Rufo v Hosking - [2002] NSWSC 1041

No judgment structure available for this case.

CITATION: Rufo v Hosking [2002] NSWSC 1041

CURRENT JURISDICTION: Common Law Division
Professional Negligence List

FILE NUMBER(S): SC 20468/01

HEARING DATE(S): 24, 25, 26, 28 June, 1, 2, 4, 29, 30, 31 July, 1, 2, 20, 21, 22, 23 August 2002

JUDGMENT DATE: 6 November 2002

PARTIES :

Michelle Rufo (Plaintiff)
Dr C.S. Hosking (Defendant)

JUDGMENT OF: Studdert J

COUNSEL : B. Donovan QC/ E. Pike (Plaintiff)
D. Higgs SC/J. Lonergan (Defendant)

SOLICITORS: Kells - The Lawyers (Plaintiff)
Colin Biggers Paisley (Defendant)

CATCHWORDS: Negligence - claim against medical practitioner - whether breach of duty of care - whether any breach causative of harm.

CASES CITED: Rogers v Whitaker (1992) 175 CLR 479
Bolam v Friern Hospital Management Committee [1957] 1 WLR 582
Wyong Shire Council v Shirt (1979-1980) 146 CLR 40
Bendix Mintex Pty Limited v Barnes (1997) 42 NSWLR 307
Wallaby Grip (Rae) Pty Limited (in liq.) v Macleay Area Health Service (1998) 17 NSW CCR 355
E.M. Baldwin & Son Pty Limited v Plane 1999 ATR 81-499
TC v State of New South Wales [2001] NSWCA 380
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
Tran v Lam (unreported, Badgery-Parker J, 20 June 1997)

DECISION: See para 281

IN THE SUPREME COURT
OF NEW SOUTH WALES
COMMON LAW DIVISION
PROFESSIONAL NEGLIGENCE LIST

STUDDERT J

Wednesday 6 November 2002

20468/01 MICHELLE RUFO v DR C.S. HOSKING
JUDGMENT

1 HIS HONOUR: In these proceedings, transferred from the District Court, the plaintiff, Michelle Rufo, sues Clifford Hosking, claiming damages for negligence. The defendant is a medical practitioner and it is the plaintiff’s case that the defendant failed to exercise due care in his treatment of her in 1992.

2 The plaintiff was born on 29 December 1977, and in early January 1992 was diagnosed to be suffering from systemic lupus erythematosus. This is an inflammatory condition in which a characteristic rash is associated with widespread internal pathology. I shall refer hereafter to the disease, shortly, as lupus.

3 The diagnosis of lupus in the plaintiff’s case was made by Dr Donald, specialist paediatrician, practising at Maitland. The plaintiff had been referred to him by her general practitioner, Dr Almeda.

4 On 8 January 1992 Dr Donald prescribed Prednisolone for the treatment of the plaintiff’s lupus. Prednisolone is a corticosteroid drug, and the commencing dose as prescribed was 50 mg per day.

5 Dr Donald subsequently became unavailable to continue the plaintiff’s treatment, by reason of going away, and her care passed to the defendant, who first saw the plaintiff at Dr Donald’s rooms in Maitland on 3 February 1992. The plaintiff thereafter continued under the defendant’s care until January 1993 when the plaintiff passed into the care of Professor Clancy.

6 The focus in this cause is on the period between 3 February 1992 and 24 August 1992 when the plaintiff was admitted to John Hunter Hospital suffering from vertebral microfractures. The evidence establishes that these microfractures were caused by the corticosteroid dosages that the plaintiff had been having. This much was conceded by the defendant in final submissions.

7 In the period from 3 February 1992 until 24 August 1992 the defendant treated the plaintiff for her lupus condition and in doing so continued the regime of corticosteroids. There is no question as to the correctness of the original diagnosis of lupus made by Dr Donald, and I am satisfied that the defendant was correct in reaching the same diagnosis when the plaintiff passed into his care. It is the management of the plaintiff’s treatment, and in particular the continued prescription of high doses of corticosteroids for her until the admission to hospital on 24 August 1992 that is at the centre of the allegations of negligence made against the defendant.

8 At the outset then it is necessary to consider the course of treatment for the plaintiff’s lupus during 1992, against the background of her signs and symptoms of that disease during the same period.

The plaintiff’s signs and symptoms and the course of her treatment by the defendant

9 The plaintiff’s response to Prednisolone after it was first administered was favourable. Dr Donald had recorded on 17 January 1992 that the plaintiff’s symptoms were then settling and that the butterfly rash (earlier recorded by Dr Donald on 2 January 1992 as being “quite impressive”) was by then “minimal”.

10 The plaintiff was seen by the defendant on a number of occasions between the beginning of February 1992 and her admission to hospital on 24 August 1992. Some of the attendances were at Dr Donald’s rooms at Maitland (where the defendant was acting as locum in Dr Donald’s absence) and others were at John Hunter Hospital. I shall deal with these attendances chronologically.

11 3 February 1992

12 17 February 1992

13 27 February 1992

14 On 27 February 1992 the defendant continued the plaintiff on the dose of 62.5 mg of Prednisolone per day.

15 9 March 1992

16 The defendant’s notes contain no record of this, but according to Mrs Rufo concern was voiced by her about Michelle’s weight. Mrs Rufo was not at the consultations that followed in April and May and I accept her recollection that it was at the consultation in March that concern was first voiced about the plaintiff losing weight. That the subject was then raised was stated in evidence by both Mrs Rufo and Mr Rufo and it was also the plaintiff’s recollection that the question of weight was raised. Dr Nanra had noted three days earlier a weight loss from 52 kgs down to 44 kgs.

17 There was one other matter which the plaintiff and her parents said was discussed on 9 March. Prior to the disease being diagnosed the plaintiff had had her first two periods but had no further period after the diagnosis was made. It was the plaintiff’s recollection that her mother drew this situation to the attention of the defendant and that the defendant said he would check the position with a Melbourne specialist. Mrs Rufo’s recollection was that this subject had come up at the earlier consultation on 27 February; Mr Rufo was of the like recollection. Whether the question was first raised on 27 February or 9 March does not matter. The defendant’s notes make no reference to this question for either date. However, I am satisfied that the issue was raised, probably on 27 February. I also accept that the defendant subsequently advised the plaintiff that the periods would resume after the treatment by corticosteroids ceased.

18 10 March 1992

“The features that suggest renal involvement include mild microscopic haematuria, perhaps borderline proteinuria, definite nocturia x 2, and a possible reduction in renal function. She has a serum Cr of .09mmol/L and this gives her a predicted Cr clearance of 66mls/min. Her measured Cr clearance is 45mls/min and when corrected for surface area goes up to over 60 and conforms with the predicted Cr clearance. She is an intelligent girl and her urine volume was at least 2.4 litres. I would therefore think that her measured Cr clearance is in fact accurate.

The degree of reduction in Cr clearance with a paucity of urine abnormalities raises the possibility of tubular interstitial disease as a manifestation of SLE in the kidney.

The fact that she has tolerated a fairly high dose of steroids before developing early cushingoid changes to me suggests that her disease was fairly active and that she was in a fairly catabolic state. I wonder if the lesions in her toes are actually microinfarcts related to lupus vasculitis.

I still have not seen her complement and C reactive protein results.

I have arranged for phase contrast microscopy of her urine and measurement of her GFR by chromium EDTA clearance through my department at John Hunter Hospital. I have also repeated her blood and 24 hr urine tests.

I plan to review her in about 2 weeks time.

In the interim I am very comfortable with her present steroid dosage.”

19 13 April 1992

20 Prompted to do so by his wife, Mr Rufo said that at this consultation he raised the subject as to whether or not there was a need for some calcium supplement. The defendant suggested that calcium tablets in a chocolate coated form could be purchased at the chemist. This was the only occasion on which the defendant addressed the question of any calcium supplement with the plaintiff or her parents and he made no recommendation as to the frequency with which or the period during which calcium tablets should be taken.

