Reported Decision : 61 NSWLR 678 New South Wales Court of Appeal CITATION : Rufo v Hosking [2004] NSWCA 391 HEARING DATE(S) : 20 May 2004 JUDGMENT DATE : 1 November 2004 JUDGMENT OF : Hodgson JA at 1; Santow JA at 14; Campbell AJA at 56 DECISION : Appeal allowed with costs. CATCHWORDS : TORT - Medical negligence - recoverability for loss of a less than 50% chance of avoiding spinal microfractures suffered in course of heavy-dosage treatment with corticosteroids against Lupus - breaches of duty of care by specialist paediatrician in substituting one corticosteroid for another so causing a heavier than the appropriate dosage and in failing to introduce a steroid sparer at the appropriate stage - more probable than not that even without these breaches microfractures would have occurred but appellant still lost a material chance that but for the negligence the fractures would not have occurred, or would not have occurred at the time or with their severity - comparison of all or nothing approach in causation and damages - causation issues - inapplicability to this situation of UK Fairchild approach to causation - relevance of expert evidence - difficulty of quantifying the lost chance - chance must be material and not speculative - relevance of possible pre-existing celiac condition in contributing to susceptibility to fractures and questions of evidentiary onus - observations on permissibility of loss of chance approach in medical negligence cases. Bennett v Minister of Community Welfare (1992) 176 CLR 408 Betts v Whittingslowe (1945) 71 CLR 637 Birkholz v R J Gilbertson Pty Ltd (1985) 38 SASR 121 Bonnington Castings Ltd v Wardlow [1956] AC 613 Chaplin v Hicks [1911] 2 KB 786 Chappel v Hart (1998) 195 CLR 232 Commonwealth v McLean (1996) 41 NSWLR 389 Daniels v. Anderson (1995) 37 NSWLR 438 Diamond v Simpson (No 3) [2003] NSWCA 373 E.M. Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434 Fairchild v Glenhaven Funeral Services Ltd [2003] 1 AC 32 Gavalas v Singh [2001] 3 VR 404 Gregg v Scott [2002] EWCA civ 1471 Hotson v. East Berkshire Area Health Authority [1987] AC 750 Jorgenson v Vener, 616 NW2d 366 (SD SC, 2000) Laferrière v Lawson [1991] 1 SCR 541 Malec v. J.C. Hutton Pty. Ltd. (1990) 169 CLR 638 CASES CITED : March v E & M H Stramare Pty Ltd (1991) 171 CLR McGhee v National Coal Board [1973] 1 W.L.R. 1 Millett v McMonagle [1970] AC 166 (HL) Naxakis v. Western General Hospital (1999) 197 CLR 269 Purkess v Crittenden (1965) 114 CLR 164 Roberts v Ohio Permanente Med Group, Inc, 668 NE 2d 480 (Ohio SC, 1996) Rogers v Whitaker (1992) 175 CLR 479 Sellars v. Adelaide Petroleum NL (1994) 179 CLR 332 Seltsam Pty. Ltd. v. McGuiness (2000) 49 NSWLR 262 Shorey v PT Ltd (2003) 77 ALJR 1104 Sutherland Shire Council v Heyman (1984-5) 157 CLR 424 TC v The State of New South Wales & Ors [2001] NSWCA 380 The Commonwealth v Amann Aviation Pty Ltd (1991) 174 CLR 64 Tran v Lam NSWSC, 9 February 1995, unreported BC 9504451 Wallaby Grip (Bae) Pty Limited (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355 Watts v Rake (1960) 108 CLR 158 Watts v Rake and Shorey v PT Ltd (2003) 77 ALJR 1104 Wilsher v Essex Area Health Authority [1988] AC 1074 PARTIES : Michelle RUFO (Appellant) Dr C S HOSKING (Respondent) FILE NUMBER(S) : CA 40125/03 COUNSEL : P BRERETON, SC/ DR K SANT (Appellant) D HIGGS, QC/ J LONERGAN (Respondent) SOLICITORS : Kells the Lawyers (Appellant) Ebsworth & Ebsworth (Respondent) LOWER COURT Supreme Court - Common Law Division JURISDICTION : LOWER COURT SC 20468/01 FILE NUMBER(S) : LOWER COURT Studdert J JUDICIAL OFFICER : - 119 - IN THE SUPREME COURT OF NEW SOUTH WALES COURT OF APPEAL CA 40125/03 SC 9475/98 HODGSON JA SANTOW JA M W CAMPBELL AJA 1 NOVEMBER 2004 Michelle RUFO v Dr C S HOSKING Judgment 1 HODGSON JA: I agree with the orders proposed by Campbell AJA, and subject to what I say below, substantially with his reasons. 2 I agree that the primary judge did not err in not being satisfied, on the balance of probabilities, that the breaches of duty by the respondent, which he found to have occurred, caused the fractures suffered by the appellant. Even when one takes into account the principles relied on by Mr. Brereton, it was well open to the primary judge not to be satisfied that, but for the negligence, the fractures would not have occurred; or that the negligence materially contributed to the occurrence of the fractures; or that the fractures were the realisation of a risk created by the negligence. 3 However, I also agree that the evidence strongly supported a conclusion that the negligence materially increased a risk, which was otherwise very substantial, that fractures would occur; and that the occurrence of the fractures was a realisation of this total risk (as distinct from the increment to the risk created by the negligence). This gives rise to the question whether the appellant is entitled to be compensated for the loss of the chance that, but for the negligence, the fractures would not have occurred (or would not have occurred at the time or with the severity of their actual occurrence). If so, then in my opinion it was an error for the primary judge to hold that the increased risk was too speculative to justify an award of damages: so long as such an increase is material, I think the Court is required to do its best to assess it. 4 It is clear that a plaintiff cannot recover damages for negligence unless it is proved, on the balance of probabilities that some actual quantifiable loss occurred as a result of the negligence. However, it is also clear that, at least in some circumstances, the loss of a chance of commercial value is regarded as an actual quantifiable loss: Sellars v. Adelaide Petroleum NL (1994) 179 CLR 332 at 355. 5 There is a real question whether the loss of a chance approach is applicable in medical negligence cases, where an adverse result is suffered, for which there was a substantial probability even without negligence, but negligence has materially increased that probability. 6 The approach was not applied by the House of Lords in Hotson v. East Berkshire Area Health Authority [1987] AC 750; but the approach adopted by the House of Lords in that case, of treating as certainty a 75% chance that the plaintiff would have suffered the disabling disease even without negligence, was considered by Clarke JA and Sheller JA in Daniels v. Anderson (1995) 37 NSWLR 438 at 527 as having been rejected by the High Court in Malec v. J.C. Hutton Pty. Ltd. (1990) 169 CLR 638 at 642-3. 7 In Naxakis v. Western General Hospital (1999) 197 CLR 269, Gaudron J considered the question at 277-281; and she rejected the view that, in a case such as that one, a plaintiff could recover damages on the basis that what had been lost was the chance of successful treatment. However, Callinan J at 313-4 considered that the loss of a chance that was real and of some substance, even though less than 50%, would attract damages. Gleeson CJ at 272 noted that the question had not been considered by the trial judge or the Court of Appeal, and had not been fully argued; and he expressed no opinion. 8 The question was not considered in Seltsam Pty. Ltd. v. McGuiness (2000) 49 NSWLR 262, where Spigelman CJ discussed the use of statistics given by epidemiological studies. 9 It seems clear that, if avoidance of the loss in question would have depended upon the plaintiff taking a particular course of action, the plaintiff must prove on the balance of probabilities that, but for the negligence, the plaintiff would have taken that course of action. The plaintiff cannot be compensated for the loss of a chance that the plaintiff might have done so: Sellars at 353. However, otherwise I think it is consistent with the principles established in Malec and Sellars to say that it is enough if the plaintiff proves, on the balance of probabilities, that he or she has been deprived of a valuable chance. 10 That chance must be inherent in the circumstances, not merely an artefact of the way evidence is presented in the case. Thus, if it appears to be a plain fact as to whether treatment would or would not have been successful, and the element of uncertainty arises merely from different expert views, then the plaintiff will not be compensated for the chance that one expert might be correct. On the other hand, if it appears that the very best medical science can do is to say that the treatment had a quantifiable chance of success, then in my opinion that can be treated as a valuable chance for the loss of which a plaintiff can be compensated. As with other questions concerning causation, a common sense approach should be taken to the question of whether a valuable chance has been lost, or whether the situation is rather one where one or other alternative would definitely have occurred, and the only uncertainty is due to imperfections in the evidence. 11 Gaudron J in Naxakis at 279-80 suggested that this approach would disadvantage plaintiffs in circumstances where the chance of successful treatment is more than 50%. If this was so, it would not in my opinion involve injustice. In any event, I doubt if it is so. Even if the occurrence of the adverse result is treated as being certainly caused by the negligence, a substantial chance that the adverse result could have resulted in any event cannot, on the Malec approach, be ignored, at least if the chance relates to the adverse result occurring at some time different from the time when it actually occurred. Further, it would be curious if the Malec approach were entirely precluded if the substantial chance related to an occurrence of the adverse result at the same time as its actual occurrence, though not precluded if it related to the occurrence of the result at some slightly later time. 12 In my opinion, the evidence in this case strongly supports the view that medical science can do no more than assert that there was a very substantial risk of the adverse result, that this risk was materially increased by the negligence, and that the adverse result was the realisation of the totality of the risk; and provide some basis for quantifying the chance that the adverse result would have been avoided if the negligence had not occurred. Accordingly, in my opinion this is a case that can be approached as one involving a loss of a valuable chance. 13 Consistently with what was said previously, this chance was less than 50%. For my part, I may have been prepared to make an assessment of the chance on the basis of the material before this Court; but both sides are in agreement that this should be undertaken by the trial judge. Accordingly, I agree with the orders proposed by Campbell AJA. 14 SANTOW JA: INTRODUCTION I have had the advantage of reading the judgments of Hodgson JA and M W Campbell AJA. I agree with each of them. I would however wish to add some observations concerning whether loss of a chance should be available as a basis for determining liability and damages in a medical negligence case of this kind as that question is an important one. 15 A principal feature of this case is that the trial judge, Studdert J, concluded that, while the respondent doctor breached his duty of care in two respects, because those breaches on balance of probabilities did not cause or materially contribute to the fracture injury to the appellant's spine, the appellant could not succeed. The appellant challenges that result. The appellant submits that she was entitled to be compensated for loss of a chance that, but for the negligence, the microfractures either would not have occurred, or would not have occurred at the time or with the severity of their actual occurrence. This is on the basis that any chance involved, though material, was below 50%. 16 There is no challenge to the first breach of the respondent's duty of care to the appellant, in substituting one corticosteroid for another (dexamethasone for prednisolone). This had the effect of increasing the steroid dosage level, when expressed in equivalent terms. There is however a challenge to the second breach found. That breach was by reason of not introducing the "steroid sparer" Imuran to the appellant's treatment regime at an appropriate stage. I agree with M W Campbell AJA that the Notice of Contention challenging that finding should not succeed and do not need to add to his reasons on that. Disposition of Appeal 17 An important question of principle underlying this case, though not itself in dispute but rather whether the facts support its application, can be stated as follows. Should medical negligence cases allow a remedy to the plaintiff whose injury, more likely than not, would have occurred without any negligence on the part of the doctor, but where that negligence nonetheless denied the plaintiff a material chance of a better outcome? To-day, opinion has decisively shifted against the simplistic approach of saying that loss in terms of compensable legal liability should depend on which party can best insure against it. Unprincipled extension of medical liability threatens to reach a point where the cost of medical indemnity insurance will become too heavy for the doctor to bear or the community to absorb in higher charges. 18 That dictates a high degree of caution in recognising any compensable liability for loss of chance. That is more especially as the High Court has yet to lay down definitively that loss of less than a 50% chance for a better medical outcome is indeed compensable. That said, there are now dicta in both directions on that subject (Naxakis v Western General Hospital (1999) 197 CLR 269). Moreover, the High Court's reasoning is available from analogous contexts, in particular contract (such as Sellars v Adelaide Petroleum NL (1994) 79 CLR 332). Also in damages generally; Malec v J C Hutton Pty Ltd (1990) 169 CLR 638. There have been a number of decisions in Australia both at intermediate appellate level and below favouring recovery in medical negligence cases. The trend so far has been the other way in Canada; Laferrière v Lawson [1991] 1 SCR 541. But in the United States the Courts' response has on the whole been more favourable, though not uniformly so; see for example Roberts v Ohio Permanente Med Group, Inc, 668 NE 2d 480 (Ohio SC, 1996); Jorgenson v Vener, 616 NW2d 366 (SD SC, 2000). 19 Courts in the United Kingdom have so far decided against loss of chance liability in medical negligence cases. The current House of Lords appeal from Gregg v Scott [2002] EWCA civ 1471 affords opportunity to reassess this difficult area. Hotson v East Berkshire Health Authority [1987] AC 750 denying compensation for loss of a chance appears to stand in the way. This is unless it be distinguishable, on the basis that, as Mance LJ explained in the Court of Appeal, Hotson was dealing with a past historic fact, not one in prospect. It was moreover a case where the adverse consequence of that past fact was inevitable (vascular necrosis from rupture of the blood vessels); with the result that negligent failure to diagnose in time a traumatic fracture of the femur had no causal effect on the necrosis. 20 Particularly influential in terms of principle has been the distinction drawn by Lord Diplock in the well-known passage in Millett v McMonagle [1970] AC 166 (HL) at 176: "The role of the court in making an assessment of damages which depends upon its view as to what will be and what would have been is to be contrasted with its ordinary function in civil actions of determining what was. In determining what did happen in the past a court decides on the balance of probabilities. Anything that is more probable than not it treats as certain. But in assessing damages which depend upon its view as to what will happen in the future or would have happened in the future if something had not happened in the past, the court must make an estimate as to what are the chances that a particular thing will or would have happened and reflect those chances, whether they are more or less than even, in the amount of damages which it awards" 21 While approved by Malec v J C Hutton Pty Ltd (1990) 169 CLR 638 the High Court added an important refinement, namely to include past events of a hypothetical character in the "what would have been" category where loss of chance or prospect hold sway. 22 This renders those past events, being of a hypothetical character, amenable to compensation on a lost chance basis though that chance be less than even, provided that the duty of care extend so far. Here we are dealing with the duty of a doctor to do what reasonable skill and judgment require. That must ordinarily be directed to achieving the best possible medical outcome, and thus to eliminating or reducing so far as practicable, the risk of things going wrong. That said I need to emphasise that doctors are not and cannot be, guarantors of outcomes. What their duty encompasses is reasonable care and skill, directed to that end. But the duty of care in other spheres may be quite different. It may in no way lend itself to such an outcome approach judged by reference to the exercise of reasonable care and skill in eliminating or reducing risks. For example one would judge the liability of a local council to the buyers of houses quite differently, where such notions of liability would not comport with the limited duty of care applicable; compare Sutherland Shire Council v Heyman (1984-5) 157 CLR 424. 23 The question, why should there be recovery for loss of a chance when less than even, turns on the nature of the duty of care imposed on the medical practitioner. It is a continuum, starting with diagnosis and the duty to advise the patient as to his or her treatment and then embracing the mode of treatment itself. Bringing to bear reasonable care and skill in advice as to risks is in order that patient consent is then informed by knowledge of the material risks of the treatment options advised. That duty operates in a context where the patient needs to make an informed decision as to the anticipated outcome. Then when it comes to managing the treatment, here that of a drug dosage regime, again reasonable care and skill is brought to bear directed to a successful outcome by maximising the chances of its achievement. This is necessarily within the scope of the patient's own informed decision about agreed treatment as well as its practical availability. We may know for example in hip replacements that a titanium hip offers a better outcome than a steel one. But cost considerations may render it practically unavailable. 24 That decision on treatment, as was the case here, may well need to be revisited where the treatment is not simply an operation, but a course of medication over a period, where competing risks have to be gauged. That is here the risk of failing to deal adequately with the Lupus as against the risk of side effects, depending on the drugs used and the dosage levels. Symptoms over time may emerge dictating adjustment to the course of medication. At the outset not all of the individual patient's reactions to the treatment may be ascertainable or even capable of reliable prediction. The doctor is therefore reasonably to be expected to keep such a course of action under review, monitoring actively its foreseeable risks, These here included the risk of microfractures from high dosage of corticosteroids, as eventuated. Moreover, each individual may react differently to the treatment. Here, for example, there was the possibility of an earlier celiac condition affecting the propensity of the bones to fracture, though there is no evidence that the doctor was aware of it at the time. All of these matters go to bringing to bear reasonable care and skill, here that of an ordinary skilled specialist paediatrician, to the task of achieving the best chance of a successful medical outcome. Given that is the purpose of medical treatment, why should not loss of a chance in achieving that end be recoverable, where treatment falls short of that standard of reasonable care and skill? It is simply the analogue of advising earlier about the prospect of risk in achieving such an outcome. 25 Professor Luntz in a penetrating article "Loss of Chance" in Causation in Law and Medicine edited by Ian Freckelton and Danuta Mendelson (1992) at 183 put the issue of principle in these somewhat stark terms: "Say that a plaintiff has a less than 50% chance of not having a leg amputated if a surgeon takes reasonable care in treating it. The surgeon fails to take care and the patient loses the leg … one might infer that the surgeon's negligence deprived the patient of the chance of saving the leg, but one could not infer that it caused the loss of a leg, since more probably than not that would have happened even if the surgeon had not been negligent. The plaintiff should be entitled to damages for that loss. Otherwise, according to those that believe that the law of torts operates as a significant deterrent, medical practitioners can be as negligent as they like when treating seriously ill patients who have less than a 50% chance of survival, since the doctors would never be liable if the patient did not survive." 26 Unless the duty of care can be invoked where negligence has reduced the chance of a successful outcome, though that chance be less than even, that indeed will be the consequence for many elderly or desperately ill people. Recovery for loss of a chance can be seen therefore as the corollary of a medical duty of care directed to achieving the best chance of a successful outcome though it call for no more than reasonable care and skill in that endeavour. Clearly, where in such a desperate case the patient's chances are in any event below 50%, the doctor is only liable if he or she fails to bring to bear reasonable care and skill in avoiding loss of the chance that is left. Judging that fairly with an appreciation of the difficulties for the doctor in making that judgment is important, as otherwise the doctor for fear of liability may choose the defensive course rather than the best one amongst limited options. 27 Suppose, therefore, in the above example there is a less than 50% chance of having the leg saved, though the chance is still significant. Suppose the treatment to save the leg involve potentially countervailing risks, because the patient is elderly and frail. It may be, for example, that the leg is close to gangrenous. In weighing up those risks, no more than reasonable care and skill is called for, but the doctor still needs to direct his or her mind to that task. So too here. In the present case, this issue finds its counterpart in the difficult decision whether and when to introduce the steroid sparer Imuran. Its benefit lay in reducing the risks of bone fracture associated with a heavy dosage of corticosteroid in the form of either prednisolone or dexamethasone. Yet Imuran had its own potential risks for kidney failure. The trial judge adjudicated upon the competing considerations, concluding that there was nonetheless a breach of duty of care in failing to introduce the Imuran on or about 10 June 1992 as a steroid sparer. 28 I agree that there is no basis for disturbing that finding on appeal. But that dilemma of competing risks concerning Imuran does emphasise the importance of not considering breach of duty of care in isolation from the chance in question. If a particular treatment offers a small, but still appreciable, chance of a beneficial outcome, it may nonetheless not be negligent to withhold it, where there are countervailing risks of sufficient magnitude from its introduction. That said, one would still expect the doctor in the exercise of reasonable skill and care to explain the treatment options with their attendant competing risks. Here it appears that the doctor did not give such advice to the child or her parents, so far as either of the breaches were concerned. 29 Thus far, as I have said, the High Court has not been faced with having to determine the permissibility of recovery for loss of a chance in a medical negligence case. In Naxakis v Western General Hospital (supra), the High Court ordered a new trial where the trial judge had withdrawn a case from the jury that would have raised that issue. The issue was whether the plaintiff had been deprived of a chance of avoiding a burst aneurysm by failure of the doctor and the hospital to diagnose it or at least identify it as a possibility requiring an angiogram. The High Court's decision was based simply on there having been sufficient evidence of negligence in causation of the injury so that the matter should have been left to the jury ultimately to determine. It was therefore strictly unnecessary to deal with the argument of lost chance. 30 Nonetheless, two of the judges, Gaudron J and Callinan J, by way of dicta, considered that issue, reaching a diametrically opposite result. Gaudron J elaborated on her views for rejecting loss of a chance (at 277-81). Callinan J expressing the contrary view that there was a place for the doctrine "particularly in cases involving the practice of what is even to-day said to be an art rather than a scientific skill" (at 313-4) and provided that "the chance lost must be a real one and of some substance, even though less than a 50% chance". 31 It is instructive to consider the reasons advanced by Gaudron J for rejecting the notion "that, in a case such as the present, a plaintiff can recover damages on the basis that what has been lost is a chance of successful treatment" (at [36]). 32 Gaudron J begins with the proposition that it is well settled that where breach of contract results in loss of a promised chance, there is an actual compensable loss. Damages will be awarded "by reference to the degree of probabilities, or possibilities, inherent in the plaintiff's succeeding had the plaintiff been given the chance which the contract promised"; Sellars v Adelaide Petroleum NL (supra) at 349. Likewise, damages may be recovered for a commercial opportunity that is lost in consequence of a breach of contract (The Commonwealth v Amann Aviation Pty Ltd (1991) 174 CLR 64). That loss of a commercial opportunity is also "loss or damage" for the purposes of s82(1) of the Trade Practices Act 1974 (Cth) (Sellars v Adelaide Petroleum NL (supra) at 348 per Mason CJ, Dawson, Toohey and Gaudron JJ at 364 per Brennan J). All of these are of course cases on damages. They are not cases about whether a particular historical event has occurred, where the issue is one of causation, at least where the event is not hypothetical. 33 Gaudron J concludes that "there is no reason in principle why loss of chance or commercial opportunity should not constitute damage for the purposes of the law of tort where no other loss is involved. However, different considerations apply where, as here, the risk eventuates and physical injury ensues" (Naxakis at [29]). But what happens if physical injury actually ensues, with the prospect of yet further injury? Is the latter recoverable by way of lost chance? Malec, cited by Gaudron J, strongly suggests it is. In Malec the plaintiff's exposure to brucellosis injured his back. Thus the negligence caused compensable injury, on balance of probabilities. But the plaintiff's successful claim in terms of lost chance was for a neurotic condition (depression) following that injury and loss of his capacity to work. The problem facing the Court was that this was a condition that could have happened in any event. 34 Precluding recovery for loss of a chance in such a case in tort would be difficult to justify, if it were nonetheless recoverable in contract. That outcome would simply lead to claims for medical negligence being brought against the doctor in contract instead of tort, relying upon an implied contractual term. It would be a term that the medical practitioner will undertake to exercise reasonable care and skill in the provision of advice and treatment, with its corollary of bringing to bear that reasonable care and skill in maximising the chances of a successful outcome, subject to patient choice and the practical availability of treatment. 35 Malec settled in the case of damages that an all or nothing approach was not to be applied to hypothetical events, even past ones, nor to future events. At 642-3 the majority said: "When liability has been established and a common law court has to assess damages, its approach to events that allegedly would have occurred, but cannot now occur, or that allegedly might occur, is different from its approach to events which allegedly have occurred. A common law court determines on the balance of probabilities whether an event has occurred. If the probability of the event having occurred is greater than it not having occurred, the occurrence of the event is treated as certain; if the probability of it having occurred is less than it not having occurred, it is treated as not having occurred. Hence, in respect of events which have or have not occurred, damages are assessed on an all or nothing approach. But in the case of an event which it is alleged would or would not have occurred, or might or might not yet occur, the approach of the court is different. The future may be predicted and the hypothetical may be conjectured. But questions as to the future or hypothetical effect of physical injury or degeneration are not commonly susceptible of scientific demonstration or proof. If the law is to take account of future or hypothetical events in assessing damages, it can only do so in terms of the degree of probability of those events occurring. The probability may be very high - 99.9 per cent - or very low - 0.1 per cent. But unless the chance is so low as to be regarded as speculative - say less than 1 per cent - or so high as to be practically certain - say over 99 per cent - the court will take that chance into account in assessing the damages." 36 The present case too turns on a hypothetical event. It asks what would have happened if a lower dosage of corticosteroids had been prescribed, or the steroid sparer introduced on 10 June 1992, in terms of the prospect of the appellant avoiding the bone microfractures that came about. While the prospect has not been quantified, and indeed may be very difficult to do so with any precision as several experts made clear, the plaintiff did indeed lose a material chance, though below 50%, of avoiding that adverse outcome that eventuated. 