principles, whether negligence that cannot be established as a necessary condition of the occurrence of harm should be accepted as establishing factual causation, the court is to consider (amongst other relevant things) whether or not and why responsibility for the harm should be imposed on the negligent party.

(3) If it is relevant to the determination of factual causation to determine what the person who suffered harm would have done if the negligent person had not been negligent:

(a) the matter is to be determined subjectively in the light of all relevant circumstances, subject to paragraph (b), and

(b) any statement made by the person after suffering the harm about what he or she would have done is inadmissible except to the extent (if any) that the statement is against his or her interest.

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

The case advanced for Mr Coote

In opening it was explained that Mr Coote's case was that he suffered a melanoma on his foot in 2009, which Dr Kelly wrongly diagnosed and treated as a plantar wart, a benign non-cancerous condition, which is usually rough and spongy. The melanoma resembled a small black mole about 3mm in diameter. When it was excised in April 2011, it was ulcerated, about 22 by 21mm,and 4.4 mm thick. Its downward penetration through the cutaneous levels of the skin had allowed the cancer cells to disseminate throughout Mr Coote's body and to metastasise, with fatal results, attempts to eradicate the melanoma with various treatments having failed.

The final submissions advanced for Mr Coote admitted of the possibility that Mr Coote was suffering both a plantar wart and an ALM in 2009. It was submitted, nevertheless, that the evidence showed, on the probabilities, that the failure to diagnose the ALM in September 2009 materially contributed to Mr Coote's situation in March 2011.

The best evidence as to the size of the tumour in 2009 was argued to be Mrs Coote's evidence, which threw up a maximum thickness of 2 mm. In the result it followed that the failure to diagnose the tiny lesion which Mr Coote had when Dr Kelly first saw him, contributed to Mr Coote having the large lethal lesion which was excised in March 2011. Dr Kelly's evidence, standing alone, would entitle Mr Coote to a verdict. Other evidence also established that on the balance of probabilities, excision in 2009 would have prevented Mr Coote suffering metastases to skin and organs, as well as relieving him from the pain and discomfort he had suffered to his foot for 18 months.

It was submitted that the evidence established that removal before metastases had enormous prognostic significance. Professor Levi's evidence that tumours grow by metastasising to local tissues, would not be accorded the meaning contended for Dr Kelly, of metastases to lymph and distant tissues. On Dr Crosland's evidence, survival from melanoma is high if caught early, with 96% alive after 5 years, but only 34% after metastatic melanoma.

It was also submitted that the epidemiological data relied on was reliable. It reflected the observation of thousands of melanoma patients around the world, commencing more than 60 years ago. It established the association between tumour growth, tumour depth, metastases and premature death

It was argued that the data established that in September 2009, Mr Coote's prognosis was 89% survival at 5 years for a tumour of less than 2mm or 79% at 10 years; or for a 2.1-4 mm tumour, 78.7% at 5 years and 63.8% at 10. In April 2011 his tumour had only a 5 year survival rate of 18.8% and for 10 years, 15.7%. This material, when considered together with the fact that detectable metastases did not occur until more than 18 months after September 2009 and with Dr Crosland and Professor Levi's opinions, established both factual and legal causation.

It followed on Mr Coote's case, that the onus which fell upon him to establish that it was more probable than not, that Dr Kelly's negligence had caused or materially contributed to his injury had been met, the standard of proof for causation being 'relatively low', as discussed in Tabet v Gett [2010] HCA 12; (2010) 240 CLR 537 at [145] per Kiefel J (Hayne, Crennan and Bell JJ agreeing).

There the High Court considered the question of causation in a medical negligence case. The plaintiff had pursued his claim on the basis of negligence which had resulted in the loss of a chance of a better outcome. That approach was rejected. It was held that a plaintiff must prove that the defendant's negligent act or omission caused the injury which resulted in the damage suffered, or as explained at [66], it must be shown 'that a difference has been brought about and that the defendant's negligence was a cause of that difference.' That was what Mr Coote sought to establish by the case pressed, that the ALM was only 2mm in diameter when he first saw Dr Kelly.