21 The defendant has made no note of this, but I am satisfied that at this particular consultation concern was expressed about the plaintiff being moody.

22 The defendant reduced the dose of Prednisolone to 40 mg per day.

23 The defendant wrote on 16 April 1992 following this consultation that the plaintiff was “starting to show signs of Cushingoidism with the development of hair on her upper lip and a slightly moon face”.

24 4 May 1992 – report of Dr Nanra

“that in spite of high dose steroids she doesn’t look very cushingoid and this usually is seen in patients with negative protein balance. I have no reason to suspect that this young girl is in such a state”.

25 Dr Nanra reported that from the renal viewpoint it was important to monitor the plaintiff’s urine for any abnormalities “at least once or twice every two or three months.”

26 11 May 1992

By this time presumably the defendant had received Dr Nanra’s report, Exhibit 2.

27 Hospital visit, 28 May 1992

28 1 June 1992

29 On 1 June 1992 the defendant determined that the Prednisolone dose should continue at 60 mg per day for four days, and according to his letter to Dr Donald of 1 June 1992 he planned that the dose be reduced then to 55 mg per day for two weeks with a subsequent reduction to 50 mg per day.

30 22 June 1992

31 By 22 June the plaintiff complained that she was very thin with a very puffed face and twig legs. The defendant’s notes contain no record of any such appearance nor does his report addressed to Dr Donald of 26 June 1992. In that report he does record the plaintiff’s ongoing emotional problems, particularly in the afternoon when the plaintiff was complaining of crying without apparent reason. It was this which prompted the split up of the daily dose and the plaintiff was referred to Dr Miller, psychiatrist, for assessment. By this time the plaintiff had been seeing a psychologist, Ms Nancy Wallace, on the initiative of the plaintiff’s parents and had seen her some five times.

32 The plaintiff was required to test her urine with multistix on a weekly basis.

33 29 June 1992 – Assessment of Dr Miller

“Nancy Wallace is certainly the ideal person to explore these issues, and the family have a good attachment to her. I have encouraged them to pursue this with her.

To help with her anxiety control, I certainly feel that Clomipramine medication was warranted and I have commenced her on a course of treatment to contain her obsessional ruminations. Hopefully, this will also lift her mood, and make her more available to Nancy’s excellent family work. I have been liaising with Nancy about her continuing intervention here, and in the background I will keep an eye on medication, and her response to this.”

34 13 July 1992

35 On this occasion the plaintiff complained of a cough and green sputum. The cough was worse at night and there was sputum at night and in the morning. The weekly urine tests disclosed no renal involvement. The doctor’s notes of this consultation record that there was “no objective sign of neuropathy”. The defendant said this was an incorrect note and that what he should have written was “no objective sign of myopathy”. The defendant said in evidence that he considered the strength in the plaintiff’s legs to be reasonable and he could recall no difficulty in the way in which the plaintiff walked. However the defendant also said that whilst he could not recall if he observed any difficulty in the way the plaintiff was walking, proximal steroid myopathy would not be unexpected having regard to the steroids the plaintiff had by then taken.

36 The evidence of the parents of the plaintiff differs from that of the defendant as to the position at 13 July. Mr Rufo said that the plaintiff told the doctor at this consultation that she was having trouble walking, and with stairs. Mrs Rufo could not recall being present at the July consultation but she gave evidence of the plaintiff’s physical deterioration in July; she said that her daughter moved slowly and with difficulty, and that her appearance deteriorated: her face was big, “she was scrawny and she had this big belly and these chicken legs. These very, very thin, thin legs.” This description accorded with the evidence that the plaintiff had given as to her condition at the consultation on 22 June 1992.

37 I have difficulty in accepting the accuracy of the defendant’s note that there was no objective sign of [myopathy] by 13 July. I think it likely that the defendant is dependent upon his records to aid his recollection, and the defendant’s notes of this and other consultations are not detailed. The evidence of the plaintiff’s parents and of the plaintiff persuades me on the balance of probabilities that the plaintiff’s appearance had altered significantly by this time, and there probably was wasting of muscles present, even though the defendant did not record it.

38 The defendant said that he asked Dr Kamal, a general practitioner who by this time had begun to treat the plaintiff, to reduce the dose of Dexamethasone to 7 mg per day once the infection then present cleared up. The defendant wrote to Dr Kamal on 14 July 1992: “I would like her to continue on 8 mg of Dexamethasone until the nasal discharge and cough has cleared in which case you will reduce it to 7 mg per day.”

39 20 July 1992 – Dr Miller’s second report

40 21 July 1992 – Dr Kamal

41 10 August 1992

42 On 10 August 1992, the defendant noted that the plaintiff had picked up over the past two to three weeks, that her teariness had gone and that the weakness in her legs had improved. He noted steroid proximal myopathy (incorrectly noted as steroid myositis) and pot belly. Despite noting that the plaintiff’s weak legs were better, the defendant said that the legs were thinner and weaker. Hence the note of steroid “myositis”. The defendant made no note of back pain.

43 The defendant’s notes are inconsistent with the evidence of the plaintiff and her father as to the extent of the back disability on 10 August 1992. The plaintiff says that by 10 August 1992 her posture was very stooped and that she had difficulty walking and with stairs. Mr Rufo supported that account and described the difficulty that his daughter had in walking to the surgery from the car park. Mr Rufo said that the plaintiff presented in the surgery bent forward and had to be assisted into position on the consultation couch.

44 I see no reason to doubt the honesty of any of the Rufo family. Nor, indeed, do I see any reason to doubt the honesty of the defendant. However, I prefer the evidence of the Rufos as to the condition of the plaintiff in terms of the plaintiff’s appearance and presentation by the time of the consultation in August 1992. I prefer their evidence for much the same reasons as I prefer their recollection of the condition of their daughter by 13 July 1992. The defendant is, understandably, largely dependent upon his notes to prompt his recollection, and the defendant’s notes are somewhat terse and imperfect. I consider the Rufos have a better recall of the position as at 10 August 1992, and that their evidence is to be preferred as to this.

45 I note that Dr Kamal recorded that the plaintiff presented to him on 11 August with pain in the lower back. The same complaint was made by her on 14 and 15 August (Exhibit G). Those complaints to Dr Kamal are consistent with the evidence of the plaintiff and her father as to the plaintiff’s condition on 10 August. The plaintiff gave evidence that Dr Kamal arranged for x-rays of her spine on 11 August 1992 but x-ray reports have not been proved. (There is a note in the hospital records for 20 August commenting that x-rays of the spine had been taken one week ago and no fractures had been seen. )

46 On 10 August 1992 the defendant reduced the dose of Dexamethasone to 6 mg per day.

47 20 August 1992 at John Hunter Hospital

The hospital records show that the plaintiff attended the John Hunter Hospital with faecal impaction and back pain on 20 August 1992.

48 Admission to hospital, 24 August 1992

49 The defendant treated the plaintiff in hospital, reducing the dose of Dexamethasone to 1 mg per day by the time of her discharge.

50 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.

51 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.

