Rufo v Hosking [2002] NSWSC 1041 (6 November 2002)

Last Updated: 15 November 2002

NEW SOUTH WALES SUPREME COURT

CITATION: Rufo v Hosking [2002] NSWSC 1041



CURRENT JURISDICTION: Common Law Division
Professional Negligence List

FILE NUMBER(S): 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: 06/11/2002

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

JUDGMENT OF: Studdert J

LOWER COURT JURISDICTION: Not Applicable

LOWER COURT FILE NUMBER(S): Not Applicable

LOWER COURT JUDICIAL OFFICER: Not Applicable

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.

ACTS CITED:


DECISION:
See para 281


JUDGMENT:


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

The defendant had had earlier discussion with Dr Donald concerning the plaintiff’s case but this was the date upon which the defendant began to treat the plaintiff. In assuming this responsibility the defendant had the advantage of access to Dr Donald’s records concerning the plaintiff and he also had pathology reports available which supported the diagnosis of lupus. The defendant wrote on 5 February 1992 to Dr Almeda that the plaintiff’s urine had shown a trace of blood on multistix and that micro urine testing was to be undertaken but from the point of view of his examination of the plaintiff on 2 February 1992 the doctor’s handwritten notes record that the plaintiff was asymptomatic. The defendant continued the dosage of 50 mg of Prednisolone per day previously determined upon by Dr Donald.

12 17 February 1992

The defendant recorded in his notes of this consultation that the plaintiff was complaining over the past few days of having a swollen face in the mornings and of being flushed and feeling hot. He also noted that the butterfly rash was prominent and that during the day the swelling went. It was at this consultation that a decision was taken to refer the plaintiff to a renal specialist, Dr Nanra. There was some issue as to whether the referral was undertaken at the initiative of the defendant or whether it was prompted by Mr and Mrs Rufo, both of whom gave evidence of attending that consultation and of the suggestion being made to the defendant that Dr Nanra be consulted. I do not find it necessary to decide whether the referral was at the initiative of Mr and Mrs Rufo or of the defendant. Dr Nanra was brought into the case and on 17 February 1992 the defendant increased the dosage of Prednisolone to 75 mg per day. I accept that his reason for doing so was that he considered the lupus recrudescent and that there was kidney involvement. The defendant reported to Dr Nanra in the letter of referral on 20 February 1992 that the plaintiff’s urine “continued to show red cells on multistix testing”.

13 27 February 1992

The defendant’s notes record that the plaintiff said she was feeling better than before and that the morning rash was not occurring. By the time of this consultation the dose of Prednisolone had been reduced to 62.5 mg per day after Mrs Rufo had reported a favourable response to the earlier increased dosage. The defendant noted that the plaintiff’s face had started to “fatten up”. The defendant wrote to Dr Almeda on 27 February following the consultation that day that he was “now convinced that [the plaintiff] is absorbing the Prednisolone”. The defendant recorded, however, that he was worried about the plaintiff’s renal function, not only because of the circumstance that there was blood in the urine on occasions but because of the creatinine clearance.

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

The plaintiff and her family had earlier lived in Dungog but by this time had moved into the Newcastle area and the plaintiff saw the defendant on this occasion at John Hunter Hospital. The plaintiff presented with a small pustule on the nose. An earlier problem of an ingrown toenail, to which reference was made in the doctor’s notes on 27 February 1992, had by this time settled. The defendant assessed the plaintiff to be improved and he decreased the dose of Prednisolone to 50 mg per day.

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

Dr Nanra reported to the defendant on 10 March 1992, having seen the plaintiff:

“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

By this time the defendant had received Dr Nanra’s report of 10 March 1992. The defendant noted that the plaintiff had had some upper lip hair depilated and that the ingrown toenail problem had settled.

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

On this date Dr Nanra wrote to the defendant, discharging the plaintiff back to the defendant’s care. Dr Nanra reported then (Exhibit 2) that the plaintiff had no evidence of renal disease, that she had no significant haematuria, no proteinuria, and that her renal function was “near normal”. Dr Nanra expressed his surprise

“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.

On this occasion the defendant noted that there was erythema at the base of the fingernails and of the toenails and that this had developed in the course of the past week. The areas affected were tender but not painful. The defendant recorded: “Everything else OK”. The defendant decided to keep the plaintiff at the then current dose of 40 mg of Prednisolone and wrote on 14 May 1992 that provided the erythema improved he was going to reduce the dose at the next consultation.

27 Hospital visit, 28 May 1992

The plaintiff developed a fever and an upper respiratory tract infection for which she attended at John Hunter Hospital and was seen by Dr Banna. It is recorded in the hospital notes that the plaintiff had increasing headache and increasing erythema, that she experienced facial flushing in the morning, and that she was tearful, with mood swings. Urinalysis raised suspicion about renal involvement. Dr Banna consulted with the defendant and the Prednisolone dose was increased to 60 mg per day.

28 1 June 1992

On this occasion the defendant saw the plaintiff at Maitland and recorded Mr Rufo’s concern about the plaintiff’s emotional lability, but the defendant in evidence said he had no recollection of how the plaintiff presented on that date. It did appear that the plaintiff had responded well to the increased dosage. The results of urine testing undertaken on 28 May were probably available to the defendant on this day but they did not indicate renal involvement, and, indeed, the doctor’s assessment (in evidence at T 669) was that the likelihood of renal involvement was “very low”. Had it been otherwise he would have referred the plaintiff to Dr Nanra.

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

The plaintiff saw the defendant at Maitland. Some fourteen days earlier, at the defendant’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 defendant, and as from 22 June 1992 the daily dose of Dexamethasone was reduced to 8 mgs.

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

Dr Miller reported on 29 June 1992 (Exhibit O). His report is a brief report and records nothing of any physical observations the doctor may have made. Reference is made in the report to the distress of Mr Rufo and to the intensity of the concern of the plaintiff’s parents. Dr Miller concluded his report:

“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

By this time the defendant had the psychiatric assessment of Dr Miller contained in the report of 29 June 1992 (Exhibit O).

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

On 20 July 1992 Dr Miller reported on a second consultation with the plaintiff and her parents, and it seems there had been an improvement in the plaintiff’s symptoms. The doctor noted the parents’ assessment to that effect. Dr Miller considered the plaintiff should remain on the medication he had prescribed for her in June for six months, and that there was no need for the plaintiff to see him again. The report contained no record of the plaintiff’s physical presentation, but Dr Miller did note that the plaintiff complained of having “jelly legs”.

40 21 July 1992 – Dr Kamal

The plaintiff saw Dr Kamal on 21 July 1992, but the doctor’s note of this visit is not revealing. The only note reads: “SLE (systemic lupus [sic] erythrematosis)”.

41 10 August 1992

Dr Hosking saw the plaintiff at the hospital and by this time her weight had fallen to 39.4 kilograms compared with her weight of 50.5 kilograms on 2 January 1992. It is to be observed that the first time the defendant personally noted any weight loss was in the hospital notes for 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.

The hospital notes record that back pain had been present for the past month, worse with movement but relieved by rest. The plaintiff was kept in hospital overnight.

48 Admission to hospital, 24 August 1992

I accept that the plaintiff experienced extremely severe back pain at home on 24 August 1992 and was taken to John Hunter Hospital and admitted. This time the plaintiff was in hospital for more than one month, being discharged on 25 September 1992. The hospital records reveal that the plaintiff had suffered vertebral microfractures and kyphosis of the spine. It is probable that the fractures accounted for the acute episode on that day, and that they occurred on or about 24 August 1992. For her back condition the plaintiff was treated by Dr Ho.

