Diamond v Simpson - [2003] NSWCA 373 - NSWCA 2003 case summary — Zoe

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Diamond v Simpson

[2003] NSWCA 373

Court of Appeal (NSW)|2003-02-20|Before: Meagher JA, Ipp JA, Young CJ, Whealy J

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Court

Court of Appeal (NSW)

Decision date

2003-02-20

Before

Meagher JA, Ipp JA, Young CJ, Whealy J

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Original judgment source is linked above.

Judgment (94 paragraphs)

[1]

CITATION : Diamond v Simpson (No 3) [2003] NSWCA 373 HEARING DATE(S) : 18, 19, 20 February 2003; 18, 19 June 2003 [Contribution Claim] JUDGMENT DATE : 16 December 2003

[2]

JUDGMENT OF : Meagher JA at 1; Ipp JA at 2; Young CJ in Eq at 3 DECISION : (1) Appeal allowed; (2) Declare that the cross defendant is liable to pay to the cross claimant one-half of the amount paid or payable to the plaintiff in respect of orders made against the cross claimant in these proceedings; (3) Liberty to apply to a Master to certify the amount of such amount if the same cannot be agreed; (4) Cross appeal dismissed with costs.

[3]

CATCHWORDS : NEGLIGENCE- Hospital- Defective birth case- Scientific evidence- Whether hospital and doctor contributed to defective birth. Evidence Act 1995 LEGISLATION CITED : Law Reform (Miscellaneous Provisions) Act 1946, s 5 Limitation Act 1969 Supreme Court Act 1970, s 75A(5) Abalos v Australian Postal Commission (1990) 171 CLR 167 Adler v ASIC (2003) 46 ACSR 504 Ahmedi v Ahmedi (1991) 23 NSWLR 288 Benmax v Austin Motor Co Ltd [1955] AC 370 Bonnington Castings Ltd v Wardlaw [1956] AC 613 Brisbane South Regional Health Authority v Taylor (1996) 186 CLR 541 Broken Hill Pty Co Ltd v Duffy (1943) 16 ALJ 374 Burrows v The March Gas & Coke Company (1870) LR 5 Ex 67 (Full Bench of Exchequer) Burrows v The March Gas & Coke Company (1872) LR 7 Ex 96 (Exchequer Chamber) Cohen v McWilliam (1995) 38 NSWLR 476 Davie v Lord Provost Etc of Edinburgh [1953] SC 34 Dearman v Dearman (1908) 7 CLR 549 Fox v Percy (2003) 77 ALJR 989 Hollman v Sampson [1985] 2 Qd R 472 The Koursk [1924] P 140 Lawrie v Meggitt (1974) 11 SASR 5 CASES CITED : Mahony v J Kruschich (Demolitions) Pty Ltd (1985) 156 CLR 522 Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705 March v E & M H Stramare Pty Ltd (1991) 171 CLR 596 Medlin v State Government Insurance Commssion (1995) 182 CLR 1 Purkess v Crittenden (1965) 114 CLR 164 R v GK (2001) 53 NSWLR 317 FF Seeley Nominees Pty Ltd v El Ar Initiations (UK) Ltd (No 2) (1990) 55 SASR 314 Seltsam Pty Ltd v McGuinness (2000) 49 NSWLR 262 Sharp v Avery [1938] 4 All ER 85 Shorey v P T Ltd (2003) 77 ALJR 1104 Simpson v Diamond [2001] NSWSC 150 Sinclair v William Arnott Pty Ltd (No 2) (1963) 64 SR (NSW) 88 Smith v Harris [1939] 3 All ER 960 State Rail Authority v Earthline Constructions Pty Ltd (1999) 73 ALJR 306 Tzouvelis v Victorian Railway Commissioners [1968] VR 112 The Volute [1922] 1 AC 129 Warren v Coombes (1979) 142 CLR 531 Watts v Rake (1960) 108 CLR 158 PARTIES : Robert Diamond (Appellant) Trustees of the Sisters of St Joseph (Respondent) FILE NUMBER(S) : CA 40962/01 COUNSEL : P L G Brereton SC and I F Butcher (A) P Hall QC and S A Woods (R) SOLICITORS : Blake Dawson Waldron (A) Makinson & d'Apice (R)

[15]