The duty of care owed by the defendant to the plaintiff

52 It is, of course, well settled that a doctor owes a duty of care to his patient. The standard of care to be observed by a doctor having some special skill or competence is “that of the ordinary skilled person exercising and professing to have that special skill”: see Rogers v Whitaker (1992) 175 CLR 479 at 487. The special skill which the defendant professed was that of a paediatric immunologist. The standard of care attracted by that status and the defendant’s relationship to the plaintiff is not, however, determined only by reference to the practice of other specialist immunologists or specialist paediatric immunologists. This was made clear in Rogers v Whitaker when the High Court declined to follow the principle in Bolam v Friern Hospital Management Committee [1957] 1 WLR 582. In their joint judgment, Mason CJ, Brennan, Dawson, Toohey and McHugh JJ said (at 487):

Bolam

53 In the course of the hearing in this case Mr Donovan of Queen’s Counsel was asked to particularise the negligence relied upon by the plaintiff. Particulars, many of which were of a general nature, were furnished during the hearing, and these included two general allegations of failing to advise. It will be necessary shortly to look more closely at the nature of the plaintiff’s case as pursued in Mr Donovan’s closing address, but as I understand it, the plaintiff’s case was directed essentially at what it was submitted amounted to a failure to exercise due care in the treatment given to the plaintiff, as distinct from a failure to appropriately advise the plaintiff of all relevant information so as to be able to choose between undergoing and not undergoing the regime of treatment which the defendant provided. Even so, Rogers makes clear that the practice of other immunologists is not necessarily definitive of the issue as to whether or not the defendant breached his duty owed towards the plaintiff, although as their Honours went on to say in their joint judgment in Rogers (at 489):

“Whether a medical practitioner carries out a particular form of treatment in accordance with the appropriate standard of care is a question in the resolution of which responsible professional opinion will have an influential, often a decisive, role to play…”

54 In Rogers, Gaudron J saw the evidence of other practitioners in cases where negligence in diagnosis or treatment was alleged as being “of very considerable significance” (at 493) but not necessarily determinative. However, her Honour considered that “at least in some situations questions as to the reasonableness of particular precautionary measures are also matters of commonsense.”

55 There has in this case been divergence of expert opinion among the specialists who have given evidence as to whether the treatment given by the defendant was appropriate and reasonable. The plaintiff here relies upon evidence that has been given by Dr Sutherland and by Dr Champion. The defendant, on the other hand, here relies upon his evidence and the evidence given by Professor Sturgess and Professor Clancy. The evidence of each of these experts warrants close attention, particularly in the context of a consideration of the various particulars of negligence expressed by Mr Donovan.

56 I find on the evidence that the occurrence of the fractures which the plaintiff sustained was a most unusual outcome in the light of knowledge in the medical profession in 1992. This was so having regard to the plaintiff’s age at the time and the period during which the plaintiff had been taking corticosteroids. This finding accords with the evidence of Dr Sutherland (T 590), Dr Champion (T 419), the defendant (T 707), Professor Sturgess (T 824) and Professor Clancy (T 893). Nevertheless it was well known in 1992 that corticosteroids could cause osteoporosis. In the respected Textbook of Pediatric Rheumatology by Cassidy & Petty (first published in 1990) the risk of corticosteroids causing osteoporosis and vertebral compression fractures was expressly stated in a passage warning of the need for caution in the use of such drugs:

“Corticosteroids should be employed in the management of pediatric 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 to infection and peptic ulceration, myopathy, behavioural disturbances and psychosis, posterior subcapsular cataracts, osteoporosis and vertebral compression fractures, and inhibition of linear growth.”

57 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.”

58 That same risk is noted in MIMS for 1992, as the defendant acknowledged (T 722). 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” (T 726).

59 The evidence establishes that it is recognised that the risk of osteoporosis and vertebral compression fractures is high in cases of post menopausal women being treated with corticosteroids, but I accept the opinions expressed in this case by Dr Sutherland (T 587) and by Dr Champion (p 6, report 2 December 1998, part of Exhibit D) that young people prior to the achievement of peak bone mass are also vulnerable to this same risk from corticosteroids.

60 I am satisfied on the balance of probabilities that the risk to the plaintiff of vertebral compression fractures due to osteoporosis caused by corticosteroids was not a far fetched or fanciful risk, but a risk which was foreseeable during the time that the defendant was treating the plaintiff prior to 24 August 1992. In determining the appropriate response by the defendant to such risk it is, of course, relevant to have regard (inter alia) to the magnitude of the risk and the degree of probability of its occurrence: see Wyong Shire Council v Shirt (1979-1980) 146 CLR 40 at 47.

61 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.

The honesty of the witnesses called

62 Mr Higgs of Senior Counsel for the defendant did not submit that I should reject the evidence of the plaintiff or that of either of her parents as being untruthful, and I do not do so. Indeed, I have already stated my assessment of the evidence of the Rufos in the context of considering the plaintiff’s presentation to the defendant in July and August 1992. Generally I found each of these witnesses to be honest and the evidence of each of them for the most part to be reliable, although I have difficulty in accepting as reliable the evidence that Mr Rufo gave as to what he claimed Professor Clancy said when Professor Clancy first began to treat the plaintiff in January 1993.

63 The defendant impressed me as a completely honest witness but, as I recorded earlier, I consider his recall of the consultations with the plaintiff in July and August 1992 to be imperfect and unreliable. The plaintiff was one of doubtless many patients being treated by the defendant at the time and it is to be expected that the defendant would have been dependent upon his notes to recall the detail of what occurred. Those notes I consider to be inadequate for such purpose. On the other hand, I am satisfied that the plaintiff and her parents had good reason to remember the detail of what occurred at each consultation and I assess their evidence as being the more reliable in this regard.

64 Stern criticism has been directed by Mr Donovan to the credibility of the evidence of Professor Clancy. Mr Rufo said that when the plaintiff first saw Professor Clancy, he accompanied his daughter to the doctor’s room at the Madison Building at Newcastle Hospital, and in the absence of his daughter he had a conversation with Professor Clancy in which the doctor was critical of the treatment the plaintiff had received from the defendant, and said he would have treated the plaintiff differently. This was denied by Professor Clancy.

65 It seems to me to be unlikely that Professor Clancy would have been quick to criticise the plaintiff’s prior treatment, and certainly when the plaintiff’s solicitor wrote to Professor Clancy seeking a report from him in December 1995 this prompted a response from Professor Clancy on 7 February 1996 which was not critical of the defendant. In that letter the doctor made specific answers to specific questions addressed to him. Not only is that response not critical of the defendant but as early as 7 September 1993, some eight months after Professor Clancy assumed the plaintiff’s care, he wrote to Dr D’Costa (part of Exhibit 9) reporting on the plaintiff’s progress. He wrote in part:

“She [the plaintiff] looks and feels well but the parents remain very upset and bitter about what they perceive as difficulties in management in the past. I have reassured them that I don’t believe there has been improper treatment but rather she had a very unusual response to fairly solid therapy.”

66 I see no reason to believe that Professor Clancy was seeking to deceive Dr D’Costa, and the above letter was written years before any action was commenced against the defendant. Indeed, a statement of claim was not issued until 1998.

67 Professor Clancy was criticised for conferring with the defendant’s solicitors, without the plaintiff’s authority, and also for communicating with them, again without the plaintiff’s authority. Professor Clancy said he did not understand he was doing anything wrong. It is not without significance that Professor Clancy’s records were produced to the Court under subpoena and no claim for privilege was made concerning the report prompted by letter from the plaintiff’s solicitors to the witness. Hence the defendant’s solicitors gained access to the letter to which I referred earlier, namely Professor Clancy’s letter dated 7 February 1996. Nor were the defendant’s solicitors advised until this hearing was in progress that the failure to maintain a claim of legal professional privilege concerning the relevant report was an error, due to oversight. Eventually the claim of privilege was not pursued.

68 Mr Donovan further submitted that Professor Clancy demonstrated bias by his willingness to be interviewed by the defendant’s solicitors, and by his correspondence with them. Further evidence of bias was to be found in a conversation which the plaintiff said she had with Professor Clancy, in which he asked her, concerning the pending action against the defendant: “Do you really want to do this? You do know what this will do to Dr Hosking.”

69 I accept that there may have been such a conversation between the plaintiff and Professor Clancy, and I accept that Professor Clancy may well be sympathetic to the defendant’s position in this cause. However, I have had the opportunity of assessing Professor Clancy during Mr Donovan’s testing cross examination of him. I did not assess the witness as setting out to deceive the Court. I regarded him generally as being an honest witness, although I do not overlook in considering his testimony the opinion I reached that the defendant has his sympathy in his capacity as a defendant in this cause.

70 No attack has been made on the credibility of the remaining witnesses in this case, and I accept that each of them genuinely holds the opinions he has expressed.