There was no issue in this case that if it was found that Mr Coote had an ALM in 2009, that if a biopsy had then been undertaken, the ALM would have been identified and treated. Mr Coote's case was that it was Dr Kelly's failure to send him for a biopsy, which had resulted in damage of the kind discussed in Tabet v Gett . For Dr Kelly it was argued that the evidence did not establish that treatment in 2009 would have resulted in any difference for Mr Coote, given the size of the lesion in September 2009.

What must thus be determined is whether it has been established on the evidence, that it was more probable than not, that had a biopsy been undertaken in 2009 and treatment for the ALM then followed, that the damage suffered by Mr Coote after the biopsy was undertaken in 2011, would not have been suffered. That damage resulted from metastasis. Mr Coote's case was that excision in 2009 would have prevented such metastasis.

It was submitted for Mr Coote that it had been established that the evidence established that in 2009 he was suffering:

"... a tiny lesion (compared to the advanced lethal lesion present in March 2011) probably , not with scientific certainty, contributed to his having a large lethal lesion and dissemination of its cells to the sentinel femoral node by late March 2011, 1 1/2 years later."

The result was said to be that an:

"'onus shifts to the defendant to prove to the same standard that that the 'miniscule (in relative terms) melanotic lesion as it then was would have irrespective of removal in September 2009 have left the plaintiff in equal plight those 1.1/2 years later."

This burden could not be met it was argued, given Dr Kelly's concessions. His evidence was:

"Q. It is pretty obvious, isn't it, that if the evidence of Mr and Mrs Coote as to the lesion were found to be reliable then the non diagnosis of what they have described has certainly led to a much worse result than would have transpired?

...

WITNESS: That statement would be true.

...

Q. Will you assume that the affidavit relates that over the six week period from the beginning of September 09 to mid October 09, Mr Coote opposes that the lesion on his foot grew in size. What do you say to that proposition?

A. I have no recollection specifically of the size of the lesion, nor have I made a note recording the size.

Q. He has deposed that the lesion during that period, was becoming darker in colour. Are you able to again say that proposition?

A. It would not be unusual for the colour of the tissue to change in response to the damage caused by the cryotherapy.

Q. He deposes that it became crustier?

A. Again, it would be not unusual for the lesion to become crusty in response to the cryotherapy.

Q. He also relates how it became to whatever degree, more raised in appearance during that period. Did you observe that phenomenon?

A. I had no specific recollection of that, no.

Q. And you made no note as to whether it had or hadn't?

A. That's right.

Q. Mr Coote describes the lesion during that period as becoming more asymmetrical in shape. Are you able to reject that proposition?

A. I have no specific recollection.

Q. And again, you made no note as to whether it had stayed the same or changed as to its shape?

A. That's right.

Q. He also says that during that period, it was flaking around the perimeter?

A. Again, that would not be unusual given the damage caused by cryotherapy.

Q. He deposes that the location, however, of the lesion, never changed throughout your course of cryotherapy. Do you agree with that?

A. That's as I'd expect, yes.

Q. Is it true that in the course of those consultations, you said nothing to Mr Coote concerning the importance of monitoring for any changes to the appearance of the lesion?

A. I have no specific recollection of what was said during those consultations.

Q. Do you deny that you were silent as to that proposition?

A. Again, I don't recall what was said during those consultations.

Q. Do you agree that you said nothing concerning the need for him to monitor the appearance of the lesion, and more specifically, as regards its size, first of all?

A. I have no specific recollection of what I said during those consultations.

Q. Nor anything concerning the edge or any thickening of the lesion?

A. My answer remains the same.

Q. Nor did you say anything to him about observing for any change in shape?

A. No specific recollection.

Q. Do you agree that you said nothing to him about being alert for any change in colour of the lesion?

A. I don't have a recollection of that.

Q. And similarly, do you agree, you said nothing to him concerning the need to observe for any change in the surfaces of the lesion or its appearance?