Tuesday 16 December 2003 ROBERT DIAMOND v CALANDRE SIMPSON AND TRUSTEES OF THE SISTERS OF ST JOSEPH (NO 3) Judgment 1 MEAGHER JA: I agree with Young CJ in Eq. 2 IPP JA: I agree with Young CJ in Eq. 3 YOUNG CJ in EQ: This is the second tranche of the appeals arising out of the birth of the first respondent ("the plaintiff"), Calandre Simpson, on 5 July 1979. The birth took place in a hospital operated by the second respondent ("the hospital"). The doctor in charge of the birth was the appellant ("the doctor"). 4 As a result of at least the appellant's negligence, the plaintiff was born in such a state that she has developed cerebral palsy. 5 The trial of the plaintiff's action came on before Whealy J and lasted for 12 weeks of hearing. 6 On the first day of the trial, the doctor admitted liability and the plaintiff thereupon discontinued against the hospital. His Honour then had to consider the question of the quantum of damages as against the doctor, and also had to consider a cross claim for contribution by the doctor against the hospital. 7 In a long and careful judgment, Whealy J found a verdict against the doctor for $14,202,042.00, see [2001] NSWSC 925. His Honour found that the hospital was negligent, but that such negligence did not cause the plaintiff's damage. Accordingly, he dismissed the cross claim. 8 The first tranche of this appeal, an appeal by the doctor against the quantum of the verdict, was heard by this Court consisting of Stein and Ipp JJA and Young CJ in Eq and on 7 April 2003, the damages were reduced to $10,998,692.00; see [2003] NSWCA 67. There was also a subsequent judgment on costs by the same panel; see [2003] NSWCA 78, delivered on 9 April 2003. 9 The present appeal seeks to have the hospital contribute to the damages that have to be paid to the plaintiff by the doctor. 10 On this appeal, Mr P L G Brereton SC and Mr I Butcher appeared for the doctor, and Mr P Hall QC and Mr S A Woods appeared for the hospital. The basis of the appeal is simply that the conduct of the hospital was negligent and was a cause of the damage suffered by the plaintiff. The doctor suggests that the hospital should contribute 50% of the amount ordered to be paid by the doctor. 11 The hospital, in its notice of contention, challenges the finding of negligent conduct. It also says that because the doctor was grossly negligent, he is not entitled to contribution at all. There is also a cross appeal by the hospital on a procedural matter, relating to whether the trial judge should have given late leave to the doctor to amend his cross claim. 12 It is convenient to consider the issues that arise on this appeal under the following heads:

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VILLAE See Intervillous. 14 The terms "hypoxic" and "vagal" are vital ones in this case. The Gould Medical dictionary defines the term "hypoxic" as "Reduction in availability of oxygen to tissue due to a decrease in the partial pressure of oxygen in the arterial blood". 15 The term "vagal" refers to or concerns the vagus nerve. This is a pneugastric nerve extending from the face to near the heart. When the vagus nerve is stimulated it emits a chemical neuro-transmitter the effect of which is to slow the heart rate. The vagal effect has a short half life so that when the vagal stimulus is removed, the chemical dissipates and the heart rate recovers. 16 In the present case, the injury was caused by unremitting bradycardia. The key question in this part of the case is whether that bradycardia had a solely vagal cause or whether there was an hypoxic cause as well and, if so, what was that hypoxic cause. 17 It must be noted that Mr Brereton put that there was no particular magic in the classic definition of hyperstimulation noted in [11]. Indeed virtually all the experts agreed that this is so. Even if contractions did not exceed 5 in 10 minutes there could still be occasioned depletion of foetal metabolic reserves. 18 Three types of forceps are referred to in this case, Wrigleys, Neville Barnes and Kiellands. It is difficult to describe the differences in words, but I will endeavour to do so. Drawings of them appear at Blue Appeal Book Vol 3, p 581. Wrigleys are curved forceps with virtually no handles: one cannot get much traction from them. Neville Barnes forceps are a standard pair of classical long forceps with a handle that one can lock and squeeze together. They cannot be used to rotate. Kiellands forceps are different in two critical ways. First, they do not have a fixed lock. Secondly they can be used to rotate the head of the foetus but they can be very dangerous as they can squash the baby's head. See Dr Clements at Black Vol 1, 194-5. 19 Eight expert medical witnesses were called by the parties. The plaintiff called Mr Roger Clements, an obstetrician, Dr Janet Rennie, a neo-natal clinician, and Dr Frederick Hinde, a specialist gynaecologist. The doctor called Professor Nicholas Fisk, an English Professor of Obstetrics and Gynaecology, described by his Honour as a foetal physiologist, Dr Robert Lyneham, a consultant obstetrician and gynaecologist, Dr John Keogh, a specialist in obstetrics and gynaecology, and Dr John Pennington, obstetrician and gynaecologist. The hospital called Professor David Ellwood, Professor of Obstetrics and Gynaecology, another foetal physiologist. 20 In summary, his Honour found the views of Mr Clements and Dr Rennie very compelling. He was very much persuaded by Dr Hinde. He preferred Professor Ellwood to Professor Fisk, and did not find much assistance in the evidence of Drs Lyneham, Keogh or Pennington. This is a matter to which I will return. 21 The only other person who needs to be described at this stage is Geraldine Ranclaud, who was the midwife/nurse involved in the delivery of the plaintiff. Sister Ranclaud was an experienced nurse. She made a statement on 1 February 1988 about the matter, but unfortunately died in 1993. Her statement was tendered at the trial, but of course, there could be no cross examination on this statement.