71 I propose to record in broad outline the medical evidence in this case.

The medical evidence outlined

72 The three expert witnesses called in the plaintiff’s case were Dr Bleasel, Dr Sutherland and Dr Champion.

Dr Bleasel

73 Dr Bleasel is a specialist neurosurgeon who examined the plaintiff on 23 January 2001 and who prepared a report of 29 January 2001 (Exhibit B). I referred earlier to the opinion expressed by the doctor, not really the subject of challenge in this cause, that he perceived there to be a causal connection between the plaintiff’s osteoporosis leading to the vertebral collapse and the corticosteroid therapy that preceded it.

74 Dr Bleasel has had previous experience with corticosteroids but has never treated patients long term with such drugs.

75 Dr Bleasel related the plaintiff’s kyphosis to the corticosteroids and also perceived that there was a relationship between the headaches and the osteoporosis, the kyphosis and the spinal fractures, and that the headaches were in part posturally induced. Dr Bleasel observed that when he saw the plaintiff she was very stooped with her head craned forward, and there was what he assessed to be a very severe degree of kyphosis.

Dr Sutherland

76 Dr Sutherland is a clinical immunologist. He was the Clinical Director of the Hunter Immunology Unit and Clinical Associate Professor of the Department of Medicine at the University of Newcastle from 1984 until 1989 when he was appointed director of the newly formed Department of Clinical Immunology at Royal Newcastle Hospital. Dr Sutherland resigned his hospital appointments in 1993 and since that time has been in private practice as a consultant specialist in clinical immunology. Since 1993 he has had almost daily experience treating patients suffering from lupus, although the doctor said that if a patient presents with primary severe lupus nephritis and is perceived to be in danger of losing renal function his practice is to refer such a patient to a nephrologist.

77 I accept that Dr Sutherland is well qualified to address the issues in this case.

78 Dr Sutherland’s reports became Exhibit C. It was his opinion, as expressed in the earlier report of 13 September 1994, that the prompt introduction of corticosteroids when lupus was diagnosed was appropriate and effective treatment, recognising that lupus nephritis is potentially life threatening and may lead to irreversible loss of kidney function and renal failure. Once kidney disease was under control it was Dr Sutherland’s opinion that vigorous attempts to withdraw the plaintiff’s corticosteroid intake were required, and he said that this regime could have commenced in the later part of March or in early April 1992. It was his opinion that steroid sparing agents should have been introduced. He also considered that use of calcium and vitamin D supplements could have been employed to address the risk of osteoporosis.

79 Dr Sutherland was in the witness box for several days and there was an adjournment of the cause in the course of the doctor giving his evidence. Before that adjournment, and in the course of cross examination, Dr Sutherland had been taken through the sequence of consultations and had acknowledged that the prescriptions of corticosteroids given from consultation to consultation were reasonable. This prompted Dr Sutherland to write a supplementary report dated 3 July 2002, and I record from that report the following:

“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:

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.

‘moon face’

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.”

80 Dr Sutherland said in the course of cross examination that he 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”.

81 After the interruption of the doctor’s evidence occasioned by the adjournment earlier mentioned, Dr Sutherland gave the following responses in questions asked about the flare up on 28 May and tests and investigations then taken:

82 When asked how he reconciled the above responses to what he had written on 3 July 2002, 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 to say was that step reasonable. As I said, at no time could I say that particular 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.”

Dr Champion

83 Dr Champion is a rheumatologist with a consulting role in paediatric rheumatology since 1973, firstly at the Prince of Wales Children’s Hospital and now the Sydney Children’s Hospital. Dr Champion’s extensive curriculum vitae was tendered, and again I accept that he is well qualified in his area of expertise. Dr Champion explained (T 356) the overlap between the disciplines of immunology and rheumatology. I need not repeat that explanation here.

84 Dr Champion’s reports became Exhibit D. Dr Champion was critical in those reports of the length of time during which what he regarded as relatively high doses of corticosteroids were maintained, and he was critical of the introduction of Dexamethasone.

85 I accept that Dr Champion has a particular interest in osteoporosis and he expressed his opinion as to the need for the regime of treatment to recognise the risks associated with the use of corticosteroids. Dr Champion wrote (report of 2 December 1998, p 7):

“Whereas there may have been justification for a high dose (50 mg/day) of Prednisone the maintenance of such a high dose as it was, was unusual to say the least and not appropriate in my view.”

86 He went on to say, as to the change from Prednisone (in fact the drug first used was Prednisolone but nothing turns on this) to Dexamethasone (at p 7 of that report):

“I consider that the change from prednisone to dexamethasone was not indicated, and was indeed ill advised particularly in the sustained high dose. As I have repeatedly indicated, the dosages of the corticosteroids were uncommonly high and there was no reason given to justify such regimen.”

87 And, later (at p 9):

“14. Considering Miss Rufo’s treatment up to and including the period upon which the osteoporosis was diagnosed, the treatment provided appears not to have been optimal. There was sustained high dose corticosteroid including a slowly eliminated steroid (dexamethasone) and in the early months, insufficient use of safer drugs such as hydroxychloroquine, and grossly inadequate consideration of the risks, particularly osteoporosis, of corticosteroid. The optimal consideration of prevention and management of osteoporosis was outlined in the above section. As acknowledged however, most physicians would have adhered to the principal points and few physicians would have achieved all of the appropriate management items.

15. It was in 1991, common practice to prescribe calcium and vitamin D supplements when treating patients with corticosteroids particularly in high risk patients. The Annal of Internal Medicine of 1990 is an appropriate reference on this issue (in more recent times there would be consideration of biphosphonate, calcitriol and oestrogen in her context, also possibly calcitonin).

16. In all the circumstances, this was not an appropriate treatment regimen prescribed from the initial diagnosis. I should qualify that statement by agreeing that the treatment was appropriate for the first week or two apart from discussions and considerations about adverse effect risks for corticosteroid.”

88 Dr Champion’s evidence was that he would have introduced Plaquenil from day one of treatment and Imuran by the time of the flare up in symptoms in May, but Dr Champion drew a distinction between “optimal” treatment and reasonable treatment. It was his 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 and that Plaquenil should have been introduced then also. Dr Champion rejected the proposition that it was reasonable management to continue without Imuran for a couple of months after 28 May.

89 It will be necessary to return to consider further the evidence of Dr Sutherland and Dr Champion when addressing the particular allegations of negligence which were pursued.

Professor Sturgess

90 Professor Sturgess is the Senior Staff Specialist in Rheumatology at the St George Hospital and the director and supervising pathologist in the immuno-rheumatology laboratory at that hospital. He is also director of the Division of Medicine there, and I accept he is well qualified in the specialist fields of rheumatology and immunology.

91 Professor Sturgess provided reports which became Exhibit 8. I extract from his report of 11 January 2000 a passage of that report which is critical of the views that Dr Champion had expressed in his report of 2 December 1998 (Exhibit D), from which I quoted earlier. Professor Sturgess wrote:

“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.

adequate

92 Addressing the criticism that Dr Champion made of the introduction of Dexamethasone, Professor Sturgess wrote:

when used in equally effective immunosuppressive doses

not

93 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 50mgs 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 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.”

94 It will be necessary for me to consider the actual evidence given by Professor Sturgess in the context of considering the various particulars of negligence upon which the plaintiff ultimately relied.

Professor Clancy

95 Professor Clancy is also a specialist immunologist. He currently holds the position of Professor of Pathology, Discipline of Immunology and Microbiology, Faculty of Medicine and Health Sciences at the University of Newcastle. He is a director of the Hunter Area Immunology Unit at Royal Newcastle Hospital. Again I accept that Professor Clancy is well qualified in his particular areas of expertise and he has been the plaintiff’s treating specialist since the beginning of 1993.

96 I referred earlier to Professor Clancy’s communication to the plaintiff’s solicitors dated 7 February 1996 (part of Exhibit 9). In that letter Professor Clancy addressed nineteen questions. I record at this point his response to question 19:

“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 the 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.”