37 At first sight Sellars v Adelaide Petroleum NL appears to stand in the way of recovery for less than even chances. The majority said: "When the issue of causation turns on what the plaintiff would have done, there is no particular reason for departing from proof on the balance of probabilities notwithstanding that the question is hypothetical" (at 353). The majority applied the Malec approach, but only to the assessment of damages: "… we consider that acceptance of the principle enunciated in Malec requires that damages for deprivation of a commercial opportunity, whether the deprivation occurred by reason of breach of contract, tort or contravention of s52(1) [of the Trade Practices Act 1974 (Cth)], should be ascertained by reference to the Court's assessment of the prospects of success of that opportunity had it been pursued." (at 353) [emphasis added] 38 The court then went back to the issue of causation saying (at 355): "…The principle recognised in Malec was based on a consideration of the peculiar difficulties associated with the proof and evaluation of future possibilities and past hypothetical fact situations, as contrasted with proof of historical facts. Once that is accepted, there is no secure foundation for confining the principle to cases of any particular kind. On the other hand, the general standard of proof in civil actions will ordinarily govern the issue of causation and the issue whether the applicant has sustained loss or damage. Hence the applicant must prove on the balance of probabilities that he or she has sustained some loss or damage. However, in a case such as the present, the applicant shows some loss or damage was sustained by demonstrating that the contravening conduct caused the loss of a commercial opportunity which had some value (not being a negligible value), the value being ascertained by reference to the degree of probabilities or possibilities. It is no answer to that way of viewing an applicant's case to say that the commercial opportunity was valueless on the balance of probabilities because to say that is to value the commercial opportunity by reference to a standard of proof which is inapplicable." 39 I consider that the reasoning in Sellars on causation and damages is reconcilable with allowing recovery for loss of a less than even chance in medical negligence cases. Sellars was a Trade Practices Act s52 case involving misleading and deceptive conduct. In such a case, while there is a duty not to misrepresent or mislead, it could not be gradated in terms of chance. There is no corresponding duty as is imposed on a doctor with regard to bringing to bear reasonable care and skill in maximising the chances of a successful medical outcome. 40 Moreover, in medical negligence cases causation must still be demonstrated at greater than 50% probability in two respects. First, the chance must be proven to exist on balance of probabilities. Second, the plaintiff must prove on balance of probabilities that if offered the chance lost, in terms of treatment, the plaintiff would have elected to have that chance. Thus "where the chance lost was a chance that the plaintiff may have acted in such a way as to receive a benefit or avert a detriment, the plaintiff must prove on the balance of probabilities that there was such a chance and that the plaintiff would have so acted" (per Badgery-Parker J in Tran v Lam NSWSC, 9 February 1995, unreported BC 9504451). That is an important control mechanism. It means that loss of a chance cannot be invoked where there is not a greater than 50% chance that the patient, properly advised, would have undertaken the particular course of treatment or operation. That is so though we are here dealing with a hypothetical event. 41 Here there is similarly no escape from showing on the balance of probabilities that the appellant would have accepted proper advice about dosage had it been given; that is, to introduce Imuran and not to substitute dexamethasone for prednisolone in the way that occurred. The trial judge gave answers in favour of the appellant to those questions. Likewise, were Chappel v Hart (1998) 195 CLR 232, regarded as a loss of a chance case, contrary to the way it had been presented at trial and contrary to the way Gaudron J categorised the appellant's loss, it would then stand as clear authority for applying the balance of probabilities to the question in that case. That question was whether the plaintiff would have chosen a more experienced surgeon had the risk (perforation of the oesophagus) been explained to her, so as to maximise her chances of a successful outcome. 42 Similarly here, the present claim can be framed in terms of losing the benefit, not of a superior surgeon with better chance of circumventing the operation's risks, but of a superior treatment regime with better chance of circumventing the risks of bone microfractures, while still curing the Lupus. In each case that better chance was less than even, but still material. There could be no question but that the better chance was a thing of value, even if its quantification posed considerable difficulty. 43 In Malec, there was no doubt that some injury occurred caused by the brucellosis on balance of probabilities, namely injury to the plaintiff's back. In contrast, in the present case the only damage is a lost chance of a better outcome. There is no associated recoverable injury brought about on the balance of probabilities. But I do not consider that distinction matters. In Malec, nothing was made of that distinction. It should not matter here, either. 44 It is concededly the case that an unqualified all or nothing approach in allowing damages for the actual harm suffered affords, in the words of Gaudron J in Naxakis at [30], "at best, rough justice". Moreover, as Gaudron J explained, problems associated with proof of causation can be exaggerated. This is when it is appreciated that, for the purposes of allocation of legal responsibility "if a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring"; citing McHugh J in Chappel v Hart. 45 However, it would be productive of injustice if the plaintiff were to receive 100% of the loss where a chance or prospect exceeds 50% (say 51%) yet receive nothing at all if such loss were, say, 49%. The fairest solution is to base compensation on whatever be the percentage, whether above or below 50%, wherever one is dealing with future events or hypothetical ones. As Luntz (supra) at 195 puts it, referring to a 1992 article: "The article that Hedigan J in Naxakis 145 found persuasive does advance reasons of policy for denying the extension of liability to loss of chance. One is obviously spurious. The article refers to two commentators and two courts that have pointed out that loss of chance leads to statistically more wrong decisions than right ones. In a group of 99 cases, of which only 33 would have survived, allowing recovery for all 99 means that 66 are wrongly decided. This is like saying that a clock that has stopped is better than one that is a minute fast, since it is right twice a day, whereas the one that is fast is never right! Most people would prefer the fast watch to the stopped one as being much more useful. In this example, the defendant would, if loss of chance were denied, never pay any compensation despite repeated acts of negligence. By requiring the defendant to pay 33 per cent of the assessed damages to all, the defendant compensates exactly the total damage that has been caused by negligence." 138 L Perrochet, SL Smith & U Collelo, "Lost Chance Recovery and the Folly of Expanding Medical Malpractice Liability" (1992) 27 Tort & Ins LJ 615. 145 [1999] VSC 389 (Vic SC, Hedigan J, 15 October 1999, unreported, BC 9906720). 46 What Callinan J describes in Naxakis at [129] as a possible approach may therefore be thought too generous to plaintiffs, if understood as allowing 100% recovery where the chance lost is merely 51% but if 50% or below allowing the full percentage. However, if Callinan J is understood as simply illustrating the outcome of the traditional approach compared to the loss of a chance approach in a medical negligence context, that example brings out the difference with clarity. 47 In Naxakis when Gaudron J explained why she rejected loss of chance as a basis for recovery in medical negligence cases, she observed that the doctrine of loss of chance would not necessarily benefit individual plaintiffs. "If damages were to be awarded for the chance lost, rather than the actual injuries or disabilities suffered, consistency would require the damages be assessed according to the value of the chance, not the injury or disability. Thus a chance which is 51% or greater but less than 100% must result in an award of damages less than would be the case if damages were awarded for the injury or disability which eventuates" at [33]. 48 While that observation is undoubtedly correct where the chance is above 50% but below 100%, several points can be made. First, the plaintiff who suffers an injury which on the balance of probabilities would have occurred anyway but nonetheless is deprived of a chance of averting that outcome as a result of the defendant's negligence, on the all or nothing rule that plaintiff would receive nothing. The plaintiff is then indubitably worse off. 49 Second, damages for future loss are customarily discounted already for vicissitudes. Likewise, damages for loss of future prospects or in relation to hypothetical past events are discounted on Malec principles. This is so even where the plaintiff proves on the balance of probabilities that the defendant did cause harm in the form of a risk that eventuated; Luntz at 186. That Malec approach to damages emphasises the unfairness in the medical negligence context of not then allowing a loss of chance approach where less than even. 50 However, Rogers v Whitaker (1992) 175 CLR 479, as Callinan J pointed out in Naxakis, was a case where the plaintiff received full damages, once it was established on the balance of probabilities that she would not have had the operation. That seems to be a corollary of the denial of any damage had it been merely established that she might not have had the operation, as distinct from would not have had the operation; compare Callinan J in Naxakis at [129]. There is much to be said even in warning cases for discounting the damages to take account of the fact that harm might still have occurred in the absence of negligence, in particular the harm of future loss of sight from not having the operation. That was not however how the case appears to have been argued. There was also the fact that the plaintiff had sought reassurance on the very risk, slight as it was, that came home. 51 Finally, I should make brief reference to recent UK authority. Currently, Gregg v Scott [2002] EWCA civ 1471 awaits the result of appeal in the House of Lords. This was a case where the defendant, Gregg, carelessly failed to diagnose Scott's cancer. It had grown larger as a result, resulting in the loss of a chance for effective remission had treatment commenced earlier. The chance lost was below 50% and the Court of Appeal denied recovery. Under the Malec approach the question, what would have occurred with earlier diagnosis, is hypothetical. It would therefore open the door to allowing recovery for the lost chance if a material chance were thereby lost. It remains to be seen whether the House of Lords allows on similar reasoning pure loss of a chance to constitute actionable damage in a medical negligence case. Earlier in the Court of Appeal Simon Brown LJ concluded that recovery should not hinge upon the accidental fact of whether the plaintiff could show a "clearly demonstrable injury upon which to hang a parasitical claim for the loss of chance". He cited against that proposition the earlier House of Lords decision in Hotson v East Berkshire Health Authority (supra). That, as I have said, was a loss of chance claim too. But it followed a past historic event, whose outcome was inevitable, as distinct from that in Malec which was not inevitable; see Jane Stapleton "Cause-in-fact and the Scope of Liability for Consequences" (2003) 119 LQR 388 at 424. OVERALL CONCLUSION 52 While intermediate courts of appeal in Australia do not yet have the guidance of a High Court decision adopting as ratio loss of chance in medical negligence, the trend of intermediate appellate and first instance authority in Australia favours that approach. There is much to be said for consistency, whereby a chance above or below 50% obtains no more and no less in compensation than the corresponding percentage, instead of an all or nothing approach. That should not open floodgates to loss of chance claims either in the medical field or more generally. First, the loss of chance must itself be established on the balance of probabilities, as also that the chance if offered would have been taken. Second, it is the very nature of the doctor's duty of reasonable care and skill that directs it to achieving the best chance of a favourable medical outcome, subject to informed patient choice and what is practically available. Duty in other spheres may have varying dimensions. 53 The present is a case where loss of a chance does afford a proper basis for compensation. It highlights the importance of considering the duty of care not in isolation, but in conjunction with a fair assessment of the difficult task facing a doctor having to choose between various options each with their own risks. 54 What is said by Professor Luntz in his article on loss of chance remains apposite: "where a medical practitioner fails to exercise reasonable care, the aim of the law generally is not to reposition the plaintiff as though no treatment had been given, but as though proper treatment had been given … whether the claim lies in contract or tort. In many instances proper treatment could have done no more than give the plaintiff a chance of cure or alleviation of a pre-existing condition. This is something of value, something for which many people would give money. The law should treat such a chance as worthy of protection" (at 197). 55 Accordingly, I would agree with the orders proposed by M W Campbell AJA. 56 M W CAMPBELL AJA: INTRODUCTION This is an appeal from a judgment of Studdert J for the respondent in an action brought by the appellant seeking damages in respect of medical treatment by the respondent which she alleged to be negligent. 57 There is also a notice of contention by the respondent in respect of one of the two allegations of negligence found by Studdert J to have been made out. Background 58 The appellant was born on 29 December 1977. She was diagnosed in early January 1992 to be suffering from systemic lupus erythematosus (lupus or SLE). This is a very serious inflammatory condition in which a characteristic rash is associated with widespread internal pathology including kidney damage. 59 The appellant's then general practitioner, Dr Almeda, referred her to Dr Donald, a specialist paediatrician. On 8 January 1992 he prescribed Prednisolone, 50 mg a day, to treat the lupus. Prednisolone is a corticosteroid drug. 60 Dr Donald becoming unavailable the appellant's treatment was then taken over by the respondent. He first saw her on 3 February 1992 and she continued in his care until passing into the care of Professor Clancy in January 1993. The respondent is a paediatric immunologist and had been in that specialty since 1969. From 1980 until 1991 he was the director of immunology at Royal Children's Hospital Melbourne and thereafter moved to Newcastle and acted as a locum for Dr. Donald. 61 On 24 August 1992 the appellant was admitted to the John Hunter Hospital at Newcastle suffering from vertebral microfractures. 62 It became common ground at the trial that the microfractures were caused by the corticosteroid dosages that the applicant had been having up to that time. The mechanism being the development of osteoporosis in the appellant's spine. 63 In his careful and detailed judgment Studdert J traced the course of the appellant's treatment by the respondent, Dr. Nanra, a renal specialist, Dr. Miller, a psychiatrist, and other care providers. I shall return to aspects of this account later. 64 Up until 8 June 1992 the appellant continued on a high dosage of Prednisolone albeit the level fluctuated depending upon her condition. 65 On that day the respondent substituted Dexamethasone for the Prednisolone and the appellant continued on that drug until after the fractures in doses to which I shall refer later. 66 For reasons to which it is unnecessary to go Studdert J found that the substitution breached the respondent's duty of care to the appellant. There has been no challenge to that finding. 67 The Judge also found that in not introducing a "steroid sparer" Imuran to the appellant's treatment regime on or about 10 June 1992 the respondent was in breach of his duty of care to the appellant. That finding has been challenged in a Notice of Contention. 68 Having concluded that those breaches of duty of care had been made out and rejected a number of other allegations, Studdert J turned to the issue of causation. He held that "the [appellant] has failed to prove damage resulting either from the failure to introduce Imuran on or about 10 June 1992 or from the prescription of Dexamethasone in June 1992". 69 This appeal challenges that finding. It is, however, appropriate to deal first with the issue raised by the Notice of Contention. Notice of Contention 70 It is convenient to begin the consideration of this issue with reference to a number of findings in Studdert J's judgment. a. The appellant was on high doses of corticosteroids for a period of 7½ months before the fractures occurred. b. It was well known in 1992 that corticosteroids could cause osteoporosis. c. The risk to the (appellant) of vertebral compression fractures due to osteoporosis caused by corticosteroids was not a farfetched or fanciful risk but a risk that was foreseeable during the time that the (respondent) was treating the (appellant) prior to 24 August 1992. d. Whilst the possibility that the administration of corticosteroids to the plaintiff for less than eight months may lead to osteoporosis and vertebral compression fractures may not have been considered to have been high, nevertheless it was a risk which, if it materialised, would be likely to have very serious consequences for the plaintiff. Vertebral compression fractures occurring in a developing body could only be assessed as major harm. 71 The Judge noted that the respected text book of Paediatric Rheumatology by Cassidy & Petty (first published in 1990) contained a passage as follows: "Corticosteroids should be employed in the management of paediatric rheumatic disease only for well-delineated indications, in the lowest dose required for achieving those objectives, and for the minimal period of time. The toxicities of the corticosteroid administration represent exaggerations of the normal physiologic effects of this class of hormones. In addition to the manifestations of Cushing's syndrome, a number of toxicities should be cited for importance in children under chronic pharmacologic treatment for rheumatic diseases: hypokalemia and alkalosis, edema, glucosuria, increased susceptibility and peptic ulceration, myopathy, behavioural disturbances and psychosis, posterior subcapsular cataracts, osteoporosis and vertebral compression fractures and inhibition of linear growth." The evidence shows that the respondent consulted this text during his treatment of the appellant. 72 The Judge also noted: "In Goodman & Gilman's The Pharmaceutical Basis of Therapeutics (8th ed., (1990)), it is stated (at 1452): 'Osteoporosis and vertebral compression fractures are frequent serious complications of corticosteroid therapy in patients of all ages.' The same risk is noted in MIMS for 1992, as the defendant acknowledged. Indeed, the defendant recognised that vertebral compression fractures were a recognised adverse effect from corticosteroid treatment of children, but he perceived such to be 'extraordinarily rare'." 73 From paragraph 8 to paragraph 49 of his judgment, Studdert J set out the course of treatment for the appellant's lupus during 1992 against the background of her signs and symptoms of that disease during the same period. 74 It is sufficient for present purposes if I refer to that material in much shortened form. 75 Dr. Donald on the 17 January 1992 found the response to the Prednisolone favourable with the rash "minimal". 76 The respondent commenced to treat the appellant on the 3 February 1992. He then found her asymptomatic although her urine had shown traces of blood on multistix. He continued the dosage of 52 mg per day. 77 On 17 February 1992 the rash was prominent and other symptoms present. A decision was taken to refer the appellant to Dr. Nanra, a renal specialist, and the dosage was increased to 75 mg per day. Studdert J accepted that the respondent's reason for so acting was that he considered the lupus recrudescent and that there was kidney involvement. 78 On 27 February 1992 the appellant was feeling somewhat better and the dosage was reduced to 62.5 mg a day. The respondent recorded however that he was worried about the appellant's renal function. 79 On 9 March 1992 the dosage was reduced to 50 mg per day. Studdert J accepted that on that day the appellant's mother had, for the first time, voiced concern that the appellant was losing weight. On that day there was also a discussion as to the appellant's periods having ceased. It is not clear whether that matter was first raised on that day or on 27 February but in any event the Judge accepts that it was raised and that the respondent subsequently advised the plaintiff that the periods would resume after the treatment with corticosteroids ceased. 80 On 10 March 1992 Dr. Nanra's report to the respondent referred to symptoms raising the possibility of tubular intestinal disease as a manifestation of SLE in the kidney and observed "in the interim I am very comfortable with her present steroid dosage". 81 On 13 March 1992 the dosage was reduced to 40 mg per day. Later the doctor wrote of that consultation that the appellant was "starting to show signs of Cushingoidism with the development of hair on her upper lip and a slightly moon face". 82 On 4 May 1992 Dr. Nanra wrote to the respondent discharging the appellant back to his care. He reported that the appellant had no evidence of renal disease and that her renal function was "near normal". He advised that it was important to monitor the appellant's urine for any abnormalities at least once or twice every two or three months. 83 On 11 May 1992 the respondent noted that there was erythema at the base of the finger nails and on the toe nails and he decided to keep the appellant on the then current dose of 40 mg, writing that if the erythema improved he was going to reduce the dose at the next consultation. On 28 May 1992 the appellant developed a fever and upper respiratory tract infection for which she attended the John Hunter Hospital and was seen by Dr. Banna. Urinalysis raised suspicion about renal involvement. Dr. Banna consulted with the respondent and the Prednisolone dose was increased to 60 mg per day. 84 On 1 June 1992 the respondent noted the appellant's father's concern about her emotional lability. But it did appear that she had responded well to the increased dosage. The doctor's assessment was that the likelihood of renal involvement at that point was "very low". On that day the respondent determined that the dose continue at 60 mg per day for four days and he wrote that he then planned to reduce that to 55 mg per day for two weeks with a subsequent reduction to 50 mg per day. 85 On 22 June 1992 the appellant saw the respondent. The judgment noted: "Some fourteen days earlier, at the [respondent's] initiative, a controversial change in drugs had occurred. Dexamethasone was substituted for Prednisolone with a dose starting at 10 mg on 8 June reduced to 9 mg on 15 June. On 22 June, 1992 a decision was taken, at the suggestion of Mr Rufo, to split the dose so that the plaintiff should take half the medication in the morning and half of it in the afternoon. That suggestion was implemented by the [respondent], and as from 22 June 1992 the daily dose of Dexamethasone was reduced to 8 mgs." 86 On that day the appellant complained that she was very thin with a very puffed faced and twig legs. The respondent's notes contain no record of that appearance but he did report to Dr. Donald on 26 June 1992 recording the appellant's ongoing emotional problems. The appellant was referred to Dr. Miller a psychiatrist for assessment. She had been seeing a psychologist, Ms Wallace. 87 On 29 June 1992 the appellant was seen by Dr. Miller who recommended Clomipramine medication and continued attendance with Ms Wallace. 88 On 13 July 1992 the appellant complained to the respondent of a cough and green sputum. The weekly urine tests disclosed no renal involvement. The doctor noted that there was "no objective sign of neuropathy" but this was said to be a mistake for "no objective sign of myopathy". The doctor considered the strength in the appellant's legs to be reasonable, however he gave evidence that proximal steroid myopathy would not be unexpected having regard to the steroids the appellant had by then taken. Having regard to the evidence of the appellant's father and some evidence from her mother as to her physical appearance Studdert J accepted that on the balance of probabilities the appellant's appearance had altered significantly by that time and that there was probably wasting of muscles present. Mrs Rufo gave evidence as to the appellant's appearance at that time and said that her face was big, "she was scrawny and she had this big belly and these chicken legs. These very, very thin, thin legs". 89 On 14 July 1992 the respondent wrote to Dr. Kamal, by then the appellant's general practitioner, saying that he would like the appellant to continue on 8 mg of Dexamethasone until the nasal discharge and cough had cleared up and then for the dose to be reduced to 7 mg per day. 90 On 20 July 1992 Dr. Miller reported that there had been an improvement in the appellant's symptoms, no doubt from the point of view of his speciality. He considered that she should remain on the medication he had prescribed for six months and that there was no need for her to see him again. 91 On 10 August 1992 the respondent saw the appellant. By this time her weight had fallen to 39.4 kg compared with her weight of 50.5 kg on 2 January 1992. The respondent was seeing the appellant at the John Hunter Hospital at that time and Studdert J notes that that was the first time the respondent personally noted any weight loss. On that day the respondent noted that the appellant had picked up over the past two to three weeks. Her teariness had gone and the weakness in her legs had improved. He noted steroid proximal myopathy and pot belly. He also noticed that the legs were thinner and weaker. There was no note of back pain, however, Studdert J accepts the evidence of the appellant and her father that she had difficulty walking to the surgery from the car park, presented to the surgery bent forward and had to be assisted into position on the consultation couch. On that day the respondent reduced the dose of Dexamethasone to 6 mg per day. 92 The appellant presented to Dr. Karmal on the 11, 14 and 15 of August with pain in her lower back and an x-ray was arranged on 11 August 1992. 93 On 20 August 1992 the appellant attended at John Hunter Hospital with faecal impactation and back pain. The hospital notes record that the back pain had been present for the past month and was worse with movement but relieved by rest. The plaintiff was kept in hospital overnight. 94 On 24 August 1992 the appellant experienced severe back pain at home and was admitted to the John Hunter Hospital where she remained until being discharged on 25 September 1992. The hospital records reveal that she had suffered vertebral microfractures and kyphosis of the spine. Studdert J considered it probable that the fractures accounted for the acute episode on that day and that they occurred on or about 24 August 1992. The appellant was treated by Dr. Ho for her back condition. 95 She was also treated in hospital by the respondent who had reduced the dose of Dexamethasone to 1 mg per day by the time of her discharge. The judgment concluded this review of the progress of the appellant's disease and treatment with the following paragraphs: "Dr Bleasel gave evidence, which I do not understand to have been challenged, to the effect that the plaintiff suffered osteoporosis by reason of the regime of corticosteroids and that the vertebral collapse was also due to the steroid therapy. I am satisfied on the balance of probabilities that the corticosteroids which the plaintiff took between the beginning of January 1992 and the time of her admission to John Hunter Hospital on 24 August 1992 caused or significantly aggravated the osteoporosis from which the plaintiff was then found to be suffering and that this condition ultimately led to the spinal fractures found following her admission to the hospital." 96 It is now convenient to examine the evidence of the doctors who dealt with this issue. Studdert J found all the doctors, including the respondent, honest. He did question the respondent's reliability in respect of some conversations as to which he relied upon imperfect notes. He rejected an attack on the credit of Professor Clancy but did observe that he thought the professor had some sympathy for the respondent. 97 Dr. Sutherland is a clinical immunologist with extensive treatment experience of patients suffering from lupus. The Judge accepted him as well qualified to address the issues in the case. 98 Studdert J took from the doctor's first report that he considered the prompt introduction of corticosteroids as appropriate and that once kidney disease was under control it was Dr. Sutherland's opinion that vigorous attempts to withdraw the (appellant's) corticosteroid intake were required. The doctor, he noted, considered that this regime could have commenced in the latter part of the March or early in April 1992 and that steroid sparing agents should have been introduced at that stage. Imuran (Azathioprine) is such an agent. 99 During a break in his cross-examination Dr. Sutherland produced a further report which said, inter alia: "As you were aware, I was taken through the individual steps in the management of Ms Rufo's illness. At each of those steps, I was challenged to express my approval or otherwise for that intervention and the rationale underlying it. At no point did I offer any direct criticism, but the exercise may have provided an insight into why a competent and well regarded clinician became involved in such an unfortunate series of events. Each of the steps was justifiable in its own right, but it seems that at no time did any one take the metaphorical step backwards, to review the entire clinical problem in a wider context. When this wider context is reviewed, it becomes apparent that there were three major causes of concern: 1. Michelle continued to require high (and therefore toxic) doses of corticosteroids for a protracted period. While doses such as 40 or even 60 mg of prednisone were bandied around, these must be seen in the context of a young woman who weighed little more than 40 kg. As I pointed out repeatedly, at some time between April and May of 1992, the ongoing necessity for high dose corticosteroids should have provoked concern, and therefore the consideration of the introduction of a second agent, as a 'steroid sparer'. 