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B. The Factual Background 22 The background facts can be shortly stated. Mrs Gail Simpson, whom I will call "the mother", was admitted to the hospital on the evening of 4 July 1979 for the purpose of giving birth to her second child. At about 8.10 am on 5 July 1979, the doctor ruptured her membranes and Syntocinon was administered to help induce labour. I will need to examine what occurred between 8.10 am and 1.30 pm that day in more detail later. For the present, I am merely outlining the background. 23 The doctor arrived at the labour ward at about 1.25 pm. He determined that the baby (the plaintiff) should be delivered by forceps. He tried five times to deliver the baby by forceps of three different types. During the final attempt with Kiellands forceps the doctor rotated the baby's head and then re-rotated it back to its previous position. The baby did not descend. During this process, the baby's heart beat reduced from about 140 beats per minute (bpm) to between 60 and 80 bpm. 24 These attempts at forceps delivery took 15 to 20 minutes. After the last attempt, the mother was taken to the operating theatre where the baby was delivered by caesarean section at 2.17 pm. There was thus about a 27 minute delay from the time that the decision was made to take the mother into the operating theatre and the time of delivery. 25 The plaintiff's condition at delivery was poor. Her APGAR was 10010 one minute after delivery. 26 The plaintiff developed cerebral palsy. It is common ground that she suffered a terminal bradycardia for at least 15 minutes, probably after 1.50 pm. There was thus a denial of sufficient blood oxygen to the brain of the plaintiff for a period in excess of 15 minutes and this is recognised as a situation where brain damage will most likely result. 27 The plaintiff sued the doctor in these proceedings which she commenced on 3 April 1987, that is, almost eight years after the event. 28 By cross claim filed on 27 February 1991 in what Whealy J, in a preliminary judgment, Simpson v Diamond [2001] NSWSC 150, called "a bland pleading", the doctor sought contribution or indemnity from the hospital without disclosing much by way of particulars as to why the contribution was sought. 29 In November 1999, the doctor's solicitors furnished the hospital's solicitors with a proposed amended cross claim. Discussions went on for some time about this. A formal amended cross claim document was provided by the doctor's solicitors on 20 July 2000. Consent to its filing was not forthcoming. On 2 March 2001, despite the hospital's arguments to the contrary, on the basis that it was prejudiced because of the death of Sister Ranclaud, Whealy J allowed the amended cross claim to be filed and it was filed on 27 February 2001. 30 In what I have described as a collateral issue, the hospital seeks to reverse that decision. 31 The trial commenced before Whealy J and lasted three months. His Honour then reserved his judgment, and on 5 November 2001, found a verdict for the plaintiff against the doctor, but dismissed the doctor's cross claim for contribution. 32 When considering his Honour's judgment I shall refer to paragraph numbers making this clear by the use of square brackets. 33 His Honour found at [1403]: "I find that the plaintiff's injury was caused solely by Dr Diamond's negligent use of forceps. This, coupled with the fact that the instrumental attempts were made in the labour ward, induced an unremitting bradycardia which continued until birth." 34 His Honour said at [1416] that he accepted on the evidence that there was never a real possibility that the mother had experienced continuous contractions during the hour prior to midday. This appears to be unassailable. His Honour continued at [1417] that he rejected the contention that the contraction frequency resulted in an interval between contractions of just under 60 seconds. He did so on the ground that the mother's evidence was to the contrary. However, as Mr Brereton submits, the mother's testimony on this issue was not likely to have been accurate. There was evidence that a mother in the position of Mrs Simpson would not have been in a position to make precise observations of the extent of her contractions, moreover, there would be a small difference in time between her experience of pain and the start and finish of each contraction. 35 His Honour also rejected at [1418] and [1419] that the entries in the fluid balance chart could have supported the Syntocinon theory because observations of the various nurses and doctors did not disclose that they had observed signs which would have been quite apparent had the fluid been administered in the way the Syntocinon theory suggested. 36 At [1423] his Honour remarked that it was obviously dangerous to attempt to reconstruct events by way of expert interpretation of hospital records. Particularly was this so where some of the records were ambiguous and Sister Ranclaud, the only person who might have been able properly to interpret them, had died before the trial. His Honour said that it was obvious that in many respects the hospital records did not provide a firm skeleton for reconstruction. His Honour said: "I remain unsatisfied and unpersuaded, despite the variations of approach, that there is any real probability that hyperstimulation occurred." 37 Regarding the contribution claim, his Honour said at [1406]: "I am satisfied that the hospital was in breach of its duty of care in relation to the dosage of Syntocinon that was administered to Mrs Simpson. This was, contrary to the doctor's instructions, at a rate 43% higher than the prescribed rate. The nursing staff was solely responsible for this breach of duty. Dr Diamond had no role in the administration of the excessive concentration."

