Causation
125In 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?"
126The 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."
127The 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
128In 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.
129The 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.
130The 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.
131It 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.
132It 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
133It 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.
134It 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).
135There 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.
136There 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.
137What 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.
138It 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."
139The 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."
140This 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."
141Despite 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
142As 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.
143It 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.
144These 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.
145That 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.
146The 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.
147What 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.
148Mr 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.
149Mr 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.
150Given 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.
151Nevertheless, 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.
152It 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.
153What 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.
154Dr 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.
155On 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.
156Professor 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.
157The 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.
158Dr 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.
159As 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.
160Professor 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.
161Professor 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.
162Professor 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
163It 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.
164Having 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.
165In 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.
166In 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."
167The 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.
168That 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.
169Mr 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.
170On 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]).
171As 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'.
172What 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.
173Even 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].)
174It follows that causation has not been established and so Mr Coote's claim must fail.