2. The ongoing need for high doses of oral corticosteroids led to a steady increase in the risk of steroid induced osteoporosis, and prophylactic treatment with oral calcium and a vitamin D preparation should have been introduced at an early stage. I mentioned that the need for a calcium supplement in such circumstances was well established prior to Michelle's illness, and I will attach a reproduction of the relevant section from a contemporary textbook to confirm this. Again as I noted, it was my opinion that there was sufficient evidence to mandate the use of vitamin D supplements as well, as shown by the abstracts that follow. 3. When Michelle lost one quarter of her body weight, this should have been regarded as a cause for major concern, and the cause for this unexplained weight loss should have been sought. Malnutrition of itself is a cause of osteoporosis, and thus possibly contributed to Michelle's problems subsequently. Certainly if her diet was deficient in calcium (the opinion of a dietician at the time), then this may have been a major risk factor for steroid induced osteoporosis. In addition, any clinical validity there may be in assessing the effectiveness of oral corticosteroid treatment by the appearance of cushingoid features such as a 'moon face' must surely have been negated by such a degree of weight loss. Thus while it is difficult (and possibly unfair) to be critical of any of the individual steps in Michelle's management, a broader view shows that that management was deficient in the lack of concern over ongoing toxic doses of corticosteroids and the apparent failure to consider alternative regimens, the failure to introduce appropriate prophylactic treatment for corticosteroid osteoporosis, and the apparent failure to react appropriately to the loss of one quarter of her body weight. Had these matters been addressed, it is quite likely that the subsequent unfortunate series of events, including the osteoporotic fractures, may have been avoided." 100 Studdert J summarised portion of Dr. Sutherland's evidence in cross examination as follows: "[H]e was critical of the treatment given before 1 June and, summarising what he said at T 349, it was Dr Sutherland's view that by April or May it was imperative to recognise the ongoing need that the plaintiff would have for corticosteroids and the inevitable toxicity associated with them. Alarm bells should have been ringing to introduce other agents, he said, referring to steroid sparers, by 'about April or May at the latest'." 101 Following questions referring to a flare up which occurred on 28 May 1992 Dr. Sutherland gave the following evidence: "Q. If in fact those tests and other clinical investigations led a person in the position of Dr Hosking at the time to the view that there was a flare-up of the disease activity but not such as it involved the kidneys, you would not be in a position because you weren't there – to pick up your language – to say that the decision not to introduce Imuran was reasonable? A. I'm not aware I've ever said it's unreasonable. I thought it was overdue, that's not the same. We talked about the clinical judgments here and that's very different from straying outside the bounds of reasonable practice and I've never suggested that. HIS HONOUR: Q. Never suggested what? A. That Dr Hosking strayed outside of acceptable clinical practice. I believe that Imuran and Plaquenil should have been started early but then to say, 'Does anybody who disagrees therefore behaving unacceptably?', obviously is a very different question. He was there and he saw a sick child. He is a reputable clinician whose judgment I value and I said that. It's a very difficult – I don't know how to answer it. Q. Just so that I can understand what you are saying though, are you telling me that you are not saying that at any stage of treating this plaintiff the doctor strayed outside the bounds of reasonable practice? A. By the standards prevailing in 1992? Q. Yes? A. Yes, I believe that that is so. That he did not stray outside the bounds of normal practice – of reasonable practice." 102 When asked how he reconciled the above responses to what he had written in his further report Dr. Sutherland responded: "I don't see any inconsistency at all and it was this that prompted me to write this second report. I was concerned that I was being taken through a process one step at a time, challenged at each individual step at a time, challenged at each individual step was outrageous, outside currently accepted standards of practice. My concern is that, as I said, nobody took the proverbial steps backwards and said, 'Just a minute'. There are three areas of major concern in this sorry story and that's why I issued that second report. Once again, we could go on for days taking me through every single step, is that step unreasonable – no. You know, can I be sure that step was wrong – no. But when you look at the whole picture and you look at what happened it's not reducible to hundreds and hundreds of little steps. It was a complex history over months that had a catastrophic outcome and I believe that these three concerns, in the medical sense, must be addressed in coming to an understanding of that series of events. So I don't think I'm being inconsistent at all." 103 Dr. Champion is a rheumatologist with a consulting role in paediatric rheumatology. Studdert J accepted that he was well qualified in his area of expertise. Dr. Champion explained the overlap between the disciplines of immunology and rheumatology. Amongst other things he said that throughout rheumatology there is a very substantial undercurrent of immunology. The doctor has a particular interest in and a large experience of osteoporosis. 104 Dr. Champion was critical of the length of time during which what he regarded as relatively high dosages of corticosteroids were maintained. He was of the view that in the exercise of reasonable treatment Imuran should have been prescribed for the plaintiff at the time of the flare up in May 1992. He rejected the proposition that it was reasonable management to continue without Imuran for a couple of months after 28 May 1992. 105 Professor Sturgess is the senior staff specialist in rheumatology at St George Hospital and the director and supervising pathologist in the immuno-rheumatology laboratory at that hospital. Studdert J considered him well qualified in the specialist fields of rheumatology and immunology. In his report of 11 January 2000 he said amongst other things: "Severe active lupus in a 15 year old girl demands high dose corticosteroid therapy. Dr Hosking also took advice from a renal physician. Renal lupus is a major factor in determining corticosteroid dosage. At each visit Dr Hosking considered the dosage and reduced the dose if the patient was well. One cannot reduce the dose of corticosteroids over just a few weeks. Experienced lupus specialists routinely continue high dose corticosteroids for months. A typical regimen would be 50mgs daily for a month, then 37.5mgs daily for a month then 25mgs daily for a month then a slower rate of reduction. The above regimen assumes that the patient rapidly responds and does not flare. If response is slow or there are flares then the dose is increased. Dr Champion argues for a 'brief' high dose course of therapy, but his approach would not be standard therapy in the lupus community. Indeed if therapy were reduced too fast, and the lupus patient had brain or renal damage, there would be an argument that the failure to use standard high dose corticosteroids would be negligent. In terms of expecting and preventing osteoporosis in this 15 year old patient with lupus, Dr Champion makes several unsupported statements. The first is that osteoporosis, was a likely and expected side effect of steroid treatment in a 15 year old. In fact, osteoporosis, and particularly fractures/kyphosis, is such an unusual and unexpected side effect of treatment in this age group that many doctors would never encounter it. I can't recall a similar case in my own experience and I use no routine osteoporosis prophylaxis. Given the rarity of osteoporosis/kyphosis without prophylaxis it is of little importance to consider the utility of preventive drugs. Dr Champion correctly states that most of the osteoporosis literature dates from well after 1991. He quotes a review from 1990 which suggests adequate calcium and vitamin D, restricting sodium, Thiazide diuretics etc. see page 6 of Dr Champion's letter. He then suggests vitamin D supplementation for which there is little or no data on efficacy in this situation." 106 Professor Sturgess continued: "Essentially my management would not have significantly differed from Dr Hosking's. In particular:- 1) I would have started with at least 50 mgs of prednisolone daily for at least a month. If she had periodic flares, as she did, I would have increased the dose without hesitation. 2) Like Dr Hosking, I would not have initially used Imuran, because of the known additional side effects which can occur. I often use Imuran, but usually try prednisolone alone at first to see if the patient will settle easily. You should know that Imuran is not without side effects of its own – in the last 18 months I would have seen patients with drug induced fever, hepatitis and leukopenia all from Imuran. It should not be regarded as an easy option. 3) I may have added Plaquenil, but I would not have expected much. It would have no benefit in terms of her renal lupus. 4) I would not have prescribed calcium, vitamin D, calcitonin, oestrogen or exercise. I would not have performed bone density testing. I consider osteoporosis a major concern in post menopausal females, but a very remote risk in 15 year old girls. Specifically I currently have 2 females under 18 on high dose prednisolone neither of whom is on anti-osteoporotic therapy. The major side effects I worry about are cosmetic, psychiatric and infective. In the first few months I worry more about not controlling the lupus than I do about the possibility of steroid side effects." 107 Professor Clancy is a specialist immunologist. He is currently Professor of Pathology, Discipline of Immunology and Microbiology at the Faculty of Medicine and Health Sciences at the University of Newcastle and Director of the Hunter Area Immunology Unit at Royal Newcastle Hospital. Judge Studdert accepted that he was well qualified in his areas of expertise. He has been the appellant's treating specialist since the beginning of 1993. 108 In a letter to the appellant's solicitors of 7 February 1996 Professor Clancy said, amongst other things: "Between the time of Michelle's diagnosis and me looking after her, one can say that her treatment was probably appropriate though it was attended by unexpected and unusual side effects. I commented at one time that the use of Imuran by itself was a little unusual in lupus, but then previous experience of steroids conditioned that. When I saw her she was on Plaquenil. I should also add that I have been forced to use significant amounts of corticosteroids on a number of occasions in Michelle, even knowing her background. I think it is very important for you to understand that this young lady has a very serious illness and her long term outcome could be compromised not by the use of steroids in the past, but by the underlying disease." 109 In a later letter of 16 July 1996 he said, amongst other things: "…My comments regarding question 11 specifically relate to this young lady. Subsequent to writing this letter I have talked with a number of my colleagues with experience in clinical immunology, and frankly none have seen the particular course that unfortunately Michelle underwent, ie in a person of this age developing symptomatic osteoporosis over the timeframe and at the dose of steroids. It really is an extremely unusual issue, though obviously older people with lower bone mass and particularly when given longer terms steroids are more likely to get this particular problem. It is thus likely that a variety of factors may well have contributed to the osteoporosis, although clearly steroids were one such factor." 110 Studdert J noted that in his oral evidence Professor Clancy was not critical of the regime of corticosteroid steroids and he did not regard it as unreasonable for the defendant not to introduced Imuran. 111 Studdert J said that he accepted the respondent's expertise in the field of paediatric immunology. He noted that the respondent acknowledged that lupus was not his specialty nor was osteoporosis. The Judge said: "Indeed he had not heard of corticosteroids causing fracture in the spine, although he was aware that steroids affected bone density and he acknowledged that they would have an effect on growing bone." 112 The judgment records that the respondent considered the outcome in this case to be extraordinarily rare and said that he did not turn his mind to the possibility of fractures when prescribing to the plaintiff over the period of 8 months nor indeed did he apply his mind to the issue of osteoporosis. He did, however, say that he knew in 1992 that glucocorticoids caused osteoporosis and he agreed that compression factors were recognised as an adverse effect of corticosteroids. Studdert J said: "As far as Imuran was concerned, the defendant did give consideration to its use but, having considered Cassidy and Petty, concluded the dangers of the introduction did not warrant its use." 113 The relevant head of negligence was "failing to reduce the high dosage of corticosteroids in particular by introducing steroid sparers Plaquenil and Imuran as early as February 1992". 114 Studdert J rejected the allegation based upon the failure to introduce Plaquenil and it may be set aside. 115 In his judgment the Judge referred to the medical evidence already mentioned and went in some detail to further material from the reports and evidence of the various doctors including the respondent. 116 I do not think it necessary or practical to go to all of that material, however, I should refer to some aspects. 117 The Judge fixed the time at which Dr. Sutherland thought that Imuran should be introduced as May 1992. He noted that Dr. Champion was of the opinion that the Imuran should have been considered "once the renal effects of the lupus were known". 118 I think the expressed reason for that view of Dr. Champion significant. Studdert J summarised it as follows: "[T]he defendant should have appreciated at the outset that there was going to be a long term requirement for steroids, and hence there was a need at the outset to build into the regime of treatment another agent to permit the reduction of corticosteroid doses to occur. He said this was particularly important because of the risk of osteoporosis." 119 Studdert J referred to the expression of caution in Cassidy and Petty set out as follows: "Specific immunosuppressive drugs have been used in the treatment of children who are seriously ill with rheumatic diseases when other modes of therapy have proved ineffective. However, few published reports have dealt with adequately controlled trials; many have been only incidental observations or case reports. In most instances these drugs are slow to begin exerting their pharmacologic effects. Therefore, they have proved more valuable in moderate – to long-term therapy than in an acute crisis. We would recommend only very circumspect use of immunosuppressive drugs in children. These agents are not presently approved for unrestricted use in children with the rheumatic diseases and should be regarded as experimental. Certain preconditions have therefore been suggested for their use in patients. Each of the agents has its own toxicities, and infection is a general concern. Little is known of the long-term effects of these drugs in children. Especially in children, the future oncogenic potential of some of these agents must be considered." 120 However he also noted Dr. Champion's comments that he did not agree with the use of the word "experimental". The judgment goes on: "In his opinion [Dr Champion's], the plaintiff was to be regarded as 'seriously ill', and he considered that a low dose of Imuran was appropriate. In his opinion the potential side effects of Imuran were quite modest compared with the threat of osteoporosis." 121 Studdert J noted that Professor Sturgess regarded the rate of reduction of steroids in the appellant's case as within the bounds of reasonable medical practice, that the Professor considered it reasonable practice to use only corticosteroids for the first six months but that would not be the case if the respondent had been treating a post menopausal patient. The Judge commented, clearly correctly, "because of the risk of osteoporosis". 122 Attention is drawn in the judgment to the acknowledgement by Professor Sturgess that by 11 May 1992 "he would have discussed the introduction of Imuran with the [appellant] and would have advised her that he thought such an introduction was "a good idea". 123 Studdert J made the following finding: "I consider it likely that had the plaintiff been told as at 11 May that it was 'a good idea' to start Imuran notwithstanding the possible side effects, the plaintiff would have accepted the advice given." 124 He also said: "I so conclude making my assessment of the plaintiff and her parents, who would, no doubt, have played an active role in decision making. I also take account of the plaintiff's compliance with the regime of medication that had been prescribed up to that point of time." 125 The Judge noted that Professor Clancy did not consider it unreasonable for the respondent not to have introduced Imuran as late as 1 July 1992. The Professor's approach to Imuran and like drugs was to delay introduction until a "plateau" amount of corticosteroid needed to control the disease became known. The Professor had given evidence in chief that: "[O]ne would like to think that by six months you would no [ sic ] that, sometimes it is three months, sometimes nine months, sometimes it is 12 months. Clearly at nine to 12 months you are starting to get a little concerned." 126 I comment that just after the passage referred to the Professor gave evidence in chief: "The information we have about corticosteroids and Imuran, and a lot of this is experience rather than something you can actually look at in a textbook or a paper, is that, and certainly my view is that Imuran is a particularly valuable drug at getting the doses of corticosteroids below a sort of magic 9 or 10 milligrams when otherwise you need 15, 16 milligrams of prednisone." 127 While Studdert J was, as he put it, not persuaded that it was unreasonable for the respondent to prescribe corticosteroids only in treating the appellant's lupus at any time prior to the flare up of May 1992, he set out a number of matters he considered of importance thereafter: "(i) The plaintiff had by this time been on high doses of corticosteroids for over four months and there had been two flare ups in her condition, the more recent of which involved increasing the plaintiff's Prednisolone dose to 60 mg per day. (ii) The inability over that period of months to reduce the dose of Prednisolone below 40 mg daily, and the inability to control the disease even at that dosage, was not a cause for optimism that corticosteroid levels could be reduced significantly and to an acceptable level in the immediate future without some change in the regime of treatment. (iii) The evidence is overwhelming that osteoporosis was a recognised adverse effect of corticosteroids and this adverse effect accompanied the continued use of such medication. I accept the evidence of Dr. Sutherland that the continued prescription of corticosteroids above a dose of 6 mg of Prednisolone per day (or its equivalent), has an adverse effect on bone density, although I also accept his view that damage of this kind probably occurred most rapidly in the first five months of treatment. (iv) Over the period of corticosteroid treatment and by the time of the May flare up the plaintiff had lost approximately seven kilograms in weight and this was a very significant proportion of her total body weight. Dr Champion described the weight loss and the amenorrhea as 'huge warning signs' as to the plaintiff's vulnerability to osteoporosis, and I accept that these features required very careful assessment, certainly by the end of May. (v) Then there was the plaintiff's emotional lability which it was reasonable to attribute to the corticosteroid intake. (vi) Whilst I find it was reasonable at the outset of treatment for the defendant to regard compression fractures as an extraordinarily rare adverse effect in the corticosteroid treatment of children – and I accept the defendant's evidence that this was his appreciation – it was not appropriate to regard the level of risk as static. I accept the evidence of Professor Sturgess that the risk of fractures occurring increased as the treatment progressed because of the plaintiff's resistance to treatment. On my understanding of the evidence, having regard to the corticosteroid doses by the end of May 1992, it was no longer correct to regard compression fractures as an extremely rare adverse possibility. It seems to me that there was good reason to consider that this risk had increased significantly. (vii) Whilst this may not have been as well appreciated ten years ago as it is today, the plaintiff was at a vulnerable stage of her development during the relevant period in terms of her exposure to osteoporosis because she was in the process of laying down new bone in her bodily growth. I accept the evidence given by Dr Sutherland and by Dr Champion on this issue." 128 The Judge noted the influence of Cassidy and Petty on the respondent's decision not to introduce Imuran and his view that the indicators for the introduction of that drug were not present. 129 In relation to reliance upon text writers the judgment referred to Professor Sturgess's comment "that it is not appropriate to look at the text book indications for Imuran and if the patient didn't fit those should not do it. It is very much a matter of weighing up the risks, the benefits and the text often mentioned the obvious reasons to do it…" 130 Turning to the weighing of risks Studdert J said: "Obviously in the present context amongst the risks to be weighed up included the risk of the progression of osteoporosis if the previous regime was continue. The defendant frankly acknowledged in his evidence that he did not turn his mind to the possibility of fractures or osteoporosis before the fractures occurred: 'Q. Let me just come back to this question. I was trying to work out what was in your mind as at 1992 when you prescribed for Miss Rufo these amounts of Prednisolone over a period of some eight months. Did you turn your mind to the possibility of fractures? A. At that time I would say no. No, because it was not high on my agenda because, as I say, it is rare. Q. Did you turn your mind to the possibility of osteoporosis? A. No." 131 The Judge set out his conclusion in a passage which demonstrates, amongst other things, that he was fully aware of the countervailing considerations: "Certainly the defendant was required to have regard to the potential side effects of Imuran in determining whether to introduce it. Moreover, I accept, as Dr Champion did, the authority of Cassidy and Petty for those treating children with lupus in 1992, and that those authors did not emphasise looking at the risk of osteoporosis. Further, I acknowledge differences of opinion as to appropriate treatment can be entertained by practitioners whilst each exercises reasonable care and skill. Moreover, I caution myself against the error of determining issues in this case by reference to hindsight. I am very conscious of the differing expert opinions that have been expressed. I realise that when Professor Sturgess gave evidence that he would have regarded the introduction of Imuran as 'a good idea' by 11 May, he was not thereby expressing an opinion that the failure to introduce it then was unreasonable, and Professor Clancy supports the defendant's treatment as provided after that time. Not so Dr Sutherland or Dr Champion. After weighing those matters I reviewed in par 169, and after reflecting on all the evidence in point, I have decided I should accept the opinion expressed by Dr Champion that the provision of reasonable treatment required the introduction of Imuran at a time after the flare up in May. I find accordingly." 132 Subsequently Studdert J fixed on an approximate date of 10 June 1992 which would have been the appropriate time for the introduction of Imuran. The Respondent's Submissions 133 The respondent's submissions began with the finding that the outcome suffered by the appellant was a most unusual one. It was put that the state of medical knowledge at that time available to a paediatrician, especially as opposed to Dr. Champion who had a special interest in osteoporosis, was such that it was not a breach of his duty of care not to be aware of and take steps to counter the admittedly foreseeable risk. It was put that it was reasonable at the outset of the treatment for the respondent to regard compression fractures as a "an extraordinarily rare adverse effect in the corticosteroid treatment of children". 134 The submission referred to Studdert J's observation that the appellant's vulnerability "might not have been as well appreciated ten years ago as it is today" and put that the main evidence in this regard came from Dr. Champion. It noted that in his report of 2 December 1998 he had observed that young people prior to the achievement of peak bone mass were also vulnerable to the same risk of osteoporosis from corticosteroids as postmenopausal women. The written submission went on "although he went on to say that 'it was thought that young people were resistant to osteoporosis in 1992'". That passage does not appear in the report and would appear to be a view as to the effect of the doctor's evidence in chief. If that be correct it was there put in not quite so clear cut a way, however, I shall come to that passage later. 135 Later in that report Dr. Champion said: "One of the problems is that there was not a great deal of normative data on bone density in adolescents in 1991. Furthermore, the potential effects of the disease itself (SLE) on bone mineral density was not adequately known in 1991. There is now (at the date of his report 2-12-98) evidence that factors associated with the disease itself were significant, indeed important, in osteoporosis in patients with SLE. I shall enclose copies of recent research abstracts from the 1988 Australian Rheumatology Association and The American College of Rheumatology Association Annual Scientific Meetings. It would have been known in 1991 that factors associated with SLE would have put an adolescent at risk. These factors which were identifiable would have included reduced physical activity. Impaired nutrition and calcium intake, relatively low oestrogen (amenorrhoea is relatively common in patients with this disease due to the constitutional effects of the illness or the drug therapy), and particularly in doses above 7.5 mg of Prednisolone (or equivalent) per day. Critical consideration of those issues would have been appropriate. I shall enclose a copy of the US National Osteoporosis Foundation Annotated Bibliography (December 1996) about corticoid induced osteoporosis. You will see that most of the papers cited are dated well after 1991. One of the reasons for this is that research on osteoporosis did not really gain must moment [ sic ] until reliable measures of bone density were available." 136 The submission then referred to recommendations the doctor made as to the optimal treatment and then set out the following passage from the report: "The above management items represent counsel of perfection as at 1991 and it should be emphasised that few physicians (including myself) would have carried out all of those precautions and principles. The high sustained dose of corticosteroid and notably the change to dexamethasone without any (written) consideration of osteoporosis prevention were the main concerns as I review all the available material." 137 The submission also went to portions of the doctor's report of 8 May 2001 which said: "Clinical practice in 1992: Dr Sturgess quoted Hodgson in a review in Endocrinology and Metabolism Clinics of North America (March 1990) where the conclusion was 'effective forms of prevention and treatment have not been identified, but … there is a good rationale for the use of calcium supplements and the maintenance of vitamin D nutrition'. … I referred in previous correspondence to a review by Lukert BP and Raisz LG entitled 'Glucocorticoid-induced osteoporosis: pathogenesis and management' published in the annals of internal medicine 1990: 112:352-363. From my research of the literature this was the most definitive review on the subject of glucocorticoid induced osteoporosis. These authors concluded that 'long-term trials of therapy for the prevention of glucocorticoid-induced osteoporosis had not been done, but reasonable recommendations include the use of glucocorticoids with a short half-life and the lowest dose possible, maintenance of physical activity, adequate calcium and vitamin D intake, sodium restrictions and use of thiazide diuretics, and gonodal hormonal replacement. In refractory cases, the use of calcitonin, biphosphonates, sodium fluoride, or anabolic steroids should be considered'. These recommendations were not highly evidence-based by today's standards, but that was a fair statement of the approved principles of prevention of glucocorticoid-induced osteoporosis at the time Ms Rufo was treated. Unfortunately, in paediatrics, there was not enough focus on osteoporosis assessment and prevention, and it would be fair to acknowledge that even experienced paediatric rheumatologists were not applying this standard of care… … A final thought: consideration may be reasonably be given to the extent to which a paediatric systems fault contributed (osteoporosis had not been a prominent topic in paediatrics despite this important and long-standing corticosteroid-influenced osteoporosis problem) to the apparent management deficiencies." 138 Attention was drawn to Dr. Champion's special interest in osteoporosis. 