97 Later, on 16 July 1996, Professor Clancy wrote (part of Exhibit 9):

no evidence of renal disease at present

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 term 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.”

98 In his oral evidence, Professor Clancy was not critical of the regime of corticosteroids and he did not regard it as unreasonable for the defendant not to have introduced Imuran. Whilst in 1993 he had a different view about it (as evidenced in a report written in 1996), Professor Clancy would not at this point of time have introduced Plaquenil with his present state of knowledge.

99 Again it will be necessary to return to the evidence of Professor Clancy in reviewing the way in which the plaintiff ultimately advanced her case on liability.

The defendant

100 The defendant is a paediatric immunologist and has been in that speciality since 1969. The defendant was the Director of Immunology at Royal Children’s Hospital, Melbourne from 1980 to 1991 before going to Newcastle and acting as locum for Dr Donald. I accept the defendant’s expertise in the field of paediatric immunology, accepting the accuracy of his curriculum vitae (Exhibit 5).

101 The defendant’s handwritten notes as transcribed became Exhibit 6. Those notes refer to the various consultations with the plaintiff and I have considered them and drawn upon them earlier in this judgment when reviewing the course of the plaintiff’s treatment.

102 The defendant said that his plan had been to maintain the initial dosage for six weeks and then to start decreasing that dosage but this was frustrated by the two flare ups or break throughs. This history was influential in the defendant’s decision to change to Dexamethasone (T 670). I shall return to the introduction of the Dexamethasone presently. The defendant was aware of the effect that corticosteroids have on bones but he had never experienced osteoporosis causing clinical symptoms in other cases in which corticosteroid doses had been prescribed.

103 The defendant acknowledged that lupus was not his sub-speciality nor was osteoporosis. Indeed, he had not heard of corticosteroids causing fracture in the spine, although he was aware that steroids affect bone density and he acknowledged that they could have an effect on growing bones.

104 Responding to the criticisms implicit in the evidence of both Dr Sutherland and Dr Champion, the defendant acknowledged that he did not start treating the plaintiff with any long term plan written down but he said it was not practicable to do so with “so many possible variations and permutations” (T 713).

105 Dr Hosking considered the outcome in this case to be extraordinarily rare and he said he did not turn his mind to the possibility of fractures when prescribing for the plaintiff over the period of eight months. Nor, indeed, did he apply his mind to the issue of osteoporosis (T 720). He did, however, say that he knew in 1992 that glucocorticoids caused osteoporosis and he agreed that compression fractures were recognised as an adverse effect of corticosteroids.

106 Dr Hosking did not consider that Plaquenil would have made a significant difference. He appreciated that it was available for use in 1992 in conjunction with steroids but it had side effects affecting the eyes and it also caused nausea. He considered it was useful in treating lupus without the complication of renal involvement and where there was little skin involvement. The defendant used this drug after the spinal fractures were sustained. He said it was his objective before then to lower the steroid dose as quickly as possible and he did not believe Plaquenil would have helped him to do this (T 747).

107 So 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 (T 749-750).

108 Again, as with the other doctors, I shall return to consider particular aspects of the defendant’s evidence in the context of assessing the various allegations of negligence pressed by Mr Donovan.

The negligence alleged

109 In the course of the hearing Mr Donovan was asked to particularise the negligence relied upon by the plaintiff. Particulars, many of which were of a general nature, were provided. There were in all seventeen matters identified. However, the plaintiff’s case was brought into sharper focus in final submissions, and I do not propose to address those seventeen matters seriatim. As I understand it, the plaintiff finally contends that the defendant was negligent in the respects which I now summarise:

(i) failing to adopt appropriate measures to reduce the high doses of corticosteroids during the period of treatment prior to the plaintiff’s admission to hospital on 24 August 1992;

(ii) failing to address the plaintiff’s weight loss;

(iii) failing to prescribe calcium, vitamin D and oestrogen supplements;

(iv) failing to advise exercise;

(v) failing to monitor bone mineral density

110 I propose to deal firstly with matters (ii), (iii), (iv) and (v).

Failure to address the plaintiff’s weight loss

111 As at 2 January 1992, Dr Donald advised Dr Almeda that the plaintiff weighed 50.5 kg and I accept that to have been the plaintiff’s weight at that time. I also accept that that was her weight when Dr Donald advised the defendant to that effect on 20 January 1992. However, I am satisfied that the plaintiff’s weight subsequently fell. Dr Nanra noted the plaintiff’s weight at 44 kg as at 6 March 1992. I accept that on 9 March 1992, at a consultation between the defendant and the plaintiff attended by the plaintiff’s parents, the plaintiff’s mother expressed concern about the plaintiff’s weight loss and raised the question as to whether a dietician should be consulted. I also accept that at that consultation the defendant advised that this would not be necessary.

112 I am satisfied that on 11 May 1992 the John Hunter Hospital notes record the plaintiff’s weight as being 43.30 kg. On 13 July 1992 the plaintiff’s weight had dropped to 40.80 kg and on 10 August 1992 it had fallen to 39.4 kg. As I observed earlier, it was on 10 August 1992 that the defendant first personally recorded the plaintiff’s weight. The defendant frankly acknowledged he did not recall whether he had noticed any drop in weight before 11 May 1992 (T 755).

113 The drop in weight above reviewed was significant. Whilst the usual effect of corticosteroids was to bring about a weight increase, the defendant attributed the loss to the lupus disease (T 657-8 and T 752). The defendant said he was more worried about the plaintiff’s kidneys than her weight (T 658), but I am persuaded by the evidence of Dr Sutherland (T 309-310), Dr Champion (T 524) and Professor Sturgess (T 860) that the weight loss should have been investigated. I accept the evidence that malnutrition of itself can be a cause of osteoporosis.

114 However, the cause of the plaintiff’s weight loss in that period was never ascertained and the evidence does not permit of a finding that had the cause of the loss been established some effective measure could have been undertaken to reverse it. There are references in the hospital notes (Exhibit L) to deficiencies in the plaintiff’s diet in the period following her admission in August 1992: see notations of 26 August 1992, 27 August 1992 and 10 September 1992. The dietician’s notes suggest that the plaintiff was avoiding all dairy products and fats and that her diet was high in fruit, vegetables and wholemeal bread and that she chose lean meat. However, the plaintiff’s evidence (T 33) was that before she went to hospital she had been eating dairy foods and fats and that she “in no way omitted dairy products from her diet”. Mrs Rufo was asked (T 280) about the plaintiff’s eating habits, and could not recall her daughter avoiding any particular foods. Mrs Rufo said that the plaintiff “would always have milk and cereal and porridge and things” and Mrs Rufo cooked the evening meals. The evidence does not permit me to conclude that the plaintiff’s eating habits accounted for the weight loss to which I have referred and, indeed, Professor Clancy said in evidence (T 937):

“We have been trying to find out why [the weight loss] for six or seven years and we haven’t come up with the answers.”

115 Absent any evidence that the weight loss could have been effectively addressed, had it been investigated as I find it should have been, the weight loss remains a relevant matter in that it was a factor that ought to have been taken into account in assessing the vulnerability of the plaintiff to osteoporosis. I shall return to this when looking at matter (i).

Failing to prescribe calcium, vitamin D and oestrogen supplements

116 I referred earlier to the opinions of Dr Sutherland and of Dr Champion as to the desirability of calcium and vitamin D being introduced into the regime of the plaintiff’s treatment.

117 In his oral evidence, Dr Sutherland opined that their introduction would have delayed osteoporosis (T 307). Dr Sutherland also said (T 308):

“I have no doubt from the reading of the literature that by 1992 calcium supplementation was regarded as a necessary part of any long term oral corticosteroid therapy.”

118 However, he added as to vitamin D, that

“the first position paper from an authoritative body saying you must give vitamin D did not come out until…1996.”

