Tabet v Mansour & Anor [2007] NSWSC 36 | Case summary

Tabet v Mansour & Anor [2007] NSWSC 36 | Case summary | Zoe

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CATCHWORDS : MEDICAL NEGLIGENCE CLAIM - six year old patient referred to first defendant paediatrician on 28 December 1990 with a history of headaches - hospital admission 29-31 December 1990 - varicella rash by time of discharge - whether first defendant negligent in treatment in failing to detect medulloblastoma - no CT scan to investigate cause of headaches. MEDICAL NEGLIGENCE CLAIM against second defendant - consulted as paediatrician on 11 January 1991 - resolving varicella rash - continuing headaches - provisional diagnosis of meningitis - hospital admission 11 January 1991 - lumbar puncture 13 January 1991 - deterioration 14 January 1991 - CT scan then reveals medulloblastoma - whether second defendant negligent in treatment - whether failure to arrange CT on 13 January 1991 causative of harm. MEDICAL NEGLIGENCE - lost chance of better outcome - entitlement to damages - assessment of value of lost chance. The plaintiff was a six year old child who was referred to the first defendant in his capacity as a specialist paediatrician on 28 December 1990 with complaints of headaches. The plaintiff was admitted to hospital on 29 December and remained there until 31 December 1990, by which time a varicella rash had appeared. The plaintiff was examined by the first defendant before her discharge from hospital on 31 December 1990, the last occasion on which the first defendant saw the plaintiff. The plaintiff consulted the second defendant, who was a specialist paediatrician on 11 January 1991, with resolving varicella rash and with complaint of continuing headaches. The plaintiff was admitted to hospital again on that date for investigation, the second defendant making a provisional diagnosis of meningitis. A lumbar puncture was performed on 13 January 1991 and on 14 January 1991 a CT was performed after the plaintiff's condition deteriorated. This procedure disclosed that the plaintiff had a medulloblastoma. The plaintiff was subsequently operated on for a subtotal removal of the medulloblastoma. The plaintiff later had extensive chemotherapy and radiotherapy. The treatment was successful but the plaintiff has been left severely disabled. The plaintiff claimed damages against each defendant, alleging negligence by each defendant in treatment and the failure to detect the medulloblastoma before it was detected. HELD - As to liability: (1) The claim against the first defendant failed - (2) The claim against the second defendant succeeded in that there was found to be a breach of duty of care in not arranging for an urgent CT on 13 January 1991 following an episode occurring on that day - (3) The failure to arrange for that procedure was not proved on the probabilities to be causative of harm, having regard to the plaintiff's pre-existing condition at that time, and to the treatment likely to have been provided if there had been a CT on 13 January 1991 - (4) The plaintiff, however, proved an entitlement to damages for loss of a chance of a better outcome and the avoidance of the damage done on 14 January. Damages: (5) There were four contributors to the totality of the brain damage from which the plaintiff suffers: (i) the medulloblastoma with its seeding and hydrocephalus - (ii) the damage that occurred on 14 January 1991 - (iii) the surgery on 16 January 1991 - (iv) the subsequent radiotherapy treatment - (6) Except for (i), each of the remaining contributors added to the brain damage preceding its contribution - (7) The contribution of the damage that occurred on 14 January to the total damage and resulting disabilities was not greater than twenty-five percent - (8) The loss of the chance of a better outcome and avoidance of the harm suffered on 14 January 1991 was quantified as a forty percent chance - (9) Damages were assessed on the loss of a chance basis at $610,000.

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Introductory outline of events 3 In the latter part of 1990, some time after the plaintiff's sixth birthday on 6 November 1990, the plaintiff became unwell and suffered from headaches and vomiting. The plaintiff's maternal grandfather and his son were general practitioners practising in the same professional rooms, and each of these doctors provided medical attention to the plaintiff and other family members from time to time. The principal family doctor was the plaintiff's grandfather (since deceased). 4 There is some issue as to when the plaintiff's grandfather first became concerned in the plaintiff's treatment for the headaches and vomiting, and it will be necessary for me to consider this question presently. However, certainly by 26 December 1990, and both parents of the plaintiff contend earlier, the plaintiff's grandfather saw the plaintiff for these problems. Notes of the medical practice conducted by the grandfather and his son record that there was a consultation on 26 December 1990: "H/V [home visit] 1/52. Vomiting, headache, no dehydration, no diarrhoea, temp 37.4, Stematil sup 5 mg. Abdo () No jaundice. No meningism. For diet." 5 Both the plaintiff's mother and the plaintiff's father gave evidence that there was a further consultation at that family practice on 28 December 1990. Dr Asaad Sheiban (the plaintiff's uncle) gave evidence to the like effect, and on that date the following entry appears in the practice record: "28.12.1990 Persistent headache + vomiting. Referred to Dr Mansour." 6 The letter of referral written by the plaintiff's uncle and dated 28 December 1990 recorded a history of headaches and vomiting for 10/7. It reads: "Thank you for seeing this little girl, who happens to be my sister's daughter. She has been [complaining of] headache and vomiting for [10 days]. No diarrhoea. Small fever Previously healthy [Previous history]: [Urinary Tract Infection] x 2 Thank you again for this quick arrangement." 7 The first defendant saw the plaintiff on 28 December at the Children's Hospital and following examination referred her to the casualty department for urine and throat swab tests. The first defendant prescribed a course of penicillin, not to be commenced until after a urine specimen had been taken. The plaintiff was not admitted to hospital, but allowed to go home. 8 The following day the plaintiff was brought back to the hospital by her parents with another referral note written by her uncle. This note reads: "Thank you for seeing this girl, who presents with [more than 10 days] of persistent vomiting and headaches. No diarrhoea. Temp 36.7. ? Small fever early on. No signs of meningism. [Abdominal] pain, but no organmyopathy or [Lymph Nodes] enlargement. [Previous history]: [Urinary Tract Infection] x 2 Yesterday she was commenced on penicillin by Dr Mansour for streptococcal infection. Still vomiting & [complaining of] abdominal pain & headache. ? Needs I.V. fluids & [blood test] - Nil by mouth." 9 The plaintiff was admitted to hospital on 29 December 1990 and remained there until 31 December 1990. In that period she was under the care of the first defendant. By the date of her discharge, a chicken pox rash had appeared and this followed upon the presentation of a rash upon the plaintiff's brother some fourteen days previously. By 31 December 1990 the tests referred to had proved to be negative and the first defendant discharged the plaintiff from hospital. 10 The plaintiff thereafter remained at home until 11 January 1991. In that period the plaintiff was very obviously suffering from chicken pox with a severe and troublesome rash but the headaches and vomiting persisted and the plaintiff was readmitted to hospital, the readmission having been arranged by either the plaintiff's grandfather or her uncle. 11 This time the plaintiff came under the care of the second defendant since the first defendant was on leave. The plaintiff was readmitted and the second defendant considered that the plaintiff, apart from having resolving chicken pox rash, was suffering from meningitis. He arranged for a lumbar puncture, and an unsuccessful attempt to carry this procedure out took place that same day. 12 The plaintiff was admitted to a ward where, unhappily, her condition did not improve. A lumbar puncture was performed on 13 January 1991 and a CT scan was carried out on 14 January 1991. This evidenced a tumour termed a medulloblastoma. A right frontal intraventricular drain was inserted to relieve intracranial pressure that developed by 14 January, and then, on 16 January 1999, Mr Johnston, assisted by Dr Maixner, operated to remove the tumour. Surgery was successful only in part, leaving an attachment in the floor of the fourth ventricle. Some spread of the tumour over portion of the cerebellum was visible. 13 What has been referred to as "seeding" occurred. When it commenced is an issue to which I will later return. However, chemotherapy treatment was undertaken between 26 February 1991 and 7 May 1991. Radiotherapy was undertaken between 20 May 1991 and 2 July 1991. 14 The plaintiff has survived but is very significantly disabled. 15 This case presents very complex issues, each of which will require close examination. 16 I will later express the allegations of negligence against both defendants in closer detail, but will broadly summarise the position now. Central to the case against the first defendant is the allegation that he should have arranged for the plaintiff to have a CT scan in the period that the plaintiff was under his care between 28 December and 31 December 1990. Had he done so, it is contended that the medulloblastoma would have been detected and it is alleged that the timing and the course of the plaintiff's treatment would have been different, and the outcome for the plaintiff would have been different also. 17 Central to the case against the second defendant is the allegation that he should have arranged a CT scan when the plaintiff came under his care on 11 January 1991, and certainly before the need for the intraventricular drain arose on 14 January 1991. Further, it is alleged against the second defendant that he should not have ordered the lumbar puncture, and that this procedure when undertaken on 13 January 1991 caused the plaintiff's deterioration on 14 January 1991. It is alleged against the second defendant that the prompt arrangement of a CT scan and the avoidance of the lumbar puncture would again have resulted in treatment different in timing and content from the treatment in fact undertaken, with a better outcome. 18 From this broad outline I will proceed to consider in closer detail the allegations that have been pursued against each of the defendants against the background of the detail of the plaintiff's presentation and treatment whilst under the care of the first and the second defendants respectively. 19 The hearing of this cause occupied thirty-six sitting days. There were many witnesses, including many experts, and there is a very considerable volume of exhibits. It would not be practicable nor useful to undertake an exhaustive review of the evidence, and I must necessarily be selective in my references to the evidence.

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The history of headaches 20 The history of headaches and vomiting available to the first defendant when he first saw the plaintiff and, indeed, whilst the plaintiff was under his care is a matter to which considerable importance was attached in the plaintiff's case. It is clear that the referral letter from Dr Sheiban alerted the first defendant to a history of headaches and vomiting for ten days, that is from about 18 December 1990 (see [6] above). However, the plaintiff's mother gave evidence that the plaintiff started vomiting and complaining of headache before 18 December 1990. Mrs Tabet's evidence was that the first complaints were closer to the plaintiff's sixth birthday than that, and, according to Mrs Tabet, she contacted her father, Dr Sheiban, either in late November or early December. Mrs Tabet said that her father then arranged for her to see the first defendant and that she and the plaintiff saw the first defendant at the hospital. Mrs Tabet had no referral letter from her father on this first occasion and, according to Mrs Tabet, the first defendant prescribed an antibiotic and advised of the need for legumes. Mrs Tabet said that she gave her daughter baked beans following this advice, and her daughter was unable to keep them down. 21 The plaintiff's father gave evidence to the effect that his wife saw the first defendant with the plaintiff early in December 1990 but Mr Tabet was not present at that consultation. According to Mr Tabet, after that visit his wife told him that the first defendant had prescribed antibiotics. 22 The first defendant gave evidence of seeing the plaintiff in a consulting room on 28 December 1990 but he had no recollection of seeing her before that date. 23 In determining whether there was a consultation with the first defendant before 28 December 1990, it is relevant to have regard to the evidence of Dr Sheiban and to the records kept in the practice of the plaintiff's grandfather and her uncle. 24 The records of the practice do not refer to any presentation to that practice by the plaintiff with complaints of vomiting and headache before 26 December 1990 and, indeed, as already recorded, the history concerning vomiting and headaches on 26 December 1990 was that they had been occurring for one week, that is from 19 December 1990. There are two earlier 1990 entries relating to the plaintiff. On 28 September 1990 there is an entry "enuresis"; and on 8 November 1990 there is an entry "fever 2 days - mild cough". There are then the two entries previously referred to on 26 December 1990 and 28 December 1990, on each of which occasions complaints of vomiting and headache are recorded. 25 Dr Sheiban Snr is deceased but Dr Asaad Sheiban gave evidence identifying the patient card records. Dr Sheiban said that it was about mid-December that the plaintiff's complaints of headache and vomiting were drawn to his attention. The referral letter on 28 December 1990 was written by Dr Asaad Sheiban, and his evidence was that he obtained a history of one week of vomiting and headache from the plaintiff's parents. 26 Dr Sheiban acknowledged in his evidence the importance of the content of the referral note, and in both the note of 28 December and the note of 29 December 1990 the complaint is consistently recorded of headaches and vomiting back to approximately 18 December 1990: ten days as at 28 December and "more than ten days" as at 29 December. 27 In the circumstances, it seems to me that the most reliable evidence as to when the complaints of headaches and vomiting began is to be found in the plaintiff's patient notes as kept in the practice of Dr Sheiban. I am satisfied on the evidence that there was a close family relationship between the plaintiff's family and her uncle and her grandfather, and if there had been a complaint of headaches and vomiting prompting an earlier referral to the first defendant, the probability is that there would have been an earlier record in the practice notes in relation to earlier complaints. Moreover, the probability is, had it been the case that there was an earlier referral, that there would have been a referral note accompanying it. Further, the referral notes that were written in late December would have recorded a different history. 28 In the circumstances, I am not persuaded by the evidence given by the plaintiff's parents that the first defendant saw the plaintiff at any time prior to 28 December 1990. I do not accept that he did so, and I accept that when the first defendant first saw the plaintiff, he had a history from the referral note which fixed the commencement date of the complaints of headache and vomiting as being about 18 December 1990.

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The course of events between 28 and 31 December 1990 29 As a background against which to consider the case as pursued against the first defendant, I will record my findings as to what occurred during the period from the plaintiff's presentation to the first defendant on 28 December 1990 and her discharge from hospital on 31 December 1990. 30 I am satisfied that Dr Mansour saw the plaintiff and her parents in an outpatients' consulting room such as he described. The plaintiff had first seen the triage nurse who recorded the plaintiff's name and address, her date of birth and the time of her attendance (see Exhibit A, p 323). 31 When he saw the plaintiff for the first time, Dr Mansour had the benefit of the history in the letter of referral. He also had a further history from both Mr and Mrs Tabet. However, for reasons earlier indicated, I do not find that Dr Mansour had seen the plaintiff at any time prior to 28 December 1990, and I do not find that the plaintiff was given any history of headaches predating the time frame in the letter of referral presented on 28 December 1990. 32 Both Mr and Mrs Tabet said that Dr Mansour examined the plaintiff on 28 December 1990, and I find that he did so. I am satisfied that the handwriting appearing on Exhibit A p 323 records Dr Mansour's notes taken on the occasion of his first consultation. He recorded a history of vomiting after meals from 18 December 1990, increasing from 23, 24 and 25 December, and he recorded that the plaintiff was complaining of frontal headaches increasing in severity from 23 December 1990. He recorded a history that the plaintiff was sleeping well at night but that she was less active. He noted the plaintiff had suffered two previous urinary tract infections but that at present she was experiencing no pain when urinating, there was no fever and her bowels were functioning normally. Dr Mansour noted a loss of one kilogram in weight in the last two weeks. Significantly, he noted that the plaintiff's brother had varicella and that his rash had appeared on 16 December 1990. On examination, Dr Mansour detected no neck stiffness and, in general, no abnormality other than noting red spots on her tonsils. Dr Mansour's notes on examination record the following: "O/E [on examination] Not distressed BP 100/ HS No neck stiffness Fundi Cranials No bruits Abdo soft BS [bowel sounds] N [normal] No tenderness Chest No lymphadenopathy Throat - red - spots on tonsils. Ears ok IMP [impression]? possibly URTI [upper respiratory tract infection] ? UTI [urinary tract infection] For msu [micro urine] c&s [culture and sensitivity] Then course of Pen V [penicillin] 125 mg tds [three times a day] 10 days" 33 As previously recorded, Dr Mansour sent the plaintiff, with her parents, to the casualty department for the tests and he prescribed penicillin. The plaintiff was allowed to go home. 34 I am satisfied from the evidence of the plaintiff's parents that they remained concerned about their daughter, that she experienced headache overnight and that she vomited on the morning of 29 December 1990. Hence, the second referral letter was obtained and presented when the plaintiff's parents took their daughter back to the hospital on 29 December 1990. 35 On 29 December 1990 the plaintiff underwent two medical examinations. The first of these was conducted by Dr Durman, and that doctor's notes appear in Exhibit A at p 324. The writing is difficult to read but the history recorded includes a note of intermittent vomiting, headaches and abdominal pain for ten days. The notes indicate that Dr Durman's examination included a neurological examination and that the fundi were normal. The headaches were recorded as being intermittent and frontal. 36 The other medical examination conducted on 29 December 1990 was not conducted by Dr Mansour but by Dr Williams. Notes of his examination appear in Exhibit B at p 553. Dr Williams noted that the plaintiff was alert and orientated. He noted that the plaintiff was not distressed but he detected in the mucosa a sign that the fluid intake may have been inadequate. Dr Williams' notes record, consistently with Dr Mansour's evidence to the like effect, that he spoke to Dr Mansour and Dr Mansour instructed him to admit the plaintiff for a trial of oral fluids. Dr Mansour further instructed, according to Dr Williams' notes, that the plaintiff be given no penicillin whilst the test results from the previous day were awaited. 37 Dr Mansour gave evidence (T 269) that when he decided that the plaintiff was dehydrated and that she should be admitted to hospital, foremost in his mind was the exclusion of a urinary tract infection, depending on the test results, and the other possibility was that this could be the beginnings of a chicken pox illness. 38 The nursing notes for 29 and 30 December appear in Exhibit B p 554:

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(c) The next note was made at 7.00 am on 30 December 1990 and it was recorded by the nurse that the plaintiff had had a good night, with no vomiting. 39 Dr Mansour examined the plaintiff at 12.15 pm on 30 December 1990. His notes at that time are to be found in Exhibit B p 554. They read: "Well, tolerating fluids. No headaches. Start light diet." Then there is an arrow indicating to proceed to "normal diet. For full blood count tomorrow." (I have been assisted by Dr Mansour's evidence at T 270 in interpreting what he has written, and I accept that interpretation, which I do not understand to have been challenged.) 40 There is then an entry on 30 December 1990 at 2.00 pm. This is a nursing note and records that the plaintiff "has had a satisfactory day". It is noted that the plaintiff has no fever and there has been no vomiting. There is a complaint of abdominal pain and of headache "getting better since prescription of Panadol at 8.30 am". It was noted the plaintiff was tolerating clear fluids well. 41 There is a further nursing note for 30 December at 10.00 pm. It is recorded that the plaintiff was given Panadol at 4.05 pm for abdominal cramps and headache and that the plaintiff had vomited and had been refusing fluids. However, she had had two ice creams. 42 The next nursing note is on 31 December 1990. It is recorded that the plaintiff complained of headache on waking at 6.00 am that morning and was given Panadol which "appeared to have the desired effect". It was noted that the plaintiff was eating breakfast and drinking well. 43 Then the plaintiff was seen by Dr Pickford at 11.45 am, according to the hospital records. Dr Pickford, who Dr Mansour identified as a resident medical officer, wrote (see p 555 Exhibit B): "Mild headache this am Nil vomits today. Feeling better. Few small vesicular lesions on neck and behind ear and symph pubis this am. Mother feels child ok to go home after the results of the culture and blood count are available. ? early varicella lesions" 44 That entry is followed by Dr Mansour's entry at 1.30 pm: "Varicella Discharge F/u [Follow up] 2-3 weeks" 45 According to Dr Mansour, before discharging the plaintiff he examined her and he saw chicken pox lesions. Dr Mansour said that he examined the plaintiff's abdomen and found no abdominal signs. Dr Mansour said that he requested the plaintiff to stand and walk to check her balance and coordination. He also said that he checked her eyes with an ophthalmoscope but that he did not record that detail because Dr Pickford had already informed him of her observations, including her observations of the eyes. At the time of deciding to discharge the plaintiff from hospital, Dr Mansour had arrived at a diagnosis that the plaintiff was suffering from chicken pox and that her preceding symptoms were consistent with that diagnosis. I accept the evidence that Dr Mansour gave as to his examination 31 December 1990, his findings and his diagnosis held at that time. 46 I accept, as Mr Tabet said, that Dr Mansour told him: "It is chicken pox. Nothing to worry about. You can take her home now" (T 40). I also accept that he told Mrs Tabet that he was going on holidays and if need be they could see a relieving doctor (T 129). Dr Mansour said that he told the Tabets that if the plaintiff remained unwell, specifically with vomiting, it may be appropriate at some later stage to do a CT scan (T 274). Mrs Tabet said there was no mention of a CT scan (T 129), but whether there was mention or not, it is clear that Dr Mansour recorded in the hospital records no suggestion, recommendation or notation about the possibility of a CT scan being done in the future. 47 Dr Mansour did not see the plaintiff again, at least for treatment, after her discharge from hospital on 31 December 1990, and I will proceed to examine the case against the first defendant having regard to the findings I have now expressed. 48 Before doing so, I record these relevant principles:

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Was Dr Mansour negligent ? 49 The negligence alleged against Dr Mansour in para 34 of the amended statement of claim was expressed as follows: "(a) Wrongly attributed Reema's signs and symptoms of persistent headache, nausea and vomiting to a pre-chicken pox condition when he knew or ought to have known that: A. Reema had been suffering from persistent headache and vomiting from at least 18 December 1990; B. Reema's brother's chicken pox rash first appeared on 16 December 1990; C. The pre-rash prodromal period for chicken pox is short, usually 24 hours, whereas Reema has signs and symptoms 13 days before her chicken pox rash appeared. (b) Failed to arrange for a CT scan of the brain when he examined Reema on 28 December 1990 or during her admission between 29 and 31 December 1990 when he knew or ought to have known that her signs and symptoms were consistent with raised intracranial pressure, the cause of which could have been a brain tumour, and (c) Failed to diagnose Reema's brain tumour." 50 Further particulars were given by letter dated 30 June 2006. I do not propose to set out the content of that letter because ultimately the case as presented focused upon the allegation that Dr Mansour was negligent in not ordering a CT scan, having regard to the plaintiff's history and presentation. It was also submitted that even if he should not have arranged for a CT scan by 31 December 1990, he should have passed on a recommendation or direction that such a scan be undertaken if the plaintiff's symptoms persisted or returned in January 1991. There were in this case many expressions of expert opinion concerning the issue as to whether a CT scan should have been carried out, and, if so, at what point of time. It will be necessary to return to this body of expert opinion when considering the case against the second defendant, Dr Gett, but I propose to review the evidence now to the extent that it addresses the issue as to whether Dr Mansour should have arranged for a CT scan to be undertaken. 51 Mr Johnston was the neurosurgeon under whose care the plaintiff came following the detection of the medulloblastoma. In his report to the defendants' solicitor, which report became Exhibit 11, he expressed the view that he would not have ordered a CT scan upon the plaintiff's presentation at the hospital on 11 January 1991. I shall return to that report when considering the case against the second defendant. However, consistently with the content of the letter, Exhibit 11, Mr Johnston was of the opinion that a CT scan was not required in December 1990. He was asked these questions and gave these answers to Dr Pincus when cross examined (T 721): "Q. Accepting for the moment your view that it would have been - I am not sure whether I have this right, my friend will correct me if I am wrong - a possible thing, would it be reasonable not to do a CT just with the history of ten days, I think you said? A. I would say that it would be reasonable not to do a CT on the basis of that, particularly in a patient that, you know, that might require or would require a general anaesthetic, who has perhaps some evidence of a developing infection. It would definitely be not a good idea to do a CT. There is not enough evidence to do it there in my mind, and there is some indication not to do it. So it's, as I think, I would take - I am not a paediatrician obviously - but I would take it to be a sort of observational position to be taken here awaiting these results." (The results to which Mr Johnston was referring were the culture results of the tests done on 28 December.) 52 And later (at T 727): " PINCUS: Q. Your view was that Dr Mansour had diagnosed chicken pox after seeing the early varicella lesions? A. Yes. Q. That explained the symptoms? A. It certainly, I would think it would. And if I may answer the, at least implied question, I certainly do not think he should have done a CT scan at this point. I definitely don't think he should have done one, that's my opinion."