139 It was accepted that the risk of fractures increased as the treatment continued but put that it continued to be a rare complication and that the cumulative dose of the Prednisolone provided in the appellant's treatment was not uncommon. 140 It was pointed out that the text Cassidy and Petty did not emphasise looking at the risk of osteoporosis. 141 The toxicities and complications that might follow the introduction of Imuran including tumours and possible fertility problems were referred to as was Cassidy and Petty's express caution. It was put that the possible complications arising from Imuran were, on one view, more serious than the complication of vertical compression fractures. 142 The complication of a decision to introduce Imuran was relied upon and also the evidence that it did not always work as a steroid sparer. The divergence of medical opinion, it was submitted, emphasised the difficulty of the decision to be made. 143 It was submitted that there was no doubt that Professor Sturgess and Professor Clancy supported the respondent's treatment despite Professor Sturgess' opinion that the consideration of Imuran would have been a "good idea". 144 The view of Studdert J that the respondent's treatment was not supported by Dr. Sutherland and Champion was challenged. It was put: "A fair reading of Dr Sutherland's evidence is that on a step-by-step basis the decision to continue with corticosteroid medication without Imuran was reasonable although he was concerned about the Respondent perhaps not taking a 'proverbial step backwards'. Dr Sutherland was adamant in denying any assertion on his part that the management of the Respondent was unreasonable. At best his 'criticism' of the Respondent was equivocal or ambiguous." 145 It was put that the respondent should be adjudged by reference to the standard of care demanded of a paediatrician at the time which in turn, of necessity, must have regard to the body of knowledge available to them. 146 It was put that Studdert J attached an unwarranted significance to Professor Sturgess' comment that the introduction of Imuran in May 1992 would be "a good idea". His use of that evidence, it was submitted, did not take proper account of the countervailing considerations to which the Professor referred. The finding of Studdert J that the appellant would have accepted the advice, if given, that it was a good idea to introduce Imuran was put to be a gross oversimplification of Professor Sturgess' evidence. Reliance was placed upon the absence of agreement between the experts as to when (if at all) Imuran should have been introduced. It was pointed out that the advice would need to be heavily qualified in view of the risks associated with the taking of Imuran. 147 It was submitted that the highest breach of duty of care could only be the failure to properly advise. It could not be said to be unreasonable to emphasise the potential risks. 148 It was submitted that Studdert J's ultimate findings largely arose from a reliance upon Dr. Champion but not entirely so. In fixing the date in June rather than May he relied upon Dr. Sutherland. 149 On the honesty of the witnesses being ultimately accepted it was submitted that this Court is in as good a position as Studdert J to decide on the proper inferences to be drawn from the facts either undisputed or as found by the Judge. 150 It was put that a recommendation as to the use of Imuran was incapable of precise definition in view of the controversy between the experts. Dr. Champion, not a paediatrician, was said to be the only doctor to criticise the respondent, at least in an unambiguous way. 151 It was pointed out that there was a risk that administration of Imuran might have given rise to far more serious complications, including life threatening ones, than the rare complication of vertebral compression fractures. On the other hand there was no choice about the administration of the corticosteroid medication, it was necessary to control the lupus. 152 It was put that it was impossible to quantify the risks on the one hand of the fractures and on the other of taking Imuran. This was said to be of particular importance in relation to the possibility of fatal complications from taking Imuran. These were issues, it was put, upon which reasonable minds could properly differ. 153 It was submitted that the highest point of the appellant's case on the issue of competing risks was the view of Dr. Champion that the potential side effects of Imuran were quite modest compared with the threat of osteoporosis. It was pointed out that this was a value judgment made in the absence, at the time, of relevant studies and with competing opinions published in various texts. 154 It was also put that the appellant had failed to establish causation since, even if there was an obligation upon the respondent to provide some advice about the availability of Imuran, it was within the bounds of reasonable practice for him to ultimately counsel against its use at the time. It was submitted that, there being no evidence from the appellant on the point, the natural inference would be that consistent with the advice the appellant would not have taken the Imuran. 155 I should mention that in the written submissions the following appears "to the extent that it is necessary (if at all) the respondent would seek to amend the notice of contention so as to add '2. His Honour erred in finding that the appellant would have started Imuran notwithstanding its possible side effects'". 156 No objection was made to the raising of the issue and I propose that the amendment be allowed. The Appellant's Submissions 157 In the written submissions reliance was placed upon the preference of Studdert J for the evidence of Dr. Champion and Dr. Sutherland formed after he had the opportunity, over a lengthy period of time, to observe them and consider their evidence. 158 It was put that the Judge had taken into account the potential adverse effects of the Imuran. Against this had to be weighed the harmful effects of the high dose steroids. Reliance was placed upon Professor Sturgess' acknowledgement that it would have been "a good idea" to consider the use of Imuran. 159 It was submitted that it was not correct to suggest that Dr. Sutherland did not criticise the respondent's course of treatment and that the Judge's summary of that evidence was correct. 160 It was put that Professor Clancy's approach of delaying the introduction of a steroid sparer until a plateau had been established did not address a case such as that of the appellant where it had proved difficult to control the lupus other than with dangerously high levels of steroids. 161 It was submitted that Studdert J's finding that it was necessary to add Imuran was in accordance with the weight of the medical evidence. 162 Mr Brereton SC who appeared with Dr K Sant of counsel for the appellant, after referring to the uncontroversial proposition that ultimately it is for the court and not the professional witnesses to be the arbiter of what reasonable care requires, Rogers v Whitaker (1992) 175 CLR 479, referred to some observations of McHugh J in Naxakis v Western General Hospital (1999) 197 CLR 269. 163 Naxakis was a medical negligence case which dealt with an issue as to whether there was evidence to support the matter going to the jury. The passages to which Mr Brereton referred included the following at 286: "To many doctors, judges and lawyers, it must seem unsatisfactory that a doctor can be condemned as negligent by a jury when he or she has acted in accordance with a respectable body of medical opinion. But as long as there is evidence that other respectable practitioners would have taken a different view concerning what should have been done by the defendant, the issue is one for the jury, provided of course the evidence is reasonably capable of supporting all the elements of a cause of action in negligence." 164 It was put that the present matter was not a case in which the court has imposed the standard of care in the absence of any professional evidence to support it. Mr Brereton submitted that, viewed as a whole, the overwhelming balance of the professional evidence, though not exclusively so, supported the view that reasonable care required the introduction of Imuran by at least 10 June 1992. 165 Mr Brereton, while conceding that before June there were valid competing considerations, put that by then the risk of steroids was so great that the competing considerations so far as Imuran were concerned paled into insignificance. 166 Following a reference from the bench as to assessment in the light of a belief at the time that osteoporosis was not a high risk in the case of young people Mr Brereton took us to a number of passages of evidence. 167 Dr. Sutherland in chief was asked a series of questions relating to Goodman and Gilman which he had agreed was a major text on the topic. He gave the following evidence (the question does not matter): "Q. In order to understand item four, I am going to have to ask you to explain what it means in context. Would you be able to do that for me? A. Yes, I alluded previously to the way in which the toxicity of corticosteroids changes with time. Unlike some other drugs where there is a known level of toxicity which is manifest throughout the duration of therapy, with corticosteroids the initial toxicity is usually very low, and therefore acceptable. As time goes on, that level of toxicity increases and begins to increase rapidly, so that the curve showing the toxicity with time becomes steeper and steeper. So that under all except the most extreme or life threatening circumstances, the time arises when that toxicity exceeds the benefits for which the drug was prescribed in the first place, and that mandates a change in management. Q. Did that occur in this case? A. It is easy in retrospect to say yes, it did. In my opinion as events evolved, by the time there was evidence of proximal myopathy, the wasting of the muscles, I believe that that was unacceptable toxicity, unless there were no other treatment modalities available." 168 For convenience I would add that the doctor also gave the following evidence relating to that text: "Q. Then the next sentence, 'The possibility of development of osteoporosis should be an important consideration when initiating and managing corticosteroid therapy, especially in postmenopausal women'? A. Yes. Q. Do you agree with that? A. Yes. Q. This young lady of course was not post menopausal, but was it still an important consideration when initiating and managing the therapy? A. Yes, it was." 169 Mr Brereton also referred, amongst other things, to the following passage in Dr. Sutherland's cross examination: "Q. We've got to 1 June. I take it from the answers that you have given to my questions that on the documentation that you have had available to you, you would not be critical – you would not suggest that the treatment provided by Dr Hosking up to and including 1 June 1992 was anything other than reasonable. Is that so? A. No. That's not what I said. You took me through a series of decisions and interventions, each of which I agreed was reasonable. At some time, and I believe that probably was in April or in May, there was an imperative to recognise the ongoing need for corticosteroids and the inevitable toxicity arising from those. So at some time in that period alarm bells should have been ringing and saying, 'We are not going to get this person off high poisonous doses of steroids and therefore we must talk about another agents [ sic ]'. And with the wisdom of hindsight, looking back on this, my opinion is that that time came at about April or May at the latest." ……… "Q. I obviously misunderstood you and it's probably my fault. I understood that just a little while ago you agreed with me that with the improvement in her symptoms as we've been over, at least up to that time before 11 May when there was this decrease in the Prednisolone from an appropriate high dose down, that you agreed with me that over that period of time at least prior to 11 May it was within the bounds of reasonable practice to keep her simply on the one drug, the Prednisolone. Have I got that wrong? A. Yes. You have got that wrong. As I said, you took me through each step and the decisions and asked me at each step whether I had criticism. I do not have criticism of those steps but sometime in about April or May it should have become apparent that this young lady was on a lot of steroid and, if not earlier when it was necessary to retain her on 40 milligrams, it is my opinion that an additional agent should have been contemplated." 170 The next reference was to the evidence of Dr. Champion. He was asked in chief to comment upon a portion of the respondent's 1999 report in which he said, amongst other things, that Immunosuppressive drugs were not indicated before the appellant had a relapse of lupus following almost complete withdrawal of steroids because of the osteoporosis. The observation was made at that stage that she was started on Imuran. The doctor's reply was: "This is not in accord with the textbook recommendations at that time, or with a number of other publications in the literature at the time… . And – and it misses of [ sic ] point of corticosteroid sparing influence. It is that which was the – would have been a substantial preoccupation among the people that I work with, and myself, being sensitively aware of impending problems with high to moderate dose steroid running along for seven months or so. The corticosteroid sparing was – was a very important issue and – and there was ample justification, probably as soon as renal lupus was – renal involvement was recognised and there were also difficulties in lowering below about 50, 50 milligrams of prednisolone. That was a reasonable and appropriate time to commence even a low dose azathioprine. The problems and threat with low dose or modest doze [ sic ] azathioprine would have been virtually nothing compared with what has happened from corticosteroid influenced osteoporosis. Of course, I realise it is easy to say that in hindsight." 171 The next reference was to a passage from the cross examination of Professor Sturgess. Mr Donovan SC, then appearing for the appellant, referring to a time period of 11 May 1992 and the use of Imuran asked a question, which in part was reply to an observation by Studdert J: "Q. I want to get the doctor to consider it first? A. Yes, I would certainly think it should be considered." Thereafter Professor Sturgess gave the following evidence: "Q. Now, the next thing is, should it have been used? A. I suppose the difficult thing is we know the final outcome, and knowing the final outcome, we would have done everything possible to reduce that prednisone, but if I put myself in the position what would I have done on 11 May, I would of talked to the family and patient about Imuran, and I've told them that there are difficulties and some side effects, and if they said well what do you think, what would you recommend, I would have said I think starting Imuran now is a good idea, it will probably help me to get your prednisolone down faster. If the family said I don't know, some of those side effects, the bone marrow damage, the risk of cancer, I wouldn't push it. I wouldn't say – I wouldn't push the patient." 172 For convenience I note that Professor Sturgess had given evidence a little earlier in his cross examination as follows: "Q. If there's been a resistance in the – let me take it a step further. Just see, where you would feel is appropriate, let us then take it through to, take you to April, get you down to 40 in April, but on 11 May her condition is such that the 40 cannot be reduced, that would I think, sorry, that would I suggest, make it more pressing to introduce Imuran about then? A. Yes. That would be the second time it would be unable to reduce the dose, and I would of thought gee I've had that lapse on prednisolone now for four months. At that point I'd almost certainly talk to her about Imuran, explaining the advantages and the disadvantages, and I would probably recommend starting Imuran." 173 Mr Brereton accepted that Professor Clancy was of another view but referred to the passage in the judgment as to the Judge's view that Professor Clancy was sympathetic to the defendant's position. 174 Mr Brereton relied upon the judgment and referred to provisions therein to which it is unnecessary for me now to go. He did emphasise the reference to the fact that the respondent in the context of very heavy use of steroids for a long time did not advert to the risk of osteoporosis and, in particular, to the matter set out in sub-paragraphs (iii), (iv) and (vi) of [72]. Conclusion and Reasons 175 It is convenient to say at once that having considered the available material and the submissions of the parties I am not persuaded that Studdert J's conclusion on the issue relating to the Notice of Contention was wrong. 176 Whilst I accept that the issue to be determined is a difficult one I found the judgment of Studdert J on this issue both free from error and convincing. 177 I consider that the thrust of the evidence of Dr. Champion and Dr. Sutherland was strongly supportive of the appellant's case. I do not agree that Dr. Sutherland's criticism of the respondent's treatment was ambiguous. 178 Dr. Sutherland was at pains to make clear that whilst each step in the treatment, considered alone, could be said to be reasonable, the respondent had failed to have regard to the overall handling of the appellant's disease. This, as the treating paediatric immunologist, was his responsibility. 179 When Dr. Sutherland said "there are three areas of major concern in this sorry story…" I do not think he was speaking only of the outcome. 180 Whilst Professor Sturgess did say that he would not criticise the respondent for not considering the use of Imuran in April or May 1992 it is clear that he would have done so himself. I refer in particular to the passage quoted in paragraph 117. 181 In Naxakis at 285 McHugh J, having noted the evidence of a surgeon that: "My opinion, from my analysis of the case, I felt there was a reasonable ground to consider the undertaking of the (operation)" said: "It is not to the point that immediately before giving this evidence (the surgeon) said that he did not think it careless not to conduct an (operation)." 182 Whilst the issue before the Court was different, the original trial being before a jury, this passage makes it clear that it was open to Studdert J and, indeed, to this Court to rely upon what Professor Sturgess would have done, if it was otherwise thought appropriate to do so, despite his lack of criticism of the respondent. 183 I think it should be accepted that Professor Clancy's evidence was solidly against the appellant's case. I do not think it can be discounted, as the appellant argued, as of little assistance on the basis that no "plateau" had been reached within six months, because the Professor's evidence made it clear that he contemplated periods as long as twelve months before that position was reached. 184 Whilst it was accepted that the doctors were honest, Studdert J did have the advantage of hearing and seeing them advance their different professional views over a considerable time. 185 Mr Higgs, whilst addressing us on the issue upon which the respondent had succeeded at trial, said: "…In particular the fact that when one comes to consider conflicting expert opinion, there does come into it issues of credit. Often opinions are intuitive, they are based on no empirical studies. That certainly was the case here because of the reference, even by Dr Champion, to his various views being expressed on theoretical grounds rather than by reference to any particular studies. So it ultimately comes down to a question of impression and one which here the trial judge had the benefit of and one which your Honour's don't have." 186 Such an approach is to some extent at odds with the respondent's written submissions, however, I accept that it is a correct, although not necessarily determinative, approach to both areas of dispute in this case. 187 Whilst it does appear that in 1992 the dangers to young people were less well appreciated it should be borne in mind that Cassidy and Petty, the text relied upon by the respondent, passages from which appear earlier in this judgment, is a textbook for Paediatric Rheumatology. The discussion of toxicities "for importance in children under chronic pharmacologic treatment for rheumatic diseases" include "osteoporosis and vertebral compression fractures and inhibition of linear growth". The emphasis is mine. Dr. Champion said that lupus was a condition which fell within this description of disease. 188 Dr. Champion had in chief pointed out that there was less experience in the use of corticosteroid sparing agents and other drugs in paediatric lupus than adult lupus because paediatric lupus was less common and less studied. He did say "…and also, in general, young people were thought to be fairly resistant to corticosteroid sparing [sic] osteoporosis, particularly those who had reached maturity, age of 20 which is the average time for peak bone mass to have been achieved …" 189 However, whilst referring to the need to keep this "balance" in mind he went on: "…but there were nevertheless two huge warning signs about osteoporotic biological vulnerability in Ms Rufo, in somebody on sustained high dose corticosteroid. One point of vulnerability was the secondary amenorrhea, hypogonadism and the second point of vulnerability was her apparently impaired nutritional state with a fair amount of weight loss. Those two together should have been substantial warnings that she would be at big risk and therefore raise the – the earlier consideration than may have been the case of, in some other individuals, of corticosteroid sparing agents." 190 Dr. Champion spoke of "substantial warnings" and Dr. Sutherland of "alarm bells [that] should have been ringing". 191 It is relevant to note that in his report of 2 December 1998 Dr. Champion did say "it would have been known in 1991 that factors associated with SLE would have put an adolescent at risk. These factors which were identifiable would have included … and particularly in doses above 7.5 mgs of Prednisolone (or equivalent) per day." 192 It is clear that in considering whether to introduce Imuran (see [57]) the respondent did not take into account the risk of osteoporosis and vertebral compression fractures being one of the toxicities specifically referred to in Cassidy and Petty a text upon which he relied. 193 Dr. Champion, Dr. Sutherland and Professor Sturgess have all referred to "hindsight" or, "in retrospect", but I do not think they are to be taken to mean that their opinions as to what should have been done are merely the product of hindsight. Rather, their use of the word shows that they were aware of the need to take the advantage of hindsight into account, at least on the issue of fault. However it is clear, for example, from the passages, which I have quoted from Professor Sturgess that it would not have been hindsight that had him thinking about Imuran in April or May 1992. Nor would that be so with Dr. Sutherland, although hindsight may well have given more certainty to his view of "April or May at the latest". 194 In Naxakis Kirby J made a pertinent observation as to 'hindsight' when he said at 295: "Although [the surgeon] conceded that his opinion had the advantage of hindsight, this necessarily had to be so. It would be true of any non-treating medical expert qualified to give evidence in such a case. It was open to the jury to disregard such a concession or to treat it as stemming from professional courtesy or collegial sympathy for [the defendant]." 195 Studdert J found that had the respondent told the appellant and her parents that the introduction of Imuran would be a good idea she would have taken the drug. That seems to me to be a finding very much dependent upon the impression formed upon him by the appellant and her parents. Accepting that finding, as I do, deals with the additional causation issue raised by amendment to the Notice of Contention. 196 It is obvious that the doctors at the trial all appreciated that the appropriate advice would need to be given as to possible risks and complications. It is clear that the trial was conducted without any attempt on either side to draw fine distinctions between prescribing the treatment and advising it. Studdert J found that the treatment should have been advised and that if the advice were given, in terms of it being "a good idea", the appellant would have taken the drug. Had it been advised and the appellant not in fact agreed to take it then the position would obviously be different. However, as Mr Brereton put in address, that simply did not occur. The Judge has made a finding, which I accept, as to what would have occurred. 197 Whilst Naxakis was concerned with a different question it does illustrate that the circumstance that a doctor acts in accordance with a respectable body of medical opinion does not conclude the issue as to whether negligence has been made out. 198 As I indicated earlier I am of the opinion that the Notice of Contention should not succeed. Causation: Overview 199 Having found that from early June 1992 there was a failure to exercise reasonable care on the part of the respondent in two respects namely: "(a) in the failure to introduce Imuran on or about 10 June 1992; (b) in the prescription then of Dexamethasone." Justice Studdert observed: "It is not sufficient for the plaintiff to prove breach of a duty of care. The plaintiff must also prove damage resulting from breach of duty in one or other or both of the respects proved: see Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307; Wallaby Grip (Bae) Pty Limited (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355; E.M Baldwin & Sons Pty Limited v Plane (1999) ATR 81-499 and TC v State of New South Wales [2001] NSWCA 380." 200 Under the heading "Causation - Has damage been proved" his Honour posed the following questions: "The damage which the plaintiff claims to have suffered is the progression of the osteoporosis to the point of the spinal fractures detected upon her admission to hospital on 24 August 1992. Would those fractures have been avoided by the introduction of Imuran in June 1992? Would they have been avoided had the plaintiff remained on Prednisolone?" 201 The first question was answered in the following passages of the judgment: "I am not persuaded on the balance of probabilities that had Imuran been introduced when I find it should have been on or about 10 June 1992, the fractures that occurred in August 1992 would have been prevented. Nor am I persuaded on the balance of probabilities that any reduction in corticosteroid dosage that may have occurred as a consequence of the introduction of Imuran would have reduced the severity of those fractures. On my assessment of the evidence, I am not persuaded on the balance of probabilities that the plaintiff did lose the chance of a better outcome because of the failure to introduce Imuran about 10 June 1992. Indeed, I think the reduction would probably have been too little too late for it to have given rise to any chance of a better outcome." 202 The second question was answered in the following passage of the judgment. "In the result, I am unable to find, and I do not find, that the introduction of the Dexamethasone in the dosages prescribed increased the risk of osteoporosis or spinal fractures that occurred beyond that which would have been accompanied the dosages of Prednisolone that the plaintiff would have otherwise have taken. Nor do I find that it is probable that the change to Dexamethasone resulted for the plaintiff in the loss of a chance of a better outcome than had the equivalent prescription of Prednisolone been continued until 24 August." 203 It is convenient to deal with a number of matters that narrow the issues to be dealt with in this Appeal. 204 First, it will have been observed that in respect of each breach Studdert J responded to an alternative allegation of loss of a chance of a better outcome. 205 Both in written and oral submissions it was made clear that the appellant's primary contention was that Studdert J was in error in holding that the appellant had not lost a chance of a better outcome as a result of the respondent's breaches of his duty of care. I propose to approach the appeal on that basis, albeit I shall say something later as to the appellant's primary case at trial. 206 Second, it was accepted at trial and on appeal that should the facts support such an approach it was available in point of law. It was not argued that the damage sustained by the appellant was not the loss of a chance but rather the compression fractures and their consequences (see, Chappel v Hart (1998) 195 CLR 232 per Gaudron J at 238, Naxakis per Callinan J at 312 and Gavalas v Singh [2001] 3 VR 404). 207 Third, there was no challenge to Studdert J's formulation of what the appellant was required to prove to recover damages for loss of the chance of a better outcome, his Honour said: "In order to recover damages for the loss of a chance of a better outcome, the plaintiff is required to prove on the balance of probabilities that there did exist a chance that the plaintiff would have had a better outcome had the negligence in treatment not occurred: see Malec v J.C. Hutton Pty Limited (1990) 169 CLR 638; Sellars v Adelaide Petroleum N.L. (1992-94) 179 CLR 333; Daniels v Anderson (1995) 37 NSWLR 438; and Tran v Lam (unreported, Badgery-Parker J, 20 June 1997). Has the plaintiff proved on the balance of probabilities that there did exist a chance that the introduction of Imuran on or about 10 June would have resulted in a better outcome, if not by avoiding the occurrence of the fractures then at least by reducing their severity? If so, then 'unless the chance is so low as to be regarded as speculative – say less than one percent' ( Malec at 643), the plaintiff is entitled to recover an appropriate award of damages referable to the quantification of the loss of the chance." 208 And, fourth, Mr Brereton indicated that there was no challenge to Studdert J's finding that "there have been no studies carried out to determine whether there is any difference in the effect that Dexathasone would have upon bone loss compared with the effect of an equivalent dose of Prednisolone". 209 I come to the significance of this concession later, however, for the moment comment that, although expressed as a matter of "studies", it is clear from the context that the Judge was not satisfied that there was any such difference. The appeal proceeded upon that basis. The Judgment 210 Studdert J considered that, before assessing the significance of the failure to introduce Imuran it was important to recognise what was required at the beginning of June 1992 to halt the progress of the appellant's osteoporosis. 