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] HCA 58; (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):

“In Australia, it has been accepted that the standard of care to be observed by a person with some special skill or competence is that of the ordinary skilled person exercising and professing to have that special skill. But, that standard is not determined solely or even primarily by reference to the practice followed or supported by a responsible body of opinion in the relevant profession or trade (See, e.g. Florida Hotels Pty Ltd v Mayo [1965] HCA 26; (1975) 113 CLR 588 at pp 593, 601). Even in the sphere of diagnosis and treatment, the heartland of the skilled medical practitioner, the Bolam principle has not always been applied (See Albrighton v Royal Prince Alfred Hospital [1980] 2 NSWLR 542, at pp 562-563 (case of medical treatment). See also E. v Australian Red Cross [1991] FCA 20; (1991) 27 FCR 310, at p 360. Further, and more importantly, particularly in the field of non-disclosure of risk and the provision of advice and information, the Bolam principle has been discarded and, instead, the courts have adopted (Albrighton v Royal Prince Alfred Hospital, [1980] 2 NSWLR at pp 562-563; F v R (1983) 33 SASR 189, at pp 196, 200, 202, 205; Battersby v Tottman (1985) 37 SASR at pp 527, 534, 539-540; E v Australian Red Cross (1991) 27 FCR at pp 358-360) the principle that, while evidence of acceptable medical practice is a useful guide for the courts, it is for the courts to adjudicate on what is the appropriate standard of care after giving weight to “the paramount consideration that a person is entitled to make his own decisions about his life (F v R (1983) 33 SASR at p 193)”

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 [1980] HCA 12; (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:

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.”

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:

“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 unreasonable?
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.”

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.

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 preventative 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.”

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

“In addition there is some confusion about dexamethasone and whether it should have been used. The key point here is whether dexamethasone is any more or less harmful than prednisolone when used in equally effective immunosuppressive doses. Dr Hosking states in his letters that he changed to dexamethasone for several reasons including a concern that prednisolone was not being sufficiently effective. He changed from 40mgs prednisolone daily to 9mgs then 8mgs dexamethasone per day. 8mgs dexamethasone is approximately equivalent (in anti-inflammatory potency) to 40-50mgs prednisolone daily so that the effect of the change was not to increase the effective corticosteroid dose by any significant degree. I am not aware of any evidence that dexamethasone is any more likely to lead to osteoporosis than prednisolone provided that they are used, as Dr Hosking did, in therapeutically equivalent doses. I have had occasion to use long term dexamethasone on 2 occasions. Neither case behaved any differently to patients treated with prednisolone.”

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):

“With respect to your letter to me of the 16th April, you essentially raised three issues. The first was with respect to Dr Nanra’s records of the 13th April where he stated ‘no evidence of renal disease at present’. That, in fact is exactly the case. Renal disease was present prior to this and presumably remitted in response to the therapy given. Therapy in lupus for renal disease has always been a controversial area with most patients being treated by most doctors with steroids and cytotoxic medication, for periods considerably in excess of those when clinical indices of renal disease are present. It must be understood that such indices are not a highly sensitive indicator of pathology within the kidney and that concept underpins the practice that is taken. Many physicians thus would have treated this patient in exactly the same way as she was, given the considerable concerns that are attached to the presence of continuing and/or progressive renal inflammation.

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

(vi) prescribing Dexamethasone.

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

(ii) 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).

(iii) 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.

(iv) 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.

(v) 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.

144 In his report dated 22 April 2000 Dr Champion stated that it was not usual practice to perform bone density monitoring in fifteen year old lupus patients in 1991-92, and he gave the reason that “there were insufficient normative data”.

145 Dr Champion acknowledged in evidence (T 365 and T 448) that there was a practical difficulty in 1992 in measuring bone mineral density because bone densitometry was not then widely available.

146 Professor Sturgess reported on 11 January 2000 that it was not usual in 1992 to perform bone density monitoring in fifteen year old lupus patients, in whom “osteoporotic fractures are so very uncommon”. In oral evidence this witness said (T 838) that bone density measuring was not available in 1992. Later (T 871-872), Professor Sturgess said this:

“My own hospital did not have a densitometer in 1992, and I’d be surprised if there was one at Newcastle Hospital. There may have been, but I’d be a little surprised, and then again we wouldn’t normally do it when we were just starting off. To do lots of densitometry, measuring bone density, we started with post menopausal women who were at the highest risk, so speaking just for myself, it would have been several years after densitometry became available that I was doing it on younger people. Now there’s lots of machines, it’s easier to get, it’s quite cheap, so now we tend to do it on many many people on prednisone. In 1992, if you could get it I think it would have only been on post menopausal women.”

147 Professor Clancy gave evidence (T 907) that the defendant was not unreasonable in not monitoring bone density, as this procedure was not available as a reliable and useful clinical tool at the time. Professor Clancy added that this was brought in on an experimental basis in Newcastle. While he initially said he thought the experimental introduction was after 1992 he conceded in cross examination that the introduction could have been in 1992 and, of course, Dr Sutherland had access to the relevant facility in that year.

148 Nevertheless, the evidence does not establish that there was generally available any relevant facility in Newcastle in 1992.

149 The evidence falls far short of satisfying me that the defendant was negligent in not monitoring the plaintiff’s bone mineral density in 1992. I find that it was not normal practice to perform such monitoring in young lupus patients in 1992 and I find further that there was insufficient normative data to be applied in any event. In addition, I am not satisfied that there was available to the defendant ready access to some facility for monitoring to be carried out.

150 I return to matter (i)

(i) Failing to reduce the high doses of corticosteroids

151 As events transpired, the plaintiff was on high doses of corticosteroids for a period of seven and a half months before the fractures occurred. It was submitted that the defendant was negligent in continuing with those high doses, and in not introducing an alternative strategy. In particular it is contended that steroid sparers should have been prescribed and that their timely introduction would have allowed the defendant to reduce the doses of corticosteroids and thus to have reduced the progress of osteoporosis. Whether the fractures would have been avoided by the use of steroid sparers is a matter that will require close consideration, but first I propose to consider whether the exercise of due care by the defendant should have led to the introduction of steroid sparers, and if so when.

152 Mr Donovan submitted that Plaquenil and Imuran should have been prescribed, and prescribed as early as February 1992. Had this been done, the defendant would have been able to reduce the doses of corticosteroids significantly.

153 Reliance is placed upon the evidence of Dr Sutherland and of Dr Champion, and I will not repeat what I have already recorded as to their respective opinions but I will nevertheless add to what I have written.

154 In Dr Sutherland’s opinion, the use of Plaquenil should have been considered as early as 17 February 1992 (T 303), at which time there had been a pleasing response to the Prednisolone. Dr Sutherland considered there was a fifty percent chance that such introduction would have achieved a major reduction in the steroid dose (T 304), but if it failed, then by May it would have been appropriate to use another steroid sparing agent, namely Imuran (T 304).

155 As Dr Sutherland made clear in his first report dated 13 September 1994, he considered it was necessary first to bring the kidney disease under control before making a vigorous attempt to withdraw the reliance upon corticosteroids. Further, it was his understanding that this point was reached in March 1992 when the results of the tests Dr Nanra ordered on 6 March 1992 became available. Dr Sutherland regarded Plaquenil as particularly useful for skin problems. Then once Dr Nanra reported in May 1992 that there was no active renal disease, and he discharged the plaintiff from his care, it was Dr Sutherland’s opinion that Imuran should also have been introduced. I referred earlier though to the concessions made by Dr Sutherland in the course of cross examination.

156 Dr Champion said that had the plaintiff been managed at Sydney Children’s Hospital, Plaquenil would have been introduced at the start of treatment and he said that Imuran would have been considered once the renal effects of the lupus were known (T 376). Dr Champion considered since there was renal involvement, the 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 (T 379).

157 Dr Champion was taken to a passage in Cassidy and Petty, 2nd ed., which expresses caution as to the use of immunosuppressive drugs (and Imuran is such a drug). The defendant also referred to this text and it is appropriate to record here what the authors said (at p 77):

“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 immuno-suppressive 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.”

158 Dr Champion did not agree with the use of the word “experimental” in the above extract. In his opinion, 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 (T 397-398).

159 In Dr Champion’s opinion the plaintiff should have been prescribed Plaquenil by January or February and Imuran as soon as kidney involvement was detected (T 401), and certainly after the flare up in May (T 496).

160 In cross examination Dr Champion conceded that the medication provided up to 11 May 1992 was “within the bounds of reasonable practice” (T 466). However, it was the opinion of Dr Champion that the flare up in May required, at that time “in the exercise of reasonable treatment”, the introduction of Imuran and also of Plaquenil (T 497). When pressed, Dr Champion disagreed with the proposition that it was reasonable to continue for another two months after that time without introducing Imuran (T 508).