119 Dr Champion said (at T 375), referring to papers on the matter, that

“although the evidence was modest for calcium and vitamin D, the theoretical basis for it was reasonable and, hence, it was a definite recommendation in medical practice where glucocorticoids were used in sufficient dose for sufficient duration and that was fairly widely known, though it would be fair to say not by any means universally applied. So there was this strong guideline in the general medical literature but was it being applied generally in medicine? Not - not enough. And was it being applied in paediatrics in those contexts? Probably very little.”

120 Later (at T 420), Dr Champion conceded that proof of the efficacy of vitamin D and of calcium was minimal in 1992 and Dr Champion agreed (T 422) that it was not the practice in 1992 for specialists treating children with lupus to use calcium and vitamin D supplements.

121 Further (T 425), Dr Champion conceded that he would not criticise the defendant as providing an unreasonable standard of care in not prescribing calcium and vitamin D for the plaintiff in 1992.

122 Then (at T 440-441) Dr Champion agreed that vitamin D was not a matter of concern if the plaintiff did not avoid sunlight and she had a normal diet.

123 Professor Sturgess would not have prescribed either calcium or vitamin D. He said it was not routine to prescribe calcium and vitamin D in 1992 (T 866-867), and Professor Sturgess, in a report of 29 March 2001 (part of Exhibit 8), referred to a review touching upon the issue of the effectiveness of calcium and vitamin D therapy to prevent osteoporosis and kyphosis. That review indicated that calcium and vitamin D therapy does not reduce fracture rates in patients treated with steroids over two years. I referred earlier to what Professor Sturgess wrote on 11 January 2000 where he stated he would not have prescribed calcium or vitamin D.

124 Professor Clancy does not consider vitamin D or calcium would have been effective preventative therapy. In his letter to the defendant’s solicitors dated 13 July 2000 he expressed his opinion to that effect, supporting it with results of a literature search.

125 Accepting as I do the evidence given by the plaintiff and her mother as to the plaintiff’s eating habits (para 114 above), I accept that the plaintiff was following a normal diet in 1992 up to the time when the fractures occurred.

126 Having regard to the evidence I have reviewed, I am not persuaded that the defendant was negligent in failing to prescribe calcium and/or vitamin D. I accept that in introducing no such prescription he did not depart from what at that time was perceived to be reasonable practice in the circumstances.

127 The plaintiff had had two periods before the introduction of the corticosteroids and then her periods stopped. This matter was brought to the attention of the defendant at either the consultation on 27 February 1992 or the consultation on 9 March 1992. Dr Champion explained (T 363) that the cessation of the periods indicated “insufficient sex hormone production and function, particularly oestrogen”. This could have been due to the lupus itself, to the plaintiff’s weight loss or to the influence of the corticosteroids. In Dr Champion’s opinion (T 364) this inadequate production could have impeded bone development and contributed to the risk of osteoporosis.

128 In May 1993, because of the plaintiff’s perceived hypogonadism, Professor Clancy advised hormonal replacement with the oestrogen Premarin. It was Dr Champion’s opinion (his report of 2 December 1998) that the defendant should have reviewed the plaintiff’s oestrogen status and considered its supplementation, and Mr Donovan submitted the defendant was negligent in failing to do so.

129 I am not persuaded that this is the case.

130 Whilst Dr Champion said (and I summarise his evidence, T 365) that these days hypogonadism would be a strong indication for prescribing oestrogen, he acknowledged that in 1992 it was perceived that oestrogen might be adverse for the disease activity of lupus.

131 To the like effect Dr Champion wrote (report 22 April 2000, p 5):

“The issue of oestrogen supplements is a difficult one and in 1991-2, even in a hypogonadal patient with osteoporosis, there would have been reservations re oestrogens. On the one hand, it would have been agreed that it was important therapy, but on the other hand there would have been slight risk of thrombosis and concerns expressed about possible exacerbation of the lupus. Currently as reflected in the abovementioned paper in the introduction, the case for prescribing oestrogen would be a good deal stronger than according to 1991-2 knowledge.”

132 In cross examination Dr Champion, in addressing medical thinking in 1992, acknowledged that there was then a prevalent notion that the administration of oestrogen to a woman would have a deleterious effect and he acknowledged further (T 448-449) that in 1992 it was reasonable to refrain from prescribing oestrogen to the plaintiff, even though he felt such restraint fell short of “optimal management”.

133 Professor Sturgess, in his report of 11 January 2000 (part of Exhibit 8), wrote:

“It would not be standard practice to prescribe oestrogen supplements to a fifteen year old lupus patient. Many experienced doctors, myself included, would be reluctant to start oestrogen in the acute phase of a SLE patient’s illness. As it later transpired, this patient was already at risk of thrombosis.”

134 Consistently with that expression of opinion, Professor Sturgess gave evidence (T 872):

“…we’d never give oestrogen to a young person, especially someone with lupus because we worry it actually makes lupus worse and in particular we think it increases the risk of thrombosis which this patient has a particular antibody making them particularly prone to thrombosis, meaning blood clots, so we’d rarely, if ever, given oestrogen to a woman with lupus.”

135 Professor Clancy’s opinion accorded with that of Professor Sturgess. He considered that the non production of oestrogen would be a small contributing factor to the risk of bone loss (T 937) but said for a whole variety of reasons that he would not introduce hormone replacement therapy in an acute situation such as that which confronted the defendant.

136 Accepting as I do the evidence of Professor Sturgess and of Professor Clancy reviewed above, and recognising the concessions made by Dr Champion on this issue, I do not consider that the defendant failed to exercise reasonable care in not considering the introduction of oestrogen as part of the regime of treatment of the plaintiff before her admission to hospital in August 1992.

Failing to advise exercise

137 Dr Sutherland said (T 319) that it was recommended in 1992 that people on high corticosteroid doses should exercise, because exercise had the potential to increase bone density and minimise the cushingoid effect of the corticosteroids.

138 In his report of 2 December 1998 Dr Champion pointed to a physical activity programme as being a matter to be addressed in the prevention and management of osteoporosis in an adolescent girl who was receiving corticosteroids. In his evidence (T 364), Dr Champion said that the management of lupus required (inter alia) physical well being and activity.

139 Professor Sturgess wrote (11 January 2000) that he would not have prescribed exercise for the plaintiff, stating:

“In a normally active fifteen year old no-one would ‘prescribe’ an exercise program.”

140 The defendant noted at the time of his consultation with the plaintiff on 3 February 1992 that the plaintiff was “doing plenty of exercise”. He acknowledged in evidence (T 774) that he made only that note about exercise but since the plaintiff was going to school this involved doing “a modicum of exercise”. He considered it would be unusual to prescribe an exercise programme for a patient who was attending school, and it seems to me that this thinking was entirely consistent with the opinion of Professor Sturgess.

141 I am not persuaded, having considered all the evidence in point, that the defendant was negligent in failing to define some specific exercise regime for the plaintiff at any time before the fractures occurred.

Failing to monitor bone mineral density

142 The defendant arranged no programme for the monitoring of bone mineral density for the plaintiff between February and August 1992. Was he negligent in this omission?

143 According to Dr Sutherland (T 312-3), he was in the habit of undertaking bone densitometry studies in persons on long term corticosteroids at that time, but he “could not find practice guidelines mandating that”, and the available technology then was not as good as that now available. Dr Sutherland was not in private practice in 1992 but was at that time director of the Department of Clinical Immunology at Royal Newcastle Hospital.

239 Even if one takes the lower of the above time estimates expressed in cross examination, it seems to me there would have been minimal opportunity, according to Professor Sturgess, to lower the corticosteroid dose between 10 June and 24 August.