A. I don't have a recollection of what was said in those consultations.

Q. And do you deny that you failed to enjoin him to observe for any change in the border, or for any bleeding or ulceration?

A. I have no recollection of what was discussed.

Q. Have you seen the diagrams annexed to the transcript of Mr Coote's evidence among D and E?

A. I'm not sure. I can't be sure.

....

Q. And you'll see at the top left, doctor, and the date 3/9/09, depicted, a small circular

A. Yes.

Q. symbol?

A. Yes.

Q. Similarly, on E, at page 100, under the date 14 October 2009, a larger and slightly

A. Yes.

Q. asymmetrical depiction?

A. Yes.

Q. As to the diagram pertaining to 3 September 2009, do you agree that that is representative of something that was observable to you at that consultation?

A. I think I've explained earlier that the word I used was "large", and I wouldn't represent that as large, no.

Q. And as to the diagram on the 14th, marked E, do you agree that that is diagrammatically representative of what was to be observed on Mr Coote's left foot on 14 October 2009?

A. Again, I have no specific recollection, however, one would expect damage from the skin consistent with the cryotherapy of the order that's described in those diagrams.

Q. Do you say, doctor, that a growth in size as represented by those two diagrams, could be attributable to cryotherapy?

A. Yes.

Q. Whilst maintaining the same or a slightly increased degree of pigmentation?

A. Damage to the skin attributable to the cryotherapy, yes. As skin dies, it discolours.

Q. In any event, you made no note whatsoever of any change in the lesion?

A. That's right.

Q. You recall, I took you to the National Health and Medical Research Council's recommendations about management of skin lesions?

A. Yes.

Q. As I understand it, doctor, you may take issue of whether they applied to the particular lesion, as you have it, but you'd agree that they are a set of very common sense propositions and guides?

A. Yes, yes.

Q. It makes sense to follow them. In fact, it would be irrational not to. Do you agree with that?

A. In the circumstances where that's what I was treating, yes.

Q. My friend asked you about whether, if this was a lesion when you treated this lesion was malignant as at September 2009, whether the delay in diagnosis must have caused a worse outcome for the patient, and you answered "yes". In that, giving that opinion, would you defer to the expertise of the dermatology?

..

Q. In agreeing with my friend's proposition, what did you turn your mind to?

A. What it meant was, what I understood the question to mean was, if a person had an identifiable cancer at that point, would delay the diagnosis of a cancer at that point, result in the worst outcome in the event that we know that's what it was, that that's if we knew that it was a cancer, yes, delay would have made the outcome worse, but I wasn't referring to the lesion that I was treating, so I didn't believe, I don't believe that I saw a pigmented lesion."

Despite Dr Kelly's evidence, it seems to me that Mr Coote's case must fail, relying as it does to a very great extent on survival rates derived from epidemiological studies.

The challenge to the use made of the epidemiological studies

As was explained for Mr Coote, the use sought to be made of the epidemiological studies relied on was in part as the result of Dr Kelly's failure to note and deal with the small black spot present on his foot in 2009. Even so, what must be considered is whether or not the case Mr Coote advanced has been established on the evidence.

It was the case put for Dr Kelly that the epidemiological data on which the case advanced against him rested, did not permit the onus which fell upon Mr Coote to be met by reasoning backwards from what was known in March 2011, namely that there had by that time been a metastatic spread from the ALM, to the conclusion that in September 2009, the melanoma had not metastasised. Nor could that be determined from the estimates variously made, as to the then thickness of the tumour. There is some force in that submission, it seems to me.

These epidemiological studies are used in clinical practice to determine not only prognosis, but also treatment. They are not used for diagnosis. Professor Levi explained that they do not establish likely prognosis, only possible prognosis. Application of these studies depends on an assessment being made of the stage and grade of the melanoma in question. Various information, including tumour thickness and whether or not metastasis has occurred, is used to determine the grade and stage of a particular tumour. That information is not known in this case. The fact that metastasis was not found until after excision of Mr Coote's lesion, does not establish that it had not occurred in 2009. It is not known whether or not the ALM had then metastasised. That possibility was not looked for then.