161 I have referred already to the evidence of Professor Sturgess, but I add to that review. Professor Sturgess regarded Plaquenil as good for skin disease and joint pains but not for kidney involvement (T 826). Professor Sturgess said that he did not regard either Plaquenil or Imuran as appropriate initial therapy (T 825), although I am mindful in the earlier reference to the report of Professor Sturgess there appears the statement that Professor Sturgess may have used Plaquenil, but he would not have expected much from it. Professor Sturgess said he regarded the rate of reduction of steroids in the plaintiff’s case as within the bounds of reasonable medical practice in 1992 (T 828).

162 Professor Sturgess said it was reasonable practice to use only corticosteroids for the first six months, but this would not have been the case if the defendant had been treating a post menopausal patient (doubtless because of the risks of osteoporosis): T 831.

163 Had Plaquenil been used, Professor Sturgess would not have expected its introduction to permit of reduction of the corticosteroid dose because of renal concern (T 832).

164 Professor Sturgess in his evidence in chief (T 832) said that he would not have considered it necessary to introduce Imuran after the flare up in May, but that evidence should be considered with evidence later given by the witness in cross examination. Professor Sturgess said (at T 864) that by 11 May he would have discussed the introduction of Imuran with the plaintiff and would have advised her that he thought such introduction was “a good idea”. There were possible side effects to be considered, as Professor Sturgess acknowledged. Not the least of those possible side effects was the risk of impairment of ovarian function and other possible side effects included leucopoenia, tumours, bone marrow damage, nausea and vomiting.

165 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. 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.

166 I referred earlier to the evidence of Professor Clancy. I add that Professor Clancy did not consider it unreasonable for the defendant not to have introduced Imuran even as late as 1 July 1992 (T 889). Whilst Professor Clancy wrote in 1996 that he would probably have introduced Plaquenil, he had changed his mind by 2002. Plaquenil he regards as a valuable drug where the patient’s disease is mild (T 943), but he does not regard it as a steroid sparer and he now sees its usefulness as a control mechanism in mild long term disease.

167 Professor Clancy explained that his approach to Imuran and like drugs was to delay introduction until a “plateau” amount of corticosteroid needed to control the disease became known (T 890). He said he would like to know that six months after treatment began (T 890). In this case that would not have been until early July 1992.

168 The above review of the opinions of the experts is not, of course, by any means an exhaustive review of the evidence that bears upon the issue as to whether the defendant was negligent in failing to introduce a steroid sparer into the plaintiff’s treatment regime. The review highlights the divergence of medical opinion and emphasises one of the difficulties in this complex case.

169 I am not persuaded that it was unreasonable for the defendant to prescribe corticosteroids only in treating the plaintiff’s lupus at any time prior to the flare up in the plaintiff’s condition in May 1992. However, when that flare up occurred and the necessity arose to review the course of the plaintiff’s treatment, it seems to me, reflecting on the evidence, that the following matters assumed importance:

(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 (T 600), although I also accept his view that damage of this kind probably occurred most rapidly in the first five months of treatment (T 601).

(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 (T 375), 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 (T 726) 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 (T 840). 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 (T 587) and by Dr Champion (T 377-378) on this issue.

170 The defendant said he was concerned during 1992 about the continuing levels of corticosteroids that the plaintiff was taking because of the toxic effect and he regarded the breakthrough in May 1992 as “disappointing” (T 748). I referred earlier to the defendant’s evidence that he concluded that the dangers of the introduction of Imuran did not warrant its use (T 749). As I observed earlier, the defendant said he was influenced in that decision by what was written by Cassidy and Petty in the extract from the text I cited earlier. The indications for the introduction of Imuran were not in the defendant’s opinion present. The plaintiff did not have cerebral lupus, the plaintiff did not have life threatening systemic disease and she did not have gross manifestations of the side effects of the steroids. So far as Plaquenil was concerned, the defendant did not consider that its introduction would have helped to lower the corticosteroid level. Hence the decision not to use immunosuppressive agents in the plaintiff’s treatment prior to August 1992.

171 Professor Sturgess in his evidence sounded what I consider to be an appropriate caution against being unduly influenced by text writers. He said (T 865):

“I would not think that it was appropriate to look at the textbook indications for Imuran and if the patient didn’t fit those to not do it. It is very much a matter of weighing up the risks, the benefits and the texts often mention the obvious reasons to do it, and there may be all sorts of, like, for instance, the texts wouldn’t usually reference cosmetic side effects but if you had a patient where that was very important, then that would be a reason to use Imuran.”

172 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 continued. 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 (T 720):

“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.”

173 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 (T 422-423), 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 para 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.

174 Dr Sutherland agreed in cross examination (T 582) that it would have been appropriate to defer the introduction of immunosuppression (on the basis that such agents had not been introduced earlier) until “the uncertainty of the events around the end of May had been resolved”, and accepting this to be so, I find that the appropriate time for the introduction of Imuran was when the plaintiff’s flu-like symptoms settled, which was within one to two weeks of 1 June 1992. Precision is impossible, but I find the appropriate date to have been 10 June approximately.

175 Although Dr Champion considered Plaquenil should also have been introduced after the flare up in May, I do not find the case for its introduction convincing. The defendant did not believe Plaquenil would have assisted in lowering the corticosteroid dose, and I find persuasive support for that belief in the evidence of Professor Sturgess and Professor Clancy. The plaintiff has not proved the defendant was negligent in not introducing Plaquenil.

176 The finding I have made concerning Imuran makes it necessary to address the issue of causation, but it is convenient before doing so to consider matter (vi).

(vi) Prescribing Dexamethasone

177 Dr Champion was of the opinion that the introduction of Dexamethasone in this case was inappropriate. Both Professor Sturgess and Professor Clancy were of the opposite opinion, but the differing opinions were reached because Dr Champion, on the one hand, and Professor Clancy and Professor Sturgess, on the other hand, took different views as to the significance of the differing half lives of Prednisolone and of Dexamethasone.

178 The controversy invites reference to the seventeenth edition of Cecil’s Textbook of Medicine where the author addresses the use of glucocorticosteroid therapy. I shall refer to that text and to Cassidy and Petty. I shall refer also to the evidence of the experts concerning the prescription of Dexamethasone presently, but I will first consider the defendant’s decision to introduce Dexamethasone and the reasons for it.

179 I accept that the decision to substitute Dexamethasone for Prednisolone was made in June 1992 following the flare up in the plaintiff’s condition, and the change was discussed with the plaintiff. According to the plaintiff, the defendant explained to her as the reason for the change that the plaintiff would not have to take so many tablets and the Dexamethasone tasted better.

180 On 1 June 1992 the defendant wrote to Dr Donald advising of the anticipated change to Dexamethasone in an equivalent dosage, stating as the reason that “many of my patients are finding it much easier to take”.

181 Later, when on 28 December 1992 the defendant wrote to Professor Clancy who was about to take over the management of the plaintiff, he stated the reasons for the change to Dexamethasone in these terms:

“Because of the slow Cushingoid Development (and because I have found it ‘useful’ in other kids – the tablets do not taste as bad as Prednisolone) I changed her to Dexamethasone.”

182 In his evidence (T 699) the defendant said:

“I had a nagging worry that instead of having the steroid equivalent of the 50s, 60s and 40s that she was on, she seemed to be more acting as though she was in the 30s to 40s. I thought a change – and she had had the two breakthroughs at that stage, and I thought that the appropriate thing to do was to try another formulation in the same, of the same drug basically to see if this could be or we could stop the breakthrough and get the dose down.”

183 Later, at T 786-787, Dr Hosking gave the following response to the following questions:

“Q. ...You see, what I want to suggest to you is that this claim of yours that dexamethasone with a different form and therefore might have a different effect was simply speculation on your part?
A. Yes.

Q. And you didn't want to put in a formal document, such as this, that you were speculating about the effects of a drug?
A. I think that could be part of it. I had - I had no evidence at that time that there was a scientific basis, if you like. What I was doing was exploring a possibility which was very unlikely to make a significant difference, but just might, and which it did.”

184 As at 1 June the defendant did not consider the difference in the half life of Dexamethasone and did not recall reading of the inadvisability of prescribing a corticosteroid with a longer half life than Prednisolone (T 674).