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C. Applicable Principles of Appellate Review 40 Mr Hall commenced his supplementary submissions with a quotation from the judgment of Isaacs J in Dearman v Dearman (1908) 7 CLR 549, 561 that "the whole duty of every Court of Appeal is to give the judgment which in its opinion ought to have been given in the first instance." He then emphasized with reference to high authority the advantage that the trial judge has. He cited extensively from the judgment of Kirby J in State Rail Authority v Earthline Constructions Pty Ltd (1999) 73 ALJR 306, 330 [90-1]. 41 Mr Hall says that whilst the Court of Appeal is required by s 75A(5) of the Supreme Court Act 1970 to rehear the matter and to form its own conclusions on the evidence recorded at the trial, in doing so the Court is obliged to take into account, and give full weight to, the trial judge's advantages. 42 Mr Hall says that in the present case the 28 days of evidence, 3 days of submissions and the large number of exhibits, the oral evidence of expert witnesses occupying over 1,500 pages of transcript, the learned trial judge was at a considerable advantage, and this Court should not disturb his findings of fact unless they were not available on the evidence. 43 He then went on to say: "The principle applies to expert witnesses in the same way that it applies to lay witnesses. The trial judge has the advantage of having seen the experts presenting their opinions, and their manner of dealing with competing opinions and propositions put in cross-examination. "In particular, where the opinion expressed by an expert is based upon their experience, and where that experience forms a legitimate basis for an inference drawn by the trial judge, the Court of Appeal ought not to set aside the trial judge's assessment of that opinion: X & Y v Pal (1991) 23 NSWLR 26, 34. "It is also submitted that where the issue under appeal is the issue of causation, an appellate court would be cautious in subjecting the learned trial judge's reasons to meticulous scrutiny in the search of error: the conclusion as to causation is one that is 'often reached intuitively': Chappel v Hart (1998) 195 CLR 232, 290 [148]." 44 Mr Brereton submits that: "Although, where a challenge is made to a trial judge's finding of primary fact, an appellate court will defer to the trial judge's position of advantage if that finding is founded on substantially on an assessment of credibility, based to a significant extent on observations of demeanour (see Devries v Australian National Railways Commission (1993) 177 CLR 472, 479 (Brennan, Gaudron and McHugh JJ), 480 (Deane and Dawson JJ)), the rationale which underlies that approach is that the trial judge is acknowledged to enjoy a position of advantage, vis-a-vis an appellate court, in assessing demeanour. Demeanour did not play a significant role in the trial judge's resolution of those factual issues which remain in dispute on the appeal. The argument turns on objective facts and inferences, and the use and analysis of expert evidence, not the acceptance of one witness over another on demeanour." 45 Mr Brereton then says that it is very necessary to make a distinction between findings of primary fact and inferences to be drawn from the primary facts. In the present case he says there is no real problem about the findings of primary fact made by the Judge, so that inhibitions put on appellate courts in cases such as Abalos v Australian Postal Commission (1990) 171 CLR 167, 178-9 do not concern the present appeal. This is the case, as was Warren v Coombes (1979) 142 CLR 531, 541, where it is clear that: "Where the question is whether particular inference should be drawn from proved facts the appellate court has the right and duty to decide the question for itself."