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Q. And in terms of the headaches, what did you assume about them in terms of their severity? A. I don't have a clear picture of that." 63 I see no persuasive reason expressed in the evidence of Mr Wallace pointing to the need for Dr Mansour to have arranged for a CT scan by 31 December. 64 As I see it, the one witness who expresses the firm opinion that Dr Mansour should have had a CT scan carried out was Dr Williams. Dr Williams is a specialist paediatrician who carries on practise at Menai. He is a former specialist at the Children's Hospital. Dr Williams considered that there was an urgent need from the time that the plaintiff first presented for a CT scan to be undertaken, and this was because of the history of headaches at that time over a ten day period. Dr Williams did not express the opinion that there was an urgent need for a CT scan on 28 December 1990 when he wrote his report on 6 November 2000 (Exhibit M) but he stated this opinion in his lengthy report of 26 May 2006: "I am of the opinion that there was sufficient signs and symptoms of an intracranial tumour and that a CT scan of the brain was urgently indicated and a lumbar puncture was contraindicated. Dr Mansour did not make definitive arrangements for follow up with the parents." (See p 11 of the report) 65 In his evidence before the Court, Dr Williams was asked these questions and gave these answers referable to the above extract from his report (at T 787): "Q. What led you to the opinion that a CT scan of the brain was urgently indicated? A. The symptoms of headache and vomiting persisting for - this is in the context of Dr Mansour or Dr Gett? Q. Dr Mansour. A. Okay. The symptoms of headache and vomiting persisting for ten days. Those were the two principal symptoms that made me think that this child had an intracranial tumour. HIS HONOUR: Q. What were the signs to which you referred in that paragraph, doctor? A. Which signs? Q. The signs of intracranial tumour? A. I am just talking about the history. Q. No, what were the signs? A. There were no signs that were listed on clinical examination, so the history led me to this opinion. Q. You didn't mean that in the strict sense, the medical sense, when you refer to there being sufficient signs? A. Sufficient symptoms I should have said." 66 Later (at T 802): "Q. What are the reasons which led you to express the opinion that a CT scan of the brain was urgently indicated in relation to Dr Mansour? A. Well, the symptoms of headache and vomiting persisting for this period." 67 Then, later (at T 804), Dr Williams opined that Dr Mansour should have suspected raised intracranial pressure on 28 December and he proceeded to say (at T 895): "A. The symptoms before Dr Mansour on 28 December 1990 was that of headaches and vomiting. The child was under his care for the next three days and in that time a prudent paediatrician should have been able to diagnose, on his clinical examination and on the history, a suspicion of raised intracranial pressure. That could have been confirmed in that period of hospitalisation. That's my opinion." 68 He was then asked these questions and gave these answers (T 895): "McCULLOCH: Q. There are two parts to that answer, if I may say so with respect; the first is that his examination should have elicited signs to confirm clinically the suspicion of raised intracranial pressure, is that correct? A. That's correct.

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McCULLOCH: Q. At the time Dr Mansour examined the patient at about 1.30 on this day, that is 31 December 1990, the appearance of the varicella rash was a significant development clinically, don't you agree? A. That's correct. Q. And where there are symptoms which are explicable by a diagnosis of chicken pox don't you agree that it was an appropriate diagnosis to make? A. I have no doubt that this is the correct diagnosis to make when the rash appeared. HIS HONOUR: Q. But you say the headaches cannot be explained by the appearance the rash? A. What I am saying is that the diagnosis was not in doubt when the rash appeared of chicken pox. What I am also saying is that the headaches and vomiting cannot be accounted for by chicken pox alone." 70 It emerged it was Dr Williams' understanding that Dr Mansour did no full neurological examination before the plaintiff was discharged but, whether a full neurological examination was conducted or not, it made no difference to Dr Williams' opinion. 71 Mr McCulloch submitted that I should attach no weight to the evidence given by Dr Williams. He submitted that Dr Williams repeatedly expressed opinions which amounted to saying what he would have done in the circumstances rather than expressing a view as to what a reasonable clinician would have done: see the cross examination T 845-846. He submitted that Dr Williams' criticism of Dr Mansour's approach was based in part upon the mistaken understanding that Dr Mansour did not do a full neurological examination before he discharged the plaintiff. Whilst that is true, what Dr Williams based his opinion on was the duration of the history of headaches and vomiting. Mr McCulloch submitted that the doctor did not give his evidence in an objective manner and that he was evasive. 72 It is plain from the review of the evidence that I have undertaken as to whether the exercise of reasonable care required of Dr Mansour that he arrange for a CT scan to be undertaken, that Dr Williams is in the minority in the view that he has expressed. Of course, it does not necessarily follow that I should not find his evidence persuasive. However, there is some substance in the submissions of Mr McCulloch recorded above. Moreover, Dr Williams wrote of "signs and symptoms" of an intracranial tumour in his report of 26 May 2006, and conceded in evidence there were no signs whilst the plaintiff was under Dr Mansour's care. In addition, in contrast to what he had written, Dr Williams ultimately said in cross examination that it was not until 31 December 1990 that a CT scan should have been undertaken. No sign emerged on that date. What did emerge then were the first of the varicella lesions. 73 The issues in this cause are not to be determined by counting the number of experts supporting a party on a particular issue, but I find myself persuaded by those witnesses who have expressed the contrary view to that voiced by Dr Williams. 74 Moreover, I am influenced by the fact as I find it that in none of the various neurological examinations conducted between 28 and 31 December 1990 were there any neurological abnormalities detected. Further, I am satisfied that the chicken pox rash was evident at the time of discharge. 75 It was Dr Mansour's evidence that during the incubation period, which can last from ten to twenty-one days, there can be a multitude of symptoms, including headache, lassitude and weakness. Dr Mansour was asked these questions and gave these answers (T 1656): "Q. See, one couldn't attribute that history of headaches from 18 December onwards till when the rash appeared as being part of the prodromal period for chickenpox? A. Using specifically the term prodromal period, you are correct.

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Q. Well, on what basis do you say that it was consistent with the emergence of varicella on the 31st? A. During the incubation period, your Honour, you can have a multitude of symptoms which are non-specific in chickenpox and that period - the incubation period can last from between 10 to 21 days and headache, lassitude, weakness can be a part of that, general non-specific symptomatology." 76 Dr Mansour's evidence that there can be symptoms during the entire incubation period referable to the varicella finds no support in the other evidence in this case, which seems to confine varicella related symptoms to the prodromal period. Nevertheless, having closely considered the evidence and the competing submissions, I am not persuaded that the exercise of reasonable care required of Dr Mansour that he arrange for a CT scan at any point of time prior to the plaintiff's discharge from hospital on 31 December 1990. 77 Was the first defendant negligent in failing to pass on a recommendation or direction that a scan should be undertaken if the plaintiff's symptoms persisted or returned in January 1991? 78 Dr Mansour said that the appearance of the chicken pox rash sufficed to account for the plaintiff's symptoms and that the plaintiff had no abnormal neurological signs. Dr Mansour acknowledged that he made no entry in the hospital records to the effect that the plaintiff should have a CT if she represented, but his evidence was that he had no concerns that the plaintiff was going to represent (T 1666). Earlier, Dr Mansour gave these answers to these questions (at T 1666): " HALL: Q. I suggest to you Dr Mansour, that you needed to make a note in the hospital records that if she re-presented to the hospital with a continuing history of headache, she should be submitted to CT scanning? A. That question, I have to pre-empt it first by stating that at the time of discharge I had concluded that the diagnosis was varicella which was causing her symptomatology. And I always do this in my practice, when any child presents with headache, I cover myself and say if headaches were to persist, severe headaches persist and no other cause to be found and neurologically to examination, the child is normal, but the headaches are persisting, then a CT scan is indicated and that's what I basically had said at the point of discharge to the parents. But in my mind, I was well and truly comfortable with the diagnosis that this is a child who had varicella with a long incubation period with symptomatology causing severe abdominal pain more than the headache, right, the abdominal pain was more than the headache.

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Q. What was the basis of the view you formed? A. That she had resolving chickenpox lesion of her skin and I was concerned that she may have varicella or chickenpox meningitis and encephalitis." 94 Whilst Dr Gett kept no detailed notes of that examination, I accept the above description as given by him to be reliable. He wrote a note to the admitting doctor, Dr Kohn: "Dear Michael, Thank you for admitting Reema who has clinical signs of meningitis. She has resolving varicella rash. She needs L.P. and IVI fluids. Thank you for your help." (See Exhibit C, 566) 95 The hospital records describe the examination findings of Dr Kohn, which I am satisfied were made after Dr Gett had referred the plaintiff for admission. Dr Kohn gave evidence as well. He had no real recollection of the examination nor of the attempted lumbar puncture but, nevertheless, I accept his notes in the hospital record as being reliable. He recorded in those notes (see Exhibit C, 576A and 577): "Developed chicken pox - rash on 31.12.90 - following 1 week prodrome of vomiting for which she was admitted under Dr Gett. At home she developed severe rash - involving chest/[abdomen]… She [complains of] cont. headaches & intermittent [abdominal] pain. 48 hr [decreasing] appetite. This morning began vomiting again x 4 - becoming lightly bile stained. Pain - controlled with Panadol. [Seen by] Dr Gett - who has requested admission." 96 Dr Kohn went on to record his examination findings: "alert orientated dozing [A note which the doctor interpreted as meaning speech intact] afebrile [Blood pressure] 110/70 [a reading I accept to be somewhat high] HR 130/min RR 24/min" 97 Dr Kohn went on to record results of his neurological examination. Pupils were examined and found to be normal. He examined various cranial nerves and he tested the neck for stiffness. 98 Accepting as I do the hospital notes in this regard as reliable, they record no sign of neurological abnormality at the time Dr Kohn examined the plaintiff. 99 The notes next record an examination by Dr Blissta on the same date. I will not record those notes in detail but they convey that on examination the plaintiff was afebrile, conscious and well orientated, and that there were no meningeal signs. Some examination of the central nervous system was conducted and, again, it showed no abnormality according to the doctor's note. 100 Whilst Dr Kohn had no recollection of attempting a lumbar puncture, the hospital note records that he carried out an unsuccessful attempt, and he discussed this result with Dr Gett. 101 The next recorded medical examination was on 12 January 1991, and this was an examination carried out by the second defendant. He said that he saw the plaintiff on his ward rounds and that he conducted a neurological examination specifically of the ocular fundi and he checked the plaintiff for neck stiffness, power and tone. Dr Gett's notes of this examination I record: "Still vomiting Afebrile Some neck guarding - probably no stiffness Hydration better [Abdomen] [No abnormality detected] Chest clear [ Diagnosis ] Viral infection Plan Defer [lumbar puncture] [for time being] Check on blood count Clear fluids - continue [intravenous infusion] { LMO (who is also [maternal] grandfather) - { Notified Dr Sheiban" 102 Dr Gett decided to defer a lumbar puncture for twenty-four hours because the plaintiff was "clearly irritable and crying" (T 408). 103 The next notes made by a doctor are notes of Dr Jones at 11.00 am on 13 January 1991. I will not record the content of the nursing notes between Dr Gett's examination on 12 January and Dr Jones' examination on 13 January 1991, except for the important notes recorded at 11.45 am, but evidencing events that occurred before Dr Jones made his examination that morning. The entry at that time is in these terms (Exhibit C, 582): "Father called out to nursing staff that Reema was staring and unresponsive. On observation by staff, [patient] responsive but irritable and drowsy and complaining of headache. Pupils noted to be unequal and [right] pupil not reactive. [Blood pressure] 131/85, other observations within normal limits. RMO notified. LP attended. [Seen by] Dr Gett, family reassured. [Patient] settled at time of report. Pupils now equal and reactive." 104 Mr Tabet gave evidence of what he had observed prompting him to call the nurse. He saw his daughter lying still and staring into space at about 11.00 am. I am satisfied it is the description of this event which prompted the attendance of the nurse and the nursing note to which I have referred. 105 Dr Jones was the registrar on duty, according to the hospital record, and that record reveals his note that he was asked to see the patient because of unequal pupils (Exhibit C, 581-582). His note relevantly reads: "Viral encephalitis Now [increasing] headache drowsy since [On examination] fundi [normal] pupils equal and [reactive] answers commands [Discussed with] Dr Gett. He wishes LP and then review of patient by himself later on today." 106 A lumbar puncture was performed at approximately 11.30 am on 13 January 1991, shortly after the above examination by Dr Jones. His note concerning that procedure and its outcome was: "LP at L3/L4 low pressure 3-4 mls of clear CSF" 107 That fluid was sent for examination. 108 The nursing notes at 1.00 pm record: "Nil further episodes of unequal pupils today. Observations stable, afebrile. Appears more settled. Given Panadol for headache at 1400…" 109 Then, at 9.40 pm it is recorded: "Neuro observations remained stable this evening pupils equal and reacting…" 110 Mr Tabet said that there was an incident about 9.00 pm on 13 January when he observed the plaintiff staring again and he called the nurse, but that is not reflected in the hospital notes. However, Mr Tabet said that a doctor attended, and this may be a reference to Dr Lane, who did examine the plaintiff on 14 January 1991. Dr Lane appears to have examined the plaintiff at 1.00 am, and he noted persisting headache not relieved by regular doses of paracetamol and codeine. Dr Lane noted that the neurological signs were stable. On examination he found the plaintiff to be afebrile. As I read the notes, he detected no neurological abnormality but there was neck guarding and stiffness. Dr Lane noted concerns of the parents for a neurological review, and concluded his note: "Dr Gett aware and will arrange neuro consult." 111 At 5.15 am on 14 January 1991 the nurse wrote (Exhibit C, 583): "Reema has had a very unsettled night. Complaining of a headache. She has had codeine phosphate sixth hourly and panadol regularly with very little effect. Viewed by Dr Lane at 1 am…and for review again about 5.45 am." 112 There are medical notes at pp 585 and 586 of Exhibit C. It is not clear what time Dr Brooks made his notes, but the notes include an entry "sent for CT scan". Dr Brooks' notes are followed by the registrar's note which does bear the date 14 January, and at that time the plaintiff was unresponsive, and it is recorded that she had been "since seizure at midday". 113 The nursing notes written at 2.45 pm on 14 January (Exhibit C, 587) probably put the notes at 585 and 586 into perspective. It is recorded that at 11.45 am the plaintiff's mother called for a member of staff to look at Reema. She was staring into space and was unresponsive on examination. Moreover, the pupils had deviated to the left side. Dr Ouvrier, a neurologist, was called and the plaintiff was taken for a scan at 12.40 pm. This was the CT scan which detected the medulloblastoma. 114 Following the scan, arrangements were made for the insertion of a ventricular drain. Dr Maixner's notes of the examination preceding that procedure appear at Exhibit C, 588. Dr Maixner first saw the plaintiff shortly after the CT scan in the EEG department, where it was clear to Dr Maixner that the plaintiff was having episodes of decerebrate posturing with extension of her limbs. The EEG was not then showing seizure activity and Dr Maixner did not consider that the plaintiff had an epileptic seizure. Following her examination, Dr Maixner proceeded to insert a right frontal external ventricular drain. 115 Dr Maixner reported (in Exhibit G, her report dated 4 July 2006) that the plaintiff had improved with CSF drainage by 15 January 1991, but the extent of any improvement and its significance is a matter to which it will be necessary to return later. On 16 January 1991 Mr Johnston carried out the operative procedure to remove the tumour. Dr Maixner's observations at operation, as recorded in Exhibit G, were that "a large tumour was found arising from the wall of the fourth ventricle on the right side. The tumour had spread in a subpial fashion over the surface of both cerebellar hemispheres and was protruding over the foramen of Magendie. I documented that an incomplete removal of the tumour was achieved." 116 I will trace the course of events following the plaintiff's surgery later in this judgment, but I now address the allegations of negligence ultimately advanced as against the second defendant which follow on the events thus far recorded.

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(iii) Dr Gett was negligent in pursuing a provisional diagnosis of post chicken pox encephalitis or meningitis, particularly having regard to the history of headaches. 119 Earlier I expressed some matters of principle to be considered when assessing the case against Dr Mansour (at [48] above). Those same principles are to be considered when assessing the case against Dr Gett, who was also consulted as a specialist paediatrician. With the benefit of hindsight, it is clear that Dr Gett's provisional diagnosis was incorrect, but Dr Gett's care of the plaintiff is not to be measured by resort to hindsight; rather the issue to be determined is whether in caring for Reema, Dr Gett exercised reasonable care, measured by reference to the standard of care required of a specialist paediatrician. 120 Mr McCulloch submitted that the differential diagnosis which Dr Gett made on 11 January 1991 was a reasonable one. I referred earlier to Dr Gett's observations, his recollection of the history that the parents gave him and to his examination. Mr McCulloch submitted that Dr Gett's examination ruled out the existence of evidence of raised intracranial pressure at that time. Dr Gett tested for neck rigidity and stiffness and it is submitted that it was reasonable, there being a resolving chicken pox rash, that Dr Gett would want to rule out inflammation of the lining of the brain by doing a lumbar puncture. Mr McCulloch submitted that Mrs Tabet acknowledged that the examination took place and she recalled that Dr Gett told her he felt stiffness on one side of the neck and this was indicative of encephalitis. Mrs Tabet agreed that Dr Gett said there was a need to rule out post chicken pox encephalitis (T 186). Hence the need for the note to Dr Kohn advising him that the plaintiff had "clinical signs of meningitis" (see Exhibit C, 566). 121 Dr Gett referred to meningitis and encephalitis as being interchangeable expressions. 122 There is support in the medical evidence for the reasonableness of Dr Gett's provisional diagnosis. 123 Dr Allen reported on 8 November 2001 (Exhibit 17) that varicella encephalitis is an uncommon complication of varicella occurring, usually, within ten days of the rash (see p 4 of his report of that date). Dr Allen described it as reasonable to express "the principal provisional diagnosis at this time as being varicella encephalitis". Dr Allen referred to a published article of Cherry and Shields (part of Exhibit 17) in which the most common initial manifestations of encephalitis were stated to "resemble an undifferentiated acute systemic illness with fever, headache or, in infants, screaming spells, and abdominal distress, nausea and vomiting." 124 Mr Johnston in his earliest report (Exhibit 11) expressed the opinion that Dr Gett's diagnosis of post chicken pox encephalitis made on 11 January 1991 was "entirely appropriate" in the absence of any signs of intracranial hypertension and no focal neurological abnormality. See also the evidence of Mr Johnston to the like effect (at T 679). 125 Professor Watson opined that "there were very good reasons to think that" the plaintiff had post chicken pox encephalitis (T 1863). 126 Dr Knight agreed that in a patient who had been exposed to varicella virus it was important for the clinician, where the presenting symptoms included headache, to include meningoencephalitis in any provisional diagnosis (T 1236). 127 Mr Wallace agreed (at T 1371) that on the information which Dr Gett had, including confirmed chicken pox, a diagnosis of chicken pox encephalitis or meningitis was utterly understandable subject to the problem of the headaches and vomiting, which he referred to as "a red light". As to that "red light", Mr Wallace said this (at T 1370-1371): "The thing that sticks in my mind about this case is that there's headache and vomiting that's come within two days of the exposure to chickenpox and, therefore, we're still in the incubation period of chickenpox and it's so easy, with hindsight every child I see with headache and vomiting has got a brain tumour, so I don't see the hundreds of patients that go in with other things such as migraine and headache and vomiting but, looking at this specific case, the red light is that there is headache and vomiting within two days of exposure to chickenpox so to my mind that means that it can't be chickenpox encephalitis. Then it goes on for two weeks…" 128 Mr Klug refrained from expressing an opinion as to whether or not the provisional diagnosis was a reasonable one (T 1704). 129 Dr Sheiban agreed if there was a possibility of encephalitis, it was reasonable to address that first (T 243). 130 Having regard to the evidence reviewed, Mr McCulloch submitted that it was reasonable for Dr Gett to form the provisional diagnosis of post chicken pox encephalitis at the time of the plaintiff's readmission to hospital on 11 January 1991. Further, he submitted, that the period of readmission was a short one and no neurological signs were detected, at least in the first forty-eight hours after readmission. Hence, Mr McCulloch submitted, that it was reasonable to maintain that provisional diagnosis until the CT scan was undertaken. 131 Mr Hall submitted to the contrary. He submitted that the diagnosis of post chicken pox encephalitis was not maintainable and drew attention to the circumstance that the plaintiff was afebrile throughout and to the further circumstance that neck stiffness was not detected following the plaintiff's readmission. Dr Kohn found no neck stiffness and Dr Blissta found no meningeal signs later on that same day. On the other hand, Dr Lane did detect neck stiffness on the examination referred to earlier (see Exhibit C, 584). 132 Having regard to the evidence reviewed, I consider that the provisional diagnosis which Dr Gett formed was an understandable one at the time he formed it, subject only to the history of headaches. As I indicated in the course of submissions, I have found this history to be a troublesome feature in the approach by Dr Gett to the formation and maintenance of his provisional diagnosis. 133 For reasons Dr Gett explained, there are no notes of his initial examination or of the history taken but Dr Gett's recollection was that he obtained a brief history from the parents and that that included a history of some headaches. That put Dr Gett on notice that headaches were a feature of the plaintiff's presentation. Had Dr Gett consulted the notes concerning the original admission, he would have seen the referral letter from Dr Sheiban recording a history of headaches commencing on 18 December 1990. Dr Gett never saw the records of the previous admission, although a reading of the record as to the readmission would have alerted him to the plaintiff's earlier admission to hospital. Dr Kohn referred to the earlier admission in the history he recorded on 11 January 1991: Exhibit C, 576A. 134 Dr Gett was asked these questions and gave these answers (T 435): "HIS HONOUR: Q. Doctor, I am still not clear as to what history you had as to when the headaches and the vomiting had started, at the time you referred her for admission and then on the day following when you saw her after she had been admitted -- A. Yeah.