185 At this point I record selected extracts from Cecil’s Textbook of Medicine (1985 edition) which attracted the attention of the various witnesses, and I quote from pp 112:

“There are a number of synthetic analogues of cortisol in clinical use today. These differ in their plasma half-life, relative anti-inflammatory potency, and salt-retaining potency. Among the glucocorticosteroid preparations in common use, cortisone and hydrocortisone have the highest sodium-retaining potency. For this reason, these agents are rarely the steroids of choice in situations requiring long-term administration, except when used as replacement therapy in adrenal insufficiency. Certain cortisol analogues such as dexamethasone are much less susceptible than cortisol to metabolic degradation. Thus, their plasma half-lives are longer, contributing to their greater relative anti-inflammatory potency. In general, the greater the plasma half-life of a glucocorticosteroid, the greater is its potency. However, almost invariably associated with greater potency is a greater degree of toxic side effects, including suppression of the hypothalamic-pituitary-adrenal (HPA) axis...”

186 Then (at p 114):

“Ever since the development of synthetic glucocorticosteroids, great effort has been made to develop agents that are extremely potent and long acting but relatively non-toxic. Unfortunately, as a general rule, there is a correlation between duration of plasma half-life, potency, and toxic side effects. For example, dexamethasone is longer acting, more potent, and associated with greater deleterious side effects than the more commonly used prednisone. From a strictly anti-inflammatory or immunosuppressive standpoint, it would be desirable to administer a high dose of a long-acting agent at frequent intervals for an extended period of time in order to induce and maintain disease remission. However, the toxic side effects of such a regimen render it unacceptable except under the most extraordinary circumstances. In situations such as the chronic connective tissue diseases, it is more appropriate to employ a short-acting agent such as prednisone in a single dose in the morning, or on alternate days. Shorter-acting agents such as prednisone are essential for the construction of long-term regimens that closely mimic the normal diurnal cortisol cycle. What then is the indication for a potent long-acting agent such as dexamethasone? While there are no absolute indications, dexamethasone is generally considered to be the steroid of choice in clinical situations in which sustained high levels of potent glucocorticosteroids are desirable for limited periods of time, as in brain edema.”

187 There appears at the foot of p 112 a table which identifies a number of glucocorticosteroids and sets out there in columns their equivalent potency per milligram, their sodium retaining potency and their plasma half life. The table of equivalent potency records 5 mg Prednisolone as having the equivalent potency of 0.75 mg of Dexamethasone. The plasma half life of both is stated to be the same at those doses.

188 The interpretation of what was written in the above extract was a matter of dispute, and I shall shortly record what the various experts had to say about it.

189 However, before doing so I also record an extract from what is written in the second edition of Cassidy and Petty – Textbook of Pediatric Rheumatology on the topic of minimising corticosteroid toxicity, which draws attention to the significance of the biological half life of corticosteroids. Dr Champion emphasised the significance of the longer biological half life of Dexamethasone in his evidence to which I shall shortly make reference. In Cassidy and Petty it is stated (at 75):

“The unavoidable but deleterious effects of corticosteroids can be minimized by employing an analogue with a relatively short half-life. Prednisone is the drug most often preferred for oral therapy. It has enhanced glucocorticoid, and therefore anti-inflammatory effects, decreased mineralocorticoid actions, and the lowest risk/benefit ratio of any of the corticosteroids in general use.”

190 At the foot of p 75 in Cassidy and Petty appears a table headed “Dose and Duration of Action of the Adrenocorticosteroid Drugs:

Table 3-18 Dose and Duration of Action of the Adrenocorticosteroid
Drugs

________________________________________________________________
Duration of
Equivalent Plasma Suppression
Dose Half-Life HPA Axis
Corticosteroid (mg) (min) (h)
________________________________________________________________
Short-actinga 24-36
Hydrocortisone 20 80-115
Prednisone 5 60
Prednisolone 5 115-250
Methylprednisolone 4 80-190

Long-actingb 48
Dexamethasone 0.75 110-280
_________________________________________________________________
a Short-acting: 8- to 12-h biological half-life.
b Long-acting: 36- to 72-h biological half-life.

191 The equivalent dosage figures for Prednisolone and for Dexamethasone in the above table correspond with those in the table in Cecil (para 187 above). The plasma half life figures do not correspond, as Cassidy and Petty state a range. Cecil’s expressed plasma half life for both drugs is within the ranges expressed in Cassidy and Petty.

192 The defendant did not consider what Cecil had written before he prescribed the Dexamethasone but he prescribed a dosage, as conveyed by Goodman and Gilman (described by him as a standard text for determining dosages), a little higher than the equivalent Prednisolone dose to begin with. He said he did this deliberately, but what the defendant intended to do was to prescribe Dexamethasone in lesser quantities, with the perceived equivalent potency of Prednisolone, and with the reductions in dosage to which I referred earlier.

193 In the opinion of the defendant, the change over would have had no difference in terms of toxic effect. I refer to the defendant’s evidence at T 698-699:

“Q. Since these events, as I understand it, you have looked at and heard evidence about it with respect to the half life?
A. Yes.

Q. In relation to the difference in the half life of Dexamethasone, over the period June to August 1992, in the doses that were prescribed for Michelle, do you have a view as to the difference in the ultimate outcome that would have occurred, compared to her having continued on with equivalent doses of Prednisolone? Do you have a view about that first, yes or no?
A. Yes, I do have a view.

Q. What is that view?
A. My view is that I gave her an equivalent dose in terms of glucocorticoid action, and I can see it would have made no difference. If we make an assumption that the Prednisolone was working as it should have been, and I changed that to Dexamethasone, it would make no difference. The main reason why people don't use it, is because of the longer half life, and the effect on the HPA [axis]. Then if you were giving it for a short time, then this would become relevant.

Michelle, however, had been on steroids for a number of months. After two or three months the HPA [axis] is no longer relevant, because it is going to take as long, it is going to take as long to recover whether you use Dexamethasone or Prednisolone. Because it is no longer at, the [axis] is no longer acting. It is a feedback mechanism. Once the dose has been present for a long time, the HP side of things gives up, if you like. It gives up, and doesn't really restart until you get to virtually no steroid present, glucocorticoid present.

Q. You have referred to the HPA [axis] giving up after a short period of time?
A. After a couple of months.

Q. On the doses of Prednisolone that Michelle was on in January and February, do I take it that by at least March that HPA access would have given up on those doses, in your view?
A. Yeah.”

194 Whilst the defendant agreed in cross examination that in theory Dexamethasone may have a more deleterious effect than Prednisolone because of its longer half life, Dr Hosking’s belief was that this was allowed for in setting the dose (T 732-733):

“Q. If then, in theory, it was possible that the dexamethasone may predispose to additional corticosteroid osteoporotic complications, was that not something you should have taken into account in 1992?
A. I guess I am hesitating because this is sort of way beyond clinical practice and what was actually happening at the time. May I - at the time, I was worried that Miss Rufo was not either absorbing or metabolizing the glucocorticoid to the extent that I was expecting her up to that time. I tried a new formulation which, in fact, one could easily say was more impressive in terms of its glucocorticoid effect, despite being given any equivalent doses, than the prednisolone. I would find it hard to argue that with - that if we are blaming the bone micro-fractures on the prednisolone, that the relatively short length of time that Miss Rufo had the prednisolone - had the dexamethasone, was not - that was a relatively small fraction of the total - total milligrams or grams of prednisolone that she had. I could work that out as a fraction but I suspect 15 percent. Unless we are hypothesising that the equivalent dose is not the equivalent dose, then, I am sorry, I - I am having trouble finding the right words. I find it hard to follow that line of reasoning. Yes, I will agree that there is a theoretical possibility that it may have had a more deleterious effect, if you like, than - than prednisolone because of its long half-life but, as I say, my belief is that that is allowed for in the equivalent dose.”

195 The defendant believed that what he was prescribing had the equivalent potency of what he had prescribed by way of Prednisolone. This was how and why he set the dose.

196 Dr Champion does not agree with the defendant. Dr Champion wrote on 2 December 1998 (part of Exhibit D):

“I was also surprised and concerned to note the change from prednisolone to dexamethasone, and the unusual reasons given for such a change. It should be understood that dexamethasone is a slowly eliminated corticosteroid of considerable potency and is usually reserved for acute contexts often in hospital rather than for maintenance therapy in a chronic disease. This would represent very powerful corticosteroid influence, potent adrenal suppression, and would have put her at even greater risk of adverse reactions than the prednisolone.”