[33]

However even here, because of inadequate records there has to be inference on these matters also. 48 As counsel reminded us, the High Court has recently considered the matter again in Fox v Percy (2003) 77 ALJR 989 and in Shorey v P T Ltd (2003) 77 ALJR 1104. In the latter case at p 1109 [32], Kirby J, who gave the leading judgment, said it was unnecessary to consider whether "the judicial authority about disturbing evidence on the basis of assessments of credibility applies, or applies with the same strictness, in the case of expert witnesses where … the honesty of the witness is not in doubt and the issue for decision at trial is the acceptability of the witness's opinion, the extent of his or her experience in the speciality and whether one expert's conclusion is more acceptable and logical than that of another expert." His Honour noted that there were differing views on that question and referred in a footnote to Ahmedi v Ahmedi (1991) 23 NSWLR 288, 291, the Earthline Constructions case at 321 [68] and referred also to Watts v Rake (1960) 108 CLR 158, 162-3. 49 However, Mr Brereton says that most significant is paragraph 42 of the judgment of Kirby J at p 1111, where his Honour notes that the error into which this Court fell in Shorey's case was to search for a single cause when the case appeared to be one where there were multiple causes, because all the plaintiff had to show was that the defendant's conduct was a cause, not necessarily the cause, of her injury. 50 Mr Brereton points out that in the Earthline case, the High Court did allow the appeal even though the trial judge had been heavily swayed by his impression of a witness on giving evidence, by taking regard to other evidence at the trial. 51 In my view, Mr Brereton's approach is correct. The Court in this case has greater liberty than in many appeals to examine the facts. This is because almost all the findings made by the judge were of inferred facts. Moreover, with minor exceptions, there were no problems as to credibility.

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D. The Opposing Arguments on Appeal 52 Mr Brereton for the appellant says that on the whole of the evidence, it is more likely than not that the plaintiff's injury was caused by two concurrent causes, one of them hypoxic rather than by one vagal cause only. 53 He further says that the trial judge erred in taking the view that he could give greater weight to the observations (or non-observations) of the clinicians than to the evidence of the scientists. 54 Mr Hall for the respondent hospital says that the decision below was one on a question of fact. The trial judge made his assessment on the evidence and his decision was well within the range. 55 The heart of the case for contribution between the doctor and the hospital is whether the latter's negligence in administering an overdose of Syntocinon to the plaintiff's mother was a contributing cause of the plaintiff's injury. 56 The learned trial judge found that the hospital was negligent in relation to the dosage of Syntocinon (see [1406]). However, his Honour held that that was not a contributing cause of the injury. 57 The doctor says that this is an error. He says his Honour should have found that that breach of duty was a cause of Calandre's injuries. The excessive Syntocinon regime produced such a level of contractions in Mrs Simpson that the reduced opportunity for replenishment of the placental villae between contractions resulted in the depletion of Calandre's foetal metabolic reserves, such that her ability to withstand the stresses of labour, including instrumentation, was impaired and compromised, with the consequence that, when otherwise she would have recovered from the forceps episode without permanent damage, she was unable to do so ("the Syntocinon theory"). 58 Mr Brereton puts it that a compelling reason for this conclusion is that the failed forceps were an insufficient explanation for the catastrophic outcome, unless some other, hypoxic, mechanism were also at work. This was the opinion, in particular, of the two foetal physiologists, Professors Fisk (for the appellant) and Ellwood (for the hospital). Although finding Professor Ellwood's approach to be "both reasonable and convincing", his Honour (contrary to both Professor Ellwood and Professor Fisk) did not accept that it was necessary to find an hypoxic explanation as well as a vagal bradycardia. Rather, his Honour accepted the evidence of the clinicians (Mr Clements and Dr Hinde), that it was not necessary to look for a second pathology. In so doing, his Honour apparently took the view that the clinicians Dr Hinde and Mr Clements "knew what they have seen", and were not concerned with the "niceties of precision" which troubled the foetal physiologists. This approach did not do justice to the scientific evidence. His Honour did not analyse the expert evidence - scientific and clinical - with the rigour required. His Honour should have concluded that the result was not explicable in the absence of a second pathology. 59 These are the basic contentions. There were, of course, arguments on the details. These are considered when matters of detail are discussed in these reasons.