That is why estimates have been made of the thickness of the tumour in September 2009 and those estimates sought to be used, in order to establish that it was probable that at that time, metastasis had not occurred.

The case finally pressed rests on Mrs Coote's evidence, that when she felt the small black spot, that it was raised only about 1mm. In considering the thickness of the tumour when Dr Kelly first saw Mr Coote, his evidence may, however, not be overlooked. Indeed, the experts had regard to his description of what he could then feel, in reaching the opinions which they expressed in their reports. They were not aware of Mrs Coote's oral evidence before giving their concurrent evidence. What all of the evidence has shown is that this was not only a most unusual lesion, given the presence of both a plantar wart and an ALM, but that it was of considerable size, even when Mr Coote first saw Dr Kelly. What impact the HPV cells had on the melanoma is not understood, but the evidence does show that this was, from the outset, a constantly growing tumour. The evidence also suggests that at certain times, it was fast growing.

What Mr Coote said was that he first felt something like a pebble in his shoe, in August 2009. He described it to have been about 3mm in diameter, 1-2mm high and he could also feel it under the skin. Mrs Coote saw a small black 2 mm spot, raised about 1mm at the same place on Mr Coote's foot. Given Mrs Coote's description of Mr Coote even then picking at this lesion, that it was at the upper end of Mr Coote's description of being raised by 1 to 2 mm high, or indeed possibly even more, also follows.

Mr Coote saw Dr Kelly on 3 September when the lesion had plainly grown. It was then about 5 to 10mm in diameter. That the ALM had also grown in thickness, is clearly possible. Dr Kelly gave no evidence about this. Nor did Mr Coote, but given Mrs Coote's evidence that he was already then picking at it, the possibility of such growth is plainly present.

Mr and Mrs Coote's evidence was that it continued growing rapidly. They later told the surgeon in May 2011, that 12 months before, it had ulcerated. That seems to have occurred after Dr Kelly's last treatment. By September 2010 Mrs Coote estimated it to have grown to 17mm in diameter and by January 2011, to 20 mm. That does not accord with Dr Hiddins' evidence that there was initially a 5mm lesion when she saw Mr Coote on 11 January and by 11 February it had grown to 10 mm, with a second 5mm lesion adjacent. Her clinical notes record a large 5 mm wart that appears to be contracting on 28 January and a large wart of 10 mm and a second wart of 5 mm on 11 February. That also does not accord with this lesion being 5 - 10mm when first seen by Dr Kelly, nor with Dr Wall's recollections.

Given that it was Mrs Coote who looked at this lesion repeatedly, when she had to put band aids on the lesion each day after each cryotherapy treatment and throughout the time that Mr Coote was using corn pads, initially one and later two, to accommodate its growing size, it seems to me that her recollection of its size at various times is likely to be more reliable than that of the doctors who saw it only relatively few times. On excision the lesion was even larger than her estimates.

Nevertheless, even accepting the basis of the case pressed for Mr Coote, it is the thickness of the ALM in 2009 which is the critical measurement relied on. That it was only 2 mm thick in September 2009 was not established. On excision in 2011 its Breslow thickness was microscopically determined to be 4.4 mm, but what must be considered is that beforehand, this lesion had been picked at in 2009 and repeatedly pared and pumiced by Mr Coote in 2010, back to the skin as Mrs Coote explained. It had been treated with cryotherapy by the three general practitioners in 2009, 2010 and 2011 and in 2011 Dr Hiddins had again pared it back three times and Mr Coote had pumiced it, not long prior to the excision. By the time that the lesion was excised, there was nothing left to be seen of the plantar wart.

It follows that the measurement of the thickness of the ALM taken on excision was a measurement of what then remained of this advanced ALM, after any further growth, after the cessation of Dr Hidden's treatments, not long beforehand. As the experts accepted, it follows that unpaired, it could then have been thicker than 4.4 mm.