197 And later in the same 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.”

198 In his evidence Dr Champion explained what he perceived to be the significance of the greater biological half life of Dexamethasone compared with that of Prednisolone (T 358-360):

“A. Well, the biological half-life is quite different, much longer in dexamethasone. Should I qualify, explain biological half-life or is the Court clear on that?

Q. Yes, yes. Then I am going to ask you to tell me what that means or what the effect is. First of all, perhaps tell us what the biological half-life means?
A. This is for a chosen pharmacological effect. It is the time, that is a pharmacological effect, that is reversible. It is the time for 50 percent of that effect to be lost, once the administration of corticosteroid has been ceased or the drug has been ceased. And for prednisolone, this is of the order of 12 to 36 hours for typical chosen pharmacological effects and, for dexamethasone, is some 36 to 72 hours so that when using dexamethasone on a multiple dose regimen or on continued therapy, the - the equivalence - the pharmacological effect would be substantially greater than even that suggested by that equivalence dosage.

HIS HONOUR: Q. Tell me, what happens to the other 50 percent in that concept? You talk about the biological half-life?
A. Yes.

Q. And the time that it takes to dissipate. What about the other 50 percent?
A. Well, it's a curvilinear function so that the loss of the next 50 percent takes the same time and the loss of the next 50 percent takes the same time. So this results in a curvilinear function or, on a long transformation, a straight line. If that means anything.

DONOVAN: Q. Just help me a little bit further. The biological half-life is longer, that means that there is more of the steroid remaining for a longer period?
A. Yes and so the pharmacological and hence the therapeutic effect is more intense and it's sustained. So both the therapeutic effect and the adverse effects tend to be substantial and this is the reason why dexamethasone is virtually restricted to short-term usage in optimal medical practice.

HIS HONOUR: Q. Short term meaning what?
A. Days. There are virtually - I did a literature search on this. I saw virtually no significant publications advocating or utilising long-term dexamethasone in modern medical practice.

DONOVAN: Q. Can I take that a little further. If, let us say, there's a certain amount taken on day one and we go over to day two and take another dose, does that mean the second dose is being taken before the first dose has been cleared?
A. Yes, before the effects have worn off.

Q. Yes, the biological effect?
A. Yes. What that means of course is that there's more major pituitary adrenal suppression when one takes dexamethasone on a longer term basis because there's not the opportunity for the natural biorhythm of cortisol production to continue. It's just a sustained suppression of it.

Q. I think you've said this but what effect does that have on, for example, side effects such as osteoporosis or those types of things?
A. Yes. Well, both the desired effects and the adverse effects would potentially be high intensity and sustained and so that when one is using dexamethasone one is always conscious of a short course or - well, conscious of just a short course and its use is restricted to certain important conditions like acute conditions such as cerebral edema.”

199 Later, Dr Champion commented upon the passage in Cecil at p 112 where the author wrote “In general the greater the plasma half life of a glucocorticosteroid the greater its potency”, and said this: (T 386):

“A. It is the biological half-life. This is clearly written by a non pharmacologist. Yes, there is no relationship between the potency and the plasma half-life of a drug.

Q. It has been put to the Court that the potency of Dexamethasone is simply related to the fact that if you adjust the dosage, then the potency is the same between that and Prednisolone. Is that correct?
A. Potency is pharmacological effect in relation to milligram dosage. Efficacy, which is what we are really on about, is the actual therapeutic effect from a given dose in relation to potential adverse effects from that dose. So that they are quite different concepts, yet they tend to get obscured. The therapeutic effect of Dexamethasone is a consequence of, in part, its potency, but its long biological half-life.

Q. Moving over to page 113, I don't want to go through this in detail, but in the section headed, "Design of Glucocorticosteroid Therapeutic Regimens", are there descriptions of the type of regimens which may be used, including even, for example, the massive one gram Methylprednisolone dose for disorders such as status asthmaticus?
A. Yes.

Q. In determining the appropriate regime, the authors refer to toxic side effects. Are they the sort of toxic side effects that you have been emphasizing must be taken into account and dealt with appropriately?
A. Yes, yes. The adverse effects of corticosteroids in short-term use, and particularly long-term use, follow like a shadow the therapeutic effect. And always, it is always a medical preoccupation to try to keep those two sides of the coin in balance in perspective.”

200 In cross examination Dr Champion stressed the importance of the pharmacological effect on the tissues as being the problem with the longer half life (T 553):

“A. Yes, there is confusion of course between the pharmacological half life, the concentration reflecting the concentration in plasma, and the biological half life, which is reflecting the pharmacological effect in the tissues. It is the latter which is so important in therapeutic and toxic effects. But there has been confusion. Indeed, in one or two of my reports I made the same confusion by reiterating without much sort, stuff that was published in the various texts.

Q. If in fact it takes longer on the cessation of Dexamethasone for the bodies own Cortisol production to be reinstated, that response would not increase the risk of osteoporosis, would it?
A. No, it is the prolonged tissue effect which increases the risk of osteoporosis...”

201 And then (T 554):

“Q. I suggest to you that there is no correlation between the HPA assess half life, and the residual effect of a drug such as Dexamethasone in the context of it increasing the risk of osteoporosis?
A. There is a relationship. It is a complex relationship, because it also, the risk of osteoporosis all depends on dose and duration of continuing therapy. Whereas these biological half lives we are talking about have a single dose effect. But the fact is that the reason Dexamethasone is not used in chronic therapy, is because there is no opportunity for the pituitary adrenal access to recover, so there is major long-term suppression of the adrenal glands. Also while the therapeutic effect may be fine, the sustained effect, catabolic effect, negative effect on bones, for example, just continues on. This is - in respect of bone, this is admittedly a theoretical concept, but it is a strong enough theoretical concept that studies would not be done with the use of Dexamethasone in long-term diseases such as lupus...”

202 And (T 555):

“Q. There is no basis upon which the correlation between the suppression of the HPA assess arising from the use of Dexamethasone, and the increased risk of osteoporosis can be quantified?
A. Well it would be difficult to quantify, because the experiments, to my knowledge, haven't been done.”

203 I turn to the evidence of Professor Sturgess.

204 Professor Sturgess considered the suitability of Dexamethasone in his report of 11 January 2000 and I have recorded earlier (at para 92 above) what Professor Sturgess wrote.

205 Whilst the professor wrote that there had been two occasions on which he had used long term Dexamethasone, in the evidence he later gave (T 849) he said that there was only one occasion on which he had given Dexamethasone rather than Prednisolone and that was with a patient who could not tolerate Prednisolone. Professor Sturgess said that that patient had been on 4 mg of Dexamethasone a day to start with, reducing to 1 mg a day at the end of six months. He had not prescribed Dexamethasone with a commencing dose of 10 mg reducing to 6 mg daily, and he said it had never been necessary for him to do so.

206 Professor Sturgess had used Dexamethasone on a long term basis for the treatment of Addison’s Disease, and his evidence was that Dexamethasone was used widely for this (T 847). He said that it was necessary to give the Dexamethasone daily and he did not agree with that experience that the half life lingered on. In the case of use of the drug for treating Addison’s Disease, the dose was small, ranging between 0.25 mg and 0.75 mg (T 847-849).

207 In the one case in which Professor Sturgess had treated his patient long term with Dexamethasone, he would have been happy to give her high doses of that drug had it been necessary, but Professor Sturgess acknowledged that he was not aware of any text that recommended the use of long acting corticosteroids for lupus, and he said that nearly every text expressed a preference for Prednisolone (T 848-849).

208 Later, in cross examination Professor Sturgess gave the following evidence (T 852-853):

“Q. Let me take this question of the Dexamethasone a step further. Do you know of any papers where dexamethasone has been used at these sort of levels, that is ten to six, over – well, actually it goes from the 8th of June through to 24 August?
A. No, no, I am not. Most people are quite happy with prednisone and prednisolone as steroid drugs. We like them, they come in a nice variety of tablet sizes, they are easy to use and we would only use an alternative if there was some reason to do it.

Q. See, what I am puzzled about is you say that you would change your view if we could produce to you a paper, experimental paper, showing the dexamethasone as worse and I am just wondering whether you are not actually turning the onus around the wrong way and that the real thing you have got to look at is not proof that it is bad but proof that it is safe at these high levels?
A. Look, I am not sure. It is a philosophical argument almost.