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(b) the period after that episode and the performance of the lumbar puncture 142 There is a division of medical opinion in this case on the issue as to whether a CT scan should have been arranged, and, if so, when. 143 Mr Johnston firmly supports the approach that Dr Gett took throughout his management of the plaintiff's treatment. Mr Johnston, in his first report, Exhibit 11, expressed the opinion that he would not have ordered a CT scan of a child with a viral illness who had no focal neurological abnormality and no raised intracranial pressure. He considered the risks associated with an anaesthetic in the plaintiff's case and came to the conclusion that a CT scan was not warranted. When asked about the opinion he expressed in his report, Mr Johnston responded to the following question in the following way (T 730): "Q. …You said, in the report of 24 January 2001, that you would not have personally ordered a CT scan at that time, meaning 11 January 1991, when the child was admitted back under Dr Gett with an unquestioned viral illness without evidence of intracranial hypertension. I put it to you that there was evidence of intracranial hypertension by that time, namely persistent headache and vomiting, from 18 December 1990? A. By evidence I mean any physical signs. Q. Well, aren't headaches and vomiting, persistent over a long period, evidence of a hypertension? A. They are evidence of a lot of things, not sufficiently specific alone to warrant, in my opinion, a CT scan, without any other evidence, and with an alternative reasonable diagnosis. That was my position then and is now. Q. The alternative reasonable diagnosis you refer to? A. The post viral encephalitis." 144 Dr Allen referred to the risk of giving CT scans. He said (at T 1155): "When one looks at the risk of CAT scans as opposed to risk of not doing a CAT scan, one needs to say CAT scans need to have a real reason to be done in children. There is actually an increased risk of tumours in children who have CAT scans. So the reason for doing the CAT scan is if there are focal neurological signs and this is very consistent…" 145 Then (at T 1172), Dr Allen gave the following evidence: "Q. Doctor, I suggest to you that at this stage, this is on the 12th, the morning of the 13th, we had this continuing history of headaches and vomiting, no sign, no diagnostic sign of meningitis and therefore the time had arrived to do a CT scan? A. The time had arrived to investigate this in an appropriate way. Now in retrospect it is easy to say that a CAT scan should have been done on 12 January. Prospectively, when one is thinking that this may be one of the post infectious phenomena now related to chickenpox, one looks at what is most likely to be the cause of - the causation of the problem. Then one determines the - which tests one does. Again, there are no focal neurological signs so one is - the clinician is not thinking this is some space occupying lesion in the brain at this moment in time. He can't because--

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Q. Doctor-- A. If I could finish? Because if it was a space occupying lesion and it was in the posterior fossa, one would expect other clinical signs to be present and they're not." 146 Dr Allen went on to say there was no contraindication to a lumbar puncture on 13 January, but I will refer more closely to that evidence presently. 147 Professor Watson did not agree that the presentation of the plaintiff on 11 January called for a CT scan, even if there was a history of headaches and vomiting on 18 December. At T 1879: "HALL: Q. If it were the fact that a patient had presented at hospital and had been admitted to hospital and presented to hospital first on the 28th, then presented on the 29th and been admitted to hospital between the 29th and 31st of January when varicella was noted and she returns - and on those earlier admissions there was a history of more than 10 days headache and vomiting, I want you to assume they present on the 11th of January 1991 with a history of continued headaches and vomiting over the interval period. When she represented would you not agree that she should have been submitted to a CT scan? A. No, I would not agree that she should have been submitted to a CT scan." 148 Professor Watson considered it appropriate for the lumbar puncture to be done when it was. I will refer to his evidence in that regard shortly. 149 I turn to record the opinions critical of the failure to carry out a CT scan before the lumbar puncture was performed. 150 Dr Hopkins considered that a CT scan should have been done on 11 January because of the continuing headache and vomiting (T 1076). 151 Dr Hopkins went on to add that it was his opinion that a general paediatrician should have arranged for an urgent CT scan to be performed on 11 January. Dr Hopkins adhered to that view in cross examination (T 1084). 152 Not surprisingly, since Dr Williams thought that Dr Mansour should have done a CT urgently when he saw the plaintiff, Dr Williams thought that Dr Gett should have done a CT as at 11 January (T 815 and T 937). Dr Williams was critical of the diagnosis that Dr Gett made and said he would not have made it (T 939). 153 Dr Knight considered that having regard to the history of headache and vomiting, a CT scan should have been done as soon as possible after the episode on 13 January. 154 Dr Knight's evidence was (T 1217): "Q. To what extent, if at all, do you say a lumbar puncture should not have been performed when it was on 13 January? A. I think the episode of dilated pupils, even though it was not sustained, was a serious observation and a clinically significant observation and it should have been combined with the history of headache and vomiting to raise even further the concern that this child had an intracranial pathology and if that is a significant consideration then a lumbar puncture is contraindicated.

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Q. What about down to the 13th, once that single focal sign had been observed could, in your view, a CT scan be postponed or to not undertake? A. No, I don't think so." 156 Then, in cross examination (at T 1258): " HIS HONOUR: Q. Do I understand your position to be this; given ten days of headaches and vomiting without a satisfactory explanation, once there was an appearance of abnormal neurological signs, on the one occasion, that was enough to warrant the CT as the next investigative technique? A. Yes, that's right. McCULLOCH: Q. But before that time do you agree, Dr Knight, that the presentation, absent those clinical neurological signs, did not warrant the use of a CT scan? A. That's slightly different, it did warrant them. The investigation would have been perfectly justified, even if it had been negative, because of the nature of the symptoms, but I don't think I could say it was poor practice to not do it at that stage. There is an important difference. Q. Thank you very much. Will you agree that so far as the symptoms of headache and vomiting were concerned, without the appearance of the focal neurological signs on 13 January 1991 it would have been reasonable to continue to observe this patient? A. Yes. Q. And will you agree that once the focal neurological signs appeared on 13 January 1991 and were seen to resolve within or by the time Dr Jones saw the patient that it was then reasonable to continue to monitor the child by observation? A. No. Q. At that point you say that a CT scan should have been undertaken? A. Yes." 157 Mr Wallace, as a neurosurgeon, considered that headache and vomiting raised the possibility of raised intracranial pressure and the need for a scan (T 1391). Mr Wallace considered there was an absolute indication for a scan on 13 January 1991 after the staring and unresponsive episode (Exhibit C, 582). As to this, Mr Wallace said (at T 1536), commenting on the combination of the nurses' notes and the notes of Dr Jones: "Q. It was what was observed by the nurse you understand, that attracted Dr Jones? A. I think Dr Jones - should I comment on my views on this?

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Q. What number of days did you have in mind? A. Well, since the start of the complaint of headaches and vomiting." 164 Dr Maixner gave evidence as to the need in her opinion for a CT scan to be carried out on 13 January. Her evidence in point was taken on the voir dire, but it proceeded to form part of the evidence in the case, and Dr Maixner said (at T 2172): "If I had been called about the child where she had an episode of unequal pupils, in the context of headache and vomiting, I would have recommended a CT scan that day, yes." 165 Dr Kellie appears also to be of the opinion that a CT scan should have been done before the lumbar puncture. This emerged in re-examination when he indicated it was not his view that in the absence of unequivocal signs of intracranial pressure a CT scan was not required before a lumbar puncture (T 649). It also emerged (at T 649) that Dr Kellie had agreed with Dr Pincus at a conference before the hearing that a CT scan should have been done earlier than it was performed. 166 The above review highlights the divergence of expert opinion in this case on this particular issue. I had occasion earlier to review the evidence of expert opinion in the case of Dr Mansour, and what I am about to record in the present context applies also in Dr Mansour's case. 167 In Bolam v Friern Hospital Management Committee (1957) 1 WLR 582 it was determined that a doctor who had acted in accordance with a practise accepted as proper by a responsible body of medical opinion skilled in the area was not guilty of negligence merely because there was a body of competent professional opinion that might adopt a different approach. The Bolam approach was not followed in F v R (1983) 33 SASR 189, in which King CJ said (at 194): "The ultimate question, however, is not whether the defendant's conduct accords with the practices of his profession or some part of it, but whether it conforms to the standard of reasonable care demanded by the law. That is a question for the court and the duty of deciding it cannot be delegated to any profession or group in the community." 168 The High Court approved of the above stated approach by King CJ in Rogers v Whittaker (supra): see the joint judgment of Mason CJ and Brennan, Dawson, Toohey and McHugh JJ at 488-489. 169 Rogers v Whittaker was, of course, a case concerning the extent of a medical practitioner's duty to warn of the possibility of adverse consequences of contemplated treatment and the decision recognises "a fundamental difference between on the one hand, diagnosis and treatment and, on the other hand, the provision of advice or information to a patient" (at 489). The judgment has to be considered in that context. However, their Honours in the joint judgment did address the relevance and probative value of expert opinion concerning treatment (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…" 170 Gaudron J said as to the role of the Bolam test (at 493): "…even in the area of diagnosis and treatment there is, in my view, no legal basis for limiting liability in terms of the rule known as 'the Bolam test' which is to the effect that a doctor is not guilty of negligence if he or she acts in accordance with a practice accepted as proper by a responsible body of doctors skilled in the relevant field of practice. That is not to deny that, having regard to the onus of proof, 'the Bolam test' may be a convenient statement of the approach dictated by the state of the evidence in some cases." 171 The Bolam approach has been introduced into the Civil Liability Act 2002 in s 5O of that statute: "(1) A person practising a profession ( a professional ) does not incur a liability in negligence arising from the provision of a professional service if it is established that the professional acted in a manner that (at the time the service was provided) was widely accepted in Australia by peer professional opinion as competent professional practice. (2) However, peer professional opinion cannot be relied on for the purposes of this section if the court considers that the opinion is irrational. (3) The fact that there are differing peer professional opinions widely accepted in Australia concerning a matter does not prevent any one or more (or all) of those opinions being relied on for the purposes of this section. (4) Peer professional opinion does not have to be universally accepted to be considered widely accepted." 172 Mr McCulloch has acknowledged in his written submissions that s 5O of the Civil Liability Act does not apply in this case. The significance of the expert evidence such as I have reviewed is to be approached with the above cited dicta from Rogers v Whittaker in mind. 173 I must determine whether the second defendant has exercised reasonable care assisted in that task by a consideration of the expressions of medical opinion reviewed such as I find persuasive. 174 What happened at about 11.00 am on 13 January 1991 introduced an additional element to be weighed by Dr Gett in the exercise of due care. Now, for the first time since the plaintiff was readmitted to hospital, and, indeed, for the first time since the plaintiff was referred for treatment to Dr Mansour, a neurological sign has been observed. The plaintiff has been observed to be staring and unresponsive and, significantly, her pupils were noted to be unequal and the right pupil was not reactive. 175 This development having occurred, was the second defendant negligent in arranging for the lumbar puncture to proceed? 176 It is to be recognised that the abnormality observed by Mr Tabet and by the nursing staff did not persist. By the time Dr Jones examined the plaintiff, the fundi were normal and Dr Jones noted the pupils were equal and reactive and that the plaintiff answered commands. 177 Dr Gett examined the plaintiff on 13 January but was unable to recall the details (T 412). He spoke to Dr Jones about doing the lumbar puncture. He said that he was still concerned about Reema's condition in that he did not have a definitive diagnosis and this was the context in which he requested that the lumbar puncture be done (T 413). 178 That decision made by Dr Gett is supported by Mr Johnston, Dr Allen and Professor Watson. 179 Mr Johnston considered that the decision was reasonable in the absence of evidence of raised intracranial pressure. Mr Johnston reported that the lumbar puncture was "a completely appropriate investigation and did not under the circumstances require prior CT scan" (see Exhibit 11). 180 Mr Johnston said in evidence (at T 676): "Q. When you recorded in your report 'there is absolutely no documentation of clinical signs of raised intracranial pressure or focal neurological disturbance', what was it you had regard to as the source of any potential documentation, if it existed? A. The thing I mentioned earlier this morning, papilledema and sixth nerve palsy, and the focal disturbance would have been any abnormality of motor function or sensory disturbance or cerebella function. I mean a number of people carried out an examination which was recorded and in no case was there the evidence of raised intracranial pressure." 181 Then (at T 678): "Q. Bearing in mind that you had assumed that there was a history given of, a ten day history of nausea, vomiting and headache, why do you say there was nothing to support a diagnosis of intracranial neoplasm? A. Because as I explained this morning the symptoms of headache, nausea and vomiting are very non-specific and can occur in a whole variety of things. So that if a patient presents with those symptoms then the purpose of the examination is to try to identify at least which system is involved, like the nervous system, gastrointestinal system, or whatever, and if the patient has a raised intracranial pressure you would expect to find some supporting evidence of the form we have discussed. In other words, the clinical signs. But as I mentioned also this morning they are not invariably present. So that the person, in a general sense, the person assessing a patient will go through the examination and will try to identify the source of these symptoms and if they don't find any signs of raised intracranial pressure they will conclude provisionally that it's not present, but they can't conclude unequivocally that it isn't present. Q. In that event, in the event you have just described, is there a role to be played in further neurological examinations from time to time? A. Yes. Q. And what is that role? A. Well, it depends. I mean if, let us say, some satisfactory other explanation is found for the signs or the symptoms particularly, then - and even a diagnosis is made then that doesn't implicate the nervous system then there isn't much point in further neurologic investigation. If the matter is still open then every possible cause has to be considered. I mean, I don't expect there are any figures on this, but if you were to think or to take, for example, all patients presenting with the symptoms of headache and vomiting, a minuscule number of those would be patients with raised intracranial pressure. Q. What do you mean by minuscule, can you volunteer a percentage? A. I tried to indicate that I couldn't. An absolute guess would be under one per cent. No, a fraction of that. Such common symptoms. The direct answer to your question though is I have no idea in actual fact." 182 Later (at T 679): "Q. Now turning to the question of the lumbar puncture, did you form a view about whether a lumbar puncture was appropriate in Reema's case on about 13 January 1991? A. Well, I thought it was. I still think it was, actually. I have seen no reason to change my position. Q. Why do you say that? A. I think that, as is clear from all the records, she had chicken pox and she then represented with these further symptoms and the diagnosis, as I have indicated here, of post chicken pox, post viral encephalitis, in the absence of raised, signs of raised intracranial pressure was a reasonable one. Therefore, a lumbar puncture to try to confirm that diagnosis was, in my view, a reasonable approach to these clinical situation." 183 Dr Allen considered that it was reasonable to do the lumbar puncture after the episode at 11.00 am on 13 January. At T 1138: "Q. Bearing in mind those entries [referring to the nursing notes and Dr Jones' notes, 581-582], what, if anything, is the significance of what was observed before the lumbar puncture was undertaken in terms of whether or not the lumbar puncture should have been proceeded with? A. When Dr Jones reviewed the patient the patient has equal and reactive pupils and has normal fundi. So when one, before one does a lumbar puncture one has to be satisfied that the patient is fit to lumbar puncture; and it is good clinical practice before one indulges and does that test to look in the fundi to make sure someone is happy with that. The episode of unequal pupils which settled rapidly, which resolved rapidly may have been either a, it could have been considered - the first question is did it really happen. If we assume that it did happen then it could be the first clinical sign that there is some other process going on. It could be that she had, in association with her encephalitis, some form of seizure, which is related to the infective process. It could be that there was some other post chicken pox event happening; for example, the commonest problem neurologically after chicken pox is acute cerebella ataxia. So there are a number of neurological things that could be causing this to happen. Because she was neurologically normal when Dr Jones saw her it is reasonable to proceed with the lumbar puncture because we still believe that this is a post infective, this is an infective phenomena, not because there is a space occupying lesion there, which becomes evident some time later. I think because of the duration of this illness now the primary diagnosis is still the primary diagnosis, and Dr Gett is trying to confirm that diagnosis for the family." 184 Dr Allen referred to what was seen about 11.00 am as "a transient neurological observation". 185 Professor Watson thought that it was reasonable to perform the lumbar puncture notwithstanding what had happened at about 11.00 am (at T 1862-1863): "Q. What view do you have about whether or not a lumbar puncture was appropriate on 13 January 1991 after there had been those signs observed at or before 11am taking into account the working diagnosis reported in the hospital notes which you've assumed as part of the history? A. I think it was a reasonable test to do. In fact, Dr Gett had intended it be done at--

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The issue of damages 194 It is the plaintiff's case that earlier detection of the medulloblastoma and the avoidance of the deterioration that occurred some twenty-four hours after the lumbar puncture would have enabled the plaintiff to make a good recovery following surgery and radiotherapy. Mr Hall relied in particular upon the evidence of Mr Wallace and Mr Klug, and submitted that but for the negligence of the defendants and each of them the plaintiff would have been able to lead a relatively normal life. Unhappily, this has not proved to be possible and the plaintiff is, and will remain, profoundly disabled. 195 Whilst the extent of the plaintiff's disabilities is not challenged by the second defendant, there is a very real issue on causation. It is the defendant's case that the plaintiff's disabilities are the consequence of the growth of the tumour and the hydrocephalus, together with the unavoidable consequences of the surgery performed by Mr Johnston and the extensive chemotherapy and radiotherapy which followed. 196 The breach of duty which has been proved is limited to the decision made by the second defendant after the abnormal episode that occurred at approximately 11.00 am on 13 January 1991. Whether that breach of duty was causative of harm presents an extremely difficult issue, but before I consider that issue, it is desirable that I address the question of the damages that would have been attracted in the event that the plaintiff was entitled to be compensated for all the harm that she has suffered as has been claimed on her behalf. 197 The parties reached agreement on most of the heads of damage in the event that the plaintiff was found to be entitled to be compensated for the effects of all the brain damage she has suffered, with all the attendant disabilities. 198 It is common ground that the plaintiff will never be capable of employment and that the plaintiff will always require full time care. 199 Dr Oakeshott, who is a specialist in rehabilitation medicine, assessed the plaintiff on 19 September 2001. He did not expect that there would be improvement in the plaintiff's condition at that time and, having seen the video evidencing activities of the plaintiff at the time of hearing, Dr Oakeshott said that the plaintiff appeared to be similar to her presentation to him in 2001 (T 1620). 200 Dr Oakeshott's evidence was not controversial. Essentially, his views were expressed in his report dated 12 October 2001 (Exhibit V). Having examined the plaintiff, Dr Oakehsott identified her disabilities, expressing the following opinion: " 1. Disabilities · Severe brain damage · Spastic quadraparesis (partial paralysis of arms and legs) · Impaired vision · Epilepsy As a consequence of her brain damage she has: · Reduced cognitive ability. I understand that testing has shown that she functions as a 7 year old at present. · Reduced word finding ability. · Impaired memory. For example, she loses things easily and often repeats herself and does not remember what she has been told. As outlined above she requires constant supervision and assistance with activities of daily living (feeding, grooming, toileting, bathing, dressing). She is unable to make any meaningful decisions in regard to herself and her future. She has no concept of money or time. She can participate in a simple conversation and respond to simple questions. She does not initiate meaningful conversations. Pain is not an issue. She does not have any headaches of significance. 2. Prognosis I consider that her present situation can be considered permanent. I do not anticipate any significant improvement or deterioration in her cognitive or physical abilities in the future. 3. Future Treatment At present she does not require any significant medical or surgical treatment apart from what she is currently receiving. She may require surgery to both feet... I suggest that a report from her treating Orthopaedic Surgeon, Dr Stephens, be obtained in this regard. I understand she will not require any further significant treatment for her treated brain tumour. However, this should be confirmed with her treating medical specialists. An opinion from her treating Ophthalmologist should be obtained in regard to whether or not any further treatment is required for her visual impairment. She will require annual review of her teeth. A report from a Dental Surgeon should be obtained in this regard. I believe she will require a general anaesthetic or intravenous sedation when she has dental reviews to allow adequate treatment to be undertaken if necessary. She will not require any further surgery to her back." 201 Dr Oakeshott identified equipment needs that the plaintiff had, including a mobile walking frame, ankle splints, a wheelchair and a computer with appropriate software. 202 Dr Oakeshott opined that the plaintiff will require twenty-four hour attendant care for the rest of her life, as well as a regime of medical care which it is unnecessary for me to detail. Dr Oakeshott's assessment was that the plaintiff will never be capable of gainful employment. 203 I accept the opinions expressed by Dr Oakeshott. In coming to this conclusion, I have been assisted by seeing the film of the plaintiff's activities (Exhibit P). 204 In view of the extent of the agreement that has been reached on the various heads of damages, I do not find it necessary at this point to consider in closer detail the extent of the plaintiff's permanent disabilities and the way in which they have affected and will affect the plaintiff's lifestyle. 205 Dr Sunny Lah, clinical neuropsychologist, made an assessment of the plaintiff on 9 May 2006, and her expert's report is dated 25 May 2006 (Exhibit 24). Dr Sunny Lah interviewed the plaintiff with her parents jointly with Professor Watson, although the two experts conducted separate examinations. Dr Sunny Lah recorded that the plaintiff attended Balmain High School in a special unit. After leaving school, the plaintiff was assessed for sheltered workshop training but was found unsuitable, although this year the plaintiff has been attending a community access programme. The plaintiff lives with her parents and her older brother, who has recently finished a combined law and science degree and is now doing a post graduate medical degree. 206 On assessment the plaintiff's overall IQ was found to be consistent with moderate mental retardation. Dr Sunny Lah had made earlier assessments in September 2001 and February 2002, and Dr Sunny Lah wrote in May 2006: "Miss Tabet is a 21 year old woman with a history of normal to advanced early development and a brain (posterior fossa) tumour diagnosed at 6 years of age. She developed complications and underwent partial tumour resection. She remained in coma for four months following the surgery. She required further intense oncological treatment (chemotherapy and very intense spino-cranial irradiation) to survive. She had a multitude of residual deficits and required ongoing multidisciplinary treatment. Previous assessment of cognitive skills consistently showed evidence [of] cognitive impairments. Miss Tabet's cognitive deficits were pervasive, rather than specific. Her IQ fell in the low Mild to Moderate Mental Retardation range on a number of assessments. In addition, speed of information processing and memory were severely impaired on neuropsychological assessments I carried out on 17 September 2001 and 26 February 2002. On current review, Miss Tabet impressed as a personable young woman. Although she seemed to have grown in her maturity since the last time I saw her, her behaviour was still rather immature for her age. Miss Tabet's responses during the interview indicated that she knew the function of money, but not its value or how money was normally managed in the society. The current assessment confirmed Moderate Intellectual Retardation, severe memory impairment, greatly reduced speed of information processing and marked difficulties with high level cognitive functions. Neurological examination performed by Professor Watson showed essentially no change over the past four and a half years. Miss Tabet lives with her parents and an older brother. She requires assistance in most activities of daily living. She attends a transition to work program three days per week. She enjoys work-related activities, but has reportedly developed some medical problems and is to be moved to a community program within a month. Overall, Miss Tabet has made little cognitive gains since her last neuropsychological assessment performed over 4 years ago. In addition, she continued to have physical/medical difficulties as per Professor Watson's findings. Based on her neurocognitive deficits alone Miss Tabet would require a considerable amount of support in daily living activities and would not be able to obtain work in a competitive work environment. As stated in my previous report, I am of the opinion that Miss Tabet's neuropsychological deficits are likely to be secondary to widespread brain damage arising from a combination of factors: complications developed before and after surgery, the primary disease itself, and the treatment required for her survival." 207 The agreement of the parties as to damages, assuming the basis recorded above, is expressed in Exhibit Z. I will not set that document out in its entirety. It contains sixty-six items. However, the major items are the subject of agreement and include:

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The President went on to cite the passage from Jamieson set out earlier, and proceeded: "See generally Sharman v Evans (1977) 138 CLR 563 at 583-584; Government Insurance Office (NSW) v Mackie [1990] Aust Torts Reports ¶81-053 at 68,214. The latter case demonstrates that care must be taken to avoid double recovery when considering both loss of earnings and loss of support. In Government Insurance Office (NSW) v Mackie, Clarke JA recognised that different cases needed to be dealt with differently. He instanced the ease of a young lady who was engaged to a wealthy man and who established that she had not planned to work after marriage. For such an injured plaintiff 'the destruction of marriage prospects could not simply be swept aside' (at 68,215). For other cases the matter might be more appropriately weighed in the scales in determining the extent of any deduction for vicissitudes." 215 In Simpson v Diamond [2001] NSWSC 925 Whealy J recognised a claim for loss of marriage benefits only by adjusting the discount for contingencies, which was set at fifteen percent (see [795] of his Honour's judgment). 216 Mr Hall, in advancing this claim, relied on the decision of Giles J in Hines v Commonwealth of Australia 1995 ATR 81-338 where his Honour awarded $400,000 for loss of support. However, the plaintiff in that case was an adult whose former fiancé was an accountant who had progressed in his profession by the time of trial. The case is to be distinguished factually from the present case where the plaintiff became burdened with her disabilities as a six year old child. 217 I do not consider it would be appropriate in this case to make a discrete allowance as a separate head of damages for loss of marriage benefits, but rather to reflect the loss in the allowance for vicissitudes in relation to the claim for loss of earning capacity. Exhibit Z discloses that the allowance for loss of earning capacity for the future has been calculated using a fifteen percent discount for contingencies, and I consider that traditional discount remains appropriate in all the circumstances of this case.

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Was the lumbar puncture causative of the plaintiff's deterioration on 14 January 1991? 226 The lumbar puncture was performed by Dr Jones at approximately 11.30 am at the L3/L4 level. As earlier stated, Dr Jones noted: "Low pressure 3-4 mls of clear CSF" 227 The nurse recorded at 1.00 pm (as earlier noted): "Nil further episodes of unequal pupils today. Observations stable, afebrile. Appears more settled. Given Panadol for headache at 1400 and Maxilon as ordered at 1400…" 228 At 9.40 pm it was recorded (again, as earlier noted): "Neuro observations remained stable this evening. Pupils equal and reacting to light. Continued to complain of headaches…vomited undigested food." 229 Then, on 14 January 1991 at 5.15 am the nurse noted (again, as earlier noted): "Reema has had a very unsettled night, complaining of a headache. She has had codeine phosphate sixth hourly and Panadol regularly with very little effect. Reviewed by Dr Lane at 1.00 am. For review again about 5.45 pm…All other neuro observations within normal limits." 230 The next entries in the hospital notes are the notes of Dr Lane, to which I made earlier reference, followed by the notes of Dr Brooks, to which, again, I made earlier reference. 231 Significant notes on 14 January 1991 are those written at 2.45 pm, commenced by noting that the plaintiff "appeared miserable and complaining of headache this morning". There follows a note of what happened at 11.45 am, and I here repeat the earlier reference to this for the sake of convenience: "At 11.45 am mother called for member of staff to look at Reema, had woken and staring into space, unresponsive on examination, pupils deviating to (L) side, nystygmus, L pupil size 6 mm, R pupil size 3 mm. Very sluggish to respond…SB Dr Ouvier. Some (?) (R) sided Todd's palsy. Fit appeared to last approx 15 minutes. Taken to scan room at 12.40 pm…" 232 It is to be observed that the deterioration evidenced by the content of the hospital notes occurred approximately twenty-four hours after the lumbar puncture was performed. 233 The CT scan was followed by the procedure carried out by Dr Maixner on 14 January and by the surgery on 16 January 1991. 234 The issue as to whether the lumbar puncture was causative of what occurred twenty-four hours later has been addressed by many of the expert witnesses in this case, and this is yet another issue as to which there has been disagreement. 235 I commence the review of the evidence in point with Mr Johnston, who formed his opinions with the advantage of being the operating surgeon on 16 January. 236 The involvement of the lumbar puncture in the subsequent deterioration in the plaintiff's condition depends upon proof that it was causative of a coning event. "Coning" is a term which has attracted criticism in the evidence because of its imprecision and there have been various definitions given as to its meaning. I do not consider it necessary to record the various definitions here, and I content myself with recording Mr Johnston's definition (at T 682): "Any movement of tissue, displacement of tissue through any part of the cranial cavity or craniospinal compartment into an area where it should not normally be." 237 One form of coning, and Dr Jones referred to this as "transforaminal herniation" (T 1426), conveys the meaning of movement of tissue through the foramen magnum in a downward direction. 238 Mr Johnston considered that the time lapse between the lumbar puncture and the plaintiff's deterioration was "strong evidence that there wasn't herniation precipitated by lumbar puncture" (T 685). Mr Johnston's opinion as to the cause of the plaintiff's presentation when he first saw her was raised intracranial pressure due to hydrocephalus attributable to tumours (T 685): "In the clinical picture as it presented itself in the hospital records to you up until the point at which you saw the patient, what in your opinion caused her presentation at the time you first saw her? A. Raised intracranial pressure. Q. Brought about in what way? A. Due to I think that what I was observing was raised intracranial pressure due to hydrocephalitis which as we have discussed is attributable to the tumours but the presentation, the fluctuation of neurologic state, the deterioration which she undoubtedly showed I think was due to raised pressure due to hydrocephalus. That and, as we have tried to clarify, that was secondary to the tumour." 239 And then (at T 686): " Q. In your opinion did the lumbar puncture contribute at all to Reema's presentation as you saw it? A. No I don't think it did. It is clearly my opinion that the lumbar puncture is an irrelevance here..." 240 Earlier, in his report (Exhibit 11), Mr Johnston had expressed his reasons for determining that the lumbar puncture did not cause the deterioration on the following day. Mr Johnston said (at pp 2-3 of that report): "As to whether the successful LP on 13th January was responsible for neurological deterioration and contributed to her long-term deficit by causing trans-foraminal herniation of the cerebellar tonsils ['coning'], I do not believe this was so for the following reasons. First, the time course and clinical picture were not at all in keeping with tonsillar herniation. This is typically an acute and dramatic decline with compromise of medullary function, particularly respiration, and either fatal or reversible with relief of the supratentorial CSF pressure increase. Although there was some non-specific evidence of deterioration after the LP this quickly and spontaneously reversed and when seen shortly afterwards by Dr. Gett her condition was thought to be stable and satisfactory. Secondly, and most important, I do not think Reema was susceptible to acute tonsillar herniation due to lumbar puncture. The mechanism is that drainage of CSF from the spinal subarachnoid space creates a transient pressure differential between the cranial and spinal compartments which is the cause of cerebellar tonsillar displacement. In Reema's case, however, there is evidence both from operative findings and subsequent MR scanning, that the spinal subarachnoid space was completely occupied with disseminated medulloblastoma which is a not unusual occurrence with this particular tumour. This prevents the mechanism described above from operating and would also account for the failed LPs and the low CSF pressure and slight amount of fluid drained at the time of the successful LP. Thirdly I believe, on the basis of the operative finding, that foramen magnum obstruction had already occurred due to the tumour itself which would prevent the coning mechanism from acting in the usual way. Fourthly, Reema did not show the kind of improvement after external ventricular drainage which I would have expected had post -LP tonsillar coning been the cause of her deterioration." 241 Mr Johnston was one of the four signatories of the report following the joint conference of experts (see Exhibit 20). That report evidences that at the joint conference the authors of the report determined that the lumbar puncture had not been a significant factor contributing to "coning". The other authors of the report were Dr Hopkins, Professor Watson and Dr Jones, and it is convenient to refer to the opinions each of these doctors expressed in evidence as to the causative significance of the lumbar puncture. 242 Dr Hopkins considered that the most likely explanation for the deterioration on 14 January was the effect of the tumour and the secondary hydrocephalus. Dr Hopkins' opinion is conveniently recorded in the following extract from his cross examination (at T 1115-1116): "McCULLOCH: Q. If I ask you to assume that the first set of neurological signs that we discussed occurring at 11 o'clock were before the lumbar puncture undertaken on 13 January, would you not agree that the picture which presents itself between 11am on 13 January and the decerebrate posturing on 14 January is due to the effect of the tumour and the secondary hydrocephalus? A. I think that is the most likely basis of those changes.

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Q. And so as far as the lumbar puncture is concerned will you agree that so far as you are concerned it remains there but only as a possibility? A. Yes." 243 It was the opinion of Dr Jones that the plaintiff's presentation following decline on 14 January was due to hydrocephalus causing raised intracranial pressure (T 1429). Dr Jones acknowledged that transforaminal herniation can be caused by lumbar puncture in the presence of raised intracranial pressure (T 1428) but the consequence of that herniation in Dr Jones' opinion is an abrupt deterioration going on to respiratory and cardiac arrest (T 1428). Transtentorial herniation, on the other hand, Dr Jones did not consider to be brought about by lumbar puncture, and he said this form of herniation "is most frequently caused by mass lesions such as extradural haematoma" (T 1428). 244 In cross examination Dr Jones opined that in this case there was neither tentorial herniation nor transforaminal herniation (T 1485). 245 Professor Watson altered his position about the significance of the lumbar puncture. When he wrote his report on 9 April 2002, Professor Watson considered that there was a coning episode after the lumbar puncture that probably accounted for twenty to thirty percent of the plaintiff's difficulties. Having read Mr Johnston's report he was influenced by it, particularly by his observations in relation to the operative findings. This took Professor Watson to the conclusion that ninety to ninety-five percent of the plaintiff's problems were inevitably the results of the tumour and its treatment and only five percent to ten percent related to coning after the lumbar puncture (see the report of 7 May 2002). However, Professor Watson changed his opinion again. This, of course, is reflected in his adoption of the content of the joint expert report, Exhibit 20. He no longer considers that the lumbar puncture was a significant factor contributing to coning. His current view is expressed at T 1856-1858: "McCULLOCH: Q. Professor Watson, what was the material which caused you to change your opinions in the way we see them recorded in the first report, second report, and in the joint experts' report? A. The material that caused me to refine and narrow the uncertainties I had expressed in my first report to the second report was the report of Dr Johnston. And I think we have just been through that. The material that led me to refine and narrow further my aetiological balance between the second report and the conference of experts was having Dr Johnston there, the treating neurosurgeon, to talk about his recall of the case, and for the first time, to my recall, to actually see some of the available scans, neuro imaging. If you like that was the completion of a journey from a less certain broad opinion canvassing, as I said up to nine mechanisms, homing in on two or three and then refining it further by my first supplementary, my second report, and finally in the conference of experts; coming to the opinion that I no longer consider the lumbar puncture a significant factor contributing to the 'Coning'.

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Q. When you said in that answer the severe and bulky tumour, what information if any, did you receive about its physical appearance or other matters which caused you to change your opinion? A. I always thought it was bulky. It's just when I saw Dr Johnston's first hand report, it was clearly even more bulky with evidence of widespread spread through the CSF space, the spinal cord, the lower brain, the hemispheres of the brain." 246 Dr Allen wrote in his report of 4 February 2002 (part of Exhibit 17): "The coning occurred some eighteen hours after the lumbar puncture. The literature shows that the coning in relation to lumbar puncture and raised intracranial pressure is usually within an hour and very rarely after twelve hours. Therefore, there is a very small risk that the lumbar puncture contributed to the coning event. Although it is impossible to exactly quantify the risks of the lumbar puncture contributing to the coning, the time frame would suggest that in percentage terms there is less than a two percent chance of it being a contributing factor." 247 What Dr Allen referred to as "the coning" was, presumably, what happened at 11.45 am on 14 January 1991, not eighteen but twenty-four hours after the lumbar puncture. In written submissions, Mr Hall is critical of Dr Allen, inter alia because his history was inaccurate, but, plainly, the longer the period between the lumbar puncture and the episode on 14 January, the less likely it became that the lumbar puncture was causative of the deterioration. 248 In cross examination, Dr Allen agreed that the possibility of a relationship between the lumbar puncture and the coning episode could not be excluded (T 1181) but he said that the greater majority of coning episodes related to lumbar puncture, some ninety-five percent of them, occurred within the first four to six hours following the procedure (T 1182). 249 In his report of 8 October 1995 (Exhibit 10), Dr Kellie wrote (at p 14): "It is apparent that Reema was developing potentially serious neurologic symptoms prior to her LP. It is also apparent that she was generally and neurologically stable/unchanged in excess of eighteen hours following the LP. Her marked neurologic deterioration occurred the day following her LP. If her LP caused her to 'cone', marked neurologic deterioration would be expected in close temporal relationship to the procedure." 250 In the course of giving evidence, Dr Kellie was asked this question and gave this answer (T 577): "Q. That wasn't the problem I had in mind. Doctor, didn't you have this problem; that you knew she had coned on 14 January 1991? A. I knew she had coned. The question of date, I think, is an open question." 251 Mr McCulloch has drawn attention to three exhibited articles, Exhibit 13, Exhibit 14 and Exhibit 15, inviting the finding that the lumbar puncture did not cause damage. 252 I made a reference to Exhibit 13 earlier. It is the article in the Mt Sinai Journal of Medicine addressing the risks of lumbar puncture in the presence of intracranial lesions. There were thirty-eight patients in the study. One patient died, but that patient had lost brain stem reflexes prior to lumbar puncture. There were four other patients who deteriorated after lumbar puncture. They were also deteriorating prior to the procedure, and they returned to the pre-procedure status within forty-eight hours. The conclusion expressed by the authors of the report were these: "The clinical data presented in this series and cited references indicate that the risk of LP, if any, is very small when there is an intracranial mass, or when a mass cannot be ruled out. The occasional deterioration seen after LP is most likely due to worsening of the underlying condition, ie, the very reason LP was performed." 253 The authors, however, concluded with this cautionary note: "Nonetheless, LP cannot be 'proven' safe by this or any other clinical series. Such proof requires additional experimental work with artificial intracranial masses (eg, extradural balloon) and LP under controlled conditions." 254 Exhibit 14 is an article "Therapy of Malignant Intracranial Hypertension by Controlled Lumbar Cerebrospinal Fluid Drainage". There were twenty-three patients the subject of the study addressed in this article. The conclusions expressed in the article were these: "Controlled lumbar cerebrospinal fluid drainage represents an effective method to control refractory intracranial hypertension in carefully selected patients. The possibility of transtentorial or tonsillar herniation can be minimised by considering lumbar drainage only in the presence of discernible basal cisterns and controlled release of cerebrospinal fluid under monitoring of ICP and vital signs. Future studies, however, are needed to completely understand the mechanisms underlying the ICP-lowering effect of controlled lumbar cerebrospinal fluid drainage." 255 Exhibit 15 is an article published in the British Medical Journal in 1993 entitled "Cerebral Herniation during Bacterial Meningitis in Children". There are dicta in this article which suggests that lumbar herniation occurring in eight out of eighteen cases may have been due to lumbar puncture because herniation occurred within thirty minutes of the procedure. 256 Having considered Exhibits 14 and 15, I am not persuaded that they assist me in addressing the issue of present concern. Nor, indeed, do I find Exhibit 13 to be persuasive on this issue. 257 Dr Knight, whilst critical of the decision to perform the lumbar puncture, reported on 22 April 2002 (Exhibit S): "As it was clear that the intracranial pressure was high prior to the lumbar puncture the relationship between the procedure, done on January 13th, and the acute deterioration on January 14th is uncertain. The coning process may have occurred as a result of the acute hydrocephalus per se." 258 Dr Knight adhered to that expression of opinion in his evidence (at T 1238): "Q. And so far as Dr Gett is concerned you do wish to criticise his care insofar as he failed to order a CT scan, is that correct? A. Yes. Q. And insofar as he directed that a lumbar puncture be undertaken on 13 January 1991? A. Yes.

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Q. Whereas what can be directly connected to the patient's presentation from the time that she went into decerebrate posturing on 17 January is the tumour and the hydrocephalus which was secondary to it? A. Yes." 259 When Dr Maixner wrote her report dated 4 July 2006 (Exhibit G), she referred to an episode of "coning" on 14 January 1991, that being her clinical diagnosis when she saw the plaintiff on that date. Dr Maixner considered the decerebrate posturing and dilated pupil evidenced "coning", which Dr Maixner described as "a loose term" (T 204). Dr Maixner said a lumbar puncture could cause coning and so could hydrocephalus secondary to tumour (T 206). Dr Maixner could not give an opinion as to which one caused the "coning" in this case (T 206). 260 This brings me to a review of the evidence supporting a connection between the lumbar puncture and the deterioration twenty-four hours later. 261 Mr Klug considered it to be highly likely that the lumbar puncture precipitated coning on 14 January. In his report dated 21 January 2004 (Exhibit W), Mr Klug wrote (at p 6) "that the lumbar puncture…was highly likely to have contributed to this instability and the severe depression of her neurologic state". He went on to explain: "I feel it is highly probable that at the time she had a lumbar puncture there was substantial raised intracranial pressure with in all probability a pressure gradient at the level of the foramen magnum relating to tonsillar and tumour herniation. A lumbar puncture with removal of fluid from the spinal subarachnoid space alters the pressure relationship and may lead to increased herniation leading to deterioration in function. Such deterioration can either occur immediately or more commonly occurs in the hours subsequent to the procedure. Under the latter circumstances such relates to the continual leakage of fluid from the needle puncture site in the lumbar spine. The term 'coning' is commonly used to describe this scenario. Although it could possibly be argued that the deterioration on that day was simply a progression of the tumour leading to increased pressure and distortion, I believe the undertaking of the lumbar puncture constituted a very significant reason why such acute deterioration occurred on that day." 262 In his evidence, Mr Klug said (at T 1679): "Q. In this particular case, if it were a fact that the plaintiff underwent lumbar puncture on the thirteenth and was seen to exhibit decerebrate posturing on 14 January 1991, what, if any, do you regard as the relationship between the lumbar puncture and that observation that she was exhibiting decerebrate posturing? A. Well, I believe that there was a relationship between the lumbar puncture and the subsequent deterioration on the following day which was associated with decerebrate posturing. I believe that the lumbar puncture, with removal of fluid, had altered what up until that time had been a reasonable stable situation and allowed progression of the pathologic processes." 263 Then (at T 1689): "Q. For more abundant caution, to what extent if at all would you implicate the lumbar puncture which was performed on 13 January with the coning episode on 14 January? A. I believe it's highly likely that the lumbar puncture did precipitate the onset of coning on the following day. Or at least greatly increased the chances of such occurring on that day." 264 In cross examination, Mr Klug did not agree that the time lapse exculpated the lumbar puncture (T 1720). He considered that although acute coning occurred within one hour, delayed coning was more common, up to twenty-four hours (T 1721). Later still in his cross examination, Mr Klug was asked these questions and gave these answers (T 1758): "Q. I want to suggest to you, Mr Klug, that there was not any coning in the way you have described it; that is importantly transforaminal herniation, or herniation of the posterior fossa contents through the foramen magnum, for three reasons. I want to put each of those reasons to you and ask you some questions about them. The first is that - I will deal with something else whilst I am waiting for that Mr Klug. It's your opinion that the coning event which you have described in your reports and about which you have given evidence was brought about by the lumbar puncture on 13 January 1991, is that correct? A. I believe that the lumbar puncture was a significant contributing factor in the onset of coning on the subsequent day.