What all of this evidence does not permit is a conclusion that in September 2009 this melanoma was either 'tiny' or 'miniscule', as was submitted for Mr Coote. Nor was it established that it was probable that it was then only 2mm thick. Professor Levi's opinion was that it then had a Breslow thickness of 2.1 - 4 mm. He gave a range, which he explained in cross-examination was as close as he believed anyone could get to an estimate, based on the available information. That range did not permit this to be considered a 'thin' melanoma, which has high prospects of complete cure on excision. Such a melanoma has a cut off of only 0.75 mm thickness.

Dr Crosland postulated that in September 2009 the ALM could have been raised by up to 3 mm, given that it was repeatedly pared. Dr Crosland's explanation that melanomas generally extend at least as far below the skin as above must also be considered.

On all of the evidence it seems likely that when Dr Kelly first saw the lesion in 2009, it was at the upper end of the thickness that Professor Levi postulated, namely 4 mm, not the lower end, 2.1 mm. It may have been more. If it was greater than 4mm, which Professor Levi accepted in cross-examination was possible, Mr Coote's prognosis was much worse than Professor Levi suggested and considerably worse than what flowed from the case finally advanced in submissions, that it had a thickness of only 2 mm.

Professor Levi agreed that the 2011 Breslow thickness of 4.4 mm would have been reduced by the treatment Dr Hiddins had earlier given the lesion in 2011 and that the lesion might in 2009 have been thicker than he had assessed, he thought by perhaps 0.1 mm to 0.2. Given Mrs Coote's evidence of Mr Coote's earlier repeated picking and paring of the lesion, that is a strong possibility.

The evidence is that Breslow thickness is one of the most important diagnostic factors in predicting life expectancy on diagnosis, but it is not infallible. Epidemiological studies undertaken in the last 20 to 30 years, show that it provides one reliable measure as to prognosis. Another important factor to be considered is metastases.

Dr Crosland's opinion was that it was entirely possible, given Mr Coote's description of the lesion, that the ALM had already metastasised in September 2009 when he first saw Dr Kelly. In that case, the 5 year survival figure was in the order of 50%, 10% greater if no nodes were then involved and 10% worse, if they were.

As to metastases, Professor Levi explained in his cross-examination the importance of the Breslow measure to be that it reflected the degree of penetration of the malignant cells into the skin's surface, which has contact with the lymphatic and blood systems, as well as being indicative of the melanoma's propensity to metastasise.

Professor Levi also explained that the appropriate treatment for the lesion in 2009 was surgical excision, which carried with it the risk of the need for a skin graft, carrying with it the risk of failure and infection. A sentinel node biopsy would also then have been required, to determine whether there had been metastases and if there was a positive result, more lymph node dissection would have been necessary. Had metastases then been found, consideration would have been given to chemotherapy and immunotherapy, although the latter would have depended on Mr Coote's eligibility for clinical trials. Had there been metastases, it is apparent that Mr Coote was even then at risk of the result he has now suffered.

Professor Levi further explained that whether or not there is metastases to other body parts from a particular melanoma, depends on the nature of the cells within that melanoma, not its size. It was the biological behaviour of the individual's melanoma cells which was the ultimate determinant of metastases. He agreed that despite what the epidemiological studies showed, it was possible for lesions with a Breslow thickness of under half a millimetre to metastasise, with fatal results and those with a 4mm thickness never to metastasize.

Professor Levi also explained that the removal of a lesion before metastases was of enormous prognostic significance for life expectancy, because it allowed for the likelihood of a cure. Removal of a melanoma did not, however, remove the chance that there had already been microscopic metastases beforehand, which had not yet lodged in an organ. When cells metastasised they spread over immediate local tissues, then beyond by lymphatics or blood spread. There is no known time duration between when this begins to happen and when the cells actually lodge and start to grow in tissue. Cells could lodge within hours or days, but not grow for long periods of time, or they could disappear entirely. Unless the melanoma was removed before metastasis had occurred, the potential to spread remained after removal.