Q. I am not sure that the Drug and Food Administration in the US would say that but--
A. I mean, the drug is, you know, licensed in all western countries for use. You know, it is widely used. I don’t think we can just assume that it is more toxic without some evidence.

Q. I know you are against me on this and you say there is no difference in the length of the effect, but assume against you that there is such a difference. Would not that indicate at least in theory that there is a likelihood of greater good and bad effects from it?
A. Well, it certainly would be true. If, for instance, dexamethasone persisted in the body for 48 hours but I gave it to someone every 24 hours, the previous dose would not have yet disappeared so I get a progressive cumulative effect, the dose would get higher and higher. We know from practice that isn’t right, the drug is gone every 24 hours, so we have to give it every day.

Q. We know from practice in giving small doses. You don’t know in practice from giving doses of between ten and six, do you?
A. No, I haven’t had the opportunity – the necessity to do that. When it is given to people with brain tumours, who often take it for several months, not just a couple of weeks--

Q. That is in circumstances where they are terminally ill, isn’t it?
A. Well, the are going to die.

Q. Yes?
A. But we certainly don’t want to accelerate that process and dexamethasone can prolong the life of a patient with brain tumours for many months. We actually give it there more than once a day because we want to – we don’t want any effect to wear off. We want the maximum effect 24 hours a day so the patient would routinely be on two milligrams every six hours, that is eight milligrams a day, for months sometimes. They are very Cushingoid but they are alive.

Q. We don’t of course know what has happened to their bones during that time?
A. No, we assume--

Q. You don’t carry out bone densitometry on them because, in a sense, it doesn’t matter because the important thing is to keep them as comfortable as possible to the end of their days without shortening it, but the emphasis is one the palliative side?
A. Yes. But I wouldn’t want you to think that – say we had someone on eight milligrams of dexamethasone for brain tumours, and we chose dexamethasone because it won’t retain salt, and give it in daily doses because it doesn’t wear off, I don’t think it would give them more osteoporosis, even though it doesn’t matter for that patient, it wouldn’t give them more bone fractures than for someone put on one hundred milligrams of prednisolone a day because they are the same. I think it turns out that dexamethasone is better for brain tumours.

Q. At the end of the day, there is nothing to show that those sort of doses would be safe on bone?
A. No, I agree with that. There is no proof that those doses are equally safe.”

209 Professor Clancy was asked about the defendant’s decision to change from Prednisolone to Dexamethasone at T 895:

“Q. In the face of the symptoms that we have been over to 1 June, do you have an opinion as to whether or not the change to Dexamethasone was reasonable or not?
A. I find that a very difficult question. The reason being that that decision is very much a clinical decision, where many factors are occurring, and I am looking at a lot of these in notes. I think it was an interesting decision, an innovative decision to address a very difficult clinical problem that was facing the physician at the time.

Q. Would you have done it?
A. I probably wouldn't have done it.

Q. Why?
A. Because I wouldn't have thought of it. I mean that as a serious answer.

Q. If it were suggested to you at the time, is it something that in your view, taking into account the warnings that one had, or the material that had been published in texts such as Cassidy and Petty advocating against the use of corticosteroid medication with a longer half life, do you have a view as to whether it was unreasonable?
A. If I was asked my opinion at the time knowing all those circumstances, I'd say, ‘That's a good idea, lets see how it goes.’

Q. As I understand your previous answers, it is your view that the equivalent dose of Dexamethasone to Prednisolone would not have any impact upon, or would not increase the risk of osteoporosis or the manifestations there of?
A. I wouldn't have considered that as an issue, no.”

210 Earlier, Professor Clancy had been directed to the evidence that Dr Champion gave concerning the therapeutic effect of Dexamethasone and he disagreed with that evidence in trenchant terms (T 893-894):

“Q. In relation to the effect of dexamethasone as opposed to prednisolone on a patient in terms of the risk of osteoporosis, particularly to an extent that has clinical manifestations such as vertebral fractures, what is the difference, if any, between dexamethasone and prednisolone, in your view?
A. There's no known differences.

Q. When you say no known difference, what do you mean by that?
A. I can think of no reason why there should be a difference and no-one has ever looked to see if there is a difference, and there is no theoretical reason why there should be a difference.

Q. You understand, don't you, that Dr Champion speaks of the therapeutic effect, I think is the term that he used, of dexamethasone with its longer half life as a factor in the increased period that the pituitary adrenal [axis] is suppressed as being a basis from which you can extrapolate like a shadow an increased risk of the toxicities which include osteoporosis. What do you say about that?
A. Well, I would say that that's a totally illogic view, and I am surprised he said that.

Q. Why?
A. Because the hypothalamus, which is the controller of endocrine glands like the adrenal gland, is a very moment-to-moment sensor of the level of steroid. The receptors that allow this to occur are geared to do that because that's what's required for life maintenance. When you, say, go to the bone, the receptors on the cells there are totally different receptors, totally different dynamics of interaction with the steroid bearing little or no relationship necessarily with any dose of steroid in the blood. It has its own pace, its own - and everybody is different in the way in which their receptors will handle it. Some people will never get osteoporosis, some will get it after a few years, some people will get muscle problems, some other people will get diabetes, so all the tissues have their own ways of handling the corticosteroid, which is quite different to the hypothalamus.”

211 Professor Clancy was asked to consider the effect of the change to Dexamethasone on the assumption that it did produce an increased risk of osteoporosis compared with Prednisolone, and as to this his evidence was as follows (T 896-897):

“Q. If you would not mind, just assume for the time being that contrary to what I understand your evidence to be, namely that there is no reason to believe that the longer half life of Dexamethasone would present an increased risk of osteoporosis than Prednisolone, and assume that the longer half life does have an impact over a long period of time, referable to the longer suppression of the HPA axis, and adopting the process of reasoning that we have touched upon as expounded by Dr Champion, that is the toxicities shadowing the therapeutic benefit and the period of time over which the HPA axis is suppressed, do you understand?
A. Yes, I understand.

Q. If you assume that worse case scenario against us, and you apply that learning to this period of time from 1 June to 24 August when the fractures were seen, and take into account her previous history and the medication that she had been on, what, if at all - even assuming the worst against us - would have been the impact in terms of an increased chance of osteoporosis over this period of time?
A. As compared with say the continued use of Prednisone?

Q. Yes?

OBJECTION. QUESTION ALLOWED.

A. In my view it would make no difference over that timeframe at all.

Q. Why is that?
A. Because of the plateau effect I mentioned, because the half lifetime in relation to hypothalamic suppression is totally unrelated to effects on tissues, and because of the timeframe of being very short, and because the - because of the total different kinetics in tissue.

Q. Lets assume that there is a relationship between the HPA axis suppression and osteoporosis as opined by Dr Champion, but that you are confining yourself to length of time and length of time alone. Does that alone allow you to come to an opinion as to whether or not the switch over from Prednisolone to Dexamethasone would have had an increased risk of osteoporosis for Miss Rufo?
A. In that timeframe?

Q. Yes?
A. I would not expect it to have any effect.”

212 Professor Clancy was cross examined at some length on the Cecil text which I referred to earlier and there are several passages in the cross examination which address this. At T 945-946 Professor Clancy gave the following responses to the following questions:

“Q. ‘In general, the greater the plasma half life of a glucocorticoid steroid the greater its potency.’
A. Yes, that determines the dosage. We are talking about dosage here.

Q. No, he is not talking about dosage, he is talking about plasma half life.
A. No, but he is really talking about dosage here because all this is determining is the dose you use for equivalents.

Q. Let me ask you the passage and see if you agree with it or not. This is all he says. ‘In general, the greater the plasma half life of the glucocorticoid steroid, the greater its potency.’ Do you agree with that or not?
A. Except you and I think different - we have different interpretations of potency.

Q. Why don't I put it this way to you. ‘In general the greater plasma half life of the glucocorticoid steroid, the greater its effect.’
A. Per equal weight.

Q. No.
A. That's what they are talking about.

Q. That's what they are talking about, okay.
A. Can I explain? That's why the ratio is so much less.

Q. ‘However, almost invariably associated with greater potency is a greater degree of toxic side effects, including suppression of the hypothalamic pituitary adrenal axis.’
A. Yes, that would be right.