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Q. Doctor, what contribution if any did the lumbar puncture on the 13th make to the coning itself? A. I think it was the cause of the coning. Coning doesn't occur unless a pressure gradient is produced at the level of the foramen magnum and in the presence of a posterior fossa tumour, if a lumbar puncture is done, the pressure is lowered below the foramen magnum and extremely high within the cranium and there is a displacement of the brain downwards. The fact that the lumbar puncture pressure was said to be low at the time that lumbar puncture was done, although a measurement isn't given, indicates that probably coning had already occurred and no cerebrospinal fluid was getting down the spine at that time. But once a lumbar puncture has been done the needle hole in the dura in the spine leaks fluid progressively out into the tissues and so there is a progressive lowering of the pressure in the spinal canal compartment which compounds the pressure gradient at the foramen magnum." 267 In cross examination, Mr Wallace expressed the opinion that it was likely that the foramen magnum was obstructed long before the lumbar puncture was done. He said that otherwise the pressure at the lumbar puncture would have been normal or high (T 1359). He said that "in this instance if the pressure was low at lumbar puncture it means that the foramen magnum was already obstructed, probably by a combination of tumour and herniation of the cerebella." 268 Dr Williams, in his report dated 6 November 2000, described the lumbar puncture performed on 11 January 1991 as "the most damaging insult", and referred to coning on that date. Dr Williams was mistaken about the history, but he had a correct history when he wrote his report dated 26 May 2006, and in cross examination(at T 864) Dr Williams made it clear that he did not consider a time lapse of fifteen to sixteen hours between lumbar puncture and the symptoms ruled out a causative role for the lumbar puncture. 269 In cross examination (at T 998) Dr Williams agreed that the deterioration on 14 January 1991 was due to raised intracranial pressure and that hydrocephalus secondary to tumour was one of the mechanisms. However, he disagreed with the proposition that the plaintiff's presentation on that date was the direct result of the tumour and the secondary hydrocephalus (T 998). 270 I do not propose to review in further detail the expert evidence that bears upon the significance of the lumbar puncture in this case. Plainly, there is a marked divergence of professional opinion:

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The consequences of the failure to arrange for a CT scan on 13 January 1991 272 I recorded earlier my finding that had Dr Gett arranged for a CT scan instead of a lumbar puncture on 13 January then the tumour and the hydrocephalus would have been detected and no lumbar puncture would have been undertaken. However, was the path chosen by Dr Gett on 13 January causative of relevant harm? That is, did the delay in detection of the tumour and the associated hydrocephalus over the period of twenty-four hours materially contribute to the harm which the plaintiff suffered? 273 Plainly, it was not for Dr Gett to carry out the CT scan. I am satisfied that the hospital protocol required that the plaintiff be seen by a neurologist or by a neurosurgeon. It would have been that practitioner's decision to determine if and when the test was performed. 274 I would draw the inference that the neurologist or neurosurgeon would be influenced by the opinion of the paediatrician but the question would remain as to when the procedure would have been likely to have been carried out had Dr Gett decided at approximately 11.30 am on 13 January that it ought to be carried out. 275 Whilst I do not overlook the evidence of Mr Klug that most CT scans are done on children without general anaesthetic in Melbourne (T 1710), the procedure, if undertaken at the Children's Hospital in Sydney in January 1991, would probably have involved a general anaesthetic. I accept the evidence that Dr Mansour gave (T 275) and that Dr Gett gave (T 480) as to this, and, of course, their evidence on this issue is supported by the evidence of Mr Johnston. 276 Dr Ouvrier was the neurologist who saw the plaintiff after her condition deteriorated on 14 January 1991. Dr Ouvrier has not been called, but Mr Johnston has given evidence that bears upon the question as to when a CT scan would be likely to have been carried out in this case, and so too has Dr Maixner. 277 Mr Johnston gave evidence (T 2094) that only emergency scans were available on the weekend. He said he had a role to play in determining whether a scan should be done urgently. He said this was "either through the registrar the resident". He was asked this question (at T 2094): "Q. If you had been asked to see Reema to arrange a CT scan on the assumption that she had had the episode recorded at 11am, would you have regarded that circumstance as necessitating an emergency scan? A. No. I certainly wouldn't have regarded as necessitating a scan on the Sunday. Depending on what actually I thought of the situation when I examined her, I might have suggested that she be put on the Monday GA list - I think there was one on a Monday afternoon - so I would have made an assessment. I would have made my own assessment or it would have been made through Dr Maixner or Dr Cook, but on the basis of what's recorded in the notes, I would certainly not have made an emergency arrangement on the Sunday.

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Q. What was it about her condition that leads you to express that opinion? A. Well it was primarily the pressure was primarily due [to] hydrocephalus, but, you know, tumour-related swelling steroids would have improved. So it an issue of which was the more important and by how much. That is very speculative, I have to say. I mean, you could certainly make an argument that they would have improved the situation and that they may have prevented the episode, but, as I say, nobody could answer that with any certainty." 282 Dr Williams was on the staff at the Children's Hospital in January 1991. He said at that time there was a need to consult a neurologist if a CT scan was considered to be necessary. It would have been Dr Gett's responsibility to call in the neurologist. The services of a radiologist, an anaesthetist and a radiographer would have been required, and Dr Williams said that takes several hours to arrange. Dr Williams' evidence (at T 2120) was this: "I would guess if the lumbar puncture was done at eleven o'clock that morning and Dr Gett then came in to see her, that around about five o'clock or six o'clock in the afternoon the CT scan could have been done under general anaesthetic." 283 When the correct sequence of events was put to Dr Williams, he said it would have taken five to six hours from the decision that had been made for a CT scan for it to be carried out. He was asked this question and gave this answer (at T 2120): "Q. Subject to the fact that they have to be called in, would you see any difficulty in having them called in and having it done? A. Oh, no. No, I see no problem, because in this particular setting, with these abnormal neurological signs and the history that had been going on for weeks, I think it was indicated clinically for it to be done as an urgent procedure at that moment." 284 In cross examination, Dr Williams indicated he was not aware as to when the plaintiff would have been listed for a CT scan if the carrying out of the procedure was not considered to be urgent (T 2122). 285 When Dr Maixner was recalled to address the issue presently under consideration, her evidence differed from that of Mr Johnston. According to Dr Maixner, and I referred to this evidence earlier, she would have arranged for a CT scan on 13 January 1991 had she been consulted (T 2172). Even though the unequal pupil incident passed, "the concern was that she would deteriorate neurologically, as she subsequently did the following day" (T 2174). 286 Dr Maixner was asked the following question and gave the following response (T 2174-2175): "Q. To what extent would the plaintiff's condition, bearing in mind you have a report of an incident of unequal nonreactive pupils, then a report by the registrar that they were now equal and reacting to light, but she was drowsy, to what extent would she then have priority in relation to treatment? A. As a neurosurgical registrar I would, she would have high priority and in the hierarchy of how we justify priority to anaesthetists and other surgeons, unless somebody is acutely dying and needed urgent anaesthetic care or surgical care, because they could be dying, she has the next immediate priority. So, the priority is judged on, in terms of organising surgical cases, anaesthetic care, are judged on saving life and then saving brain function and organ function. So she would have very high priority." 287 Once the scan was undertaken, the case would have called for urgent treatment. Dr Maixner said (at T 2175): "… the child, with that history and the CT scan that she subsequently had, dictates that she has severe intracranial hypertension. So she needs urgent relief of that. The choice of what you do that day would be dependent on the surgeon, in other words, meaning that the simplest way to relieve the pressure is to insert a drain and that gives you immediate pressure relief. However, the treatment that she ultimately needs is removal of the tumour and that will control the fluid build up in the brain in most cases anyway. Some surgeons would do that as an urgent procedure on the same day that the case is presented to them, depending on availability of theatres and appropriate staff. And other surgeons would delay that until they have a theatre set up that is appropriate to deal with the problem. But either/or she would need urgent relief of intracranial pressure. Either a drain gets put in and you wait a day or two and do the tumour more at your leisure, if you like, or the tumour would be removed that day, in which case you would have drained the fluid at the same time and that is where there is a surgeon preference. But she needed urgent treatment, irrespective of what type." 288 Plainly, Dr Maixner's approach, had she been the decision-maker, would have been different from that of Mr Johnston. Dr Maixner said that she was the only neurosurgery registrar on call at the relevant time, unless she was on duty at the hospital or on leave (T 2170). (I observe that Dr Maixner was on duty on the following day, as her involvement in the plaintiff's treatment evidences.) Had Dr Maixner become involved, I accept that the plaintiff's case would have been treated by her as being urgent, but surgical action would have been dependent upon the view taken by the surgeon, as Dr Maixner acknowledged. 289 My impression of Dr Maixner is that she is a very confident medical practitioner, anything but incapable of making a decision to act in what she perceived to be a patient's best interests. I do not ignore her advancement since 1999 but her capacity to decide and to act was probably similar when Dr Maixner treated the plaintiff. I refer to the transcript of her evidence (at T 2180-2182): "Q. And Dr Maixner you also said that you were very junior at the time? A. Yes, but I happened to have been a very good junior doctor too, which is why I don't have a problem saying to you that as the neurosurgical registrar at the time I was quite capable of making decisions regarding whether somebody needs urgent neurosurgical treatment or not and what potentially are the diagnoses leading up to it or not. This case was actually at the end of my year at the children's hospital and as the neurosurgery registrar I was quite skilled, for that stage of my training, in looking after those sorts of patients. I could pull out a list of other patients with differential diagnoses not too dissimilar. I have no problem saying that they are decisions I would have made as a registrar. That I have no difficulty saying. Q. And would you agree that in respect of this patient, apart from you being called, it's possible that a call may have been made direct to Mr Johnston? A. That's possible. Q. Would you agree that in so far as a call was made to you that it's likely that you would have telephoned Mr Johnston to tell him of this development, that is you had been called to see a patient with unequal pupils? A. What would have been the likely scenario, because of the way the unit was run, is that I would have been called to see the patient, I would have seen the patient, organised the scan, seen the results of the scan and conveyed the results of the scan and of the patient to Mr Johnston. And if necessary, in the interim, organised urgent therapy for the child, but it wouldn't have sounded like she would have needed me to organise being intubated and those sorts of things. I would have conveyed it at the end of my assessment and judgment of the patient and the results of the scan. Q. Do you agree that on 13 January 1991, on the assumption I ask you to make that it was a Sunday, if the patient was considered ultimately by those who made the decision that she was not urgent, that she would have waited until the next available GA list? HIS HONOUR: For what?

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McCULLOCH: Q. For the CT scan? A. If the patient was deemed by those people looking after her not to be urgent then that would be correct. First of all I am not sure she needed a GA, but even so then it's up to the team looking after the patient to decide the degree of urgency for the scan and so, for instance, if her medical team at that day thought that she required a scan urgently they would have organised it and would have been able to have it on the same day. Q. I am sorry, I interrupted you, I didn't mean to. A. That was the end. Q. Is this an accurate description of the relationship between you and Mr Johnston at this hospital in January 1991; that in so far as you had been called to see this patient as the registrar, neurosurgical registrar you would have made a clinical assessment and then contacted Mr Johnston to have him make a decision about what was to happen next? A. Okay. No. The way my relationship with Mr Johnston and the other consultants at the hospital at that stage was that, as what happened on the next day when I did see the patient, was that I would assess the patient, organise the scan, see the scan, convey to Mr Johnston what were the results of the scan and the state of the patient and for something like that it would have, that would have been a recommendation to put in the drain. Either I would have suggested to Mr Johnston or he would have said, "Can you put in a drain", and I would have put the drain in. I suspect, I can't recall definitively, but I would - the way that that operation report is written, which it would have been my writing and it would have been that I would have put the drain in unsupervised. That's a sign of the trust and the relationship between Mr Johnston and myself at that stage. Q. Once Mr Johnston approved it, I take it? A. He would have to. Unless the patient was acutely dying and I could not contact him he would normally approve the operation. It was exceptionally rare, or occasionally happened, that I would take a patient to theatre and contact him when I am halfway through the case, that would be exceptionally rare, because it would, I would have wanted his approval that that was the right management decision and given that he was the consultant in charge and I was the registrar." 290 As I have earlier observed, Mr Johnston and Dr Maixner have disagreed on how the plaintiff should have been treated on 13 January 1991. Mr Johnston found no fault in Dr Gett's decision as to how the plaintiff was to be treated on that date, and in this particular respect I have already expressed a finding to the contrary. However, I accept what Mr Johnston has said as to how he would have acted had Reema's case been referred to him on 13 January. 291 Whether Mr Johnston would have been called in or some other neurosurgeon, is uncertain. According to the hospital protocol, there may have been yet another decision-maker involved. It may have been Dr Ouvrier or some other neurologist who would have seen the plaintiff on 13 January had Dr Gett decided a CT scan was warranted. It cannot be assumed that a neurologist would have shared Dr Maixner's opinion as to the urgent need for a CT scan, but if a decision had been taken for a scan to be carried out, then I find that this could have been arranged to be performed later that day, even allowing for the need for an anaesthetic to be administered. 292 Mr Hall was given leave on 9 November 2006 to reopen the plaintiff's case to introduce a further report from Mr Wallace. This report, dated 29 September 2006, addressed the issue raised by Mr Johnston as to when a CT scan would have been arranged if called for on 13 January and what the likely course would have been thereafter. 293 The report from Mr Wallace was in the following terms: "In reply to your letter of 20.09.2006, I believe these propositions are absurd. It does not matter what the day of the week is in a situation like this: a child with raised intracranial pressure from a posterior fossa tumour needs an urgent burr hole and insertion of an intraventricular catheter to control intracranial pressure followed by an urgent CT scan or MRI scan, irrespective of the time of day or the day of the week, followed by surgery for tumour removal at the first available opportunity, irrespective also of the day of the week or the time of the day. On the history alone, this child needed urgent intervention in the way of a burr hole and insertion of an intraventricular catheter or drain, on an emergency list and certainly not on the next available elective list. It matters not a jot how difficult it is to get people onto an operating list, as a situation like this demands immediate intervention." 294 The above report has to be read in conjunction with the letter from the plaintiff's solicitor inviting the opinion of Mr Wallace in relation to matters about which at the time instructions were given it was anticipated Mr Johnston was going to give evidence on 21 September. The points expressed for the consideration of Mr Wallace were these: "1. 13 January 1991 was a Sunday. 2. A CT scan on that day for this patient would not likely be done until the next day. 3. Based on the CT scan taken, (-since lost-) and what was in the hospital notes the plaintiff's condition did not need the insertion of a drain urgently and would have had her placed on the next surgery list. 4. It was not a simple matter to get people into lists and it couldn't be certain the drain would have been inserted in the next list." 295 It is not clear from his report that Mr Wallace read the evidence actually given by Mr Johnston on 21 September 2006 or that he was informed of its content before he wrote his short report. However, there was ample opportunity for Mr Wallace to have learned what Mr Johnston said. 296 Mr McCulloch objected to the introduction of the report by Mr Wallace and he objected to the references in the report in both the first and second paragraphs to the need for a burr hole. I do not treat the report as evidence to be considered in the case against the second defendant of a procedure which he should have taken steps to have done. I treat this report by Mr Wallace though as affording evidence that in this specialist's opinion there was an urgent need for some measure to be taken to relieve raised intracranial pressure. 297 I do not find helpful the language used by Mr Wallace in asserting that the propositions for which Mr Johnston's evidence provided support "were absurd". Mr Johnston was not cross examined to suggest that his evidence was "absurd", and, of course, Mr Hall is not to be criticised for this. However, this report from Mr Wallace does raise the issue as to whether Mr Johnston's evidence given on 21 September should be regarded as truthful, and the letter also has to be considered when assessing overall the reliability of Mr Johnston's evidence. 298 Elsewhere in this judgment I have expressed my favourable assessment of Mr Johnston as a witness, and a consideration of the recent short report from Mr Wallace does not cause me to alter this assessment. I am, moreover, satisfied that the evidence which Mr Johnston gave as to how he would have treated the plaintiff was truthful evidence. 299 Indeed, I do not find ultimately that I am assisted by the report of Mr Wallace dated 29 September 2006. I am concerned to determine how soon a CT scan could and would have been arranged in this case, and what measures thereafter would have been put in place, and when, for the relief of raised intracranial pressure. Absent any involvement in procedures undertaken at the hospital where the plaintiff was being treated, I do not find Mr Wallace's views persuasive on the issues just identified. Mr Johnston is not a defendant in this cause. What is relevant in the present context is how he would have acted if consulted on 13 January, and Mr Johnston did not share Dr Maixner's view as to the urgency of the situation. 300 Had the plaintiff been given the opportunity of a CT scan on 13 January and treatment thereafter as advised, I am satisfied such opportunity would have been taken. One or other of her parents was constantly in attendance at the plaintiff's bedside and I find both parents wanted the plaintiff to have such treatment as was considered necessary. I consider it to be more probable than not that if Dr Gett had decided, as I find he should have, that there was an urgent need for a CT scan following the incident at 11.00 am on 13 January 1991, such a scan would have been carried out on that same day. This would certainly have happened if Dr Maixner was approached, accepting as I do her perception as to what was required and when. I conclude from her evidence that CT scans are routinely arranged by the registrar on duty or on call, and I infer that it would have been more likely that the registrar would have been first approached to arrange the CT rather than to have called in a senior neurosurgeon to make the necessary arrangement. Dr Maixner's evidence (at T 2181) was that "the likely scenario, because of the way the unit was run, is that I would have seen the patient, organised the scan, seen the results of the scan and conveyed the results of the scan to Mr Johnston." I accept that evidence. Even if it had been necessary for Dr Gett to request Mr Johnston to arrange for an urgent CT scan, notwithstanding the evidence Mr Johnston gave, I think it likely that he would have acceded to Dr Gett's request. What treatment Mr Johnston would have determined upon thereafter is another matter. 301 The evidence does not enable me to find as a probability that the course of treatment proposed by Dr Maixner would have followed the discovery of the tumour, had a CT scan been done on 13 January. This is so because of the conflicting evidence of Dr Maixner and of Mr Johnston. 302 I consider there is a real chance that a decision would have been made to insert a drain as a matter of urgency but this may well have depended not only on whether Dr Maixner became involved, but, if she did, how persuasive her view was with the neurosurgeon who undertook the plaintiff's case. Had that neurosurgeon been Mr Johnston, he would have taken a different approach, as disclosed by his evidence, and I accept Dr Maixner's evidence that even if she disagreed with the surgeon's decision she would generally have to accept it (T 2176). 303 The hypothetical course of events under consideration would have occurred on a Sunday, but it was possible for the measures that were actually taken on the following day to have been taken on 13 January, so that it was possible not only for a CT scan to have been performed but also for a drain to have been inserted on the Sunday as well. 304 Had Mr Johnston been consulted on the Sunday, his evidence was that he would probably have put the plaintiff on steroids, and whilst I am unable on the evidence he gave about this to find as a probability that the deterioration on 14 January would have been avoided, it is possible such prescription would have been effective. Absent the introduction of a drain, it is likely that steroids would have been prescribed as soon as the presence of the tumour was disclosed. I do not overlook the possibility in evaluating the significance of the evidence Mr Johnston gave about the treatment he would have given to the plaintiff that he may not have been the neurosurgeon consulted. However, in the absence of any evidence from some other neurosurgeon who may have been called in to treat the plaintiff, and having regard to Mr Johnston's status at the hospital, I treat his evidence as reflecting the likely neurosurgical approach to the plaintiff's case at this particular hospital. 305 Mr Johnston gave the following evidence as to the possible efficacy of steroid prescription in the plaintiff's case:

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(ii) at T 2111-2112 Mr Johnston gave the further evidence set out earlier (at [281]). 306 Having regard to the evidence given by Dr Maixner and Mr Johnston, and in particular having regard to how Mr Johnston said he would have treated the plaintiff, I am not persuaded on the balance of probabilities that if Dr Gett had called for a CT scan at 11.00 am on 13 January, as I have found he should have done, the discovery of the tumour through that procedure would have led to the plaintiff being treated in such a way as would have avoided such brain damage as occurred on 14 January 1991. It follows that the plaintiff's claim in respect of such damage that it was caused by the negligence of the second defendant must fail. Nevertheless, I am satisfied on the balance of probabilities that had a scan been called for at 11.00 am on 13 January 1991 the scan would have been performed urgently ([300]) and the medulloblastoma would have been detected by it, and treatment would have been commenced on 13 January to reduce pressure, either by drainage or prescription of steroids. I consider the use of a drain would have given the plaintiff a chance of a better outcome than the prescription of steroids, but in assessing the value of the lost chance I must heed the superior role Mr Johnston would have had in the decision-making process if he became the treating surgeon. Whichever of the two forms of treatment would have been undertaken, the plaintiff was deprived of the chance of having it by the second defendant's breach of duty and was consequently deprived of the chance of a better outcome. Another factor to be weighed in the assessment of the value of the lost chance is that the detection of the tumour would have eliminated the time lost in carrying out the EEG on 14 January (Mr Johnston, T 2107) and the time occupied in performing the CT on that day. I accept, as Mr Johnston acknowledged (also at T 2107) that "the earlier the intervention by neurosurgeons the better the likely result". 307 The findings I have just expressed will lead me to a consideration as to whether the plaintiff is entitled to be awarded damages for loss of the chance of a better outcome concerning any brain damage suffered on 14 January 1991, but before such consideration it is desirable that I assess the significance of what occurred on that date. 308 The events of 14 January must be viewed in context:

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The plaintiff's condition immediately prior to 11.00 am on 13 January 1991 309 An MRI performed on 26 February 1991 showed that by that time there was wide dissemination of the tumour throughout the subarachnoid space. The report following this MRI reads in part: "In the head scans it can be seen that there is marked meningeal enhancement surrounding the entire brain. Although it is possible that some of this is post operative, enhancing masses can be seen in the superior cerebellar cistern, in the crural cistern, and in the middle cranial fossae anteriorly on both sides. Nodular enhancement is seen anterior to the medulla, and there is a vermian mass which protrudes through the craniotomy and is surrounded by irregular enhancement. The entire spinal cord is surrounded by an enhancing sheath of tissue, with some large nodules posteriorly at T8/9 as well as some smaller ones all along the back of the cervical cord. Several enhancing nodules are seen in the lumbar canal as well, one just behind L3, one at L1/2, and two to the right behind L1." 310 Mr Johnston reported on 6 July 2003 (part of Exhibit 11) that seeding had already occurred at the time of the surgery which he performed on 16 January 1991 and he also referred in that report to the preoperative CT scan which showed this. Unfortunately, the films have been lost. They were available to the four doctors who conferred for the purposes of preparing the joint experts' report, Exhibit 20. Mr Johnston said further in his report that seeding was visible on inspection of the subarachnoid space over the cerebellar surface. It was his view, expressed in the same report, that seeding would have occurred prior to 30 December 1990. 311 Mr Johnston referred to the wide dissemination of the tumour through the subarachnoid space, as shown by the February MRI (T 667), and was asked about the significance of this (T 667): "Q. What if anything did that inform you as to the likelihood that the tumour had seeded before say the end of December 1990? A. Well I've said in a report somewhere and I adhere to that opinion that it had probably done so before then given that the extensive nature of the dissemination but it's not something on which I would be prepared to make any sort of dogmatic statement as to when it happened. But the degree of seeding was such that I thought that it had been there for some time. I could make two other points on that. Do you want me to do that?