Conclusion

It was accepted for Dr Kelly that if it was established on the evidence, that on the balance of probabilities, the failure to excise the ALM in 2009 had permitted it to metastasise, that not already having occurred to that point, then causation would have been established. His case was that this had not been shown on the evidence, with the result that causation had not been established. It was urged, as discussed by the High Court in Tabet v Gett , that the loss of a chance of a better medical outcome, which may have resulted from Dr Kelly's failures, was not compensable.

Having carefully considered all of the evidence as to the thickness of this lesion in 2009, I am not satisfied that it has been shown to be probable that the ALM was only 2mm thick in 2009, when Dr Kelly first saw Mr Coote. Further, it has not been shown to be probable that this ALM had not already metastasised, at that time. It appears probable that even then, it had a thickness of 4 mm, or more. Given the rapid growth of the lesion to 3 September 2009, a growth consistent with Mr and Mrs Coote's description of continued growth between September 2009 and March 2010, estimated by Mrs Coote then to be about 17 mm in diameter and 20mm by January 2011; its thickness in September 2009 and in 2011; when considered together with the metastases detected after excision in 2011, the first time that metastases was investigated, it is not possible to conclude that it is probable that the ALM had not already metastised in September 2009.

In the result, it cannot be concluded that it has been shown that it was probable, that had the ALM been excised in 2009, that Mr Coote would have had a greater life expectancy than 5 or 10 years, or alternatively a normal life expectancy, or that his life expectancy was significantly reduced, as the result of Dr Kelly's negligence, the claims advanced in the statement of claim.

In coming to these conclusions, I have had regard to the use which it is accepted may be made of epidemiological studies. That was discussed by Spigelman CJ in at [78] - [101] in Seltsam Pty Ltd v McGuiness [2000] NSWCA 29; (2000) 49 NSWLR 262 . Amongst his Honour's observations pertinent to this case were:

"78 Epidemiology is, as I have noted above, concerned with the study of disease in human populations. It is not, of itself, directed to the circumstances of an individual case. For the purpose of determining whether exposure to a particular substance is the legal cause of a particular disease, epidemiology only provides evidence of possibility.

79 Evidence of possibility, including expert evidence of possibility expressed in opinion form and evidence of possibility from epidemiological research or other statistical indicators, is admissible and must be weighed in the balance with other factors, when determining whether or not, on the balance of probabilities, an inference of causation in a specific case could or should be drawn. Where, however, the whole of the evidence does not rise above the level of possibility, either alone or cumulatively, such an inference is not open to be drawn

80 The common law test of balance of probabilities is not satisfied by evidence which fails to do more than establish a possibility. See especially the unanimous joint judgment of the High Court in St George Club Ltd v Hines (1961-62) 35 ALJR 106 at 107 where the court referred to Bonnington Castings Ltd v Wardlaw (1956) AC 613 as authority for the following proposition :

"In an action at law a plaintiff does not prove his case merely be showing that it was possible that his injury was caused by the defendant's default."

...

94 In circumstances where the aetiology of a disease is uncertain, or subject to significant scientific dispute, the Courts are not thereby disenabled from making decisions as to causation on the balance of probabilities. As Herron CJ said in EMI (Australia) Ltd v Bes [1970] 2 NSWR 238 at 242:

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

98 The Courts must determine the existence of a causal relationship on the balance of probabilities. However, as is the case with all circumstantial evidence, an inference as to the probabilities may be drawn from a number of pieces of particular evidence, each piece of which does not itself rise above the level of possibility. Epidemiological studies and expert opinions based on such studies are able to form "strands in a cable" of a circumstantial case."