Q. As well as the greater plasma half life, do you understand there is a greater biological half life?
A. It depends what biological activity you are talking about.

Q. Well, let me ask you this. This comes from Dr Chaitow.

OBJECTION (DR CHAITOW IS NOT BEING CALLED; SHOULD NOT BE PUT).

Q. Can you answer this question. Do you understand there is a greater biological half life or not?
A. Well, as I said, with respect to what biological activity?

Q. Any biological activity.
A. They are all going to be different. I mean it all depends on tissue receptors and how they handle this.

Q. Is there a greater biological half life in relation to some biological activity?
A. There probably is.

Q. You are not sure of that?
A. No. I don't think anyone else is, either.

Q. You don't think other experts could say that; is that what you say?
A. I have never seen anybody quantitate those sorts of activities in man at all.”

213 He gave the following evidence at T 954-955:

“Q. Then the next sentence, ‘However, the toxic side effects’?
A. That sounds reasonable. At the equivalent doses it would be quite reasonable.

Q. The last one, ‘However, the toxic side effects of such a regimen render is unacceptable, except in the most extraordinary circumstances.’ Do you agree with that sentence?
A. Yes, to be perfectly honest I think this is ambiguous. I think we are getting an ambiguous outcome of this.

Q. Do you agree with the sentence or not?
A. Well, I could agree with it in one context, and disagree with it on another.

Q. You had better tell me in what context you disagree?
A. I disagree with it in the sense that what I read this as talking about is dose equivalences. A drug is more, if you have got 10 milligrams each, a more potent drug is going to have more effect. So therefore you reduce that dose to get an equivalent effect.

Q. You wouldn't agree then--
A. There is nothing intrinsic. It is an intrinsic difference in potency per unit weight.

Q. You wouldn't agree then that with Dexamethasone you have a situation where let us say it has an effect for 72 hours?
A. Yes.

Q. That is the top of its biological half life, as stated. You wouldn't agree that there is a situation where you give Dexamethasone on the first day, and you have got, lets say, ten milligrams. You give it on the second day and you have got a carry over from the first 24 hours into the second day and so on, and a carry on into the third day until you get to the end of the 72 hours?
A. It doesn't work like that, because these half lives are all determined on single dose starters.

Q. I appreciate that. But if they are all determined on single dose starters, when you start on the second day an additional amount, you are adding it to an amount which is already there continuing on, aren't you?
A. Yes, but you get increased metabolism, the clearance rates are changing. In fairness there is not a simple answer.

Q. There is not a simple answer, but certainly if not precisely as I have put it to you, there is a real possibility of there being more of the drug in the system?
A. Yes.

Q. With a longer acting?
A. Yes, there would be.”

214 I am satisfied on the evidence that there was no text writer of whom the defendant was aware, or indeed who the evidence identifies, who supported the long term use of Dexamethasone in the treatment of lupus. Nor did the defendant draw on his personal experience or the experience of any other practitioner to decide upon the course of the long term prescription of Dexamethasone for the plaintiff. Dr Hosking’s evidence does not convey to me that he actually read what Cecil wrote in advising against the long term use of Dexamethasone. Dr Hosking said that he did not recall reading what Cassidy and Petty had written in the extracts set out above before prescribing Dexamethasone (T 674). It is the case, as the defendant very fairly acknowledged, that he did not consider at all the difference in the half life of Dexamethasone compared with that of Prednisolone. It follows that he did not consider the significance of the greater half life, although, of course, he has done so since, and I have referred to his evidence about that, which accords with the evidence of Professor Sturgess and with the evidence of Professor Clancy.

215 I am not persuaded that there was good reason to change from Prednisolone to Dexamethasone. That it may have tasted better does not seem to me to have been a reason warranting the change and the evidence does not suggest that the plaintiff was unable to tolerate Prednisolone. I accept what Dr Champion said (T 361) about the absence of a cushingoid effect being no reason to change to Dexamethasone and, indeed, the evidence satisfies me that there had been an appreciable change in the plaintiff’s appearance by the end of May.

216 Mrs Rufo gave evidence, which I regard as reliable, that one of the factors that led to the plaintiff going to see Nancy Wallace was the change in the plaintiff and Mrs Rufo perceived one of the reasons for that change to be that the plaintiff was being given a hard time at school and was being teased because of her physical appearance. I refer to the evidence of Mrs Rufo at T 277:

“Q. I'm just going to go back to Nancy Wallace for the moment. What were the factors which led to your daughter Michelle being referred to Nancy Wallace?
A. Because of this change in Michelle, the Jekyll and Hyde. It was really a change in Michelle.

Q. Were there any physical changes that she had at that time?
A. Yes. At that time she had a big face and she was being teased at school. She was spat on. She was kicked. She was abused, verbally abused.

Q. Just let me ask you this then: Was one of the reasons why she was taken to Nancy Wallace because of her reaction to the shape of her face?
A. Yes, that was one of them. We weren't coping. We just weren't coping as a family.”

217 Mrs Rufo fixed the date of the first appointment with the psychologist as being in May, and whilst there is no report from this psychologist in evidence, that time setting is consistent with Dr Miller’s introduction. As I earlier observed, by the time the referral to Dr Miller was arranged, the plaintiff had already seen Ms Wallace some five times.

218 The defendant said, in the passage I referred to earlier (para 180), that in changing to Dexamethasone he was “exploring a possibility”, but I do not consider the decision was an appropriate one, absent a careful consideration of the properties of Dexamethasone compared with those of Prednisolone, including the longer half life of Dexamethasone and the possible adverse significance of this. I find there was no such comparison made before the Dexamethasone was prescribed.

219 I do not find that there was any failure to exercise reasonable care on the part of the defendant before early June 1992. However, for the reasons above stated, I find that there was such failure in early June in the following respects:

(a) in the failure to introduce Imuran on or about 10 June 1992;

(b) in the prescription then of Dexamethasone.

220 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 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 and TC v State of New South Wales [2001] NSWCA 380.

Causation – Has damage been proved?

221 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?

The failure to introduction Imuran

222 Before assessing the significance of the failure to introduce Imuran, it is important to recognise what was required as at the beginning of June 1992 to halt the progress of the plaintiff’s osteoporosis.

223 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 6 mgs per day could adversely affect bone density (T 600). I refer to Dr Champion’s evidence (T 532-533):

“Q. ...Do I take it that firstly ideally, as I think you have told us beforehand, in order to avoid a real chance of ongoing osteoporosis, you want to achieve a low maintenance dose of Prednisolone in the order of 6 milligrams a day or less?
A. Yes.

Q. Am I correct in assuming that if Miss Rufo is receiving more than 6 milligrams, there is the likelihood of ongoing osteoporosis?
A. Yes.

Q. That's the reason you're aiming for 6 milligrams?
A. Yes.

Q. Even if you were to achieve as low a rate as 20 milligrams a 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 it 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 sufficient cause for concern too, that it may not make a huge difference over a limited timeframe.”

224 It follows from the above evidence that above a daily dose of 6 mgs of Prednisolone, it was likely that osteoporosis would have progressed. Certainly a dosage of 20 mgs 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 mgs 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.

225 Both Dr Sutherland and Dr Champion gave evidence of the impact of Imuran (and Plaquenil) had these steroid savers been introduced earlier in point of time than I have found the exercise of reasonable care required that the defendant should have introduced Imuran. Nevertheless, I propose to refer extensively to the evidence that both doctors gave relevant to the issue of causation I am now considering. I am going to address firstly the impact of Imuran.

Dr Sutherland

226 In his report dated 13 September 1994 (at p 5) Dr Sutherland wrote:

“The key issue here is the probable outcome, had Michelle been weaned off her high dose oral corticosteroids as soon as there was evidence that her lupus nephritis was under control. As already stated, this time cannot be ascertained with precision, but may well have been in March or April. It seems certain that her osteoporosis would have been much less at that stage, and on the balance of probabilities, not of sufficient severity to cause crush fractures and the subsequent kyphosis. From subsequent events, it seems likely that control of other manifestations of her lupus would not have been possible with hydroxychloroquine alone, making it likely that azathioprine would have been introduced several months earlier than it was.”