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E. Expert Evidence 60 The solution to the very awkward problems presented to the Court in this case lies in the proper interpretation of the expert evidence and analysis of records compiled at the time of the plaintiff's birth. 61 There is no doubt as to the eminence and qualification of all the experts who gave evidence in this case. However their evidence was not entirely consistent. In particular, there was tension between the clinicians and the scientists which I have already noted and will discuss in the appropriate part of these reasons. 62 It must be remembered that "the parties have invoked the decision of a judicial tribunal and not an oracular pronouncement by an expert": Davie v Lord Provost Etc of Edinburgh [1953] SC 34, 40. The Court must decide the issue of fact before it, aided by the expert evidence. Where expert evidence is contradictory, the Court resolves the conflict applying "logic and commonsense to the best of its ability in deciding which view is to be preferred or which parts of the evidence are to be accepted": Hollman v Sampson [1985] 2 Qd R 472, 474. 63 Mr Brereton says that the requirement is for a trial judge to evaluate the reasons given by the expert witnesses for their views. A judge is not entitled merely to pick the most impressive of the expert witnesses put before him or her. 64 It must be remembered further that, whilst under the Evidence Act 1995 it is admissible for experts to give evidence of opinion close to the ultimate issue, the closer they approach the ultimate issue the more careful judicial scrutiny should be: R v GK (2001) 53 NSWLR 317, 326; Adler v ASIC (2003) 46 ACSR 504, 633. 65 In Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705 at 729 and following, Heydon JA, when a member of this Court, gave detailed guidance as to the way in which courts should approach expert evidence. He said [59] at p 729, with respect to the expert in that case, Professor Morton: "a prime duty of experts in giving opinion evidence [is] to furnish the trier of fact with criteria enabling evaluation of the validity of the expert's conclusions." 66 He pointed out that that view had been accepted by a large number of judicial and academic writers. His Honour then continued at 731 [64]: "The basal principle is that what an expert gives is an opinion based on facts. Because of that, the expert must either prove by admissible means the facts on which the opinion is based, or state explicitly the assumptions as to fact on which the opinion is based. If other admissible evidence establishes that the matters assumed are 'sufficiently like' the matters established 'to render the opinion of the expert of any value', even though they may not correspond 'with complete precision' the opinion will be admissible and material; see generally Paric v John Holland Constructions Pty Ltd [1984] 2 NSWLR 505, 509-510; Paric v John Holland (Constructions) Pty Ltd (1985) 59 ALJR 844, 846."

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A. Because fortunately there are very few cases like this. Q. Would you agree that there is no scientific explanation which explains a continued sustained vagal bradycardia? A. There is no scientific explanation because it would be extremely difficult to do a study which, under the circumstances of what we are discussing addressed this question." 71 The impression I obtained from these passages is that Dr Hinde was relying on his own experience rather than objective experience from literature. 72 Mr Brereton submits that the opinion of Dr Hinde that forceps alone can lead to sustained bradycardia is based purely and simply on an observation of forceps being followed by bradycardia in rare cases in the past. This involves the unstated and unproven assumption that in those cases, there was a causal connection; and, therefore, the supposition that there could have been such a connection in the plaintiff's case. However, neither Dr Hinde nor the hospital has put forward any factual matters at all which would allow evaluation of the opinion about causation in those earlier cases, or as to how conclusion could be drawn from them applicable to the plaintiff's case. While in some cases a temporal association may be sufficient to permit a causal relationship to be inferred, the evidence of the foetal physiologists means that this is not such a case. 73 Thus, it is put that his Honour did not direct his mind to the expert evidence in the way dictated by authority and considered in Makita v Sprowles (supra). 74 There is a lot of force in this submission. 75 His Honour seems to have considered that there was some dichotomy between "scientific certainty" expected from the perspective of a foetal physiologist and the observations of the clinician "who knows what he has seen"; see [1448]. 76 I agree with the submission of Mr Brereton in this regard: "This does not do justice to the role of scientific evidence. Here, two eminent foetal physiologists - one on each side of the record - agreed that a second pathology was necessary to explain the outcome. It was not enough to discount that to find that clinicians, not even able to describe particular cases on which their professional opinion depended, thought otherwise. This was no question of 'searching for scientific certitude'; two scientists on opposing sides said that the outcome was not possible without a second pathology, and his Honour should have so found. In a field of specialised knowledge (foetal physiology), the opinion shared by experts on both sides (and as well by Dr Lyneham and Dr Keogh) ought to have been accepted; at the least, it should not have been put aside without compelling reasons. The evidence of the decisions - Mr Clements and Dr Hinde - did not provide such a basis."