211 He said: "Dr Champion gave evidence which I accept and from which I conclude that to avoid a real chance of ongoing osteoporosis, it would have been necessary to reduce the corticosteroid dose of Prednisolone (had the plaintiff remained on it) to 6 mgs per day. Dr Sutherland also considered that a dose of Prednisolone above 6mgs per day could adversely affect bone density." 212 A quoted passage from Dr. Champion's evidence contained the following: "Q. Even if you were to achieve as low a rate as 20 milligrams per day, you still have a level of Prednisolone in your view that is going to in all likelihood cause ongoing osteoporosis? A. Yes Q. Can you tell me, as between the 20 milligrams that she was on and the 60 milligrams a day that she was on to begin with after the flare-up, is there a precise correlation between the adverse effect upon the bones in terms of osteoporosis and the dosage? Or is there a bell curve, or is it a flat line or whatever? A. I cannot answer that. The fact is that on theoretical grounds it is likely that there would be an important proportionality, a dose effect consequence. But the actual studies would be extraordinarily difficult to perform, to prove that beyond reasonable doubt. So that we have to run with basic pharmacological principles that there will be a dose response effect on loss of bone density, until a fracture threshold is reached. Q. In saying that, can you give us an idea as to whether or not 60 milligrams of Prednisolone a day is twice as bad as 30, or is that too crude a way of looking at it? A. Well it is substantially worse than 30, but 30 might be a sufficient cause for concern too, that it may not make a huge difference over a limited timeframe." 213 The Judge concluded: "It follows from the above evidence that above a daily dose of 6mgs of Prednisolone, it was likely that osteoporosis would have progressed. Certainly a dosage of 20mgs per day was likely to cause ongoing osteoporosis. As I understand Dr Champion's evidence, it is not possible to say that a dose of 40 mg would double the progress of the disease compared with a dose of 20 mgs, and, indeed, if the dose was as much as 30 mgs, the increased risk of a dose above that may not be very significant, at least over a relatively short period." 214 Dr. Sutherland, had given evidence as to it being more probable than not that crush fractures would have been avoided had the appellant been weaned off high dose corticosteroids by March or April. Studdert J, however, went to other points of his evidence as follows: "Q. I want you to assume that in March/April the Plaquenil and Imuran was introduced, and that the steroid was reduced to about 15 milligrams. What period of time would that have taken from 40, which she was on at that time? A. Of the order of five months, if it went without hiccups or other disease flares on the way through. Q. I will come back to that May issue in a moment, when she went to hospital. If that had been done, would that have made a difference to the likelihood of the fractures which she suffered? A. Yes, it would have made a difference to the likelihood or the risk. Q. Would it have been more probable than not that they would not have occurred? A. I can't answer that. HIS HONOUR: Q. Are you able to give a professional opinion as to how that effect could be measured then? A. I would be a worthwhile favourable effect. The problem is the natural history of this has not been well studied. Therefore, to take an individual who has been on high dose steroids, and then reduced by 5 milligrams a month for four or five months, must have been a help. I don't believe it is possible to put a number on it, or other than a vague term like 'worthwhile' or 'helpful.' There are, in the literature, reports of, for example, 20 percent increase in bone density with the withdrawal of steroids. But then we come back to that other question; would that have prevented the fracture, and I don't know if it is possible to answer that." …… "Q. I just take you to page 5 of your report and you will see in the third paragraph you are talking about March or April of 1992 and you said, 'It seems certain that her osteoporosis would have been much less at that stage', that's March or April, 'and on the balance of probabilities not of sufficient severity to cause fractures and subsequent kyphosis'. Do you see that? A. Yes, I do. Q. Now that's talking about March or April? A. Yes. Q. Are you able to say whether the same would have been so, that is on the balance of probabilities in May or June, or is it getting more difficult then? A. It's getting very difficult, if not impossible." 215 Studdert J observed: "Plainly the last of the above responses would not support a finding on the balance of probabilities that the introduction of Imuran in June would have avoided the crush fractures that occurred." 216 The judgment quoted the following passage from the evidence in chief of Dr. Champion (I have omitted an unresponsive answer): "A. The objective is to get the Prednisolone down to 6 milligrams per day, or of that order, without losing control of the lupus. It's a difficult objective in a severe disease, that's why the adjunctive therapy with hydroxychloroquine initially and the probable requirement of azathioprine after renal recognition would have occurred. Small, steady reductions while adjusting the azathipronine dose, assuming tolerability, aiming over three months or so to get the Prednisolone well under 6 milligrams per day. HIS HONOUR: Q. You're going to chip away at 5 milligrams at a time? A. If there is difficulty, yes. There are many suggestions that you reduce about 10 milligrams at a time but the smaller the reduction the more easier it is to effect without a reduction, without relapse. …… DONOVAN Q. What I was trying to establish was how often you would anticipate that you could reduce the Prednisolone making use of the Plaquenil and the Imuran as the adjunctive therapy? A. That mostly works out favourably and you expect to achieve substantial reduction within two to four months. Q. When you say 'substantial reduction', can you give me a range of what you mean by that in terms of numbers? A. I think it's very difficult. Q. That's why I use the word 'range' to try and make it a little easier? A. There would be a reasonable expectation of getting to about 15 milligrams of Prednisolone by four months. Q. Assume that had occurred and, taking into account the other factors that you've mentioned, can you indicate whether that would have had any effect on the likelihood of the kyphosis and fractures which she suffered or the degree of kyphosis and fractures that she suffered? A. It would definitely have reduced the rate of progression of osteoporosis. It follows that it would have reduced both the risk of osteoporotic vertebral compressions and the extent of - that is the number of vertebrae affected and the degree of compression. Q. I'm going to take you to another question and I'll see if you can answer it. In terms of the risk of any kyphosis and fractures, and I'll just use those lay terms rather than the way you've described it for the moment, are you able to say whether on the probabilities she would have escaped with no injury? A. Purely from the corticosteroid reduction alone I could not say that that would be more probable than not. Q. Without [ sic ] other factors would have been necessary for you to reach a view that more probably than not she would have escaped any spinal collapse? A. She would have needed a major therapeutic response to hydrochloroquine and azathioprine within weeks of commencement of the azathioprine such that the Prednisolone was down to about 6 milligrams per day within two or three months. Even then there are these other nutritional and hormonal issues that would need to be taken into account. Q. Let me go back to your previous scenario, that is the 15 milligrams in three to four months. I think I get that right, tell me if I'm wrong? A. Yes. Q. In four months. If that was achieved and if her nutritional situation was remedied, would that lead to a more probable than not conclusion that she would not have had any fractures at all? A. I cannot say that because there is one very big unknown and that is what was her bone density like at the time of commencement of the lupus. Since we do not know that - if it were very low because of genetic, developmental and other factors - and the question that's been raised about celiac disease - then even that improved regimen I can't say would more probably than not have prevented fractures. All I can say is there would have been a substantial reduction in risk. Q. And a reduction in the extent of injury? A. It follows that - it includes, yes - you would expect, with that achievement as proposed, a reduction in the number and extent of vertebral compressions." …… "Q. Supposing the Imuran and Plaquenil - perhaps I should reverse that in order - were introduced at a later time, April/ May, so that the 6 milligrams in three months or the 15 milligrams in four months were moved back closer to the event. Would that have had, first, any effects on the risk and, second, any effect on the extent? A. Are we still employing the dexamethasone? Q. No, for the moment I want to leave that to one side? A. Well, the issue there is that is it too late. It would have to be some reduction of risk but there would be less reduction of risk than with the first, that is the earlier, scenario we discussed. Q. And less reduction in extent? A. Yes. Q. I don't suppose there's any point in my asking you what extent? A. No, it's too speculative I think." 217 Studdert J concluded that the later Imuran was introduced the less the chance of fractures being avoided. 218 As summarised in the judgment the evidence of Dr. Sutherland and Dr. Champion as to the likely extent of reduction was as follows: "Had the Imuran been introduced in March or April when the plaintiff was on 40mg per day, Dr Sutherland thought it would have taken five months to reduce the dosage to 15mg, barring setbacks. Dr Champion considered it would have been 'a reasonable expectation' to reduce the dosage to 15mg in 4 months. This being so, it seems to me to be altogether unreasonable to have expected that a dosage as low as 15mg per day could have been achieved by 24 August had Imuran been introduced on 10 June. As I see it, Dr Champion put the plaintiff's case at it's highest in opining that it was 'a fair expectation' that the plaintiff's dose of Prednisolone might have been reduced to [ sic ] 30 mg per day by 24 August. In examination in chief, Dr Champion said that had the plaintiff been on a dose of Prednisolone of 50 mg as at 22 June (in fact she was then on 8 mg of Dexamethasone per day - the equivalent of 53.4mg of Prednisolone), he considered it was 'a fair expectation' that the plaintiff's dose of Prednisolone might be reduced to 20mg per day with the help of Imuran." The judgment went on: "However, it would not have been possible to start reducing the corticosteroid dose as soon as the Imuran was introduced and, in speaking of a reduction to 20 mg per day, Dr Champion had in mind the introduction of Imuran a little earlier than I find it should have been introduced. In cross examination Dr Champion did say (T 512) that the steroid sparing effects of Imuran took 'weeks to months' to occur, but he considered that by the end of May there would have been compelling reasons to introduce Imuran with a dose of 50 mg and to increase that quickly to 100 mg, provided it was well tolerated. It would have taken one to two weeks on this approach to reach a dose of 100 mg. According to Dr Champion, it would have been a reasonable approach (and one consistent with the regime set out in table 7-35 in Cassidy and Petty (at p 299)) to wean the plaintiff off Prednisolone at the rate of 2½ to 5 mg per week (T 515). Assuming the defendant had introduced Imuran as I have found he should have done on about 10 June 1992, and assuming it would have been possible to start to reduce the corticosteroid dose two weeks later, that is by 24 June 1992, then taking the more conservative reduction rate of 2.5 mg referred to in Cassidy and Petty , this would have left the plaintiff on a dose of at least 30 mg of Prednisolone per day as at 24 August 1992. That dosage would still have remained well above that required to arrest ongoing osteoporosis according to Dr Champion. Of course, a lower end dose may have been achieved by heavier weekly reductions of, say, 5 mg per week had this proved possible but I consider that such a rate of reduction would have been an unlikely outcome even if the Imuran dosage had been rapidly pushed to 100 mg. There was a risk of rebound to be guarded against." 219 Studdert J's view that the appellant's case derived no assistance on this issue from the evidence called in the respondent's case was not challenged. 220 Professor Sturgess said in cross-examination that the introduction of Imuran would not have affected the Prednisone [sic] dose for six to eight weeks leaving, as the Judge concluded, minimal opportunity to lower the corticosteroid dose between 10 June 1992 and 24 August 1992. 221 Professor Clancy's evidence was that benefits would not be expected for four to six weeks after introducing Imuran. He did not think in the available time that Imuran would make a substantial difference. He also expressed this concept as "would not make much difference". 222 The passages from the evidence of Professor Clancy set out in the judgment included the following: "Q. Are you able to give us an idea each month or each six weeks or fortnight as to what you would be attempting to aim for in terms of a reduction in the dose of Prednisolone? No doubt it would be a range? A. Yes. I think I would like to think that I could reduce by five to ten milligrams a month, that sort of range. So the maximum would be then getting down to around about 30 of Prednisone. But the realistic expectation - and real life is not what you want - might be 40 to 50 milligrams, given the track record of what we have already seen… Q. The five to ten milligrams that you would aim or hope for per month, would that have been in any way slowed down because of the flu like symptoms that did present in mid July? A. Yes, it would." 223 Studdert J considered that it was unlikely that the introduction of Imuran on about 10 June 1992 would have achieved a reduction in dosage below 30mg of Prednisolone or its equivalent and that the dose may have been closer to the equivalent of 40mg of Prednisolone. 224 He reached the first conclusion I set out in [146] above. 225 Dealing with the claim based on loss of a chance the judgment went on: "Had the dose of corticosteroid been lowered to the equivalent of 30 mg of Prednisolone by 24 August 1992, is it probable this would have resulted in the chance of a better outcome for the plaintiff? Certainly the dose would have been 10 mg less than the Prednisolone equivalent of the dose of Dexamethasone that the plaintiff was actually taking by that time. How is the significance of that difference to be determined in the present context and in the relevant time frame? There is no expert evidence that directly addresses this question. I bear in mind the evidence of Dr Champion to which I earlier referred (at para 223), but I do not find that this really assists me here, particularly in the limited time frame. A dose of 30 mg per day would still have been five times the dose which it would have been necessary to achieve to arrest the progression of osteoporosis. Moreover, the reduction in dosage to 30 mg had it been achieved would only have been achieved very close to the time that the fractures actually occurred." 226 Studdert J reached the second conclusion I have set out in [146] above. 227 The Judge then asked the question "was the prescription of Dexamethasone causative of harm?" 228 The judgment conveniently sets out the dosage prescribed as follows: "The initial dose of Dexamethasone, commencing on 8 June 1992, was 10 mg per day. (According to the Cassidy and Petty table (see para 190 above) this was the equivalent of a daily dose of 67 mg of Prednisolone). On 15 June 1992 the Dexamethasone dose was reduced to 9 mg per day (on the same table this was the equivalent of 60 mg of Prednisolone). On 22 June 1992 the daily dose was reduced to 8 mg per day (the equivalent on the same table of 53.4 mg of Prednisolone). There was a further reduction of the dose of Dexamethasone to 7 mg per day on 20 July 1992 (the equivalent of a dose of 46.7 mg of Prednisolone). There was a further reduction in the dose of Dexamethasone on 10 August 1992 to 6 mg and that remained the dose until the fractures occurred. (This was the equivalent of 40 mg of Prednisolone according to the Cassidy and Petty table.)" 229 It was pointed out that had Dexamethasone not been introduced it would have been necessary to have continued on Prednisolone. Studdert J considered, leaving aside the effect of Imuran, that: "It is probable … that the doses of Prednisolone would have been expressed as to the equivalents I have set out above." 230 The judgment stated that had Imuran enabled the reduction of the corticosteroid level this would have applied to either Dexamethasone or Prednisolone at the corresponding level. The Judge gave the following example: "If, for example, the defendant, by the introduction of Imuran, had been able to reduce the Prednisolone level by 20 August 1992 to 30 mg per day, and from my assessment of the evidence I do not find this likely, then since the plaintiff was taking Dexamethasone instead of Prednisolone there would have been a corresponding reduction of the Dexamethasone dose down to 4.5 mg." 231 Studdert J then said: "Hence in addressing the issue as to whether or not the introduction of Dexamethasone was causative of harm, I am concerned to consider whether, by reason of its different properties, the substitution of Dexamethasone for Prednisolone caused harm over and above that which necessarily accompanied the equivalent dose of Prednisolone." 232 As I have set out above the Judge concluded that it did not and made the finding to which I have referred [147]. 233 As that finding is not challenged I do not need to go to the reasoning process by which it was arrived at, beyond noting that Dr. Champion considered that the use of an equivalent dose of Dexamethasone rather than Prednisolone "probably slightly" increased the risk of fractures in the relevant time frame whereas Professor Sturgess, Professor Clancy, Dr. Sutherland and the respondent considered there was no increase. 234 It is apparent from the judgment that any increased risk following from the respondent's prescription of Dexamethasone at a dosage equivalent somewhat above the actual dose of Prednisolone was not considered. I will return to this issue later. 235 An issue dealt with in the judgement appears from the following passage: "Mr Donovan submitted that it was a legitimate approach in this case when considering causation to begin with the assumption that the plaintiff had normal bone density when her treatment on corticosteroids commenced. Mr Donovan submitted this was an appropriate approach because the plaintiff was, before overtaken by the lupus, a healthy young woman who did a lot of exercise. Unfortunately, however, there is no evidence of the plaintiff's bone density before treatment commenced. No measurement of bone density was taken and that is not a matter that calls for criticism, but it does not seem to me that I can properly infer that the plaintiff had normal bone density in the absence of evidence to that effect." 236 Studdert J refers to the opinion of Professor Clancy that the appellant has celiac disease and that in the professor's opinion this was a major factor in the progression of the osteoporosis to fractures. 237 The judgment, amongst other portions of the evidence in chief of Professor Clancy on this topic, sets out the following: "Q. Given the advent of these new tests and the leading to the ultimate diagnosis that you have made of celiac disease, are you able to express an opinion as to the likelihood or otherwise of that in some way contributing to this unusual outcome in this patient from January to August 1992 when Miss Rufo was under the care of Dr Hosking? A. Yes, yes, I can. Q. What is the likelihood? A. In my view, I have no doubt that it was the major cause - it was the reason for the gap, the difference, and I believe it was the major cause of this rapid bone loss, in conjunction with steroids that she required for her treatment." 238 It is noted that in cross-examination the Professor acknowledged that he was aware that Dr McElduff, an endocrinologist to whom he referred the plaintiff, did not agree with the diagnosis of celiac disease. 239 The Judge concluded that the appellant had failed to prove damage resulting from the failure to introduce Imuran on or about 10 June 1992 or from the prescription of Dexamethasone in January 1992. The Appellant's Submissions 240 The written submissions put that Studdert J should not have examined each breach separately but rather compared the treatment the appellant actually received as apposed to that she would have received without negligence. 241 Such a comparison, it was put, showed that the appellant had received a relatively higher dose of corticosteroids than she should have done during the period 10 June 1992 to 24 August 1992. It was submitted that the spinal fractures due to osteoporosis were "exactly what would be expected to follow from excessive use of corticosteroids". 242 It was submitted: "In those circumstances, the Respondent bore the onus of showing that the Appellant would have suffered the same outcome in any event, or alternatively had no chance of a better outcome on the lower dose regime. Such a conclusion would fly in the face of (a) common sense, (b) the uncontroversial finding that the spinal fractures were caused by osteoporosis due to corticosteroids, and (c) the finding that the effect of the corticosteroids was accumulative." 243 The fractures suffered on 24 August 1992 being caused by the corticosteroids prescribed by the respondent were, it was submitted, precisely the type of damage which would be expected to be caused by the negligence found and within the very scope of the risk created by such negligence. 244 In that situation, it was put, causation was to be inferred in the absence of any sufficient reason to the contrary and the respondent bore the onus of excluding his negligence as a contributory cause. 245 It was submitted: "(a) Breach of a duty coupled with an incident of the kind that might thereby be caused is enough to justify an inference, in the absence of any sufficient reason to the contrary, that in fact the result did occur owing to the act or omission amounting to the breach. (b) Once a plaintiff demonstrates that a breach of duty has occurred which is closely followed by damage, a prima facie causal connection will have been established. Notwithstanding the burdens of proof imposed by law upon the parties, states of fact may be proved by the evidence as the case advances, or appear as inferences which the evidence supports, which authorise or even demand findings in favour of a party unless or until some further or other state of fact is made to appear by evidence. There are presumptions of fact, as distinct from presumption of law. In particular:- If the disabilities of the plaintiff can be disentangled and one or more traced to causes in which the injuries he sustained through the accident play no part, it is the defendant who should be required to do the disentangling and to exclude the operation of the accident as a contributory cause." 246 I deal later with the comparisons which the appellant submits should have been made between what happened and what would have happened had the respondent's treatment not departed from the standard of reasonable care. 247 It was submitted that the difference between the actual dosage of corticosteroids and the hypothetical reasonable dose materially contributed to the outcome. It was put that the effect of corticosteroids being dose related and cumulative commonsense dictated that the excess over and above the hypothetical reasonable dose contributed to the outcome. 248 A distinction was drawn between halting osteoporosis, which would require a dose at or below 6 mg a day, and averting fractures or reducing the severity of fractures. 249 Reliance was placed upon what was said to be Dr. Champion's evidence that reasonable and prudent practice would have resulted in a reduction to about 20 mg a day. This would have reduced the osteoporosis and with it the risk of vertical compression. 250 Whilst the reference to "reasonable and proper practice" is an appropriate inference from the effect of Dr. Champion's evidence he did not expressly put the matter that way in the referred to passage. He did give evidence: "Q. Assume this; a reasonable expectation of getting to about 15 milligrams of Prednisolone by four months? A. Yes. Q. Assume 50 on 22 June? A. Yes. Q. What level of Prednisolone would you expect to be achieved by way of reduction, assuming no complications of course, by 24 August? …… Q. No, nine weeks, from 22 June to 24 August? A. Right, yes, nine weeks. Q. Do you need a pen to do it? A. No, no. There is no mechanic [ sic ] answer possible. There are too many assumptions, but obviously one would be aiming and hoping to achieve reduction realistically to 15 milligrams or less. But a fair expectation might be of the order of 20 milligrams of Prednisolone by then. But, as was shown in reality later, faster reduction was achievable, albeit with the risk of flare. Q. Could you just repeat that, I didn't quite hear? A. The reduction without flare, you reasonably expect to get to about 20 milligrams a day by then, but you would be aiming for less. If you aim for less, aiming for 10 milligrams or less, the increased risk of flare comes, although that is offset by the co-prescription of the earlier Hydroxychloroquine and Azathioprine." 251 The submission also referred to the following evidence in chief from Dr Champion: "Q. You have in front of you a table that I have prepared. Would you please ignore the right-hand column, but taking the 20 which you have expected would be achieved, could you tell me please what sort of extent or degree of reduction of the risk would there have been between the actual Dexamethasone used, and the expectation which you would otherwise have expected? A. Compared with what actually was prescribed, the proposed alternative schedule of Prednisolone and its reduction would represent probably roughly a half, halving of the corticosteroid effect. Clearly that would, over a period of two months, reduce the osteoporosis, so the risk of vertebral compression – that is the risk of reaching the threshold for spontaneous vertebral compression – would be reduced, would have been reduced. That is not to say that it would necessarily have been prevented. But the risk of significant vertebral compression would have been reduced, and any vertebral compression would probably therefore have been less involving fewer vertebral bodies, and less compression of the affected vertebral bodies." 252 It is relevant to note the following question and answer: "Q. Are you able to give any indication by percentages or otherwise of how much less the extent of vertebral compression would have been? A. No, I think that's beyond, it would be too speculative." 253 Attention was drawn to Dr. Champion's view that "it is likely that there would be an important proportionality, a dose effect consequence". 254 In respect of Dr. Champion's evidence as follows: "Q. In saying that, can you give us an idea as to whether or not 60 milligrams of Prednisolone a day is twice as bad as 30, or is that too crude a way of looking at it? A. Well it is substantially worse than 30, but 30 might be sufficient cause for concern too, that it may not make a huge difference over a limited timeframe." It was submitted that his answer was "far from acceptance that a reduction of the dose of the type achievable on any of the hypothetical scenarios referred to above would have produced no benefit, or chance of a benefit, in respect of the ultimate outcome". 255 It was put that Dr. Champion emphasised that to maintain prednisolone at 40 mg per day for prolonged periods was particularly dangerous. 256 It was put that Studdert J was in error in declining to infer that the appellant had normal bone density before taking the steroids. In particular it was submitted that in the absence of any finding in favour of celiac disease the respondent has not adduced the necessary evidence to displace the inference of causation. Reliance was placed upon Watts v Rake (1960) 108 CLR 158. 257 It was also submitted: "Some further support for the view that the period after 10 June was particularly deleterious for the Appellant can be gained from the observations of deterioration in her appearance, and myopathy. While the evidence did not - as His Honour said - establish a direct relationship between myopathy and bone loss, it favoured the view that there was some general relationship, and again common sense suggests that if the corticosteroids in use after 10 June were exacerbating the side effects in one respect, they would likely have been in another also." 258 It is convenient to say that I do not consider that this proposition can be made out in view of the finding, well supported by the evidence, that the appearance changes and myopathy could result from an appropriate level of dosage. 259 It was put that what the appellant had to establish to recover damages was no more than that, as a result of the breaches of duty, she had lost the chance that the vertebral fractures of her bones would have been either averted or reduced in severity. 260 It was also submitted that a regime which reduced the corticosteroid dose must necessarily reduce the risk of the vertebral compression fractures and increase the chance of the appellant either averting the injuries or at least having less severe injuries. 261 Mr Brereton, in his additional submissions, drew attention to what he put followed as the necessary consequences of the findings of negligence. Apart from the reduction in corticosteroid dosage to follow the introduction of Imuran he relied upon the fact: "…Dexamethasone was given in a dose which was higher than the Prednisolone equivalent which would otherwise have been administered." 