227 Whilst in the above passage Dr Sutherland spoke of the probability of avoiding crush fractures had the plaintiff been weaned off high dose corticosteroids by March or April, the evidence that he gave (T 319), on the assumption that Plaquenil and Imuran were introduced in March/April, was 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. 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.”

228 Dr Sutherland was then asked (T 326) about the introduction of the steroid sparers in May or June:

“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 crush 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.”

229 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.

Dr Champion

230 When he was asked about the introduction of steroid savers – and his evidence was given in the context of the use of Plaquenil at the outset and the later introduction of Imuran – Dr Champion said (T 402-403):

“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 azathioprine 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 reaction, without relapse.

Q. How often are you going to chip?
A. Depends on progress, depends on the dosage of azathioprine. But the question is would this be sufficient to have saved her from osteoporotic vertebral compressions? It would have reduced the risk but it's reasonable to state, I believe, that without the other considerations in regard to nutrition, general health, oestrogens, it would have been less likely. In other words, the Prednisolone--

OBJECTION. NOT RESPONSIVE.

HIS HONOUR: Let's hear what the doctor is saying.

WITNESS: In other words, hugely important as such Prednisolone reduction is with the assistance of the adjunctive drug therapies, it's still not the full picture. To maximise the likelihood of her maintaining adequate growth and bone structure, the nutritional and hormonal aspects would need to be taken into consideration as well.

HIS HONOUR: That doesn't seem to be responsive, having heard it through. Put the question again Mr Donovan.

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 would 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 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 hydroxychloroquine 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.”

231 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.”

232 It follows from the above evidence, and logically, that the later the Imuran was introduced, and the later it therefore became possible to reduce the corticosteroid level, the less the chance of avoiding the fractures which occurred.

233 It would follow, accepting Dr 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 1992 could have produced prior to 24 August 1992.

234 What was the likely extent of reduction of the corticosteroid dosage that would have been achieved by the introduction of Imuran on or about 10 June? The time available to achieve any reduction in such dosage was limited to a period of just under eleven weeks up to 24 August. Had the Imuran been introduced in March or April when the plaintiff was on 40 mg per day, Dr Sutherland thought it would have taken five months to reduce the dosage to 15 mg, barring setbacks (para 227 above). Dr Champion considered it would have been “a reasonable expectation” to reduce the dosage to 15 mg in four months (para 230 above). This being so, it seems to me to be altogether unreasonable to have expected that a dosage as low as 15 mg 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 its highest in opining that it was “a fair expectation” that the plaintiff’s dose of Prednisolone might have been reduced by 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 53.4 mg of Prednisolone), he considered it was “a fair expectation” that the plaintiff’s dose of Prednisolone might be reduced to 20 mg per day with the help of Imuran (T 416-417).

235 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 (T 516). It would have taken one to two weeks on this approach to reach a dose of 100 mg (T 517). 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).

236 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 (see para 223 above). 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 to100 mg. There was a risk of rebound to be guarded against (T 514). I also have regard to the evidence of Professor Sturgess and of Professor Clancy to which I shall now refer.

237 The plaintiff’s case derives no assistance on this causation issue from the evidence introduced in the defendant’s case.

Professor Sturgess

238 As I understand the evidence of Professor Sturgess, the introduction of Imuran would not have had an immediate effect. According to Professor Sturgess, it takes six to eight weeks to build up the dosage of Imuran to a level at which one can then start to reduce the steroid dose. In his opinion, the Imuran would start to work once a dose of 75-100 mg a day had been reached and the patient had been on that dose for two to four weeks (T 832). Professor Sturgess said he would not have altered the steroid dose for eight to ten weeks after the introduction of Imuran (T 833). Later, in cross examination (T 869), Professor Sturgess said Imuran would not have affected the Prednisone dose for six to eight weeks.

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):

“Q. If Imuran were introduced on 1 June, can you give us an idea as to how that would impact upon the rate at which you would be able to reduce the prednisolone? Assume that she continues on prednisolone for the time being after 1 June. What impact would that have on the ability to reduce the prednisolone?
A. The drugs work in totally different ways. Whereas prednisone shuts off the production of the nasty hormones that cause problems, Imuran works on cell division, so it is a very slow acting drug. You would not expect benefits or being able to take advantage of the Imuran being there, I would say for four to six weeks.”

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.

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.”

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] HCA 20; (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):

“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.”

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):

“Q. Putting aside that it was Dexamethasone, what effect would the increased dosage or equivalent dosage have on the bone loss?
A. If the dose had been increased in equivalence, then it is reasonable to expect that that would have accelerated the bone loss further. If the dose was equivalent to the previous dose of Prednisolone, then the bone loss would have been ongoing, but I'm not aware that Dexamethasone is in any way protective or otherwise.

HIS HONOUR: Q. Is what?
A. Is protective. I don't know that one steroid is better for the bone than the others. I doubt it is true.”

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):

“Q. Could I ask you this, that you say, for example, instead of switching to Dexamethasone this girl continued on taking Prednisolone --?
A. Yes.

Q. -- At dosages that were the same, as it were, prescribed in the form of Dexamethasone but taking into account this conversion factor we have just been over, the Dexamethasone would not make any difference to the ultimate outcome or the ultimate outcome in terms of osteoporosis in all likelihood simply related to the dose of corticosteroid irrespective as to which one was used. Would you agree with that?
A. I would agree with that, yes.”

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:

“Q. In terms of operation on bone, do you think dexamethasone has any difference to prednisolone?
A. No, I don’t. When it – when the letters asked me about this, I did as thorough a literature search as I could. I couldn’t find any human data, like from treating patients. I couldn’t find any human experiments and I couldn’t find any animal experiments indicating any difference in the way dexamethasone works on bone and the way prednisone, prednisolone or betamethasone work on bone.”

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):

“Q. Lets go to something else. I want you to assume this; that up until June when there is a change, the patient shows a little bit of puffiness of the face, and a bit of hair on the face. There is a bit of a moon face, a bit of hair on the face, but according to the doctor who is treating her, she shows no other signs. I want you then to assume this – if you want to make notes feel free, because it may be long. I want you to assume that by mid July she has the proximal myopathy. I want you to assume all these other things happened I am going to read to you. So she has the proximal myopathy in July, she develops a buffalo hump by July. Then over the next period up to 10 August she develops the following, a pot belly; legs become like chicken legs; difficulty walking, particularly climbing stairs; develops back pain. By 10 August the person is hunched over and walks very slowly, to a degree that when she goes to the doctor she has to be lifted by the doctor and her father on to the examination couch, and has to be propped up by the doctor as he examines her. So held up, she cannot lie down straight, held up. If you assume all those things came on in that later period after the change, would you not conclude that there was a likelihood – not a certainty, but a likelihood – that other changes were going on inside her which could not be observed?
A. Oh yes, if those were the external features.

Q. Indeed, one of those features or effects would also be osteoporosis. Indeed, bearing in mind the severity of what I have just explained to you, you would have a suspicion that there would be a risk of rapid osteoporosis occurring in conjunction with those rapid features that occurred outside?
A. Yes, the critical ones being the back pain and the hunched posture.

Q. Assume that she has been on equivalent doses of both the first steroid, the Prednisolone, and the later steroid, obviously I am talking about the Dexamethasone. Would you not for starters consider that it may have been the Dexamethasone which has a causal link or contribution with those rapid changes?
A. No, I wouldn’t. I have seen exactly this situation in patients of my own that I have had on one drug, Prednisolone continuously, and I have seen no side effects for three, four, five, six months. Then in the space of a matter of weeks I have seen a lot of side effects develop. That is very well described.

Q. The question was would you consider it? I take it the answer is no?
A. No, that’s correct.

Q. You wouldn’t even consider it?
A. No, I would think it was the cumulative effect of doses.”

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):

“Q. Is it a significantly longer half life or are we talking about one or two hours' difference?
A. The impact of - it would be significantly longer because you would certainly get more hypothalamic suppression, which would mean it would be significantly longer.

Q. You assert, I think, that that does not change the effect that the dexamethasone has in terms of good curative effects or bad adverse effects?
A. Yes. There's not a relationship between plasma half life and the effect on tissue function.”

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.

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.”

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.

2. Costs reserved.

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LAST UPDATED: 06/11/2002