[182]

Q. And when you referred to its dissemination in that last answer throughout the subarachnoid space, were you there referring to the head only or to the rest of the nervous system? A. The head and the spinal cord, over the spinal cord. " 312 And then (at T 668): "Q. Mr Johnston, what did you observe at operation about the extent to which the tumour had spread, and I'm referring in this question to the spread of the primary mass? A. The primary mass was occupying a very dilated fourth ventricle and it had basically obliterated all the normal anatomy. I mean in this situation with a very big tumour as in this case and in most posterior fossa tumours and midline tumours in children there's no specific identification of the foramen of Magendie or the foramen of Luschka laterally. I mean everything's disported by the large tumour which has largely destroyed the normal anatomical landmarks that you would see if you were exposing the normal brain." 313 Mr Johnston said that what he saw at surgery was tumour in the subarachnoid space over the cerebellar hemispheres (T 688). 314 Mr Johnston was asked to express an opinion as to whether an earlier diagnosis of the medulloblastoma on 11 January 1991 would have made any difference, and he said that it would not (T 691). He gave this reason (T 691): "A. Because I think the situation would have been unchanged; that hydrocephalus was present, was probably present although that is a very treatable component and that given the nature of tumour growth it was very unlikely or impossible really I think, that the tumours had dramatically increased in size or significantly in any way increased in size between 11th and 14th. I mean, if I had thought that there was that sort of problem present then I would not have delayed the operation myself from 14 to as far 16th: Trying to get the hydrocephalus under control. Generally speaking with posterior fossa tumour, medulloblastoma and papilledema which are similar in being midline malignant tumours of children it was my practice when the presentation was less acute, had the patient maybe just had raised neuro pressure, papilledema to drain CSF by third ventricularlostomy or a shunt and wait a week or two before doing the actual definitive tumour removal that was fairly standard practice and one that I continued right up until when I retired and was widely used." 315 The notes relating to the surgical procedure as taken by Dr Maixner are to be found in Exhibit B, 413. They refer to the spread of the tumour over the surface of both cerebella and they also record that the tumour was protruding through the foramen Magendie. 316 Dr Kellie is a paediatric neurological oncologist who became involved in caring for the plaintiff late in January 1991, some ten or eleven days after Mr Johnston had operated to remove the tumour. His various reports were admitted into evidence as Exhibit 4. Dr Kellie considered the age of the tumour, taking as a starting point the size of the primary tumour determined on surgery. That tumour was approximately three and a half centimetres in diameter (T 501). Dr Kellie said (T 501): "…understanding that for a medulloblastoma to reach three and a half centimetres in diameter that tumour, starting from the very first malignant cell, must have undergone 35 or so doublings from one to two to four to eight and so on to create a mass of that duration - a mass of that size would require around 35 doublings. We know that the doubling time for medulloblastoma is in the order of 20 to 27 days. It may not be a linear equation but that gives some insight into the likely time course, going back to the very first cell of origin." 317 Hence, according to Dr Kellie, the tumour took 700 to 945 days to develop to its size at the time of surgery (T 501). 318 Dr Kellie said that it was not possible to determine simply by reference to the size of the primary tumour whether seeding had occurred or, if so, to what extent (T 502). 319 Dr Kellie's attention was drawn to the surgical reports and other hospital records. Consideration of those records increased the likelihood of seeding, and I refer to the evidence (at T 502-503): "Q. You saw, didn't you, in the course of your treatment of this patient the various surgical and other reports that were in the hospital records that have been authorised or prepared under Dr Johnston's supervision? A. Correct.

[185]

Q. And does that finding at surgery say anything about the likelihood of the tumour having seeded before the end of December 1990? A. It makes - it makes the likelihood of seeding more probable but that still relies ultimately on the investigations directed at the spine and the spinal fluid." 320 Studies done in February 1991, referred to by Dr Kellie (at T 506), disclosed that the tumour was seen to have invaded vascular tissue (T 505) and MRI scans of the brain and the spine showed very gross nodular evidence of disease in many areas around the brain stem and up and down the spinal cord (T 506). (This analysis appears to be consistent with the report set out above (at [309])). Dr Kellie said that a number of the nodules measured more than one centimetre across (T 508), and that led Dr Kellie to conclude that it was likely that nodules existed before 30 December 1990. He opined that had a scan been performed at that time nodules would have been identified. It followed that there must have been seeding by that date (T 508). 321 Associate Professor Berry reported on 28 October 2003 (part of Exhibit X) that he did not consider on the balance of probabilities that the plaintiff had evidence of seeding in late 1990 and early January 1991. His assessment of the probabilities he stated as "based on the literature where in the majority of cases, gross evidence of seeding is not evident at the time of diagnosis". He went on to add that there was in the plaintiff's case an absence of symptoms or signs suggestive of seeding up to 13 January 1991. Of course, Professor Berry did not see the plaintiff for the first time until May 1991, and he acknowledged that it was very difficult to know when seeding occurred (T 1821). He further acknowledged that even where there is seeding there are commonly no signs of this (T 1822). 322 Associate Professor Smee's opinion was that he considered it "exceedingly unlikely" that the extensive metastatic deposits shown on the MRI in February 1991 would have become apparent over a short period of time (see Associate Professor Smee's report of 24 September 2003, part of Exhibit 22). 323 I find myself persuaded on the balance of probabilities by the evidence of Mr Johnston and of Dr Kellie which I have above reviewed. I accept the evidence of Mr Johnston and of Dr Kellie which I have above reviewed as to the extent of the tumour and as to seeding, and hence I am satisfied that the primary tumour was extensive as at 13 January 1991 and that there was seeding at that time. I find on the probabilities that there was seeding before the end of December 1990, by which time I am also satisfied that the tumour itself was very advanced.

[189]

Q. And the longer she remained unconscious, the more certain, I take it, that she suffered brain damage? A. Yes, that's a fair assumption." 326 The hospital records (Exhibit C, 590-605) report observations and assessments of the plaintiff between the time that the drain was put into position and the surgery carried out by Mr Johnston on 16 January. In his evidence, Dr Jones analysed those notes. He concluded that after the insertion of the drain there was significant improvement (T 1431). Later, in cross examination (at T 1502-1503) Dr Jones said this: "I think, in my opinion, she recovered quite well but not completely following relief of her intracranial pressure, but she deteriorated at the time of excision of the tumour and, in my opinion, a lot of the post operative state was - well it followed temporally the excision of the tumour, and I am of the opinion that it was caused by events at the time of the excision of the tumour." 327 I accept, as Dr Jones opined, that there was improvement in the plaintiff's condition after the drain was inserted and before Mr Johnston carried out the surgery on 16 January, but I am also satisfied that recovery to the extent hoped for after the insertion of the drain did not occur. The evidence of the plaintiff's parents was that their daughter remained unconscious. That, of course, is a lay assessment, but I accept their evidence with that qualification. Moreover, in accepting that evidence I am mindful that either Mrs Tabet or Mr Tabet was by the plaintiff's side throughout the relevant period. 328 Mr Johnston considered that brain damage did occur on 14 January and so, too, did Dr Kellie, in evidence to which I shall shortly refer in considering the causative significance of the operation carried out on 16 January. 329 Dr Knight expressed the opinion that the episode on 14 January was the culmination of raised intracranial pressure and that brain function was severely affected by compression of the brain stem. I refer to his evidence (at T 1223): "A. I think the episode on the 14th was the culmination of a period of raised intracranial pressure and it was a critical time where the pressure was such that brain function was severely affected by compression of the brain stem. And the evidence that recovery from that took place in my mind can be looked at through the intensive care observation and examination. Does that answer your question?

[192]

The causative significance of the operation and subsequent treatment 335 The tumour excision on 16 January was incomplete. The tumour found arose from the wall of the fourth ventricle and there was spread along the subpial surface of both cerebellar hemispheres. Tumour was protruding through the foramen of Magendie. After the procedure there was a small amount of the tumour left on the wall of the fourth ventricle. 336 Post operatively the plaintiff returned to the intensive care unit and remained there until 27 January 1991. 337 In his report dated 24 November 2001 to which I will refer again later, Mr Johnston identified the surgery as one of a number of contributors to her "late and severe morbidity". 338 Dr Kellie became involved in the plaintiff's care from ten or eleven days after the surgical removal of the tumour. He was involved in the "staging", being the investigation to determine the extent of the disease at the primary site and at seeding sites. Various tests were carried out, including an MRI of the brain, an MRI of the spine, a bone scan, two lumbar punctures, and a bone marrow examination. A plan of treatment was put in place that involved chemotherapy and radiation treatment. Chemotherapy was commenced on 22 February 1991 and it continued until 23 April 1991. Radiation treatment began on 20 May 1991 and it continued for six weeks. 339 Dr Kellie gave evidence that the deterioration on 14 January caused some damage (T 581) but his evidence did not identify that damage. He did express the view that the plaintiff had coned, but it was an open question as to when this occurred, according to Dr Kellie (T 577). He said it was possible that the plaintiff's loss of vision and her quadriparesis were caused by the coning (T 628) but other possible causes were the tumour itself and cerebellar mutism (T 629). 340 Dr Kellie considered that the plaintiff had severe cerebellar mutism (T 532). This is a syndrome which Dr Kellie said has only been recognised more recently than 1991 but it is caused by surgical splitting of the cerebellum. Dr Kellie gave the following evidence (T 521-522): "McCULLOCH: Q. Dealing with some of those in turn, what is the nature, physically of the defect that occurs in the cerebellum in the process you have described at surgery? A. At the time of surgery if the middle of the cerebellum is split open there runs a substantial risk, and it's now published at the rate of 15 to 20 per cent of children having this type of surgery, who experience profound mutism after surgery. The onset can be within the first 24 hours, the first 48 hours, but the duration can be for days, weeks or even in excess of a year. That phenomenon is associated with often profound ataxia, balance difficulties. The other problems that I mentioned, irritability and feeding difficulties, and patients rarely make a full recovery. One of the important associations of the cerebella mutism syndrome is late neurocognitive decline. That decline is seen in children who have cerebella surgery but have not ever had radiation.

[199]

Q. Impaired memory? A. Yes." 341 Mr Hall submitted that the evidence of Mr Klug and of Mr Wallace should be preferred to that of Dr Kellie on the issue of cerebellar mutism. Mr Klug did not consider cerebellar mutism was a permanent condition, based on his own experience (T 1682). He did not consider that the plaintiff was suffering from that condition (T 1685). Mr Wallace was also of the view that cerebellar mutism was a transient event (T 1348). 342 Mr Hall submitted that Dr Kellie should be regarded as biased and, accordingly, other than objective. That submission does not accord with my assessment. I do not lose sight of the fact that it emerged in evidence that Dr Kellie spent some hours in conference with Dr Pincus before he was called as a witness in this case. The evidence that Dr Kellie gave as to the time that he spent in preparing to be a witness to my mind showed only a conscientious approach to giving evidence, as did the extensive presentation of supporting articles (Exhibit 8). I also add that Dr Kellie gave evidence unhelpful to the second defendant as to "coning". 343 I accept the evidence that Dr Kellie gave in relation to cerebellar mutism. Dr Kellie had the advantage, not shared by Mr Klug or Mr Wallace, of having been closely involved in the plaintiff's treatment and of having had the advantage of regular observation of the plaintiff. 344 Dr Kellie considered the impact of the plaintiff's post operative treatment. The plaintiff was classified as a high risk patient who needed higher doses of radiation because of her high risk features. 345 In 1991 there were known side effects from radiotherapy of the type that the plaintiff underwent. Dr Kellie described those side effects as "massive" (T 510). He said that the best documented side effects were, indeed, at a lower dose than that required in the plaintiff's case, and he said that there was far less documentation concerning the side effects at the higher dose that the plaintiff needed (T 510). He said "At the lower dose of radiation therapy, the outcome for a six year old is very, very serious in terms of neurocognitive outcomes, intellect, hearing, growth, stature, hair density, dentition, the works" (T 510) 346 Dr Kellie said that the white matter loss from the brain appears to be proportional to the dose used and the loss of white matter results in attentional difficulties and interferes with global IQ function (T 511). 347 Dr Kellie gave the following evidence concerning the effect of lower dosage treatment (T 513-514): "We know that the application of 3600 centigray to the whole brain is devastating in a six year old. Published data shows that most of those children do not attend normal school, they have 25 to 30 percent IQ loss, they experience major problems with their hearing, dentition, risk of second cancer, short stature, endocrine failure. 3600 to the brain of a six year old is extremely damaging. The question that you ask though is how does it compare with a higher dose and it becomes inseparable to work out what are the additional disabilities determined by the presence of tumour on the surface of the brain. In other words, the reason that a child receives an even higher dose of radiation therapy is also likely to impact on those factors that I've just mentioned. So it's not possible to separate out the reasons for giving the higher dose that might also impact on outcome versus the higher dose only. There has never been a randomised study comparing 5000 whole brain with 36 whole brain which would be required to answer your question.

[205]

There's a risk of thyroid underfunctioning or failure because of the impact of the spinal dose entering through the neck and exiting through the front of the neck and there's a risk of thyroid cancer. There is well-documented cardiac complications relating to the spine dose of radiation going in through the chest and coming out through the heart and there is an ever present risk of cardiac failure which may occur many years after treatment was delivered. There is a risk of scoliosis and spinal structural abnormalities and we're appreciating more now there is an ever increasing risk of second malignant tumour relating to 3600 centigray. Those tumours might involve the brain, the skin, the bones or the coverings of the brain." 349 Both Dr Berry and Dr Smee expressed the opinion that the side effects are generally proportional to the total dose of radiation (see the evidence of Dr Berry at T 1819; to the like effect, Dr Smee at T 1819). 350 I am satisfied, having considered the evidence of Dr Kellie, Dr Smee and Dr Berry, that the side effects brought about by the radiation therapy in the plaintiff's case were greater than they would have been had lesser doses of such therapy been appropriate. 351 In expressing his agreement with Dr Berry about the impact of the heavier dosage of radiation in the plaintiff's case, Dr Smee said this (at T 1819): "We don't have any evidence that 50 [Gray] is worse than 36 [Gray] principally because it's not been a usual practice and, therefore, it's not been well documented but anyone in the field would know that, you know, 50 is greater than 36 and the outcomes certainly would be different in the adult situation. I've certainly seen patients who have 60 to the whole brain or 50 to the whole brain and they don't do very well…I agree with Dr Berry from the point of view that there's just not any evidence but the assumption is that the more you give the greater the likelihood of deficit." 352 I am satisfied that the surgery which the plaintiff was required to undertake caused brain damage, and I am also satisfied that the radiation treatment caused further brain damage.

[206]

Entitlement to damages for loss of a chance 353 The plaintiff's primary case was that she was entitled to damages for negligence resulting in brain damage, and even if restricted to harm suffered on 14 January, the ultimate damage was not divisible. Hence, it was submitted that the assessment of damages should be approached on this basis. For reasons stated earlier in this judgment (at [301]-[306]), I am not satisfied that the plaintiff has proved such entitlement. However, Mr Hall has advanced a claim in the alternative to be compensated for the loss of a chance of a better outcome. 354 This alternative claim is resisted by Mr McCulloch. It is submitted that this claim was not squarely raised on the pleadings or during the hearing. I do not accept this submission. Whatever its shortcomings, the amended statement of claim filed in Court on 28 July 2006 expressed a claim (in para 38) for damages in the alternative for "the loss of an opportunity to avoid injury, loss and damage". 355 The written submissions for the defendant dated 1 December 2006 properly acknowledge that the issue of the claim for loss of a chance was raised during Mr Hall's opening address in which the transcript records the following (at T 29): "McCULLOCH: Sorry, there was one other matter. I just invite my learned friend at some stage to make plain whether or not his client does now in fact advance a pure loss of chance case. It wasn't apparent to me in his opening and the dialogue that he really in fact is. It's a matter I have spent some time looking at and if I don't need to, I don't need to deal your Honour with that issue. HALL: I'm not abandoning that, if that's what my friend is asking. And to me, as I understand their case, it's an alternative, pose the question of damages. In other words, we say there was actual damage, that's reflected in our condition. If that's not the case, then we say there is a loss of chance. Our primary case is actual damage." 356 Unquestionably, the principal focus at the hearing was on what Mr Hall referred to in opening as the "primary case", but it was never my understanding that the "loss of a chance" claim was abandoned, and hence my invitation to counsel for written submissions on that issue on 9 November 2006. Both sides have presented written submissions on "the loss of a chance" issue and I consider that justice requires the consideration of such claim. 357 Mr McCulloch submitted that an action is not maintainable for damages for loss of the chance of a better medical outcome in medical negligence cases, and he cited in support of that submission the decisions of the House of Lord in Hotson v East Berkshire Area Health Authority (1987) AC 750 and in Gregg v Scott (2005) 2 AC 176. Reference was also made to dicta of Gaudron J in Naxakis v Western General Hospital (1999) 197 CLR 269. Mr McCulloch submitted that Rufo v Hosking (cited earlier at [221]) was wrongly decided. 358 It is to be observed that the authorities upon which Mr McCulloch relied were all considered in Rufo, although the House of Lords had not dismissed the appeal from the Court of Appeal in Gregg by the time judgment was delivered in Rufo. 359 There is no decision of the High Court which is directly in point. In Malec v J.C. Hutton Pty Limited (1990) 169 CLR 638 the High Court was concerned with the assessment of a plaintiff's damages and not the issue of liability. In Naxakis, to which Mr McCulloch referred, the facts were these: a young boy, following admission to hospital, was diagnosed as having suffered a subarachnoid haemorrhage. Shortly after his discharge from hospital it was found that he had suffered a major intracranial bleed from a burst aneurism. It was contended at trial that there was negligence in the failure to perform an angiogram whilst the plaintiff was in hospital. There was no medical evidence that directly supported that proposition, and the trial judge directed the jury to find a verdict for the defendant. A new trial was ordered. 360 In these circumstances, the remarks of Gaudron J and of Callinan J, to which I am about to refer, are strictly obiter. Gaudron J said as to the notion of the lost chance approach (at 279-280 [33]-[34]): "[33] Moreover, the lost chance approach is not one that necessarily works to the benefit of the individual plaintiff. If damages were to be awarded for the chance lost, rather than the actual injuries or disabilities suffered, consistency would require that damages be assessed according to the value of the chance, not the injury or disability. Thus, a chance which is 51 per cent or greater but less than 100 per cent, must result in an award of damages less than would be the case if damages were awarded for the injury or disability which eventuates (See Hotson v East Berkshire Area Health Authority [1987] AC 750 at 759-760, per Sir John Donaldson MR, who would have adopted the loss of chance approach in that case and who said: 'As a matter of common sense, it is unjust that there should be no liability for failure to treat a patient, simply because the chances of a successful cure by that treatment were less than 50 per cent. Nor, by the same token, can it be just that if the chances of a successful cure only marginally exceed 50 per cent, the doctor or his employer should be liable to the same extent as if the treatment could be guaranteed to cure. If this is the law, it is high time that it was changed'. [34] Additionally, the lost chance approach cannot easily be applied in conjunction with the traditional balance of probabilities approach. As already indicated, the lost chance approach requires proof that a valuable chance has been lost. A chance would have no value if the defendant could establish, on the balance of probabilities, that the pre-existing condition would have resulted in the injury or disability in question in any event. Thus, if proof on the balance of probabilities were also retained, damages for loss of a chance would be awarded only in those cases where the plaintiff cannot establish, on the balance of probabilities, that the risk would not have eventuated and the defendant cannot establish that it would. There is, thus, limited practical significance for an approach which allows for loss of a chance if the traditional approach is also retained."

[207]

361 To the contrary, Callinan J said (at 312-313 [128]-[130]): "[128] On the evidence here the jury were entitled to hold that the failure, the treating doctor's omission either to undertake an angiogram or the failure to give any consideration to the undertaking of it, materially contributed to the appellant's condition. They would also be entitled to take an alternative view that the second respondent's conduct, although it might not be possible to say (on the balance of probabilities) that it definitely materially contributed to the plaintiff's final condition, at least caused him to lose a valuable chance (the value of which it was for them to assess) of avoiding being in the condition that he now finds himself. There is still, in my opinion, room for the operation of the loss of chance rule (Chaplin v Hicks [1911] 2 KB 786. See also Sellars v Adelaide Petroleum NL (1994) 179 CLR 332 at 349-350, per Mason CJ, Dawson, Toohey and Gaudron JJ.) (particularly in cases involving the practice of what is even today said to be an art ("Medicine is the most distinguished of all the arts, but through the ignorance of those who practice it, and of those who casually judge such practitioners, it is now of all the arts by far the least esteemed." Hippocrates, Law, bk 1.) rather than a scientific skill), enabling a plaintiff to recover damages to be equated with, and reduced to the value of the chance he or she has lost, rather than the damages which would be appropriate if it has been proved on the balance of probabilities that the plaintiff's condition owes itself to the defendant's acts or omissions. [129] It must be acknowledged that this approach is not without its difficulties. If the chance that has been lost is a 51 per cent or greater chance, why should not the plaintiff be taken to have proved his or her case on the balance of probabilities? I think that in such a situation, the plaintiff has, and should recover his or her damages in full. Rogers v Whitaker ((1992) 175 CLR 479) is, in one sense, such a case. The Court there accepted on the balance of probabilities, that the plaintiff would not have had the operation to which she submitted, and which caused the problems for her that it did, if she had been warned of the risk that the Court thought material there. Perhaps the plaintiff's damages there might have been reduced, and indeed significantly so, if what had been established there, was that she might not have had, as opposed to, would not have had the operation.