262 This goes to the aspect of Dexamethasone use which was not dealt with in the judgment. 263 He laid emphasis upon the cumulative effect of corticosteroid use as referred to the passage in the judgment where Studdert J said: "I understand it to be common ground between the experts that the corticosteroids which the plaintiff took from the time the treatment began had a cumulative effect, and on my assessment of the relevant medical evidence in this case I do not consider it appropriate to relate the changes in the plaintiff's appearance simply to the change of drug." 264 He also referred to the common ground that the greatest impact of steroid treatment on bone loss was in the first few months of treatment and put that the appellant was exposed to an increased vulnerability by June 1992. 265 Mr Brereton went on: "That situation demanded steps to conserve her remaining bone mass to reduce the dose and add a steroid saver instead, in effect she was given an increased dose as a result of the switch to Dexamethasone and steroid saver was not added. Between 10 June and 24 August at a time when her remaining bone mass should have been conserved, it was instead further compromised to the extent that on 24 August she suffered these multiple fractures. She lost the vital lost portion of her bone mass during that period after the May flare-up had been brought under control. That's why we attach particular significance to that latter period of the administration." 266 Mr Brereton set out to make good three propositions of law to which, he put, Studdert J had not adverted. They were: "The first is that causation is to be inferred where a breach of duty is followed by damage within the scope of a risk which was increased by the breach of duty in question. In other words, if the breach of duty increases the risk of the damage and the damage incurs, it will be taken to have caused that damage. The second proposition is that where it is asserted that the plaintiff would have ended up in the same condition; either at the same time or at some later time in any event responsible, then the defendant bears the onus of disentangling the causes and of demonstrating how and to what extent the damage is attributable to the non-negligent cause. The third proposition which in our submissions is the complete answer to this case and which takes it beyond the inferences which flow from those first propositions is that where damage is the result of an accumulation of doses, some of which are negligent and some of which are non-negligent, then so long as the negligently administered dose was not de minimus it was a material contributing cause to the ultimate result." 267 I come to the authorities upon which he relied later. 268 From the judgment of Hayne J in Chappel v Hart, Mr Brereton referred to the following passage at 282: "The search for causal connection between damage and negligent act or omission requires consideration of the events that have happened and what would have happened if there had been no negligent act or omission. It is only by comparing these two sets of facts (one actual and one hypothetical) that the influence or effect of the negligent act or omission can be judged." 269 This, he submitted, was the approach, which Studdert J should have adopted but did not. He put that the Judge had examined the two breaches in isolation without considering their effect together. 270 It is convenient to say that there is substance in this observation if the effect of the prescription of Dexamethasone was to increase the dose of corticosteroids that the appellant received by a material amount above that which she would have received had she continued on Prednisolone. There is no substance in it if Studdert J were correct in treating the only relevant question being as to whether Dexamethasone was more damaging to bone density than Prednisolone when prescribed at an equivalent dose. If he were correct then the effect, on his unchallenged finding, was nil and it would add nothing to whatever followed from the failure to introduce Imuran. 271 Mr Brereton then handed up a table which set out at Scenario 1 the amount of Prednisolone equivalent prescribed to the appellant as found in the judgement. Scenarios 2 to 6 allowed for different rates of reduction and other changes in circumstances. 272 He submitted that scenarios 3, 4 or 6, showed that the appellant should have received something in the order of 3000 mg of steroid equivalent during the relevant period instead of nearly 4000. 273 Mr Brereton accepted that no medical witness had dealt directly with a question as to what difference it would have made if the appellant had received 3000 instead of 3900 mg of Prednisolone equivalent. He relied on the following evidence from Dr. Champion as set out, with a preliminary observation, in the judgment: "He was then asked the following questions and gave the following answers which assume particular relevance in view of my finding that the time when, in the exercise of reasonable care, Imuran should have been introduced was not until about 10 June (T 404): Q. Supposing the Imuran and Plaquenil - perhaps I should reverse that in order - were introduced at a later time, April/May, so that the 6 milligrams in three months or the 15 milligrams in four months were moved back closer to the event. Would that have had, first, any effects on the risk and, second, any effect on the extent? A. Are we still employing the dexamethasone? Q. No, for the moment I want to leave that to one side? A. Well, the issue there is that is it too late. It would have to be some reduction of risk but there would be less reduction of risk than with the first, that is the earlier, scenario we discussed. Q. And less reduction in extent? A. Yes Q. I don't suppose there's any point in my asking you what extent? A. No, it's too speculative I think." 274 He submitted that the effect of that passage is that there would have been some reduction in risk. 275 Mr Brereton put, without objection as to the calculation, that scenario 2 showed that the appellant received 8.2 per cent more steroid than she should have, scenario 3 - 26.6 percent more, scenario 4 - 16.7 per cent more, scenario 5 - 67.2 per cent more and scenario 6, 34.3 per cent more. 276 He submitted that the differences could not be said to be de minimus and that application of the principles in Bonnington Castings Ltd v Wardlow [1956] AC 613, even without reliance on what he called the Chappel v Hart type inference, made a conclusion of causation in favour of the appellant inescapable. 277 Mr Brereton also submitted that Studdert J had erred in failing to proceed on the basis that the appellant entered into the treatment process with a normal bone density. He relied upon Watts v Rake and Shorey v PT Ltd (2003) 77 ALJR 1104 and put that, having not determined that Professor Clancy's diagnosis of celiac disease was correct, the Judge should have inferred on the state of the evidence that the bone density was normal. The Respondent's Submissions 278 It was submitted that Studdert J did not examine the two breaches separately but rather whether the acts of negligence or either of them caused damage. Attention was drawn to the language used by the Judge under the heading "Causation - Has damage been proved?" (see [145]) 279 The point was made that the breach of duty of care in relation to Dexamethasone related to the "possible adverse significance of this" [emphasis added] and did not depend upon whether there was any actual adverse significance. 280 It was submitted that the process of reasoning in the judgment demonstrated consideration of the question whether damages resulted from one or other or both of the breaches proved. 281 Reference was made to the finding that above a daily dose of 6 mg of Prednisolone it was likely osteoporosis would progress and that 20 mg per day was likely to cause ongoing osteoporosis. Dr. Champion's evidence that it was not possible to say that the dose of 40 mg would double the progress of the disease compared with a dose of 20 mg was relied upon. As was his evidence that with a dose as much as 30 mg, the increased risk may not have been very significant, at least over a relatively short period. 282 Reference was made to the finding that it was unlikely for a reduction of the corticosteroid medication to be achieved below 30 mg of Prednisolone or its equivalent and indeed that the dose may have still have been closer to the equivalent to 40 mg of Prednisolone. It was pointed out, by reference to the actual breach of duty of care found by the trial judge, the time available to achieve any reduction in dosage was limited to a period of just under 11 weeks up to the 24 August 1992. 283 Reference was made to the time it would take for the steroid sparing effect of the Imuran to come into effect as discussed in the judgment. It was noted that on a more conservative reduction of 2.5 mg per week of Prednisolone (or its equivalent), the appellant would have been left on a dose of at least 30 mg of Prednisolone per day as at 24 August 1992. 284 Submissions were made as to the introduction of Dexamethasone to which it is unnecessary to go. 285 It was asserted that it was not possible to infer on the probabilities that the appellant's bone density was normal before treatment, particularly in view of the possible diagnosis of celiac disease. 286 It was submitted that it was only in the context of the consideration of Imuran being introduced earlier than 10 June 1992 that the "very big unknown - … and that is what was [the appellant's] bone density like at the time of the commencement of the lupus" became relevant. This being a reference to Dr. Champion's statement of his view that had Imuran being introduced in April it would have been four months of treatment with Imuran giving rise for a reasonable expectation of getting the dosage down to about 15 mg. The point was made that even then he was unable to say whether on the balance of probabilities the appellant would have had any fractures at all because no one knew her bone density at the commencement of the lupus. 287 The submission goes on "but if the introduction of Imuran occurred later (such as in June) the issue there is that it is too late. There would be some reduction of risk but the extent of the reduction would be 'too speculative' to quantify". It is convenient to say at this point that I agree with Mr Brereton's submission that, as put, this submission depends upon an interpretation of Dr. Champion's evidence, which I do not think it bears. In fact the doctor asked a rhetorical question when he said "…the issue there is that is it too late" [emphasis added]. 288 The submission put that the appellant was wrong in suggesting the respondent bore the onus of proof of showing that the appellant would have suffered the same outcome in any event, or alternatively had no chance for a better outcome, on the lower dose regime. I deal with the submissions on this point later. 289 It was put that Studdert J had not misstated the legal test in relation to the burden of proof for causation nor did he ignore his capacity to draw inferences. It was submitted that no demonstrable error in the reasoning process had been demonstrated and continued: "All relevant matters were expressly considered by the trial judge. Furthermore, an appellate court needs to take into account the unexpressed considerations that go into a trial judge's conclusion, it being the task of an appellate court to afford respect to the endeavour of the trial judge to give the correct and lawful conclusion to the puzzle presented to him. No judicial reasons can ever state all the pertinent facts. Nor can they express every feature of the evidence, which causes the decision to prefer one factual conclusion over another." 290 The written submissions contained detailed criticism of the appellant's submissions in relation to the comparisons to be made and I shall deal with the relevant parts of those submissions later. As mentioned above the appellant relied upon an amended schedule. 291 It was submitted that it was open to Studdert J to adopt the more conservative rate of reduction of 2.5 mg per week rather than 5 mg per week, which was the top of the range put by Cassidy and Petty. Attention was drawn to the flu like symptoms suffered by the appellant during the period as an example of "flare-up" which Dr. Champion and Dr. Sutherland agreed it was important to avoid, as did Professor Sturgess and Professor Clancy. It was submitted that it was appropriate for Studdert J to take the danger of flare-up or rebound into account. It was put that these factors were not taken into account in the appellant's analysis of the role of Imuran. 292 At this point of the submissions reference was made to the fact of Imuran, as a psytoxic drug, having a number of side effects militating against its introduction unless absolutely necessary. However, Studdert J had found it should have been introduced by the 10 June 1992 and the issues flowing from this fact go rather to the notice of contention than to questions of causation. 293 The submissions point out that the appellant received a total cumulative dose of 9095.3 mg of Prednisolone, or its equivalent, by the 24 June 1992 the date by which it was put that the introduction of Imuran would have supported the commencement of reduction. It was put that the appellant's comparison tables ignore the total cumulative dose of Prednisolone correctly given up to this date and ignore the uncontested evidence that the osteoporosis causing dose was the total dose since day one. 294 It was also submitted that the appellant's tables ignore the finding that the maximal bone loss is higher within the first few months of treatment. 295 It was submitted that the appellant's argument that the appellant received 1.5 times the correct dose was an unfair representation of the evidence and the treatment. It was put "at best it could have only have been a very small percentage reduction in the overall cumulative dose of corticosteroid medication that could have been achieved even if the Imuran had been introduced on 10 June 1992 (something of the vicinity of 3% reduction if that)". 296 It was put that Studdert J's rejection of the argument based upon the link between myopathy and bone loss was based upon an analysis of the evidence and there being no detection of myopathy in the early months. 297 The written submission concluded with the following passage: "As conceded by the appellant in argument from a practical point of view the best she could ever hope for would have been a judgment on the footing of a lost chance. As outlined above and observed by his Honour the introduction of the Imuran on 10 June 1992 would have simply have been too little too late particularly in the limited time-frame available for the medication to bring about a reduction in the dose of Prednisolone. The ultimate hypothetical lowest dose was probably about 30 mg per day (and perhaps higher) which still would have been five times the dosage necessary to achieve an arrest of the progression of the osteoporosis." 298 In his additional submissions Mr Higgs began by going in some detail to the judgment and the evidence referred to therein. His purpose being, he said, to show that irrespective of the test that was to be applied the evidence that was adduced by the respondent in an attempt to disentangle the complicated matrix that needed to be considered was in fact disentangled to a degree and analysed by Studdert J properly so as to entitle the Judge to come to the conclusion that he did. 299 He drew attention to the loss of weight referred to by Professor Clancy and the fact that no cause could be found for it. That, he put, was a factor taken into account by Studdert J in deciding the ultimate issues. He also drew attention to the appellant's perceived hypogonadism and the concern at that time that it would be inappropriate to provide oestrogen supplementation. The submission noted Professor Clancy's opinion, which was similar to that of Professor Sturgess, that the non-production of oestrogen would be a small contributing factor to the risk of bone loss. There was no finding that supplementation should have been provided. 300 Whilst Mr Higgs conceded that logically Studdert J came to address the various issues separately, the Judge always had, it was submitted, in the forefront of his mind that what he had to ultimately determine was whether the dosage, because of the failure to introduce Imuran and because of the introduction of Dexamethasone with its different properties, had the combined result of materially contributing to the damage. 301 It was put that on any view the appellant was receiving an equivalent dose of Prednisolone as part of her proper treatment in excess of the critical 6 mg per day. 302 In turning then to the Dexamethasone Mr Higgs pointed out that Studdert J ultimately came to the view that in the relevant short time frame the fact of the prescription of the Dexamethasone made no difference. Mr Higgs accepted that there were two aspects to it. There was the dosage which had been referred to in argument, that is, an increase, and the different quality of Dexamethasone. It is unnecessary to go to the question of different quality. It is convenient to deal with the other issue later. 303 Mr Higgs made the point that the appellant's case never focused on Imuran being introduced on or about 10 June 1992 which made it difficult to know what the expert's views would have been if directed to that date. He submitted that the reduction that could have been effected from April or May was not applicable. It was put that Studdert J was correct when he said: "…the later the Imuran was introduced and the later it became possible to reduce the corticosteroid level, the less the chance of avoiding the fractures which occurred. It will follow, accepting Champion's evidence set out above, that it would be even more difficult to determine what possible effect the introduction of Imuran, on or about 10 June could have produced prior to 24 August 1992." 304 It was then submitted that the effect of Dr. Sutherland's and Dr. Champion's evidence, correctly understood, was that the contention that no more than a reduction of 2.5 mg per week would have been achieved, even with Imuran, was correct. He also pointed to the views of Professor Sturgess and Professor Clancy. 305 Mr Higg's submissions then returned to the issue of increased dosage following upon the prescription of Dexamethasone. It is convenient to deal with that issue and the submissions in relation to it later. Supplementary Submissions 306 After the hearing of the appeal the respondent supplied requested additional appeal book references and also filed Supplementary Submissions. 307 The appellant then filed a Reply to those submissions and requested that if the Court receives the respondent's submissions it consider the appellant's reply with them. 308 Both sets of submissions deal with the issue as to the quantity of Dexamethasone prescribed. They are relevant and helpful. I propose that they be received. 309 I deal with the matters raised in the submissions later. Consideration 310 It is convenient to begin by examining the first two of the three propositions of law Mr Brereton placed at the forefront of his submissions. 311 The first was that causation is to be inferred where a breach of duty is followed by damage within the scope of a risk which was increased by the breach of duty in question. 312 Mr Brereton put that the starting point for this proposition was the judgment of Dixon J, as he then was, in Betts v Whittingslowe (1945) 71 CLR 637. Dixon J said at 649: "It is not necessary to inquire whether their Lordships meant more than that the breach of duty coupled with an accident of the kind that might thereby be caused is enough to justify an inference, in the absence of any sufficient reason to the contrary , that in fact the accident did occur owing to the act or omission amounting to the breach of statutory duty." [The emphasis is mine.] 313 Mr Brereton then went to Bennett v Minister of Community Welfare (1992) 176 CLR 408 where Gaudron J said at 420, after referring to the above passage from Betts: "And although it is sometimes necessary for the plaintiff to lead evidence as to what would or would not have happened if a particular common law duty had been performed, generally speaking, if an injury occurs within an area of foreseeable risk, then, in the absence of evidence that the breach had no effect, or that the injury would have occurred even if the duty had been performed , it will be taken that the breach of the common law duty caused or materially contributed to the injury." [References have been omitted and the emphasis is mine.] 314 Mr Brereton then referred to the judgments in Chappell v Hart which he submitted supported his proposition, albeit with some difference of emphasis between the views of McHugh J, and possibly of Hayne J, on the one hand and Gaudron and Kirby JJ on the other. 315 I do not need for present purposes to go to those judgments for I respectfully agree with the view of Mason P, with whom Priestley JA agreed in part and Beasley JA agreed, in TC v The State of New South Wales & Ors [2001] NSWCA 380 as to their effect relevant to the issues in this appeal. He said at 58: "For at least part of the appeal, the appellant submitted that this passage endorsed Lord Wilberforce's statement in McGhee v National Coal Board that the onus of proof shifts in cases such as the present. The judgment of Kirby J in Chappel v Hart (1998) 195 CLR 232 at 273-4 was also invoked as authority for this proposition. Contrary decisions or dicta of this Court in Bendix Mintex Pty Ltd v Barnes (1997) 42 NSWLR 307, Wallaby Grip (Bae) Pty Ltd (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355 and E M Baldwin & Son Pty Ltd v Plane (1999) AustTortsR ¶81-499 were said to be wrongly decided. I cannot accept this submission. I remain of the view that Australian law has not adopted a formal reversal of onus of proof of causation in negligence, even negligence involving breach by omission. A robust and pragmatic approach to proof of causation permits, but does not compel, a finding of liability in cases of negligence by omission which (as Gaudron J points out in Bennett ) is necessarily based upon a hypothetical enquiry. A defendant who exposes a plaintiff to a risk of injury or who, by omission, fails to take reasonable steps to avoid or minimise that risk is not liable unless the risk comes home in the sense that the court is ultimately satisfied on the balance of probability that the defendant's breach caused or materially contributed to the harm actually suffered. I explained my reasoning in Bendix Mintex at 311-318. There (at 316) it was noted that the majority of the High Court in Bennett (Mason CJ, Deane J and Toohey J at 416) adverted to the questions (a) whether there might be no real distinction between breach of duty and causation and (b) whether a failure to take steps which would bring about a material reduction of the risk amounts to a material contribution to the injury. Their Honours said: These questions have been considered in Canada in the context of a possible shift in the onus of proof … but it seems that the problem still awaits final resolution. I also observed (at 316) that the passage in Gaudron J's judgment in Bennett that is set out above: … would appear to take Mason J's principle [in Sutherland Shire Council v Heyman (1985) 157 CLR 424 at 467] beyond the field of a duty to take care to protect the plaintiff from foreseeable injuries due to the acts of third parties or accident. What is less clear is whether her Honour was embracing the idea that in such circumstances the onus shifts to the defendant (cf at 420 footnote (23)) or whether she was merely endorsing a legitimate method whereby the trier of fact could validly move from evidence of risk to finding of probable cause of damage. Bennett was a case of negligence by omission. In Bendix Mintex I concluded that the ultimate legal onus of proof rested with the plaintiff. It is not sufficient that a plaintiff prove that the defendant negligently exposed the plaintiff to a risk of injury: liability depends upon the plaintiff persuading the trier of fact that it was probable that the risk came home (see at 318). Beazley JA was of like view (see at 339). I do not think that later High Court authority has concluded otherwise as regards reversal of onus of proof. If anything, there has been an endorsement of the traditional view as to the plaintiff bearing the ultimate legal onus, albeit in a context that has emphasised the propriety of a trier of fact taking a robust and pragmatic approach to causation. The passage in Kirby J's judgment in Chappel (at 273-4) upon which the appellant relies treats McGhee per Lord Wilberforce and Bennett per Gaudron J as authority for a shifting of the evidentiary onus in proper cases. I respectfully agree. Nothing in the other judgments in Chappel support a reversed onus of proof as a legal proposition. Indeed (on my reading) they reject it (see per Gaudron J at 238-9, per McHugh J at 244-5, per Gummow J at 257-9, per Hayne J at 281-2). Chappel (like Bennett ) is a case of negligence by omission." 316 Mr Brereton also referred to Naxakis. He acknowledged that that case dealt with an issue as to whether a jury should have been directed to return a verdict for the defendant. However, he pointed out that Gaudron, Kirby and Callinan JJ addressed the causation issue and sought support from their observations. In TC v State of New South Wales Mason P at [68-72] dealt with the relevant judgments as follows (references are omitted and the emphasis is that of the President): "Three of the justices returned to the topic in Naxakis v Western General Hospital & Anor . Again I set out the passages with emphasis added. Gaudron J said (at 278-9): It has been suggested that to allow compensation for the loss of chance would alleviate problems associated with proof of causation. There is, in my view, a tendency to exaggerate the difficulties associated with proof of causation, even in medical negligence cases. For the purposes of the allocation of legal responsibility, "[i]f a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring". And in that situation, the trier of fact — in this case, a jury — is entitled to conclude that the act or omission caused the injury in question unless the defendant establishes that the conduct had no effect at all or that the risk would have eventuated and resulted in the damage in question in any event . Kirby J said (at 296): Once the jury took the first step, and concluded that Mr Jensen did not, as he should have, consider aneurysm and the need for an angiogram, it would have been a small step for them to conclude that the failure to consider this alternative diagnosis was a cause of the second haemorrhage suffered by the appellant with its grave results. Where, as here, a plaintiff demonstrates that it was open to a jury to conclude that the respondents were in breach of their duty of care to him and this breach was closely followed by his damage , a prima facie causal link is established. It may be displaced and it may be rejected ; but it cannot be ignored in considering a motion for judgment for the defendant for want of evidence. Callinan J said (at 312): In Chappel v Hart McHugh J was one of two dissentients in a Court of five members of this Court, but I do not take his Honour's observations that I am about to quote and adopt as being in any way affected by that dissent: "Before the defendant will be held responsible for the plaintiff's injury, the plaintiff must prove that the defendant's conduct materially contributed to the plaintiff suffering that injury. In the absence of a statute or undertaking to the contrary, therefore, it would seem logical to hold a person causally liable for a wrongful act or omission only when it increases the risk of injury to another person. If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contributed to that injury occurring." On the evidence here the jury were entitled to hold that the failure … materially contributed to the appellant's condition. This recent body of High Court learning is analysed by Spigelman CJ in Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262 at 278-280. Davies AJA agreed with Spigelman CJ. I respectfully agree with what the Chief Justice has written. I shall set out pars 105-109 and 119. 105 The Respondent relied on an observation by McHugh J in Chappel v Hart (at 244-245 [27]) where his Honour, noting that "increases" in this context includes "creates", said: …"If a wrongful act or omission results in an increased risk of injury to the plaintiff and that risk eventuates, the defendant's conduct has materially contributed to the injury that the plaintiff suffers whether or not other factors also contribute to that injury occurring. If, however, the defendant's conduct does not increase the risk of injury to the plaintiff, the defendant cannot be said to have materially contributed to the injury suffered by the plaintiff." 106 Although his Honour's was a dissenting judgment, this passage has subsequently been referred to with approval. (See Naxakis v Western General Hospital per Gaudron J, and per Callinan J). 107 The starting point of McHugh J's analysis was that it had been established on the balance of probabilities that the conduct did create or increase the risk of injury, "and that risk had eventuated". 108 This starting point is the very matter in issue in the present case. Was there evidence on the basis of which the trial judge could conclude, on the balance of probabilities, that there was an increased risk of injury and that that risk had "eventuated" in the specific disease of the Respondent? 109 If there was such evidence then, to use the words of both Gaudron J (and Callinan J), the tribunal of fact was "entitled" to find that the conduct which increased risk, materially contributed to the injury - entitled, but not, of course, required to so find. … 119 There is a tension between the suggestion that any increased risk is sufficient to constitute a "material contribution", and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well established to be qualified by the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The "possibility" or "risk" that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X. Par 119 of Seltsam was recently approved by the Queensland Court of Appeal in Batiste v State of Queensland [2001] QCA 275. Thomas JA (with whom McMurdo P agreed) said (at [10]): It remains the law that it is still necessary for a plaintiff to prove that a defendant's conduct materially contributed to the sustaining of the injury. I agree." 