Professor Clancy

240 Professor Clancy was also of the opinion that the introduction of Imuran would not have permitted of the immediate reduction of the corticosteroid dose. Professor Clancy considered it would be four to six weeks before there would be any benefit from introducing Imuran. He responded to the following question with the following answer (T 890):

241 Later in his evidence (T 898), Professor Clancy said he would like to think he could reduce the dose of Prednisolone (after the above time lapse) by 5-10 mg per month. It would follow from this that assuming Imuran had been introduced about 10 June 1992 it would not have been until the middle of July at the earliest that the dose of Prednisolone could have been reduced by reason of such introduction. It is difficult to see how on this timetable the introduction of Imuran would have reduced the Prednisolone dose, had the plaintiff remained on that drug, much below 40 mg by the time the spinal fractures occurred.

242 This certainly seems to be the view of Professor Clancy considering the following evidence given by him (T 897-898):

“A. …..Firstly, had she continued at 60 milligrams of Prednisolone, even with the introduction of Imuran, and taking into account the symptoms that she had exhibited both before and during this period - if I can remind you of the flu like symptoms in July - to what extent within reasonable bounds would you be aiming for in terms of a reduction of the dose of Prednisolone per day from 1 June to the end of August?

HIS HONOUR: Assuming the introduction of Imuran on 1 June?

HIGGS: Q. Yes, assuming the introduction of Imuran?
A. Over that timeframe the Imuran would not make much difference. That is assuming that Imuran has as much steroid saving effect at these high doses, compared with the much lower doses that we have our experience with. I have commented on that. This is a clinical decision which has got to be focused on on a particular individual. Given the fact that she had known sustained activity, activity that was enhanced in the presence of respiratory tract infections, I would be extremely cautious, very wary, I certainly didn't want to see an exacerbation, given the comments we made before. Over that period, we are talking six, seven, eight weeks, is it?

Q. I think it is about twelve weeks from 1 June to the end of August. It is June, July, August, three months.
A. And we are on say 60 milligrams of Prednisolone, or 65 equivalent?

Q. Say she didn't switch to the Dexamethasone, she is on the 60 milligrams of Prednisolone. Can you give us an idea, in terms of each month or fortnight or whatever, that you would be aiming for in terms of within reasonable bounds in terms of reducing the Prednisolone?
A. Okay, I think if you could get to the mid 40's or something like that over that timeframe you would be doing well and that would be cautious and reasonable. Of that order anyway. I mean it is a very variable thing.

Q. That is with Imuran?
A. That's with or without Imuran. I truly don't believe Imuran would, in this circumstance, make a substantial difference. Not in that timeframe.

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. Say, for example, compared to what you would have hoped for, the doctor treating Miss Rufo at the time did not switch her to Dexamethasone, and continued her on Prednisolone. In the symptoms which presented, including the flu like symptoms in the middle of July, he aimed at reducing her at the rate of no more than 5 milligrams a month. I appreciate that you might have a different view, but are you able to express an opinion as to whether or not that regime would have fallen within the bounds of reasonable practice?
A. Yes, and was consistent with what could be done in the clinical scene at the time.

243 On my analysis of the evidence, I consider it unlikely that the introduction of Imuran on about 10 June 1992 would have achieved a reduction of the corticosteroid dose below 30 mg of Prednisolone or its equivalent, and, indeed, the dose may still have been closer to the equivalent of 40 mg of Prednisolone. (The plaintiff was in fact taking 6 mg of Dexamethasone as at 24 August and that was the equivalent of 40 mg of Prednisolone.)

244 Having reviewed and reflected upon all the relevant medical evidence on this question (not of course limited to the extracts above set out), I am not persuaded on the balance of probabilities that had Imuran been introduced when I find it should have been on 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.

245 Whilst the plaintiff’s primary submission was that the evidence established on the balance of probabilities that the defendant’s negligence caused the fractures, or at least resulted in the fractures being worse than they otherwise would have been, it was also submitted on behalf of the plaintiff that the defendant’s negligence deprived the plaintiff of the loss of a chance of a better outcome from the steroid related osteoporosis and the resultant fractures. In response, the defendant submitted that even if, contrary to his principal submissions, breach of duty of care and causation were established, there was no evidence upon which the loss of a chance could be quantified. Alternatively, it was submitted that any loss of chance was “miniscule”.

246 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).

247 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.

248 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?

249 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.

250 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.

The introduction of Dexamethasone

251 Was the prescription of Dexamethasone causative of harm?

252 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.)

253 Had Dexamethasone not been introduced when it was, it would have been necessary for the plaintiff to have continued on Prednisolone and it is probable, subject to a qualification to which I shall refer, that the doses of Prednisolone would have been those expressed as the equivalents I have set out above. The qualification is that the introduction of Imuran in June could have led to reduction of the corticosteroid dose, but I have considered this earlier. Had Imuran enabled the reduction of the corticosteroid level, this would have applied to Dexamethasone or Prednisolone. 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.

254 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.

255 The review of the medical evidence earlier recorded (paras 177-214 above) reveals the marked difference of professional opinion between Dr Champion on the one hand and Professor Sturgess, Professor Clancy and the defendant on the other hand as to the relevant properties of Dexamethasone. 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.

256 Dr Champion was asked to address this very question (T 407):

257 The plaintiff’s case on this issue derives no support from Dr Sutherland who, as I understand his evidence, did not regard Dexamethasone as being more harmful than Prednisolone in terms of causing bone loss. I refer to evidence that Dr Sutherland gave when asked to consider the defendant’s decision to introduce Dexamethasone (T 324-325):

258 Dr Bleasel referred to Dexamethasone as being “sharper and more dramatic” in its effect than Prednisolone. His own experience of its use was short term and he used that expression in terms of use over a period of four or five days. Dr Bleasel expressed his puzzlement at the defendant’s decision to change from Prednisolone to an equivalent dose of Dexamethasone, and having done so was asked these questions and gave these answers (T 265):

259 It would not appear from the above responses that Dr Bleasel held a different opinion from the experts called in the defendant’s case as to whether or not the prescription of Dexamethasone carried with it an increased risk of osteoporosis compared with the risk accompanying the prescription of Prednisolone.

260 It was the defendant’s view that the Dexamethasone was no more harmful in the doses he prescribed than Prednisolone would have been in the doses of that drug he would have prescribed in the event that the plaintiff had remained on it (see paras 193-194 above).

261 Professor Sturgess did not consider that the change to Dexamethasone altered the outcome as to the progress of the osteoporosis and the occurrence of the fractures (T 836-837). Nor did Professor Sturgess consider that Dexamethasone had a different effect from Prednisolone on the plaintiff’s bones. In response to this question Professor Sturgess gave this answer:

262 Professor Sturgess did not see a necessary relationship between proximal myopathy (which became significant in July 1992) and osteoporosis (T 842).

263 In the course of cross examination Professor Sturgess was asked about the changes in appearance which seemed to occur rapidly after the introduction of the Dexamethasone. Professor Sturgess did not consider that these changes were to be attributed to the Dexamethasone but rather to the build up of the corticosteroid effect over the entire period of treatment. Professor Sturgess was asked these questions and gave these answers (T 844-845):

264 Professor Sturgess stressed the need to distinguish between the potency and the efficacy of a drug, and said (T 846):

“We do have to distinguish between potency and efficacy. So a drug is more potent if milligram for milligram comparison says it is more effective. But we adjust for that so that the efficacy of the drug, once you adjust the doses, can be the same efficacy of two drugs, even though one is more potent than the other.”

265 Turning to Professor Clancy, it was his opinion that the risk of osteoporosis associated with the use of Dexamethasone was no greater than that associated with the use of an equivalent dose of Prednisolone. Moreover, even assuming, as Dr Champion opined, and contrary to Professor Clancy’s opinion, there was a relationship between the suppression of the HPA axis and osteoporosis, Professor Clancy still did not consider that the changeover from Prednisolone to Dexamethasone would have increased the risk of osteoporosis in the time frame from June to August (T 897). I referred earlier to the evidence given as to these matters at T 893-894 and T 896-897, and to this see paras 210-211 above. I will not repeat those extracts from the transcript.