The further evidence which it was contended for Mr Coote showed that he would have been in a different position, but for Dr Kelly's negligence, was submitted to be:

a) The description of the lesion given by Mrs Coote bespeaks a small lesion not raised above the skin by more than 1 millimetre and thus with less than 2 millimetres thickness.

b) The photo of the lesion taken on 28 March 2011 proved the existence o a very advanced melanoma.

c) With metastases to 2 lymph nodes by April 2011 it was accepted by the Professors McCarthy that it had been growing for quite a while to get to that size and in Professor Bill McCarthy's opinion it was likely to have been developing for more than 12 months.

d) Some of the medical experts accepted that applying wart treatments to the lesion could/would have a harmful effect and stir up the tumour. Professor Stan McCarthy said that the melanoma may have grown more rapidly because the treatments which were applied to it. The treatment applied and recommended by Dr Hiddins may have caused the melanoma to grow more rapidly.

e) This logic would apply to the cryotherapy applied by the defendant, Dr Wall and Dr Hiddins as well as to the plaintiff's paring of the lesion in 2010. These treatments could have accelerated the growth and metastases of the melanoma which in Professor Stan McCarthy's opinion had since September 2009 grown quite rapidly

f) Metastases to the lymph nodes was not detected until March 2011. Up to this time there was no evidence of palpable lymph nodes.

g) Metastases to the skin were not detected until April 2011.

h) Metastases to the lungs and spleen were not detected until November 2011 and January 2012. A CT scan performed on 7 April 2011 did not detect any evidence of metastatic disease in the brain or lungs or abdomen.

i) In relation to ALM it is generally agreed that there is no survival difference between superficial melanoma, nodular melanoma when these are corrected for thickness. Therefore prognoses in respect of these categories may be considered to be similar.

That evidence of metastases was not found until after excision of the ALM does not establish that it is probable that there was no metastasis before September 2009. On the expert evidence, to reach the size the ALM had reached in March 2011, it had been growing for a considerable period. The mere lapse of time between September 2009 and excision in 2011 does not establish that it was probable that there was no metastasis before September 2009.

Mr Coote seeks to establish from the evidence as to the size of the lesion in September 2009, that it is probable that it had not metastasised to that point. On the expert evidence, the thicker the lesion was, the more likely that it had metastasised. I have already dealt with the size of the tumour when first seen by Dr Kelly in 2009. The evidence suggests that this ALM was then 4mm thick or more and that it was growing quickly, before any treatment was sought or given. While it is possible that the cryotherapy which Dr Kelly applied affected the growth and metastasis of this ALM, on the evidence there is a high likelihood, on the approach advanced for Mr Coote, that given its size, it had metastasised even before Dr Kelly saw it.

On the evidence I cannot conclude that it has been shown on the probabilities that Mr Kelly suffered the consequences of the ALM which he contracted, because of Dr Kelly's failure to treat the melanoma in 2009 (see Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 at [30]).

As French CJ discussed in Amaca Pty Ltd v Booth [2011] HCA 53 at [41]:

'Causation in tort is not established merely because the allegedly tortious act or omission increased a risk of injury[50]. The risk of an occurrence and the cause of the occurrence are quite different things'.

What had to be established is that that it was probable that the risk created by Dr Kelly came home, that is that the failure to diagnose and treat the ALM caused or materially contributed to the injury which Mr Coote later suffered. Unlike the conclusion reached in Sydney South West Area Health Service v Stamoulis , I am not satisfied that it was here shown that it was probable that if this ALM had been excised in 2009, that Mr Coote would not have suffered the consequences of the ALM which he contracted, which has had such a devastating impact on his life expectancy.

Even if there had been a diagnosis made in September 2009, Mr Coote would have required excision of the lesion. He would then also have faced all of the risks of the excision which he later received. That it is possible that his outcome would have been better, so far as the consequences of metastasis is concerned, had excision occurred in 2009, may be accepted, but that it is probable that he would have had a better outcome, has not been shown. Unquestionably there was a chance of this, but it is settled that Mr Coote may not be compensated for the loss of such a chance ( Tabet v Gett at [46].)

It follows that causation has not been established and so Mr Coote's claim must fail.