317 The respondent's submissions, by reference to TC v State of New South Wales made the point that the legal onus remained upon the plaintiff and emphasised the nature and extent of the evidence which Studdert J was entitled to take into account in deciding whether that onus had been discharged. 318 I do not consider that the first of Mr Brereton's propositions established that Studdert J had fallen into error in the approach he adopted or in the conclusion that he reached. 319 The second proposition is that where it is asserted that the plaintiff would have ended up in the same condition, either at the same time or at some later time in any event due to some other cause for which the defendant is not responsible, then the defendant bears the onus of disentangling the causes and of demonstrating how and to what extent the damage is attributable to the non-negligent cause. 320 Mr Brereton took as his starting point Watts v Rake (1960) 108 CLR 158. In that case Dixon CJ said at 160: "As to the second and third of these answers, there is undoubtedly a presumptio hominis in the plaintiff's favour which any tribunal of fact should insist that the defendant should overcome. If the disabilities of the plaintiff can be disentangled and one or more traced to causes in which the injuries he sustained through the accident play no part, it is the defendant who should be required to do the disentangling and to exclude the operation of the accident as a contributory cause. If it be the case that at some future date the plaintiff would in any event have reached his present pitiable state, the defendant should be called upon to prove that satisfactorily and moreover to show the period at the close of which it would have occurred." 321 Menzies J said at 163: "It was for the appellant as plaintiff to prove his damages, and merely to prove his present condition and his incapacity to work would not prove that these things resulted from the accident. It was not, however, for the plaintiff to disprove that his pre-accident ill health would eventually cripple and incapacitate him. Prima facie, where a plaintiff was in apparent good health before an accident and is in bad health thereafter, the change would be regarded as a consequence of the accident and it is for the defendant to prove that there is some other explanation for it, e.g., that the plaintiff has aggravated his condition by some unreasonable act or omission. Similarly, although it is of course material to ascertain what was the pre-accident condition of the plaintiff who alleges that his post-accident ill health is due to the accident, it is for the defendant to prove that before the accident the plaintiff was in a condition that, without the accident, would have led to his post-accident state of health." 322 Windeyer J agreed with both judgments. 323 In Purkess v Crittenden (1965) 114 CLR 164 Barwick CJ, Kitto and Taylor JJ said at 168: "It was, in effect, pointed out that it is not enough for the defendant merely to suggest the existence of a progressive pre-existing condition in the plaintiff or a relationship between any such condition and the plaintiff's present incapacity. On the contrary it was stressed that both the pre-existing condition and its future probable effects or its actual relationship to that incapacity must be the subject of evidence (i.e. either substantive evidence in the defendant's case or evidence extracted by cross-examination in the plaintiff's case) which, if accepted, would establish with some reasonable measure of precision, what the pre-existing condition was and what its future effects, both as to their nature and their future development and progress, were likely to be. That being done, it is for the plaintiff upon the whole of the evidence to satisfy the tribunal of fact of the extent of the injury caused by the defendant's negligence." 324 In Shorey v PT Ltd (2003) 77 ALJR 1104 Kirby J said at 1111: "So far as the evidentiary presumption is concerned, this is the presumptio hominis to which Dixon CJ referred in Watts . It stands in a plaintiff's favour and 'any tribunal of fact should insist that the defendant should overcome [it]'. The presumption was explained in these terms: 'If the disabilities of the plaintiff can be disentangled and one or more traced to causes in which the injuries he sustained through the accident play no part, it is the defendant who should be required to do the disentangling and to exclude the operation of the accident as a contributory cause. If it be the case that at some future date the plaintiff would in any event have reached his present pitiable state, the defendant should be called upon to prove that satisfactorily and moreover to show the period at the close of which it would have occurred.' The other judges in Watts agreed with Dixon CJ's approach. The principles so stated have been re-stated by the Court since then. They are settled doctrine. They were not contested in this appeal. Indeed, they represent no more than the application of common sense to decisional reasoning. If it be the case that these principles were not expressly relied on at trial or in the Court of Appeal, it matters not. They are simple rules, applicable to judicial reasoning, whether at first instance in a trial, or in a re-hearing on appeal when the issue concerns the effect on damages of multiple causes." 325 Callinan J referred to the passage quoted in [14] above as the rule stated in Purkess v Crittenden. 326 In Diamond v Simpson (No 3) [2003] NSWCA 373 Young CJ in Eq, with whom Meagher and Ipp JJA agreed, accepted the applicability of the principles in Watts v Rake, Purkess v Crittenden, and Shorey v PT Ltd but, on the evidence in the matter, did not consider it necessary to rely upon them. 327 With respect I consider that Studdert J fell into error in failing to apply these principles in the determination of the issue whether the breaches of the duty of care he found established were a cause of the appellant's present state. 328 As set out above Professor Clancy considered that the appellant suffered from celiac disease. As to that the Judge said: "Whether or not that diagnosis is correct, I do not determine. On the other hand, I do not find such diagnosis has been excluded, and it would readily account, in conjunction with the high doses of corticosteroids which were given, for the osteoporosis progressing to fractures. The possible diagnosis that has been advanced by Professor Clancy is one matter to be taken into account in determining whether or not it would be appropriate to infer that the plaintiff's bone density was normal before treatment commenced. It seems to me that the inference Mr Donovan invites me to draw is one which I ought not draw on the balance of probabilities, and I do not do so." 329 The evidence of Dr. Champion [161] and Professor Clancy [183] makes it clear that the condition of the appellant's spine before she commenced taking corticosteroids and the possible effects of celiac disease on the spine are important factors in the likelihood of compression fractures following treatment by corticosteroids. There was evidence that the appellant was "in apparent good health" before the onset of the lupus. 330 Studdert J did not, as in my respectful view he should have done, approach his assessment on the basis of the presumptio hominis referred to by Dixon CJ and Kirby J. 331 I do not consider that it can be drawn from the judgment that the error did not alter the conclusion to which Studdert J would have arrived had it not been made. 332 Mr Brereton also submitted that the Watts principle should be applied in respect of an argument based upon the relevant damage occurring as a result of the appropriately prescribed level of corticosteroids. 333 There is, however, a good deal of evidence as to the likely effect of particular quantities of corticosteroid and the effect of differing levels of dose. 334 As the respondent's submissions point out in Watts Dixon CJ did say: "That being done it is for the Plaintiff upon the whole of the evidence to satisfy the tribunal of fact of the extent of the injury caused by the Defendant's negligence." 335 Unlike the celiac disease issue there is on this issue positive evidence from which the Judge could conclude that properly prescribed corticosteroids had been a cause of the damage. 336 In these circumstances I do not consider that error has been established in this regard. The Change to Dexamethasone 337 It is convenient at this point to turn to the appellant's claim that Studdert J omitted to take into account the additional consumption of corticosteroid that resulted from the change to Dexamethasone at the level the respondent prescribed. 338 As Mr Higgs observed in address there were two aspects of the breach as to the prescription of Dexamethasone. One was the allegation that the Dexamethasone was causative of the damage by reason of its different quality. That was dealt with by Studdert J and may now be set aside. 339 The other aspect was that which depended upon the consumption of a greater quantity of corticosteroid by reason of the amount of Dexamethasone prescribed. 340 Studdert J did not deal with this aspect. Mr Higgs put that "this was not the way the case was run." However, the issue was raised in particulars and in evidence and in my view the appellant is entitled to rely upon it at least upon the question of causation. 341 Mr Higgs put that the "small difference" that resulted would not affect the ultimate outcome and that if there was an error it should be regarded as a de minimus slip. 342 On 8 June 1992 when the change to Dexamethasone commenced the appellant was on 55 mg Prednisolone a day (see [29]). On that day the dose became 10 mg Dexamethasone. 343 The respondent agreed that his handwritten notes contained a notation "change to Dexamethasone equivalent" and "(1:6)". He later agreed that on his ratio 10 mg of Dexamethasone was equivalent to 60 mg of Prednisolone. 344 The respondent gave evidence: "Q. In relation to the delivery of cortisone to the [appellant] with respect to the initial dose of Dexamethasone that you proposed to prescribe for Michelle, what was your intention in terms of the potency with respect to Cortisone as compared to Prednisolone. Was it more or less the same? A. For the initial few days I intended it to be not less than and fractionally more. So it was approximately, these ratios that are given there are very approximate, I might add. I was worried that if I had made a mistake in the other direction, then she may well have had another breakthrough. I felt that the benefit to risk ratio would be better to slightly over do it rather than under do it and then bring it down reasonably fast." 345 It would seem probable that the increase in Prednisolone equivalent from 55 to 60 (on the ratio used by the respondent) was to guard against the possibility of error and that there would not have been such an increase had the appellant remained on Prednisolone. That the respondent refers to an increase supports the view that the appellant was on 55 mg before the change. 346 The pattern of subsequent reduction does not suggest that the dosage was reduced further or faster than it would have been had the appellant remained on Prednisolone. 347 I set out above [173] the passage from the judgment which records, amongst other things, the equivalent doses of Dexamethasone and Prednisolone as taken from the table in Cassidy and Petty. At the hearing the respondent accepted that 1:6.67 was the appropriate ratio. This accords accurately enough with Cassidy and Petty, Goodman and Gilman and Cecil's Textbook of Medicine (1958 edition). The respondent did point out that the figures were approximate. 348 At the hearing of the appeal there was no challenge to the figures as set out. However, in its supplementary submissions the respondent has gone to other ratios given in evidence by the medical witnesses. In response to that the appellant has noted, amongst other things, that Dr. Sutherland gave evidence: "Q. First of all, I wanted to take you to the first paragraph, where you state some equivalents between Prednisolone and Dexamethasone? A. Yes. Q. I think you indicated over the lunch hour that you accepted the Goodman and Gilman ratio, rather than the one you have stated? A. Yes, the ratio from Goodman and Gilman is expressed in a different way, .75 milligrams of Dexamethasone being equivalent to five milligrams of Prednisolone. If you correct that, in fact it is more than 5 to 5.5, it is six point - - Q. Six seven? A. 6.67. That is a standard authority on the subject. I have no problem with that. Q. When we come to the Dexamethasone, the dosage that is prescribed with the 10 milligrams of Dexamethasone becomes 67 equivalence of Prednisolone? A. Approximately, yes." 349 The respondent volunteered, whilst being cross examined, that Goodman and Gilson was the standard text. 350 I accept that the figures are to some extent approximate but, nevertheless, consider that I should adopt the table accepted by Studdert J. 351 When the appellant was receiving 10mg of Dexamethasone she was receiving the equivalent of 67 mg of Prednisolone. That is 12 mg a day more than the 55 mg of Prednisolone she was receiving at the time of the change to Dexamethasone and 6 mg per day more than the respondent appreciated he was prescribing. The difference would reduce at lower figures. 352 Having regard to my views as to the Notice of Contention it is unnecessary for me to consider at this point whether the additional dosage occasioned by the change to Dexamethasone was itself sufficient to lead to a finding for the appellant on the issue of causation. The increase is to be considered together with the excess dosage level resulting from the failure to introduce Imuran. 353 I should, however, note that I do, on the evidence, regard it as more than a de minimus amount and consider that it should have been taken into account. 354 In view of the conclusions set out above it is appropriate for the Court to reach its own decision on the issue of causation having, in doing so, appropriate regard to the findings of Studdert J. 355 To consider this question it is appropriate to adopt the unchallenged formulation of Studdert J [152] as to proof of damage for loss of a chance. 356 It is also appropriate to adopt the approach enunciated by Hayne J in Chappel v Hart when he said at 282: "The search for causal connection between damage and negligent act or omission requires consideration of the events that have happened and what would have happened if there had been no negligent act or omission. It is only by comparing these two sets of facts (one actual and one hypothetical) that the influence or effect of the negligent act or omission can be judged." 357 The first step in carrying out this comparison is to determine the amount of corticosteroid consumed by the appellant over the period from 10 June 1992 to 24 August 1992. This amount is known and appears from the first column of the appellant's amended table as set out below: Scenario 1 Scenario 2 Scenario 3 Scenario 4 Scenario 5 Date Actual 2.5 mg/wk 2.5 mg/wk 5 mg/wk 5 mg/wk Scenario 6 wef 22/7 wef 24/6 wef 22/7 wef 24/6 18.6.92 66.7 55 55 55 55 55 (10 dex) 17.06.92 60 50 50 50 50 50 (9 dex) 24.06.92 53.36 50 47.5 50 45 45 (8 dex) 01.07.92 53.36 50 45 50 40 45 (8 dex) 08.07.92 53.36 50 42.5 50 35 41.25 (8 dex) 15.07.92 53.36 50 40 50 30 37.50 (8 dex) 22.07.92 46.67 47.5 37.5 45 25 33.75 (7 dex) 29.07.92 46.67 45 35 40 20 33 (7 dex) 05.08.92 46.67 42.5 32.5 35 15 29.25 (7 dex) 13.08.92 40 40 30 30 10 25.50 (6 dex) 20.08.92 40 37.5 27.5 25 10 21.75 (6 dex) a 3921.05 3622.5 3097.5 3360 2345 2929 358 The second step is to determine the amount of corticosteroid that probably would have been consumed by the appellant over the relevant period had the two breaches of duty not occurred. This is the hypothetical figure to which Hayne J referred and the table offers a number of alternatives which I propose to consider. 359 Before doing so I should note that Mr Higgs submitted that "the mathematical precision that is attempted to be foisted upon the Court by these tables…is not the preferred approach". He drew attention in particular to the flu like symptoms the appellant was suffering in early June (sic) 1992. 360 My own view is that, given that the appellant's actual consumption is known, a good deal of evidence has been given as to possible reduction rates and the factors affecting them and the availability in the texts of recommended reduction rates, it is not inappropriate to present the material in this way. That is not to say that in reaching conclusions other factors including those creating uncertainty and doubt should not be taken into account. 361 At this point it is convenient to consider two issues which have a broad application to any calculations. 362 The first is what period would elapse before the introduction of Imuran on 10 June 1992 would have begun to allow a reduction in Prednisolone dosage. Of course, the excess directly flowing from the change to Dexamethasone would commence at once. 363 After referring to Dr. Champion's views as to the time it would take after the introduction of Imuran to begin the reduction of Prednisolone (2 weeks), Studdert J said: "Assuming the defendant had introduced Imuran as I have found he should have done on or about 10 June 1992, and assuming it would have been possible to start to reduce the corticosteroid dose two weeks later, that is by 24 June 1992, then taking the more conservative reduction rate of 2.5 mg referred to in Cassidy and Petty, this would have left the plaintiff on a dose of at least 30 mg of Prednisolone per day as at 24 August 1992." 364 Whilst it is not suggested in the judgment that this example necessarily reflects the Judge's view of the probable time period before reduction can begin, nonetheless, it is not suggested that it is not within reasonable limits. 365 This commencement date is used in scenario 3 and scenario 5. 366 The judgment refers to the view of Professor Sturgess that it takes six to eight weeks to build up the dosage of Imuran to a level at which reduction can commence. Studdert J noted that in cross examination the Professor said that Imuran would not have affected the Prednisolone dose for six to eight weeks. 367 Professor Clancy considered that there would be a four to six week period before there would be any benefit from introducing Imuran. 368 Scenarios 2 and 4 use a commencement date of the effect of Imuran based on six weeks. 369 The evidence showed that the appellant tolerated Imuran well when it was later introduced. There is no definite finding on this point. Having regard to the matter referred to in the last sentence I consider it reasonable to adopt the period used by the Judge in his example. This view is also supported by the circumstance I refer to later at [319]. 370 The second matter is the appropriate rate of reduction per week to consider. Studdert J said: "According to Dr. Champion, it would have been a reasonable approach to (and one consistent with the regime set out in table 7-35 in Cassidy and Petty (at p 299)) to wean the plaintiff off Prednisolone at the rate of 2-1/2 to 5 mg per week." 371 As noted above [308] the Judge took the figure of 2.5 mg for his example. He also said: "Of course, a lower end dose may have been achieved by heavier weekly reductions of, say, 5 mg per week had this proved possible but I consider that such a rate of reduction would have been an unlikely outcome even if the Imuran dosage had been rapidly pushed to 100 mg. There was a risk of rebound to be guarded against (T514)" 372 Mr. Brereton submitted that the risk of rebound had been allowed for by Dr. Champion in suggesting a reduction at 5 mg at a time rather than 10 mg. The judgment set out the following passage from Dr. Champion's evidence: "HIS HONOUR: Q. You're going to chip away at 5 milligrams at a time? A. If there is difficulty, yes. There are many suggestions that you reduce about 10 milligrams at a time but the smaller the reduction the more easier it is to effect without a reaction, without relapse." 373 Support for the view that 5 mg may well have been obtainable comes from the evidence of the respondent who was familiar with the appellant's response to treatment. He said: "So my thinking was: I will overlap a little and then come down at a fairly rapid rate, which I did, at an equivalent of 5 mg per week, which I did from there on basically." 374 It is also relevant to note that the appellant was in hospital following the fractures until 25 September 1992. At the time of the fractures the actual dose was 6 mg of Dexamethasone per day. By the time she left hospital the respondent had reduced it to 1 mg per day. 375 Had I been approaching this issue entirely afresh I would have been inclined to accept as a matter of probability a figure somewhat higher than the most conservative and less than the top of the suggested range. As it is I consider that I should adopt the figure found by Studdert J. 376 However, in doing so I consider that the possibility of "flares" has been appropriately provided for and that no further allowance, in considering probabilities, need be deducted from the conclusion as to the likely reduction in overall consumption. 377 These considerations lead me to conclude that the probable reduction in consumption is of the order of that set out in scenario 3 of the appellant's table. That is a reduction of approximately 825 mg of Prednisolone equivalent. On the undisputed figures put by Mr Brereton the result is that the appellant received 26.6 percent more corticosteroid between 10 June 1992 and 24 August 1992 than she would have done had the breaches of duty not occurred. 378 Although not directly relevant to my approach to the issue of overall excess consumption the following calculation is consistent with the conclusion I have reached. If the pre Dexamethasone dose of 55 mg of Prednisolone is notionally reduced at the same rate as the Dexamethasone dose was in fact reduced over the eleven week period, there is a difference in consumption of, in broad terms, 650 mg of Prednisolone equivalent. 379 The third step is to determine whether more probably than not this excess caused the appellant the loss of a chance of suffering less damage to her spine than in fact occurred. 380 A difficulty with dealing with this step is that the medical experts were not asked to deal with a situation in which there was an excess flowing from the change to Dexamethasone, an excess flowing from the failure to introduce Imuran and an approach that did not take into account the possibility of osteoporosis due to celiac disease. 381 For ease of reference I repeat the passage from Dr. Champion's evidence in chief set out at 157: "Q. Even if you were to achieve as low a rate as 20 milligrams per day, you still have a level of Prednisolone in your view that is going to in all likelihood cause ongoing osteoporosis? A. Yes. Q. Can you tell me, as between the 20 milligrams that she was on and the 60 milligrams a day that she was on to begin with after the flare-up, is there a precise correlation between the adverse effect upon the bones in terms of osteoporosis and the dosage? Or is there a bell curve, or is it a flat line or whatever? A. I cannot answer that. The fact is that on theoretical grounds it is likely that there would be an important proportionality, a dose effect consequence . But the actual studies would be extraordinarily difficult to perform to prove that beyond reasonable doubt. So that we have to run with basic pharmacological principles that there will be a dose response effect on loss of bone density, until a fracture threshold is reached." Q. In saying that, can you give us an idea as to whether or not 60 milligrams of Prednisolone a day is twice as bad as 30, or is that too crude a way of looking at it? A. Well it is substantially worse than 30, but 30 might be a sufficient cause for concern too, that it may not make a huge difference over a limited timeframe." (The emphasis is added) 382 Whilst the proposition advanced in the emphasised passage lacks the support of studies, as a matter of probabilities, I consider that it lends substantial support to a common sense view that the excess of Prednisolone equivalent resulting from the breach of duty did cause a loss of chance. 383 Studdert J accepted the evidence of Dr. Champion and Dr. Sutherland that a daily dose of above 6 mg of Prednisolone could adversely affect bone density. 384 Dr. Champion's evidence makes it clear that the process is a dosage related one. Studdert J clearly accepted that when he said: "It follows from the above evidence, and logically, that the later the Imuran is introduced, and the later it therefore became possible to reduce the corticosteroid level, the less the chance of avoiding the fractures which occurred." 385 Dr. Sutherland gave evidence: "Q. So she was on 40 milligrams from 13 April through to the end of May? A. I believe it would have been reasonable to expect a reduction of 5 or 10 milligrams at monthly intervals down to a dose of perhaps 15 milligrams per day." ..… Q. I will come back to that May issue in a moment, when she went to hospital. If that had been done, would that have made a difference to the likelihood of the fractures which she suffered? A. Yes, it would have made a difference to the likelihood or the risk. Q. Would it have been more probable than not that they would not have occurred? A. I can't answer that. Q. HIS HONOUR: Are you able to give a professional opinion as to how that effect could be measured then? A. It would be a worthwhile favourable effect. The problem is the natural history of this has not been well studied. Therefore, to take an individual who has been on high dose steroids, and then reduced by 5 milligrams a month for four or five months, must have been a help. I don't believe it is possible to put a number on it, or other than a vague term like "worthwhile" or "helpful". There are, in the literature, reports of, for example, 20 percent increase in bone density with the withdrawal of steroids. But then we come back to that other question; would that have prevented the fracture, and I don't know if it is possible to answer that." 386 Professor Clancy accepted the importance of a change of level of 6 mg of Prednisolone equivalent when he said: "…and certainly my view is that Imuran is a particularly valuable drug at getting the dose of corticosteroids below a sort of magic 9 or 10 milligrams when otherwise you need 15, 16 milligrams of prednisone [ sic ]." 387 He did not consider this importance continued at higher level as he made clear when he said: "My view is that in terms of the corticosteroid induced side effects that we are obviously worried about in the longer term, we are on pretty much a plateau when you are between 30 milligrams, 40 milligrams and 50 milligrams. Again I am not aware of any data that 30 milligrams is better or worse for causing long-term side effects than 50 or 60 milligrams. I mean it is not helpful to try and split hairs and say 5 milligrams, 5, 7-milligram dose at those levels is going to make any difference…" 388 This later view was directly challenged by Dr. Sutherland who said: "Q. I will just hand that to you and ask you whether you agree with that statement. (Shown) I'm sorry, perhaps I should ask you this; it seems to me that Professor Clancy's view is that there is not sufficient evidence to conclude that a higher dose leads to more bone loss than a lower dose? A. That would seem to be what he is claiming. Q. Do you agree with that, and if so why, or if not why not? A. No, I don't agree with that, and it flies in the face of all the published material on this. I had come today anticipating that it was accepted that bone loss was an inevitable side effect of corticosteroid therapy, and that it was related to the duration of therapy, and to the total dose, the cumulative dose, and so I didn't arm myself with a whole series of reports to that effect." 389 The view of Studdert J as set out in [329] is consistent with the position of Dr. Champion and Dr. Sutherland on this issue and I should adopt the same approach. 390 The respondent noted that Dr. Champion was aware of the doses of Dexamethasone received by the appellant and relied upon the following evidence which he gave in chief: "Q. I want you to assume that Ms Rufo has received the Prednisolone from January, I think about the 9th, of 50 milligrams per day, through to 17 February, when she goes to 75 milligrams per day, with a reduction to 50 milligrams from 9 March, 40 milligrams per day from 13 April. She continues on 40 milligrams per day until 28 or 29 May, when she goes to 60 milligrams per day. She then reduces to 50 milligrams per day by 22 June. On 22 June, she is prescribed the 10 milligrams per day of Dexamethasone, and continues on that. Assume that she was reduced from the 50 milligrams of Prednisolone down to where she had been before to 40 milligrams of Prednisolone, assume that this is what would have happened otherwise during the period June, July, August. That is the alternative scenario. Would, in those circumstances, the prescribing of the Dexamethasone have increased the risk of fractures above that which it would otherwise have been? A. Otherwise had been, being 40 milligrams of Prednisolone? Q. Yes? A. Only slightly. Probably slightly. In other words, the total regimen of Prednisolone equivalence is quite sufficient in a vulnerable person to produce multiple spinal fractures." 391 However, at that point Dr. Champion was dealing with quality not quantity. It is common ground that Studdert J was dealing with qualitative differences. His observations in his judgment show how he understood Dr. Champion's evidence: "... Ultimately the critical question here is whether the substitution of Dexamethasone in June 1992 increased the risk of bone loss and fractures above that which would have accompanied the prescription of Prednisolone between June 1992 and the time the fractures occurred. Dr. Champion was asked to address this very question." 392 In the appellant's supplementary submissions it was put that the use of "Only slightly. Probably slightly" did acknowledge some increase in the risk of fracture . However, as pointed out above, this evidence related to the quality of Dexamethasone not the quantity of the drug. Studdert J rejected a qualitative difference and I do not understand that finding to be challenged. In any event it clearly reflected the great preponderance of the evidence on that topic. 