[57]

G. The Syntocinon Argument 78 The doctor's principal argument as ultimately formulated was that it was necessary to find a second cause, an hypoxic cause over and above any damage caused by the negligent use of forceps. Indeed, there was evidence particularly from Professors Fisk and Ellwood that it was necessary to find an hypoxic explanation as well as a vagal bradycardia. However, his Honour rejected this view. 79 The doctor says that that second cause is to be found in hyperstimulation of the mother by the hospital administering Syntocinon in a dose of 10 units in 700 mls in lieu of 1000 mls thus initially increasing the dose by 43%. 80 The effect was, so the argument ran, that hyperstimulation so used the foetus' metabolic reserves that when the forceps caused bradycardia there were insufficient reserves to recover as would normally happen if there was abuse of a foetus by forceps. 81 The argument was boosted by evidence that more than one of the eminent medical experts said they did not know of any case where there was unremitting bradycardia brought about by non-hypoxic causes alone. 82 However, there was also substantial evidence from clinicians that they had observed cases where one vagal cause might suffice. 83 His Honour completely rejected the Syntocinon theory. Mr Brereton says that his Honour was in error in doing so. Mr Brereton says that properly considered the expert evidence of Professors Fisk and Ellwood must have been accepted and was not, when properly analysed, affected by the view of the clinicians. 84 Some passages from his Honour's reasons, eg [1445-7] might lead one to think that his Honour favoured the view that if an hypoxic explanation was necessary Professor Elwood's view that that explanation was to be found through the forceps impinging on or occluding the umbilical cord was to be preferred. However, his Honour did not so find, indeed I believe eventually this was common ground. 85 The argument was that hyperstimulation brought about by administering Syntocinon in 700 mls in lieu of 1000 mls so used up the foetus' metabolic reserves that it was unable to replenish when there was vagal bradycardia caused by the last pull of the forceps. 86 At [1414] the learned Judge said that the excess dose of Syntocinon "was clearly capable of producing hyperstimulation as defined. The question is: 'did it'?" 87 A crucial piece of evidence in this case is the partogram kept by the hospital staff to record the progress of labour. 88 The partogram is printed to record a number of different matters including the Foetal Heart Rate (FHR) and Contraction Frequency and Duration. It is basically on squared paper with numerals on the left hand side, sometimes adjacent to the lines between squares and sometimes, as is the case of Contraction Frequency and Duration amidships between the dividing lines. 89 Vertical lines map out the time scale in quarter hour periods for FHR and half hour periods for Contraction Frequency and Duration. 90 The partogram records the foetal heart rate with crosses at various times during the day, the last being 12.45 pm and all the crosses are on the line for 140 beats per minute (bpm). It is almost certain that the baby's heart rate did not remain constant at 140 bpm. On the evidence the possibility of that occurring is extremely remote. Mr Hall did not seriously contest this. It is probable that the crosses are intended to indicate that the foetal heart rate was in the normal range of 120-160 bpm. To this extent the partogram is not entirely accurate. 91 The part of the partogram that is of particular importance is contained in Appendix 1. That part shows the "contract frequency and duration" and the "oxytocic dose". 92 The oxytocic dose section of the partogram shows that, at 9.30 am on the day of Calandre's birth, the Syntocinon dose commenced at a rate of 20 dpm. At 10 am the rate was increased to 30 dpm, at 10.30 am it was increased to 40 dpm and at 11.00 am it was reduced to 30 dpm. Dosage at 30 dpm continued until 12 noon. 93 Mr Brereton submitted that the hospital's administration of Syntocinon, contrary to the doctor's instructions, at a rate 43% higher than the prescribed rate, occurred during the period from 11.00 am to midday. This submission is borne out by the partogram. 94 The partogram is capable of being of even greater significance in regard to the frequency of contractions during the critical period between 11.00 am and midday. 95 There is a dispute between the parties as to the meaning of the partogram in regard to this aspect. Mr Hall submitted that the partogram indicates that, between 11.00 am and midday on the day in question, Mrs Simpson experienced continuous contractions, or contractions of 60 seconds each, every two minute period. Mr Brereton submitted, on the other hand, that, during that time, the partogram indicates that Mrs Simpson experienced contractions of 60 seconds every one to two minutes. 96 I have pointed out that the classic definition of hyperstimulation is five contractions or more in a ten minute period (subject to the comment in [17] above). The likelihood of hyperstimulation occurring increases as the frequency of contractions within this period increases. 97 Thus, if Mrs Simpson experienced 60 second contractions every one to two minutes in the one hour period from 11.00 am to midday, that would be powerful evidence of hyperstimulation (as the contractions were then likely to have exceeded five contractions in every ten minute period over this time). 