Section 5O of the Civil Liability Act

It is not necessary to deal with this defence, given the conclusions I have reached. Suffice it to observe that given the view I have reached as to the presence of the black mark on the lesion which Mrs Coote described, it cannot be accepted that if Mr Coote had established his case on causation, that this defence could have been established by Dr Kelly.

The defence depended on acceptance that the lesion was non-pigmented when Dr Kelly first saw the lesion. I have not accepted that this was the case. On the expert evidence, this being so, Dr Kelly's treatment did not adhere to what was widely accepted in Australia by peer professional opinion as competent professional practice. It follows that this defence would fail, had causation been established.

Conclusion

While it has been established that Dr Kelly owed Mr Coote a duty of care, and that he was in breach of that duty, that the breach of that duty was causally related to what Mr Coote has suffered as the result of contracting the ALM which was excised from his foot only in March 2011, has not been established. That it is probable that excision in September 2009 would have made a difference for Mr Coote, has not been shown.

It follows that there must be judgment for Dr Kelly. The usual order would be that costs follow the event. The parties should approach if they wish to be heard on costs.

Orders

For now, I make the following orders:

1. Judgment for the defendant.

2. The usual order would be that costs follow the event. The parties should approach if they wish to be heard on costs.

**********

Decision last updated: 14 March 2012

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Medium Neutral Citation:	Coote v Dr Kelly [2012] NSWSC 219
Hearing dates:	27 February 2012, 28 February 2012, 29 February 2012, 1 March 2012, 2 March 2012, 5 March 2012
Decision date:	14 March 2012
Jurisdiction:	Common Law
Before:	Schmidt J
Decision:	1. Judgment for the defendant. 2. The usual order would be that costs follow the event. The parties should approach if they wish to be heard on costs.
Catchwords:	TORTS - negligence - medical negligence - whether general practitioner made a wrong diagnosis - a lesion on the foot diagnosed as a plantar wart - whether there was a misdiagnosis of the lesion - whether it was an acral lentiginous melanoma (ALM) - whether there was failure to consider ALM as a differential diagnosis - whether there was failure to refer the plaintiff for specialist investigation - whether there was a failure to perform a punch biopsy of the lesion - plaintiff suffered a plantar wart and also had an ALM - duty of care owed - negligence established - whether there would have been a different outcome if ALM had been earlier treated - causation not established - section 50 of the Civil Liability Act - judgment for defendant - costs EVIDENCE - admissibility and relevance - opinion evidence - medical evidence - objections to expert evidence EVIDENCE - witnesses - credit - credibility of evidence - reliability of evidence
Legislation Cited:	Civil Liability Act 2002 Evidence Act 1995 Uniform Civil Procedure Rules 2005
Cases Cited:	Adeels Palace Pty Ltd v Moubarak (2009) 239 CLR 420; [2009] HCA 48 Amaca Pty Ltd v Booth [2011] HCA 53; (2011) 86 ALJR 172 Dasreef Pty Ltd v Hawchar [2011] HCA 21; (2011) 243 CLR 588 Onassis and Calerropolous v Vergiottis [1968] 21 Lloyds LR 403 Seltsam Pty Ltd v McGuiness [2000] NSWCA 29 (2000) 49 NSWLR 262 Sherry v Australasian Conference Association (trading as Sydney Adventist Hospital) [2006] NSWSC 75 Strong v Woolworths Ltd [2012] HCA 5 Sydney South West Area Health Service v Stamoulis [2009] NSWCA 153 Tabet v Gett [2010] HCA 12; (2010) 240 CLR 537
Category:	Principal judgment
Parties:	Malcolm Coote (Plaintiff) Dr Steven Kelly (Defendant
Representation:	Counsel: Mr M Williams SC with Mr O'Keefe Mr J Morris with Mr T French Solicitors: Stacks Goudkamp (Plaintiff) Norton Rose Australia (Defendant)
File Number(s):	2011/339988
Publication restriction:	None