[208]

[130] On the other hand, in other cases, there is a risk, it might be said, that in almost every instance there is a lost chance of some kind, perhaps even a 1 per cent or 5 per cent chance, and on that basis every plaintiff will succeed to some extent. The answer to this must be that the loss of a remote, or very slight chance should not attract an award of damages. The chance lost must be a real one and of some substance, even though less than a 50 per cent chance." 362 Plainly, the above dicta of Callinan J do not lend support to Mr McCulloch's submission. In his judgment in Naxakis Gleeson CJ made mention (at 272 [5]) of there having been reference made in argument to the possibility that the plaintiff's case might be put on an alternative basis, namely relating to the loss of a chance, but the Chief Justice observed that that question had not been addressed at the trial or in the Court of Appeal and it was not fully argued before the High Court. Hence the Chief Justice expressed no opinion about that issue. 363 It is to be noted that each of the members of the Court of Appeal made specific reference to Naxakis in Rufo. 364 The facts in Rufo were as follows: a fourteen year old child was diagnosed as suffering from systemic lupus erythematosus, which is an inflammatory condition with a characteristic rash and which condition is associated with widespread internal pathology. The plaintiff was treated with prednisolone, which is a corticosteroid drug. Later another corticosteroid was substituted. The defendant did not prescribe Imuran or some steroid sparer when it was found at the trial that a steroid sparer should have been introduced directed to the risk of spinal fractures being occasioned by the long term use of corticosteroids. The plaintiff suffered spinal damage but at first instance it was held that the plaintiff had failed to prove damage resulting from the failure to introduce Imuran or the substitution of the second corticosteroid. 365 The plaintiff presented her case in two ways: firstly, that the defendant's negligence was causative of the fractures that occurred; and, secondly, that the defendant's negligence deprived the plaintiff of the loss of a chance of a better outcome from the steroid related osteoporosis and resultant fractures. The plaintiff failed on both grounds. On appeal, it was held that the plaintiff was entitled to recover damages for the loss of a chance of a better outcome had the negligence in treatment not occurred. 366 It is to be observed that in Rufo it was accepted at trial and on the appeal that if the facts supported it, the claim based upon the loss of a chance was available (see the judgment of Campbell AJA at 693 and in particular at [206]). Campbell AJA said (at 693-694): "[207] Third, there was no challenge to Studdert J's formulation of what the appellant was required to prove to recover damages for loss of the chance of a better outcome. His Honour said (at [246]-[247]): '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 Ltd (1990) 169 CLR 638; Sellars v Adelaide Petroleum NL (1994) 179 CLR 333; Daniels v Anderson (1995) 37 NSWLR 438; and Tran v Lam (Badgery-Parker J, 20 June 1997, unreported). 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'… [405] Adopting a robust and pragmatic approach to the primary facts of this case (March v E & M H Stramare Pty Ltd (1991) 171 CLR 506 at 515, per Mason CJ; Wilsher v Essex Area Health Authority [1988] AC 1074 at 1090, per Lord Bridge; Wallaby Grip (BAE) Pty Ltd (in liq) v Macleay Area Health Service (1998) 17 NSWCCR 355 at 364, per Beazley JA) it seems to me that, more probably than not, the excess of corticosteroid consumed after 10 June 1992 in the context of the osteoporotic and vulnerable state of the appellant's spine caused the loss of a chance that the appellant would have suffered less spinal damage than she in fact did. [406] Also, as a matter of common sense, it seems to me that the chance lost would be more than speculative or remote and, indeed, would be 'of substance', albeit falling short of a fifty one per cent chance." 367 Hodgson JA expressed his substantial agreement with the reasons of Campbell AJA and went on to say (at 679-680): "[3] However, I also agree that the evidence strongly supported a conclusion that the negligence materially increased a risk, which was otherwise very substantial, that fractures would occur; and that the occurrence of the fractures was a realisation of this total risk (as distinct from the increment to the risk created by the negligence). This gives rise to the question whether the appellant is entitled to be compensated for the loss of the chance that, but for the negligence, the fractures would not have occurred (or would not have occurred at the time or with the severity of their actual occurrence). If so, then in my opinion it was an error for the primary judge to hold that the increased risk was too speculative to justify an award of damages: so long as such an increase is material, I think the Court is required to do its best to assess it. [4] It is clear that a plaintiff cannot recover damages for negligence unless it is proved, on the balance of probabilities that some actual quantifiable loss occurred as a result of the negligence. However, it is also clear that, at least in some circumstances, the loss of a chance of commercial value is regarded as an actual quantifiable loss: Sellars v Adelaide Petroleum NL (1994) 179 CLR 332 at 355. [5] There is a real question whether the loss of a chance approach is applicable in medical negligence cases, where an adverse result is suffered, for which there was a substantial probability even without negligence, but negligence has materially increased that probability." 368 His Honour concluded (at 681 [12]) that there was a chance that the adverse result could have been avoided if there had been no negligence and that the chance was compensable. 369 Santow JA also expressed his agreement with the judgment of Campbell AJA and with the judgment of Hodgson JA. His Honour referred to the reasoning on causation and damages in Sellars v Adelaide Petroleum NL (supra at [221]) as being "reconcilable with allowing recovery for loss of a less than even chance in medical negligence cases" (at 687 [39]). His Honour proceeded (at 687-688 [40]): "Moreover, in medical negligence cases causation must still be demonstrated at greater than 50 per cent probability in two respects. First, the chance must be proven to exist on balance of probabilities. Second, the plaintiff must prove on balance of probabilities that if offered the chance lost, in terms of treatment, the plaintiff would have elected to have that chance. Thus 'where the chance lost was a chance that the plaintiff may have acted in such a way as to receive a benefit or avert a detriment, the plaintiff must prove on the balance of probabilities that there was such a chance and that the plaintiff would have so acted': Tran v Lam (Badgery-Parker J, 20 June 1997, unreported) at 27. That is an important control mechanism. It means that loss of a chance cannot be invoked where there is not a greater than 50 per cent chance that the patient, properly advised, would have undertaken the particular course of treatment or operation. That is so though we are here dealing with a hypothetical event." 370 His Honour later (at 688 [45]) expressed his preference for the percentage approach: "However, it would be productive of injustice if the plaintiff were to receive 100 per cent of the loss where a chance or prospect exceeds 50 per cent (say 51 per cent) yet receive nothing at all if such loss were, say, 49 per cent. The fairest solution is to base compensation on whatever be the percentage, whether above or below 50 per cent, wherever one is dealing with future events or hypothetical ones." 371 His Honour conducted a review of relevant authorities, including Naxakis (supra), Sellars v Adelaide Petroleum NL (supra) and Malec v J.C. Hutton Pty Limited (supra). His Honour considered the English cases of Gregg v Scott (supra) and Hotson v East Berkshire Area Health Authority (supra), and concluded (at 690-691): "[52] While intermediate courts of appeal in Australia do not yet have the guidance of a High Court decision adopting as ratio loss of chance in medical negligence, the trend of intermediate appellate and first instance authority in Australia favours that approach. There is much to be said for consistency, whereby a chance above or below 50 per cent obtains no more and no less in compensation than the corresponding percentage, instead of an all or nothing approach. That should not open floodgates to loss of chance claims either in the medical field or more generally. First, the loss of chance must itself be established on the balance of probabilities, as also that the chance if offered would have been taken. Second, it is the very nature of the doctor's duty of reasonable care and skill that directs it to achieving the best chance of a favourable medical outcome, subject to informed patient choice and what is practically available. Duty in other spheres may have varying dimensions. [53] The present is a case where loss of a chance does afford a proper basis for compensation. It highlights the importance of considering the duty of care not in isolation, but in conjunction with a fair assessment of the difficult task facing a doctor having to choose between various options each with their own risks. [54] What is said by Professor Luntz in his article on loss of chance remains apposite, at 197: 'where a medical practitioner fails to exercise reasonable care, the aim of the law generally is not to reposition the plaintiff as though no treatment had been given, but as though proper treatment had been given … whether the claim lies in contract or tort. In many instances proper treatment could have done no more than give the plaintiff a chance of cure or alleviation of a pre-existing condition. This is something of value, something for which many people would give money. The law should treat such a chance as worthy of protection.'" 372 In the passage above extracted, Santow JA referred to the trend of intermediate appellate authority. His Honour did not refer specifically to two cases of intermediate appellate courts to which Mr Hall has drawn my attention: Gavalas v Singh (2001) 3 VR 404 and Chang v Australia Meat Holdings Pty Limited [2001] QCA 51. In Gavalas it was held by the Court of Appeal in Victoria that the plaintiff was entitled to be compensated for the loss of the chance of the complete removal of a tumour had it earlier been detected in a timely fashion. In Chang it was held by the Queensland Court of Appeal that damages were recoverable for the loss of a chance to avoid Q fever by appropriate vaccination. It is to be observed however that the latter decision concerned the failure of the defendant employer to advise its employee to consult his GP for advice as to vaccinaton. It was not a medical negligence case. 373 I referred earlier to the decision of the Court of Appeal in State of New South Wales v Burton: 221. In that case the plaintiff was a police marksman who was fired upon, but not hit, during a farm siege and he developed post traumatic stress disorder after this incident. It was held at first instance that the State was negligent in failing to provide counselling after the incident but on appeal it was determined that the PTSD was not caused by the failure to take counselling, but by the shooting itself. It was in this context that the Chief Justice and Hunt AJA said what was set out earlier at 221. However, the matter was remitted to the trial court to assess the relevant harm, which was the loss of the chance of a better outcome had there been due counselling. In the course of his judgment the Chief Justice cited Rufo v Hosking in the following context: "25 The PTSD was not caused by the failure to have counselling, or take other ameliorative steps. It was caused by the shooting. The relevant loss in this case is the loss of a chance of a better outcome. The focus of attention must be on the extent to which the Respondent's condition would or could have been improved had earlier counselling been provided. 26 Any such reassessment should not extend to the loss of a chance that the Respondent would not have suffered PTSD at all. I do not understand Dr Wright to advance the proposition that that was a significant factor. 27 The onus was throughout on the Respondent, as plaintiff, to establish the existence and extent of the loss of the chance. On the basis of his Honour's findings it appears that there was a loss of such a chance and that, as a matter of causation, the Respondent has suffered some loss or damage. (See e.g. Sellars v Adelaide Petroleum NL (1994) 179 CLR 332 at 355; Olympic Holdings Pty Limited v Lochel [2004] WASC 61 at [122]-[123]; Rufo v Hosking (2004) 61 NSWLR 678 at 680.)" 374 The place of "the loss of a chance" claim in the medical negligence field was very recently considered by McClellan CJ at CL in Halverson & Ors v Dobler [2006] NSWSC 1307. The Chief Judge had before him four related claims. The principal claim was by the patient, and three family members also sought damages for nervous shock suffered by reason of the their relative's medical outcome. The patient suffered a cardiac arrest and hypoxic brain damage allegedly as a result of the negligent treatment afforded to him by the defendant, his general practitioner. The claim advanced was that the defendant should have recognised the cardiac problem before the occurrence of the catastrophic event. One of the ways in which the principal plaintiff advanced his case was for the lost chance of a better outcome. It was claimed that the defendant was negligent in not arranging for an ECG at a particular time. The Chief Judge gave very close attention and consideration to relevant authorities and identified what he perceived to be difficulties associated with the loss of a chance approach in a personal injuries case as contrasted with a claim for a lost commercial opportunity. Nevertheless, his Honour acknowledged he was bound to follow Rufo. 375 His Honour found however that had the timely ECG been administered there was at least a sixty-five percent chance of detection of pathology so as to avoid a cardiac arrest. In these circumstances, his Honour determined that the plaintiff was entitled to full recovery of damages. His Honour said (at 73-74 [248]): "The Court of Appeal's decision is, of course, binding on me. [The decision referred to was the decision in Rufo.] However, it was concerned with a chance that was assessed to be less than 50%. Santow JA (at 688-690) suggests that the loss of a chance analysis should also apply where the chance is greater than 50%. If this is the correct approach to causation it would displace the presently accepted standard of proof in medical negligence cases. The other judgments in the case are confined to defining a principle where the chance is less than 50%. Hodgson JA expressed (at 681) the view that the loss of a chance analysis should only apply to chances of less than 50%, while in cases where the plaintiff can prove causation on the balance of probabilities (i.e. where the chance is greater than 50%) Malec should continue to apply so that damages are assessed taking into account the percentage chance that the injury would have occurred in any event. Accordingly, insofar as "loss of a chance" presently has a place in personal injury cases on the current state of the law in New South Wales it is in cases where the plaintiff cannot prove causation on the balance of probabilities, and accordingly the lost chance is less than 50%. This is consistent with the view expressed by Callinan J in Naxakis, and with the approach adopted by Spigelman CJ in Burton." [(supra), cited at [221(vii)]]. 376 I am bound by the decision in Rufo. Unlike Halverson, the present case is one in which I consider the chance lost was less than a fifty percent chance. Hence, I conclude, notwithstanding Mr McCulloch's submissions to the contrary, that I am required to determine the claim made by the plaintiff for the loss of the chance of a better outcome, applying the principles to be found in Rufo. I have found that the plaintiff did suffer brain damage on 14 January 1991. In order to recover damages for the loss of the chance of a better outcome, the plaintiff has to prove on the balance of probabilities that there did exist a real chance that the plaintiff would have had a better outcome had the negligence in treatment not occurred. It is, of course, also encumbent upon the plaintiff to prove that if offered the opportunity of a CT scan and treatment subsequent to that, that opportunity would have been taken. I have earlier in this judgment expressed findings to such effect (see [300] and [306]). 377 I am satisfied on the probabilities as to the following:

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(iv) the subsequent radiotherapy treatment. 383 The four contributors each caused brain damage, but not the same damage at the same time. Save for contributor (i), each of the remaining contributors added to the brain damage that preceded its contribution. 384 The plaintiff would, of course, have had to undergo the surgery and the chemotherapy and radiation treatment to address the plaintiff's pre existing condition whether or not a CT scan had been carried out on 13 January 1991 and whether or not the decline on 14 January had been avoided. The surgery undertaken on 16 January 1991 was no different from the surgery that would have been required had the decline on 14 January been avoided and the radiotherapy would have been no different either absent that decline. Because I find there was seeding before 14 January, any delay in the commencement of chemotherapy and radiotherapy referable to what occurred on that day did not assume significance. 385 The assessment of the value of the lost chance cannot be attempted without proper regard to the determination of the damages to which the plaintiff would have been entitled had the plaintiff proved on the balance of probabilities that the second defendant's negligence caused her brain damage such as was sustained on 14 January 1991. 386 Had there been such proof, it seems to me that it would have been altogether wrong in principle to approach the assessment of damages on the basis that the totality of the plaintiff's brain damage and all her disabilities represented her compensable loss. To do so would ignore what was likely to have been the outcome whether the decline on 14 January had occurred or not. 387 Whilst a defendant must take a plaintiff as he finds her, he is not responsible for harm that the plaintiff would have suffered in any event: see Hole v Hocking (1962) SASR 128, cited in Burton (supra) as illustrating this fundamental principle. 388 In Hatton v Sutherland (cited earlier at [221]), a case concerning psychiatric illness due to work stress, the judgment of the Court of Appeal was delivered by Hale LJ. The judgment addressed issues of apportionment and quantification (at pp 17-18) in paragraphs which I now set out: "[36] Many stress-related illnesses are likely to have a complex aetiology with several different causes. In principle a wrongdoer should pay only for that proportion of the harm suffered for which he by his wrongdoing is responsible (see eg Thompson v Smiths Shiprepairers (North Shields) Ltd [1984] 1 All ER 881, [1984] QB 405, Holtby v Brigham & Cowan (Hull) Ltd [2000] PIQR Q293 and Rahman v Arearose Ltd [2001] QB 351, [2000] 3 WLR 1184). Thompson's case and Holtby's case concerned respectively deafness and asbestosis developed over a long period of exposure; not only were different employers involved but in Thompson's case some of the exposure by the same employer was tortious and some was not. Apportionment was possible because the deterioration over particular periods of time could be measured, albeit in a somewhat rough and ready fashion. [37] It is different if the harm is truly indivisible: a tortfeasor who has made a material contribution is liable for the whole, although he may be able to seek contribution from other joint or concurrent tortfeasors who have also contributed to the injury. In Rahman's case, Laws LJ quoted the following illuminating discussion from Prosser and Keeton on Torts (5th edn, 1984) pp 345-346: 'If two defendants, struggling for a single gun, succeed in shooting the plaintiff, there is no reasonable basis for dividing the injury between them, and each will be liable for all of it. If they shoot the plaintiff independently, with separate guns, and the plaintiff dies from the effect of both wounds, there can still be no division, for death cannot be divided or apportioned except by an arbitrary rule… If they merely inflict separate wounds, and the plaintiff survives, a basis for division exists, because it is possible to regard the two wounds as separate injuries… There will be obvious difficulties of proof as to the apportionment of certain elements of damages, such as physical and mental suffering and medical expenses, but such difficulties are not insuperable, and it is better to attempt some rough division than to hold one defendant [liable] for the wound inflicted by the other. Upon the same basis, if two defendants each pollute a stream with oil, in some instances it may be possible to say that each has interfered to a separate extent with the plaintiff's rights in the water, and to make some division of the damages. It is not possible if the oil is ignited, and burns the plaintiff's barn.' [38] In Bonnington Castings Ltd v Wardlaw [1956] 1 All ER 615, [1956] AC 613, the employee was exposed to harmful dust, all of it at work, but some of it in breach of duty and some not: the employer was held liable for the whole of the damage caused by the combination of the 'guilty' and 'innocent' dust. The question of apportionment was not argued. The problem there, as in McGhee v National Coal Board [1962] 3 All ER 1008, [1973] 1 WLR 1, was whether the claimant could prove causation at all, given the possible contribution of both 'guilty' and 'innocent' dust to his illness. [39] As Stuart-Smith LJ commented in Holtby's case [2000] 3 All ER 421 at 428 (para 20): '[The claimant] will be entitled to succeed if he can prove that the defendants' tortious conduct made a material contribution to his disability. But strictly speaking the defendant is liable only to the extent of that contribution. However, if the point is never raised or argued by the defendant, the claimant will succeed in full as in the Bonnington case and McGhee's case.' Clarke LJ went further and placed at least the evidential burden of establishing the case for apportionment upon the defendant (at 433 (para 35)): 'It seems to me that once the claimant has shown that the defendants' breach of duty has made a material contribution to his disease, justice requires that he should be entitled to recover in full from those defendants unless they show the extent to which some other factor, whether it be "innocent" dust or tortious dust caused by others, also contributed.' But he acknowledged that these cases should not be determined by the burden of proof: assessments of this kind are 'essentially jury questions which have to be determined on a broad basis'. [40] Hence the learned editors of Clerk and Lindsell on Torts (18th edn, 2000) at para 2-21, state that 'Where it is possible to identify the extent of the contribution that the defendant's wrong made to the claimant's damage then the defendant is liable only to that extent, and no more…'" 389 Then, Hale LJ went on to say at [41]-[42]: "Hence if it is established that the constellation of symptoms suffered by the claimant stems from a number of different extrinsic causes then in our view a sensible attempt should be made to apportion liability accordingly. There is no reason to distinguish these conditions from the chronological development of industrial diseases or disabilities. The analogy with the polluted stream is closer than the analogy with the single fire. Nor is there anything in the Bonnington case or McGhee's case requiring a different approach. [42] Where the tortfeasor's breach of duty has exacerbated a pre-existing disorder or accelerated the effect of pre-existing vulnerability, the award of general damages for pain, suffering and loss of amenity will reflect only the exacerbation or acceleration. Further, the quantification of damages for financial losses must take some account of contingencies." 390 In State of New South Wales v Burton (also earlier cited at [221] and [373]), Basten JA was in the minority, deciding there was sufficient evidence to prove the severity and duration of PTSD could have been reduced by timely counselling. However, considering that it was likely that the plaintiff would have suffered a level of post traumatic stress disorder absent the defendant's negligence, his Honour concluded that the matter should be remitted to the trial court to apportion the harm occasioned to the negligent failure to provide treatment. 391 In the course of his judgment Basten JA said (at [71]): "…although it is sufficient that tortious conduct of a defendant materially contributes to an injury suffered by the plaintiff, there may be other causes and, in assessing loss, there are circumstances where it is appropriate to visit on the defendant liability for a proportion only of the loss suffered." 392 His Honour later said (at [73]-[74]): "…where it is appropriate to apportion loss, that can only be done if the injury is in some sense divisible. In Bonnington Castings Ltd v Wardlaw [1956] AC 613, the medical condition contracted by the worker was caused by exposure to silica dust. The worker was exposed to dust both tortiously and without any breach of duty. There being only one injury, to which the tortious exposure made a not insignificant contribution, causation was established. There was no apportionment, presumably because the injury was treated as indivisible, although as noted by Stuart Smith LJ in Holtby v Brigham & Cowan (Hull) Ltd [2000] 3 All ER 421 at [41], the point was not argued in Bonnington itself. 74 It is possible, in principle, that a single injury will be divisible if an approximate division can be made between different causes…" (His Honour then went on to cite from Hatton v Sutherland para [41] and [42] from that judgment which I have set out above.) 393 Consistently with the authorities referred to above, it seems to me that the totality of the harm suffered by this plaintiff is properly to be regarded as divisible notwithstanding the difficulties of division. As I remarked earlier, each of the contributors caused brain damage at different times, and each of the contributors (ii), (iii) and (iv) added to the brain damage preceding its occurrence. 394 In Seltsam Pty Limited v Ghaleb [2005] NSWCA 208 the worker was exposed to asbestos by successive employers and he sustained asbestosis related pleural disease (ARPD). This was treated as a divisible disease, being a disease increasing in severity through an ongoing process of successive events causing harm. In his judgment in Seltsam, Ipp JA said (at [34]): "In the case of ARPD, the disease is the consequence of inhaling asbestos fibre in circumstances where each successive inhalation of asbestos inflicts a further and separate form of harm on the victim. As each infliction of harm is an independent event, where ARPD has cumulatively been brought about by different tortfeasors over different periods, each tortfeasor is separately liable for the separate damage each has caused. Such tortfeasors are not jointly, concurrently or severally liable to the victim. The damage for which each is liable has to be separately proved and separately assessed." 395 Earlier (at [33]), his Honour identified a hearing impediment increasing in severity by exposure to excessive noise over a lengthy period as a divisible disease, where each successive exposure to noise separately increased the hearing loss. 396 See also Patrick Operations Pty Limited v Comcare [2006] NSWCA 142, another case involving successive occasions of exposure to asbestos. 397 The differences in the disease process in asbestosis and in progressive hearing loss are to be acknowledged, but nevertheless it seems to me that the analysis of those processes is apt for adoption when the discrete contributions to the plaintiff's ultimate condition and disability in the present case are given due recognition. 398 With the principles to be extracted from Hatton and from Burton to be found in the passages from the judgments to which I have referred, I propose as best I can to apportion responsibility as between the four contributors I have found here, even though the medical evidence emphasises the difficulties in this task. These difficulties are illustrated by the following extracts from the evidence:

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Later (at T 1836), Dr Smee added: "…I mean the reality is that this child's ultimate cognitive outcome is a sum of all the events that took place. If you take one event out of that then there is a likelihood that it might have been a little different but it is very difficult to quantify what the contribution of each of the events is." Dr Smee's answer last quoted followed immediately upon an answer that Dr Berry gave to the effect that the damage would have been less had the incident on 14 January been avoided, and he referred to the difficulty of "assigning a figure", saying only that it would have been "proportionately less". 399 Mr Wallace did not address the issue of the cause or causes of the plaintiff's present condition in his report, Exhibit U, but he gave evidence as to his experience in treating cases of medulloblastoma in children and of the perceived outcome in cases treated. Based on that experience, he considered the significance of the deterioration on 14 January. The experience of Mr Wallace has been that children recover relatively well from medulloblastoma tumours and are able to attend normal schools and to lead normal lives. To be left with an IQ as low as that which the plaintiff has differed in the experience of Mr Wallace from the cases of children he treated suffering from medulloblastoma in 1990 and 1991 (T 1352). 400 Mr Wallace said that the plaintiff's reduced IQ of less than 60 was "partly attributable possibly and in a very large degree to the coning that occurred after lumbar puncture" (T 1352-1353). Mr Wallace attributed the plaintiff's incapacity to care for herself to the coning episode (T 1355). He attributed the plaintiff's inability to work to the same cause (T 1355). 401 Mr Wallace considered that the plaintiff had suffered brain stem damage to a greater degree than could be attributed to radiotherapy and he attributed this increased harm to the coning episode (T 1540). Mr Wallace did not think it likely that the brain stem damage was due to the tumour. 402 Mr Klug addressed the issue of the causes of the plaintiff's present condition in his report dated 21 January 2004 (Exhibit W). He stated at p 9 of that report: "a) I would be of the opinion that the child suffered a severe brain injury prior to the release of intracranial pressure on the 14th January 1991. Although it is not possible to exclude some contribution from her condition prior to the lumbar puncture, it would be my belief that the principal damage occurred between the time she had the lumbar puncture and when the ventricular drain was inserted. b) I feel it is improbable that as a result of the surgery performed on the 16th January 1991 this person suffered any additional direct damage to her brain. I also feel it is unlikely that the subsequent hydrocephalus and the need for definitive treatment, namely a ventriculo-peritoneal shunt, contributed to further brain damage which was reflected in the ultimate functional outcome. c) I feel it is most probable that the subsequently required radiotherapy has been responsible in its own right for significant morbidity. It is well recognised that radiotherapy of the type undertaken on this child at this period of life is very frequently associated with substantial morbidity." 403 Mr Klug gave evidence of having had extensive experience in the treatment of children with medulloblastoma and he said he followed up his patients (T 1677). He expressed a familiarity with operative procedures and the effect that chemotherapy and radiation treatment have on children who have suffered medulloblastoma. 404 In his opinion, the failure to detect the tumour before 14 January meant that the course of radiotherapy was delayed and longer than it otherwise would have been (T 1679). However, I observe as to this evidence that, having considered the evidence of Dr Smee and Dr Berry, I am satisfied that the nature and the course of the radiotherapy which the plaintiff received would have been no different had the plaintiff's condition been detected twenty-four hours earlier than it was. 405 Returning to the evidence of Mr Klug, in his experience the majority of children the plaintiff's age live essentially normal lives and many are capable of living independently and of working in an unskilled or in a semi-skilled occupation following effective treatment for medulloblastoma (T 1681). Mr Klug said that such patients have disabilities related to the treatment but many of them are able to live independently. He added, however, that some children do require twenty-four hour per day care (T 1681). 406 Mr Klug did not consider that radiotherapy was causative of significant motor impairment (T 1764). As to the spastic ataxia, balance and coordination impairment, he thought that the tumour and the hydrocephalus alone could have been addressed by a successful operation, so he attributed these disabilities to coning. Moreover, he considered the acute decline on 14 January contributed to the memory impairment, but the radiation treatment was the more dominant factor in relation to this disability. 407 Neither Mr Wallace nor Mr Klug was involved in the plaintiff's treatment and each of these witnesses became involved in this case after being qualified to express an opinion for the purposes of giving evidence. 408 It seems to me that much caution has to be exercised in applying evidence based upon the general experience of Mr Klug and of Mr Wallace to the particular case of this plaintiff, and it is important to pay due regard to the evidence of those doctors who were involved in the plaintiff's treatment. 409 Dr Williams expressed the opinion that "the major brain damage occurred when coning was precipitated by lumbar puncture" (p 12 of his report of 26 May 2006, Exhibit M). Chronologically then, Dr Williams attributed major significance to the decline on 14 January. However, Dr Williams acknowledged in that same report: "I do not have expertise in the outcome of medulloblastoma". 410 Mr Johnston had this to say as to the cause of the plaintiff's disabilities (see Mr Johnston's report, Exhibit 11, dated 24 November 2001): "Her long term problems are altogether attributable to the severity of her initial problem, its secondary effects (particularly hydrocephalus and epilepsy) and the long term effects of the several treatments, surgery, chemotherapy and radiotherapy, all of which I believe were important contributors to her late and severe morbidity." 411 It is to be observed in that report that Mr Johnston did not include as contributing to the plaintiff's long term problems the decline on 14 January 1991, but he acknowledged in evidence, to which I have elsewhere referred, that there was brain damage that occurred at that time. That brain damage cannot be ignored. 412 I have earlier reviewed Dr Kellie's evidence bearing upon the effects of the brain surgery and the radiation treatment (at [338]-[348]). I also have regard to the evidence of Dr Berry and to the evidence of Dr Smee concerning the impact of the heavier dosage of radiation that was necessitated in the plaintiff's case (see [349]-[351] above). 413 Dr Jones addressed the issues I am presently considering in his report of 16 November 2001 (Exhibit 19). On p 21 of that report, Dr Jones wrote: "Given the extent of the tumour and the widespread metastasis present, it is most likely that the cerebellar signs are due to the tumour itself and the operation required to remove it. It should be noted that she was mute after operation and this is quite frequently seen in operations of this nature which are of necessity, extensive because of the nature of the tumour. As her optic fundi did not show any swelling at any time preoperatively, it is my opinion that the delay in diagnosis had minimal or no effect on her visual acuity. However, she had extensive meningeal metastasis and these could have adversely affected her visual cortex and could have affected her optic nerves also. Her vision has been further complicated by the occurrence of cataracts in her eyes. These are almost certainly due to the side effects of radiotherapy. Her endocrinological problems have been also a side effect of the radiotherapy. This is quite a common problem in patients who have craniospinal radiation. Similarly, her scoliosis is secondary to the irradiation of her spine and nothing to do with either the delay in diagnosis or the episode of coning. Intellectual retardation is frequently seen in patients with medulloblastoma treated by craniospinal radiation and this has been a cause of great concern to all treating neurosurgeons. There have been attempts made because of this to reduce the amount of craniospinal radiation that these patients get and to supplement radiation with intensive chemotherapy. Unfortunately because of the great tumour bulk in the metastasis that Reema Tabet suffered from, it was necessary to give a maximal dose of radiotherapy as well as a maximal dose of chemotherapy." 414 In evidence Dr Jones attributed the plaintiff's intellectual deterioration in the main to the very high radiation dose (at T 1429): "Q. In relation to any damage to the brain what is it that you say indicates to you the type of damage which was sustained and the point at which it was sustained? A. In my view the deterioration that occurred on the 14th of January was almost completely reversed by relieving the intracranial pressure. Reema deteriorated, she wasn't as responsive after the major operation but she improved. I would say that the major cause of her intellectual deterioration is the very high dose of radiation - craniospinal radiation that she had. The tumour itself was significant because following her radiotherapy she developed multiple defects where the tumour had been and her hydrocephalus was, I think, a much lesser concern although she did have modestly raised intracranial pressure for some time post-operatively and she required a shunt which has subsequently caused problems so there are problems relating to her hydrocephalous as well." 415 In his report of 27 September 2002, Dr Jones considered the MRI films taken on 24 January 1995. One of the images showed that the left temporal lobe lesion did not involve the medial aspect, and Dr Jones wrote that it was not the part of the temporal lobe that would be damaged in uncal herniation. 416 Commenting on this in his evidence, Dr Jones said (at T 1430): "What does that lead you to conclude about the cause then of the plaintiff's presentation with brain damage? A. I would ascribe her memory problems as due to the radiotherapy and not due to damage to the temporal lobe.

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Q. Why do you say that? A. Because the medial side of the temporal lobe looks undamaged." 417 As I understand his evidence, Dr Jones attributed the spastic ataxia largely to the radiation treatment, but the deterioration on 14 January was a probable contributor (T 1514). The impaired vision, the memory loss and the speech problems were due to the radiation treatment (T 1514-1515). 418 Earlier in cross examination Dr Jones agreed that whether damage was caused in the episode on 14 January depended on whether there was marked improvement after the drainage (T 1455). Dr Jones opined that any such damage was "mainly of a temporary nature" because of the degree of recovery (T 1466). 419 With reference to the evidence of Dr Jones, I am by no means convinced that the deterioration that occurred on 14 January was almost completely reversed by the relief of intracranial pressure, and, accordingly, I do not find that the damage occurring on 14 January was "mainly of a temporary nature". Subject to that qualification, I found Dr Jones' evidence to be generally persuasive. He was a careful witness who prepared extremely thorough reports (see Exhibit 19). 420 I referred earlier to the evidence of Professor Watson in considering whether the lumbar puncture was causative of what occurred on 14 January (see [245]). Dr Watson reported on 9 April 2002: "I agree that the motor disability, dysarthria and ataxia are significant. However I am sure that they arise from damage to the descending motor pathways from the brain and also the cerebellar structures. I am of the opinion that the cerebellum was so extensively involved by the tumour that this would of itself account for many of the problems, particularly with its attempted removal followed by the radiotherapy." (See p 20 of the report of 9 April 2002, being part of Exhibit 23) 421 Professor Watson's view was ultimately stated as being that the plaintiff's disabilities were due to the severe and bulky tumour, the surgery, the radiotherapy and, possibly, the chemotherapy. 422 At T 1858 Professor Watson said: "…that I now had arrived at the opinion that Miss Tabet's plight was the result of her extremely severe and bulky brain tumour, the neurosurgery done to try to debulk the tumour and the radiotherapy, possibly the chemotherapy. But no longer did I think the so-called coning or slow coning was an appreciable factor in contributing to her current plight." 423 Professor Watson considered that the surgery caused inevitable direct damage and vascular damage to the cerebellar cortex. It followed inevitably that the microvascular supply of the cerebellar cortex was significantly disrupted. 424 In rejecting the proposition put in cross examination that the surgery caused no additional damage, Professor Watson pointed out that parts of the plaintiff's cerebellum were removed and placed on slides for the pathologist (T 1902). 425 In his report, Exhibit R (at p 8), Dr Hopkins endeavoured to attribute the various problems the plaintiff had to various causes, and he also dealt with this in his evidence (at T 1022-1023). Dr Hopkins attributed the speech and motor disability to "direct involvement of the descending pathways from the brain and cerebella structures by the tumour, by the hydrocephalus, and by damage occurring to these parts of the brain by the coning." (Report Exhibit R, p 8) 426 The plaintiff's visual handicap he attributed to optic atrophy caused by raised intracranial pressure due to the tumour and hydrocephalus. Dr Hopkins wrote that the plaintiff's intellectual disabilities were attributable "in a significant part" to her radiotherapy. He thought that the coning episode (and I treat this as a reference to the decline on 14 January) may also have contributed. His evidence (at T 1109) was the radiotherapy was likely to be the predominant cause of the impaired intellectual ability, but, according to Dr Hopkins, the predominant cause of the plaintiff's brain stem dysfunction and disabilities, other than the intellectual disability, were the hydrocephalus and the tumour itself (T 1117). 427 To the extent that the views of Mr Johnston and of Dr Kellie differ from the views of Mr Wallace and Mr Klug on the importance to be attached to what happened on 14 January, I prefer the opinions of Mr Johnston and Dr Kellie, particularly having regard to their involvement in the treatment of the plaintiff. I add that I was much impressed by each of these witness whilst he was present in the witness box. I am mindful that neither Mr Wallace nor Mr Klug treated the plaintiff. Moreover, it seems to me that the evidence of Mr Johnston and of Dr Kellie is supported by the opinions expressed by Dr Jones and Professor Watson. Whilst I do not find, contrary to Dr Jones' opinion, that the damage that occurred on 14 January was mainly temporary, and whilst I do accept, contrary to Professor Watson's opinion, that the damage that occurred on that date was significant, I found the evidence otherwise given by Dr Jones and Professor Watson to be generally persuasive and consistent with the evidence of the two treating doctors. I am also influenced by the evidence of Dr Hopkins in the importance he attached, in terms of contribution to the plaintiff's condition, to the tumour itself and the hydrocephalus. Also to be weighed in the apportionment of responsibility to the event of 14 January 1991 is the evidence of Associate Professor Berry and the evidence of Associate Professor Smee and their conclusions about the role of the various contributors recorded at [398] above. 428 The above review of the medical evidence emphasises the difficulty in the task of apportionment. I have not attempted to record an exhaustive summary of the medical evidence. That would simply be impracticable having regard to its volume, but I have considered all the medical evidence closely. I do not accept that the event of 14 January played the dominant role which Mr Wallace and Mr Klug attribute to it in relation to the plaintiff's mental impairment and motor function disabilities, but I do accept that that event caused damage that contributed to those disabilities. Whilst Mr Johnston and Dr Kellie did not define the harm caused by the decline on 14 January, Dr Hopkins and Dr Jones in combination provided support for the view that that decline contributed to the plaintiff's intellectual impairment and her motor damage. The evidence of Professor Smee and Professor Berry also support that view. 429 Having considered all the medical evidence, I think it probable that the event of 14 January made some contribution to the plaintiff's ultimate disabilities, particularly her cognitive loss and her ataxia, her loss of balance and her coordination impairment. However, I find on the probabilities that the contribution made by the event of 14 January 1991 to the above specified disabilities and to her disabilities generally was significantly less than the combined contribution of the remaining contributors. It is impossible to be precise about the matter, as reflection on the medical evidence reveals, but I find on the probabilities that the contribution of the event of 14 January 1991 to the aggregate brain damage and resulting disabilities with which the plaintiff has presented to this Court is no greater than twenty-five percent. 430 In the result, had the plaintiff here proved an entitlement to be compensated in full measure for the harm sustained on 14 January 1991, then it would not have followed that the plaintiff established an entitlement to the total damages assessed at [220], bearing in mind the basis of that assessment. To have awarded such sum, or anything like it, would have been to award far too much. Twenty-five percent of $6,092,586 is $1,523,146.50, and it would have been inappropriate to have awarded more than that. 431 The calculation last made suggests a degree of precision belied by the approach to its assessment, which approach I have exposed. The assessment of the measure of the contribution of the decline on 14 January 1991 has not been based on any firm expression of medical opinion stating a percentage contribution, because there is no such evidence. (At a time prior to the conference of experts, Professor Watson opined in his report of 9 April 2002 that the "coning" event probably accounted for 20-30% of the plaintiff's disabilities, but he subsequently changed his mind about this.) Moreover, I acknowledge that in reaching the monetary amount last stated above, it has not been possible to proceed to that assessment in a precise way either. This follows from there being four contributors to the ultimate extent of the brain damage from which the plaintiff presently suffers, with all its resultant disabilities. However, I have made the assessment as some guide in my task of endeavouring to arrive at a fair allowance for the loss of the chance of avoiding the brain damage that did occur on 14 January 1991. 432 It is not possible to isolate any one of the various components of the total assessment considered in [207]-[220] above, and to regard it as referable only to what occurred on 14 January. The major heads of damage are the care costs, past and future, and I consider it probable that each of the contributors has increased the need, the damage occurring on 14 January, to no greater extent than in the proportion indicated. Similarly with general damages, each of the contributors has added to the various elements to be considered in connection with the non economic aspects. 433 In providing for future economic loss by the traditional approach, allowance would have to be made for the role of each of the contributors in determining to what extent the loss of capacity referable to the decline on 14 January was likely to be productive of economic loss, but the evidence here does not provide any more precise method of compensating for this head of damages than that reflected in the approach taken. 434 I have earlier expressed the conclusion that by reason of the negligence I have found, the plaintiff lost the chance of a better outcome, and of avoiding the brain damage that occurred on 14 January 1991, a chance I have measured at forty percent ([378] above). I use the figure stated at [430] above as a guide towards placing a monetary value on the lost chance, recognising the imperfections in the manner of its calculation when doing so. Ultimately then, the sum which I award is $610,000, which approximates to forty percent of the assessment arrived at in [430].

[226]

Costs 435 The plaintiff has failed against the first defendant but has succeeded against the second defendant. Mr Hall has submitted that it would be appropriate in the circumstances of this case for the Court to make an order in the nature of a Bullock order or a Sanderson order, resulting in the burden of the successful defendant's costs being shouldered by the second defendant. 436 The general rule that costs should follow the event is now expressed in Pt 42 r 42.1 of the Uniform Civil Procedure Rules. Departure from that general rule and a decision on whether or not a Bullock order or a Sanderson order ought to be made involves the exercise of the Court's discretion. It would not be proper to make an order, the effect of which was to make the second defendant responsible for payment of the first defendant's costs simply because the second defendant unsuccessfully resisted the plaintiff's claim against him. The plaintiff would have to show that the costs the subject of any order were reasonably incurred by the plaintiff as between the plaintiff and the second defendant. It would not be enough, in my opinion, for the plaintiff to show, if such was the case, that it was reasonable to sue the first defendant as well as the second defendant. It seems to me that the plaintiff would need to be able to point to some conduct of the second defendant such as would make it fair to impose some liability on him for the costs of the first defendant. This was the approach adopted by Blackburn CJ in Steppke v National Capital Development Commission (1978) 21 ACTR 23 at 30-31, cited with approval by Gibbs CJ in Gould v Vaggelas (1983-85) 157 CLR 215 at 230. 437 I am guided in considering the present application by what Gibbs CJ said in Gould in the following passage (at 229-230): "The ground on which a Bullock order may be made is, in my opinion, more accurately stated in a passage in Sanderson v. Blyth Theatre Co. [1903] 2 K.B. 533, at p. 539, which was cited with approval in Bullock v. London General Omnibus Co. ([1907] 1 K.B. 264, at p. 272) and Hong v. A. & R. Brown ([1948] 1 K.B. 515, at p. 522), viz., that the costs which the plaintiff has been ordered to pay to the defendant who succeeded, and which the plaintiff recovers from the defendant who has failed 'are ordered to be paid by the unsuccessful defendant, on the ground that ... those costs have been reasonably and properly incurred by the plaintiff as between him and the [unsuccessful] defendant'. In Johnsons Tyne Foundry Pty. Ltd. v. Maffra Corporation, ((1948) 77 C.L.R., at pp. 572-573), Williams J. stated the principle in a similar way and Starke and Dixon JJ., in giving their reasons for making a Bullock order, both relied on the circumstance that the attitude adopted by the successful defendant had induced the plaintiff to join the other defendant ((1948) 77 C.L.R., at pp. 559-560, 566). In my respectful opinion the true position was clearly stated by Blackburn C.J. in Steppke v. National Capital Development Commission ((1978) 39 L.G.R.A. 94, at p. 100; 21 A.C.T.R. 23, at pp. 30-31), when he said that 'there is a condition for the making of a Bullock order, in addition to the question whether the suing of the successful defendant was reasonable, namely that the conduct of the unsuccessful defendant has been such as to make it fair to impose some liability on it for the costs of the successful defendant'". 438 In the same case, Wilson J said (at 246-247): "A Bullock order is a term - derived from the decision of the Court of Appeal in Bullock v. London General Omnibus Co. ([1907] 1 K.B. 264) - used to describe an order requiring an unsuccessful defendant to pay the costs which have been awarded in favour of a successful defendant. Such an order may be made where the costs in question have been reasonably and properly incurred by the plaintiff as between him and the unsuccessful defendant: Bullock ([1907] 1 K.B., at p. 269); Johnsons Tyne Foundry Pty. Ltd. v. Maffra Corporation ((1948) 77 C.L.R. 544, at p. 572); Altamura v. Victorian Railways Commissioners ([1974] V.R. 33). The making of such an order is a matter for the discretion of the trial judge." 439 In Gould Brennan J expressed the position thus (at 260): "Although the making of a Bullock order is in the discretion of a trial judge, the mere joinder of two causes of action against separate defendants in the one action is insufficient to support the making of an order against an unsuccessful defendant when the other defendant is exonerated. A judicial discretion can be exercised to make a Bullock order against an unsuccessful defendant in an action brought against two or more defendants for substantially the same damages only if the conduct of the unsuccessful defendant in relation to the plaintiffs' claim against him showed that the joinder of the successful defendant was reasonable and proper to ensure recovery of the damages sought: cf. Johnsons Tyne Foundry Pty. Ltd. v. Maffra Corporation ((1948) 77 C.L.R. 544, at p. 566)." 440 The second defendant's conduct of this cause was focussed on denying that he was negligent and on denying there was any act or omission by him such as was causative of harm to the plaintiff. The second defendant did nothing to point to fault by the first defendant or to encourage the plaintiff to join the first defendant in the proceedings. I do not conclude that costs incurred in the proceedings between the plaintiff and the first defendant are to be regarded as having been reasonably and properly incurred by the plaintiff as between the plaintiff and the second defendant. Hence, I do not consider it would be proper to make a Bullock order or a Sanderson order concerning the costs of the successful defendant. 441 Costs should follow the event in respect of the proceedings between the plaintiff and the first defendant and in respect of the proceedings between the plaintiff and the second defendant, and I will make orders to this effect.

Tabet v Mansour & Anor

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