266 In Professor Clancy’s opinion there is no relationship between the plasma half life of a drug and its effect on tissue function. Professor Clancy said this (T 944):

267 I have considered closely the evidence of the witnesses called in the defendant’s case to see whether there is support for the expression of opinion of Dr Champion that there was a slight increase in the risk of osteoporosis and fractures brought about by the use of Dexamethasone. I find no such support in the evidence of the defendant, Professor Sturgess or Professor Clancy.

268 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.

269 Indeed, it is the opinion of Professor Clancy that the plaintiff has celiac disease and in his opinion this was a major factor in the progression of the osteoporosis to fractures. Professor Clancy’s evidence as to celiac disease was as follows (T 904-906):

“Q. Doctor, in your reports, you mention celiac disease as being something which, in your opinion, Miss Rufo suffers from?
A. That's correct.

Q. As I understand it, initially when you made that diagnosis, there was some debate, if I can describe it that way, as to whether or not that particular diagnosis was correct, is that right?
A. There was no clinical debate, no.

Q. What is the basis for that diagnosis?
A. The basis is, firstly, the presence of a specific antibody called IGA antigliadin antibody which has a - it is a special antibody which has a 90 to 92 percent sensitivity and specificity for the diagnosis. Secondly, she had malabsorption involving all the usual things that can be malabsorbed which could not be explained in any other way, that is B12, iron - vitamin B12, iron and folic acid. Thirdly, she had a biopsy at a time when she was on fairly heavy immunosuppression, by Methotrexate and Imuran, which was abnormal but did not show the loss of the height of the villus which are the folded lining of the mucosa of the small bowel almost certainly because of the suppression by the drugs she was on at the time that didn't stop the cells being there that caused the problem but stopped the cells secreting the hormones that caused the problem and, fourthly, she did very well on a gluten-free diet, which is the test with practically or nil complete loss of the abnormal antibody which is what you would expect in a person with celiac disease, so when you put these things together again, the celiac disease has undergone transformation. It used to be thought of as someone who had flat mucosa, somebody who had all sorts of gut symptoms, but recently with the demonstration of these new diagnostic tools, we are finding it is present in about one in 150 people, it is more common in people with lupus and we are finding much more subtle presentations, clinical presentations.

Q. You have said that the tests are new. Were these tests that were used in order to make the diagnosis, which I think that you made some time after 1997, from memory, were they tests that were available in 1992?
A. No, no.

Q. When she, that is Miss Rufo, came under your care in 1993, were you mindful or on the lookout for malabsorption problems in view of her previous history?
A. Not - not particularly, no. Not particularly because she - no, not particularly at that time.

Q. And, in any event, one of the things that prompted you to undertake tests for celiac disease, amongst other things, was the result of a bone density study that is referred to in one of Dr McGill's reports of 2 October 1997 that showed at that time, under your care, with minimal prednisolone being prescribed, a minor decrease even at that time, a minor further decrease in her bone mineral density?
A. Yes, that's right. There were this combination of malabsorption indices.

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.

270 In cross examination, Professor Clancy acknowledged he was aware that Dr McElduff, an endocrinologist to whom he referred the plaintiff, does not agree with the diagnosis of celiac disease.

271 It was put to Professor Clancy that he introduced the diagnosis of celiac disease to assist the defendant. That the professor denied and I have no reason to doubt the sincerity of the opinion which Professor Clancy has formed to the effect that the plaintiff has celiac disease. 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.

272 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.

273 Mr Donovan submitted that the conclusion was warranted that the changes in the plaintiff’s appearance noted after the plaintiff changed from Prednisolone to Dexamethasone should be attributed to the impact of the latter drug. In this connection there was the myopathy first recorded by Dr Hosking on 10 August 1992, but which Mr Donovan submitted I should find became manifest shortly after the introduction of Dexamethasone. The plaintiff complained that she had “twig legs” by 22 June, which, of course, was only fourteen days after the plaintiff started to take Dexamethasone. Earlier I recorded my finding that there was probably muscle wasting present by 13 July (see para 37 above).

274 The evidence of Professor Sturgess referred to earlier (see para 263 above) seems to me to stand in the way of Mr Donovan’s submission and I see no reason to reject this evidence of Professor Sturgess. I find no contradictory evidence from Dr Champion. I understand it to be common ground between the experts that the corticosteroids which the plaintiff took from the time her 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.

275 Nor does the evidence establish to my satisfaction a direct relationship between myopathy and bone loss. Professor Sturgess did not see any necessary link between the two, although both evidenced “the deleterious effects” of steroids. A patient could, in the opinion of Professor Sturgess, have a lot of osteoporosis and quite good muscles, and vice versa (T 842). According to Dr Champion, generally speaking maximal bone loss referable to corticosteroids occurs “within the first few months” of treatment (T 370 and T 524). To the like effect, Dr Sutherland considered that the most rapid loss of bone density occurred in the first five months of the disease (T 601). As Mr Higgs submitted, if there was necessarily a relationship between bone loss and myopathy, the latter ought to have been detectable in those early months.

276 I find on the evidence that there have been no studies carried out to determine whether there is any difference in the effect that Dexamethasone would have upon bone loss compared with the effect of an equivalent dose of Prednisolone. (I use “equivalent” in the sense previously considered and by reference to the Cassidy and Petty table set out at para 190 above.) I am faced with a divergence of medical opinion on the issue between experts, all of whom I have assessed as being impressive, honest and highly qualified. After lengthy consideration of this issue, I am not persuaded that I should prefer the evidence of Dr Champion that the use of Dexamethasone made the plaintiff’s outcome worse, albeit only “slightly”, to the contrary evidence relied upon by the defendant and reviewed above. 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 the spinal fractures that occurred beyond that which would have accompanied the dosages of Prednisolone that the plaintiff would otherwise have taken.

277 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. This follows from the conclusion expressed in para 276.

278 The evidence establishes that the plaintiff has endured much pain and suffering since August 1992 and I accept that the plaintiff’s disabilities since that time have had and will continue to have a marked impact upon the plaintiff’s lifestyle and her ability to pursue gainful employment. However, it follows from the findings I have reached that the plaintiff 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.

279 Accordingly, the plaintiff’s claim must fail and judgment is to be entered in favour of the defendant.

280 I will reserve costs to afford the parties the opportunity to make submissions on this question.

Formal orders

281 1. Verdict and judgment for the defendant.

**********

Last Modified: 11/07/2002

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Citations

Rufo v Hosking [2002] NSWSC 1041

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CITATION:	Rufo v Hosking [2002] NSWSC 1041
CURRENT JURISDICTION:	Common Law Division Professional Negligence List
FILE NUMBER(S):	SC 20468/01
HEARING DATE(S):	24, 25, 26, 28 June, 1, 2, 4, 29, 30, 31 July, 1, 2, 20, 21, 22, 23 August 2002
JUDGMENT DATE:	6 November 2002
PARTIES :	Michelle Rufo (Plaintiff) Dr C.S. Hosking (Defendant)
JUDGMENT OF:	Studdert J

COUNSEL :	B. Donovan QC/ E. Pike (Plaintiff) D. Higgs SC/J. Lonergan (Defendant)
SOLICITORS:	Kells - The Lawyers (Plaintiff) Colin Biggers Paisley (Defendant)
CATCHWORDS:	Negligence - claim against medical practitioner - whether breach of duty of care - whether any breach causative of harm.
CASES CITED:	Rogers v Whitaker (1992) 175 CLR 479 Bolam v Friern Hospital Management Committee [1957] 1 WLR 582 Wyong Shire Council v Shirt (1979-1980) 146 CLR 40 Bendix Mintex Pty Limited v Barnes (1997) 42 NSWLR 307 Wallaby Grip (Rae) Pty Limited (in liq.) v Macleay Area Health Service (1998) 17 NSW CCR 355 E.M. Baldwin & Son Pty Limited v Plane 1999 ATR 81-499 TC v State of New South Wales [2001] NSWCA 380 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 Tran v Lam (unreported, Badgery-Parker J, 20 June 1997)
DECISION:	See para 281