393 In the passage set out in [326] Dr. Champion says that whilst 60 mg a day is substantially more than 30 mg "it may not make a huge difference over a limited time-frame". This is not to say that it may not make a difference which can be regarded as more than speculative. (Malec v J C Hutton Pty Ltd [1990] 169 CLR 638 per Deane, Gaudron and McHugh JJ at 643, Gavalas v Singh per Ormiston JA at 409 or, for that matter, "of some substance" Naxakis per Callinan J at 313). 394 Mr. Higgs referred to Studdert J's finding that even with a dosage of 30 mg it is five times the level that you would want to achieve to avoid the progression of osteoporosis. However, that circumstance of itself does not rule out harmful effects from a relatively small amount. 395 The importance of the acceptance of the possibility of celiac disease is illustrated by Dr. Champion's evidence: "Q, Let me go back to your previous scenario, that is the 15 milligrams in three to four months. I think I get that right, tell me if I'm wrong? A. Yes. Q. In four months. If that was achieved and if her nutritional situation was remedied, would that lead to a more probable than not conclusion that she would not have had any fractures at all? A. I cannot say that because there is one very big unknown and that is what was her bone density like at the time of commencement of the lupus. Since we do not know that – if it were very low because of genetic, developmental and other factors – and the question that's been raised about celiac disease – then even that improved regimen I can't say would more probably than not have prevented fractures. All I can say is there would have been a substantial reduction in risk. Q. And a reduction in the extent of injury? A. It follows that – it includes, yes – you would expect, with that achievement as proposed, a reduction in the number and extent of vertebral compressions." 396 It is convenient whilst referring to this evidence to deal with an argument advanced by the respondent based upon the use of the word "speculative" in the passage from Dr. Champion's evidence which immediately follows the last quoted section. 397 The passage is: "Q. Supposing the Imuran and Plaquenil – perhaps I should reverse that in order – were introduced at a later time, April/May, so that the 6 milligrams in three months or the 15 milligrams in four months were moved back closer to the event. Would that have had, first, any effects on the risk and, second, any effect on the extent? A. Are we still employing the dexamethasone? Q. No, for the moment I want to leave that to one side. A. Well, the issue there is that is it too late. It would have to be some reduction of risk but there would be less reduction of risk than with the first, that is the earlier, scenario we discussed. Q. And less reduction in extent? A. Yes. Q. I don't suppose there's any point in my asking you what extent? A. No, it's too speculative." 398 The reference to "too speculative" is to be understood, amongst other things, in the light of the "very big unknown" to which he has drawn attention. 399 Further, the reference to "too speculative", is not directed to the chance of less damage but rather to the extent of the damage. The fact that the extent of the damages may be difficult to quantify does not defeat the claim (Luntz – Assessment of Damages for Personal Injury and Death, 4 ed 101; Chaplin v Hicks [1911] 2 KB 786). 400 It is also convenient to note that, as Studdert J found, the cause of the appellant's weight loss was never ascertained. The evidence was not available, whether provided by the respondent or not, for it to be inferred that the disability of the appellant could be traced to a cause in which the breaches of duty played no part (Watts v Rake). 401 Further, any osteoporosis occasioned by malnutrition would make the appellant more vulnerable to the effects of a smaller excess of corticosteroid than would otherwise have been the case. Causation, not duty, is the relevant issue. 402 The respondent contended that the appellant's tables of calculations ignored the effect of the dosage consumed before 10 June 1992. It was put that the effect being cumulative the amount of any proven excess for the period after 10 June 1992 should not be compared with the appropriate therapeutic dose after that time but against the whole therapeutic dose consumed. 403 The appellant submitted that since it was common ground that the greatest loss of bone density was in the early months "the greatest significance ought to have been attached to minimising jeopardy to such of the appellant's bone density as remained". Whilst expressed in terms more appropriate to duty, the concept of vulnerability applies equally to questions of causation. 404 In the absence of a proper basis for treating the appellant's spine as other than normal prior to the onset of the lupus, the known consequences of corticosteroid treatment and the fractures of 24 August 1992 it can be inferred that by June 1992 the appellant's spine was in a very vulnerable condition. 405 Adopting a robust and pragmatic approach to the primary facts of this case (March v E & M H Stramare Pty Ltd (1991) 171 CLR 506 per Mason CJ at 515; Wilsher v Essex Area Health Authority [1988] AC 1074 per Lord Bridge at 1090, Wallaby Grip (Bae) Pty Limited (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355 per Beazley JA at 364) it seems to me that more probably than not the excess of corticosteroid consumed after 10 June 1992 in the context of the osteoporotic and vulnerable state of the appellant's spine caused the loss of a chance that the appellant would have suffered less spinal damage than she in fact did. 406 Also as a matter of common sense it seems to me that the chance lost would be more than speculative or remote and, indeed, would be "of substance", albeit falling short of a fifty one per cent chance. 407 In that last regard it is appropriate to note Dr. Champion's evidence: "Q. That's why I use the word 'range' to try and make it a little easier. A. There would be a reasonable expectation of getting to about 15 milligrams of Prednisolone by four months. Q. Assume that had occurred and, taking into account the other factors that you've mentioned, can you indicate whether that would have had any effect on the likelihood of the kyphosis and fractures which she suffered or the degree of kyphosis and fractures that she suffered? A. It would definitely have reduced the rate of progression of osteoporosis. It follows that it would have reduced the risk of osteoporotic vertebral compressions and the extent of – that is the number of vertebrae affected and the degree of compression. Q. I'm going to take you to another question and I'll see if you can answer it. In terms of the risk of any kyphosis and fractures, and I'll just use those lay terms rather than the way you've described it for the moment, are you able to say whether on the probabilities she would have escaped with no injury? A. Purely from the corticosteroid reduction alone I could not say that that would be more probable than not ." [The emphasis is mine.] 408 Also relevant is Dr. Sutherland's evidence: "Q. I just take you to page 5 of your report and you will see in the third paragraph you are talking about March or April of 1992 and you said, 'It seems certain that her osteoporosis would have been much less at that stage', that's March or April, 'and on the balance of probabilities not of sufficient severity to cause fractures and subsequent kyphosis'. Do you see that? A. Yes, I do. Q. Now that's talking about March or April? A. Yes. Q. Are you able to say whether the same would have been so, that is on the balance of probabilities in May or June, or is it getting more difficult then? A. It's getting very difficult, if not impossible." 409 Studdert J commented upon that passage at [160]. 410 In my opinion the appellant is entitled to a verdict on the basis of a lost chance that she might have suffered less damage than she in fact did. 411 It remains to consider the appellant's claim to a verdict on the basis that she has proved causation of the damage suffered by her on the balance of probabilities. 412 Having regard to the views I have earlier expressed it is a prerequisite to the success of such a claim that Mr Brereton's third proposition be accepted as valid and applicable to the facts of this case. 413 The proposition is as follows: "The third proposition which in our submission is the complete answer to this case and which takes it beyond the inferences which flow from those first two propositions is that where damage is the result of an accumulation of doses, some of which are negligent and some of which are non-negligent, then so long as the negligently administered dose was not de minimus it was a material contributing cause to the ultimate result." 414 I cannot accept the proposition or the submission that it provides the complete answer to this case without depending upon inferences as Mr Brereton conceded his earlier two submissions had done. I should explain why I hold this view. 415 Mr Brereton went first to E.M. Baldwin & Son Pty Ltd v Plane (1998) 17 NSWCCR 434. In that case Fitzgerald AJA extensively reviewed the case law on the question of causation. Meagher JA, except as to an issue of apportionment, and Beazley JA agreed with Fitzgerald AJA. 416 There are some references within that review which, at first sight, appear to support Mr Brereton's submission. However, upon examination that is not so as the Judge's summation makes clear. He said at 473: "As the cases referred to illustrate, issues with respect to causation can arise in a variety of circumstances and lead to different approaches. A plaintiff's damage might probably result from a single cause, or some combination of possible causes, which might have occurred concurrently or sequentially, and some of which might be unidentifiable. All relevant circumstances, including an increase in the risk to the plaintiff from the defendant's breach of duty and the character and sequence of events, must be considered in deciding whether a defendant's breach of duty which is a possible cause of the plaintiff's damage probably materially contributed to that damage. Circumstances are relevant for this purpose if they assist in establishing or strengthening a causal connection between the defendant's breach of duty and the plaintiff's damage according to expert opinion or by the application of logic, common sense or experience. Unusually, a conclusion that a defendant's breach of duty materially contributed to a plaintiff's damage might be rejected by reference to policy considerations or value judgments. The differences of opinion evident in some of the cases are for the most part, less related to questions of principle and more attributable to conflicting views of the primary facts, and, in some instances at least, the conclusions to be drawn from expert evidence. In the present matter, Jsekarb's epidemiologists were at the centre of the scientific controversy." 417 The proposition is in conflict with the passage from the judgment of Mason P in T C v The State of New South Wales which I set out at [261]. 418 In particular, whilst the passage was directed to the question of formal reversal of proof, Mason P said at 58: "I cannot accept this submission. I remain of the view that Australian law has not adopted a formal reversal of onus of proof of causation in negligence, even negligence involving breach by omission. A robust and pragmatic approach to proof of causation permits, but does not compel, a finding of liability in cases of negligence by omission which (as Gaudron J points out in Bennett ) is necessarily based upon a hypothetical enquiry. A defendant who exposes a plaintiff to a risk of injury or who, by omission, fails to take reasonable steps to avoid or minimise that risk is not liable unless the risk comes home in the sense that the court is ultimately satisfied on the balance of probability that the defendant's breach caused or materially contributed to the harm actually suffered." 419 That passage in my opinion has equal applicability to the proposition Mr Brereton advances. 420 Also relevant is the passage from the judgment of Spigelman CJ in Seltsam Pty Ltd v McGuinness at 278-280 quoted with approval by Mason P and set out above at the end of [262]. 421 For convenience I repeat the following passage of Mason P's judgment, which includes portion of the quotation: " '119 There is a tension between the suggestion that any increased risk is sufficient to constitute a "material contribution", and the clear line of authority that a mere possibility is not sufficient to establish causation for legal purposes. The latter is too well established to be qualified by the former. The reconciliation between the two kinds of references is to be found in the fact that, as in Chappel v Hart and in the cases that suggest the former, the actual risk had materialised. The "possibility" or "risk" that X might cause Y had in fact eventuated, not in the sense that X happened and Y had also happened, but that it was undisputed that Y had happened because of X.' Par 119 of Seltsam was recently approved by the Queensland Court of Appeal in Batiste v State of Queensland [2001] QCA 275. Thomas JA (with whom McMurdo P agreed) said (at [10]): 'It remains the law that it is still necessary for a plaintiff to prove that a defendant's conduct materially contributed to the sustaining of the injury.' I agree." 422 Mr Brereton relied upon Bonnington Castings Ltd v Wardlaw [1956] AC 613. Fitzgerald AJA summarised that case in Plane at 452 as follows: "In Bonnington Castings Ltd v Wardlaw [1956] AC 613 which was referred to in Tubemakers (1976) 50 ALJR 720 the plaintiff (pursuer) had inhaled silica dust concurrently from two different work activities, one of which involved negligence on the part of the employer and the other of which did not. The House of Lords held that the effect of the silica dust was cumulative and that the plaintiff had established, as was necessary, that the silica dust from the activity which involved negligence on the part of the defendant had probably materially contributed to his disease." 423 In Bonnington Castings Ltd v Wardlaw Lord Reid said at 620-623: "In my judgment, the employee must in all cases prove his case by the ordinary standard of proof in civil actions: he must make it appear at least that on a balance of probabilities the breach of duty caused or materially contributed to his injury. … It appears to me that the source of his disease was the dust from both sources, and the real question is whether the dust from the swing grinders materially contributed to the disease. What is a material contribution must be a question of degree. A contribution which comes within the exception de minimis non curat lex is not material, but I think that any contribution which does not fall within that exception must be material. I do not see how there can be something too large to come within the de minimis principle but yet too small to be material. … In my opinion, it is proved not only that the swing grinders may well have contributed but that they did in fact contribute a quota of silica dust which was not negligible to the pursuer's lungs and therefore did help to produce the disease. That is sufficient to establish liability against the appellants, and I am therefore of opinion that this appeal should be dismissed." 424 Lord Keith of Avonholm said at 626: "I think the natural inference is that had it not been for the cumulative effect the pursuer would not have developed pneumoconiosis when he did and might not have developed it at all. The inference, of course, would have been different if it could be shown that the pursuer could not have inhaled any particles given off from the swing grinding operations, or that the particles negligently released from the swing grinding operations were released at intervals so infrequent, or in quantities so insignificant, even if taken cumulatively, as to make it unreasonable to regard them as a material contributing cause of the pursuer's disease. But that, in my opinion, the defenders are unable to show. On the whole evidence, I consider that the pursuer has discharged the onus that is upon him of showing that the defenders' fault was a material contributing cause of his illness." 425 The case establishes as Beazley JA, with whom Sheller JA and Sheppard AJA agreed, said in Wallaby Grip (Bae) Pty Limited (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355 at 313: "A plaintiff must show more than that it is possible that injury was caused by the defendant." 426 The basis upon which a conclusion in favour of the plaintiff (pursuer) was reached was stated by Lord Bridge in Wilsher v Essex Area Health Authority [1988] 1 AC 1074 at 1086 as follows: "Their Lordships concluded, however, from the evidence that the inhalation of dust to which the pursuer was exposed by the defenders' breach of statutory duty had made a material contribution to his pneumoconiosis which was sufficient to discharge the onus on the pursuer of proving that his damage was caused by the defenders' tort." 427 In Wilsher Lord Bridge also referred to another dust case of cumulative effect in McGhee v National Coal Board [1973] 1 W.L.R. 1. He said at 1086: "In McGhee v National Coal Board [1973] 1 W.L.R. 1 the pursuer worked in a brick kiln in hot and dusty conditions in which brick dust adhered to his sweaty skin. No breach of duty by his employers, the defenders, was established in respect of his working conditions. However, the employers were held to be at fault in failing to provide adequate washing facilities which resulted in the pursuer having to bicycle home after work with his body still caked in brick dust. The pursuer contracted dermatitis and the evidence that this was caused by the brick dust was accepted. Brick dust adhering to the skin was a recognised cause of industrial dermatitis and the provision of showers to remove it after work was a usual precaution to minimise the risk of the disease. The precise mechanism of causation of the disease, however, was not known and the furthest the doctors called for the pursuer were able to go was to say that the provision of showers would have materially reduced the risk of dermatitis. They were unable to say that it would probably have prevented the disease. ……… A distinction is, of course, apparent between the facts of Bonnington Castings Ltd. V Wardlaw , where the 'innocent' and 'guilty' silica dust particles which together caused the pursuer's lung disease were inhaled concurrently and the facts of McGhee v. National Coal Board [1973] 1 W.L.R. 1 where the 'innocent' and 'guilty' brick dust was present on the pursuer's body for consecutive periods. In the one case the concurrent inhalation of 'innocent' and 'guilty' dust must both have contributed to the cause of the disease. In the other case the consecutive periods when 'innocent' and 'guilty' brick dust was present on the pursuer's body may both have contributed to the cause of the disease or, theoretically at least, one or other may have been the sole cause. But where the layman is told by the doctors that the longer the brick dust remains on the body, the greater the risk of dermatitis, although the doctors cannot identify the process of causation scientifically, there seems to be nothing irrational in drawing the inference, as a matter of common sense, that the consecutive periods when brick dust remained on the body probably contributed cumulatively to the causation of the dermatitis. I believe that a process of inferential reasoning on these general lines underlies the decision of the majority in McGhee's case." 428 After setting out a number of passages from the opinions Lord Bridge concluded: "The conclusion I draw from these passages is that McGhee v National Coal Board [1973] 1 W.L.R. 1 laid down no new principle of law whatever. On the contrary, it affirmed the principle that the onus of proving causation lies on the pursuer or plaintiff. Adopting a robust and pragmatic approach to the undisputed primary facts of the case, the majority concluded that it was a legitimate inference of fact that the defenders' negligence had materially contributed to the pursuer's injury. The decision, in my opinion, is of no greater significance than that and to attempt to extract from it some esoteric principle which in some way modifies, as a matter of law, the nature of the burden of proof of causation which a plaintiff or pursuer must discharge once he has established a relevant breach of duty is a fruitless one." 429 I come later to a consideration of this conclusion in Fairchild v Glenhaven Funeral Services Ltd [2003] 1 AC 32. 430 In Plane Fitzgerald AJA dealt at some length with the case of Commonwealth v McLean (1996) 41 NSWLR 389. It is convenient to repeat the following passages from Plane at 452: "In The Commonwealth v McLean (1996) 41 NSWLR 389, the principle that a finding that a defendant's breach of duty materially increased the risk to a plaintiff can in appropriate circumstances rationally support a conclusion that the defendant materially contributed to the plaintiff's injury was accepted even though any connection between the defendant's breach of duty and the plaintiff's damage was indirect. The plaintiff suffered post traumatic stress disorder consequent upon a collision between two vessels, the HMAS Melbourne, on which he was a seaman, and the HMAS Voyager. It was held that the defendant was liable to the plaintiff for his stress disorder, to which he had a psychiatric predisposition, because damage of that type to the plaintiff was reasonably foreseeable by the defendant (at 403, 404, 406). The plaintiff claimed that his stress disorder also caused an increase in his consumption of alcohol and cigarettes, which had caused his throat cancer. Although a jury verdict in favour of the plaintiff on this aspect of the case was set aside by this Court on appeal because the jury had been misdirected with respect to other issues (which included foreseeability and remoteness of damage), what was described as a ' Bonnington Castings v Wardlaw direction on causation ' was upheld (at 407-411). The critical circumstance in the dispute with respect to causation in The Commonwealth v McLean (supra) was that the plaintiff would have consumed alcohol and cigarettes even if the collision had not occurred and caused his stress disorder. The defence submission was that the plaintiff was accordingly at risk of throat cancer even if his stress disorder had not caused him to increase his consumption, and objection was taken to the trial judge's direction to the jury that ' ...where the defendant's breach of duty contributed to a potentially harmful situation, thereby increasing the risk of injury, you are entitled to find that the injury resulted from the defendant's breach of duty if the defendant's contribution was, in your judgment, significant.' In their joint judgment, with which Santow AJA relevantly agreed, Handley and Beazley JJA said at 410 - 411: 'If the jury concluded that the plaintiff's excessive smoking and drinking were caused by his stress disorder and were involuntary, they were entitled to find, on Professor Tattersal's evidence, that his stress disorder had caused his throat cancer. The defendant's submission that the plaintiff might have contracted throat cancer in any event raised a question on which medical science provided no clear answer. Some of the plaintiff's consumption was not caused by the tort because the "but for" test was not satisfied. However on the jury's findings a significant part of his total consumption would not have occurred "but for" the tort. It seems to us that the rule in Bonnigton Castings v Wardlaw ([1956] AC 613) and the related cases applies ... They supply a principle for deciding responsibility where injury results from a noxious substance or situation where only some of the exposure was caused by the tort. ... The defendant did no more than 'suggest' that the plaintiff's consumption of alcohol and tobacco, without any increase due to the tort, could have caused the cancer in any event. In our judgment the direction to the jury that they were entitled to award damages for the cancer if they found that the increase in consumption caused by the tort was significant was correct.'" 431 The emphasised passage contrasts with the present matter in that here there is a good deal of evidence doing much more than suggesting that the appellant's condition was wholly caused by the appropriately prescribed medication. 432 In this context it is to be born in mind that, whilst the effect of the corticosteroid is cumulative and dose related, it does not produce an injury which is "indivisible" and not dose related in the sense that once triggered the disease does not vary in severity according to the victim's exposure history. 433 The evidence established that the extent of the injury is dose related which distinguished the present matter from a mesothelioma case even where it is accepted that the greater exposure to asbestos the greater likelihood that the disease will be triggered. (See Jane Stapleton Cause-in-Fact and the Scope of Liability for Consequences [2003] 119 LQR 388). 434 This circumstance, as well as others to which I shall refer, leaves the present case outside the modified approach to the proof of causation adopted in Fairchild. 435 Fairchild, which was not referred to in argument, was heard with two other cases all involving employees who had developed mesothelioma caused by exposure at work to asbestos dust. All of the employees had been exposed to asbestos dust during periods of employment with more than one employer. The Court of Appeal held that each employee failed because he could not establish, on the balance of probabilities, which period of exposure had caused the disease. 436 The House of Lords upheld the appeals, applying to a closely defined set of circumstances "a modified approach to proof of causation" which it was held was justified in such cases. 437 A feature of the case is that a majority of the House expressly departed from the view of McGhee's case propounded by Lord Bridge as set out at [365] above. Lord Bingham of Cornhill said at 68: "For reasons given above, I cannot accept the view (considered in the opinion of my noble and learned friend, Lord Hutton) that the decision in McGhee [1973] 1 WLR 1 was based on the drawing of a factual inference. Nor, in my opinion, was the decision based on the drawing of a legal inference. Whether, in certain limited and specific circumstances, a legal inference is drawn or a different legal approach is taken to the proof of causation, may not make very much practical difference. But Lord Wilberforce, in one of the passages of his opinion in McGhee quoted in paragraph 20 above, wisely deprecated resort to fictions and it seems to me preferable, in the interests of transparency, that the courts' response to the special problem presented by cases such as these should be stated explicitly. I prefer to recognise that the ordinary approach to proof of causation is varied than to resort to the drawing of legal inferences inconsistent with the proven facts." 438 It is to be noted that Lord Hutton made the observation at 89: "Courts in Australia have also taken the view that the decision in McGhee was arrived at on the basis of an inference." He cited Birkholz v R J Gilbertson Pty Ltd (1985) 38 SASR 121. 439 It is unnecessary to pursue the point for, as Stapleton pointed out at 398: "…This McGhee/Fairchild 'material contribution to the risk of injury' principle does not assist C where not all sources of risk were created by D, not all sources of risk were tortious, the context was not one of employer's liability and the agents of risk were of divergent natures" 440 In this case not all causes of risk were tortious and the context was not one of employer's liability. 441 McGhee and Bonnington Castings Ltd v Wardlaw were not cases in which all causes of the risk were tortious; however, that was a requirement for the application of the principles enunciated in Fairchild Lord Bingham said at 68: "I would in conclusion emphasise that my opinion is directed to cases in which each of the conditions specified in (1) – (6) of paragraph 2 above is satisfied and to no other case." 442 Lord Rodger of Earlsferry said at 119: "Sixthly, the principle applies where the other possible source of the claimant's injury is a similar wrongful act or omission of another person, but it can also apply where, as in McGhee , the other possible source of the injury is a similar, but lawful, act or omission of the same defendant." 443 However, the other opinions did not support an enlargement beyond the circumstances of the three cases. 444 Lord Bingham did say at 68: "It would be unrealistic to suppose that the principle here affirmed will not over time be the subject of incremental and analogical development. Cases seeking to develop the principle must be decided when and as they arise." 445 Having regard to the authorities to which I have earlier referred (and the way in which the case has been argued) it is not appropriate to approach this appeal as one that may be decided upon a development of the principles enunciated in Fairchild. 446 Having regard to my earlier expressed views and the rejection of Mr Brereton's third proposition, I agree with Studdert J that the appellant did not establish, on the balance of probabilities, that the breaches of duty caused or materially contributed to the injury to the appellant's spine. Proposed Orders: 447 It should be noted that Counsel agreed that if there is a finding of liability in favour of the appellant on the basis of loss of a chance the matter should be sent back to the primary judge to assess the chance and assess the damages on the basis of the evidence at the trial. 448 For the above stated reasons in my opinion the following orders should be made: (1) Appeal allowed with costs. (2) Judgment below be set aside. (3) In lieu thereof, verdict for the appellant. (4) Matter remitted to the primary judge to determine damages on the basis of the loss of a chance and conformably with the judgments of the Court. Should the primary judge be unable for any reason to hear the remitted matter it is to be heard by a judge nominated by the Chief Judge at Common Law. (5) Defendant to have a certificate under the Suitors Fund Act if otherwise qualified. (6) Respondent granted leave to amend Notice of Contention. ********** Last Modified: 11/01/2004 DISCLAIMER - Every effort has been made to comply with suppression orders or statutory provisions prohibiting publication that may apply to this judgment or decision. The onus remains on any person using material in the judgment or decision to ensure that the intended use of that material does not breach any such order or provision. Further enquiries may be directed to the Registry of the Court or Tribunal in which it was generated.