98 The proposition that contractions occurred for 60 seconds every minute (advanced by Mr Hall) would mean that there would have been continuous contractions, that is, there would have been no break whatever between contractions. There was evidence that continuous contractions with no interval between would have been contrary to foetal life. This appears to have been accepted by his Honour. The partogram does not support such a construction and I would reject it. 99 That part of the partogtram to the right of the words "Time" and "Hours" shows the time in hourly periods, namely from 8.00 am to 3.00 pm (see Appendix 1). 100 The numbers "1" to "6-10" in the "Contraction Frequency & Duration" section represent time periods measured in minutes . Thus, the blocks in the horizontal column to the right of "6-10" are intended for filling in where the patient has contractions every six to 10 minutes. 101 It follows, according to the natural meaning of this part of the partogram, that the blocks in the horizontal column to the right of the number "5" are to be filled in when the patient has contractions every five to six minutes. 102 Thus, the number "20" where it appears under the 10.30 am vertical column to the right of the number "5" indicates that, every five to six minutes between 10.30 am to 11.00 am, Mrs Simpson was experiencing contractions that endured for 20 seconds each. 103 It follows further, that the blocks in the horizontal column to the right of the number "4" are intended to be filled in when the patient has contractions every four to five minutes, those to the right of the number "3" when the patient has contractions every three to four minutes, those to the right of the number "2" when the patient has contractions every two to three minutes, and those to the right of the number "1" when the patient has contractions every one to two minutes. 104 Thus, the number "60", where it appears in two places between the 11 am and 12 midday columns, indicates that, every one to two minutes, from 11 to 11.30 am and from 11.30 am to 12 midday, Mrs Simpson was experiencing contractions of 60 seconds each. 105 Further, the number "60", where it appears between the 12 midday and 1.00 pm columns, indicates that, every two to three minutes from 12 midday to 12.30 pm, Mrs Simpson was experiencing contractions of 60 seconds each. 106 In other words, I consider that the natural meaning of the partogram supports Mr Brereton's submissions. The partogram is compelling evidence that for an hour, from 11.00 am to midday, Mrs Simpson experienced contractions of 60 seconds every 1 to 2 minutes. Contractions at such a rate are readily capable of causing hyperstimulation. 107 Mrs Simpson testified that, in the period between 11.00 am to midday, she was experiencing contractions of a minute on and a minute off. Whealy J accepted her evidence on this issue. His Honour dealt with the conflict between her evidence and the partogram by observing, "the entries in the partogram may have been a simple error later corrected". 108 It is not clear to me what is meant by the reference to a later correction of an error. Importantly, however, the only basis of finding that the partogram contained an error was his Honour's preference for the oral testimony of Mrs Simpson. But, as I have noted, the accuracy of Mrs Simpson's evidence on this issue was inherently suspect as she would have found it extremely difficult to make precise observations of the duration of her contractions and, in any event, there would have been a small difference in time between her experience of pain and the start and finish of each contraction. 109 The partogram is evidence emanating from the hospital itself. It is the hospital's own document. It falls to the hospital to establish that it is inaccurate. 110 The hospital, however, led no evidence to the effect that the partogram was likely to be inaccurate in regard to the duration and frequency of contractions over the relevant period, it led no evidence rebutting the natural meaning of the partogram and it led no evidence suggesting that the partogram contained an error. Moreover, the partogram contains no inherent improbabilities or contradictions in regard to this issue. 111 In the circumstances, I consider that his Honour erred in rejecting the natural meaning of the partogram and in failing to find that, during the period 11.00 am to midday, 60 second contractions took place every one to two minutes.

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H. The Medical Evidence 112 It is now necessary to examine the evidence of the expert medical witnesses called by the parties in a little more detail. I will review the evidence of the doctors in the order in which they were called to give evidence. 113 The vital evidence is in relatively short compass for a case which lasted as long as this one did, but I regret to say my notes indicate that there is more than one passage which was read to us three times in the course of the five day appeal hearing. 114 The reason why it is necessary for counsel to concentrate on this material and for me to have to abstract it in so much detail is that it is the only way of noting the differences in the vital medical evidence and in isolating the real differences between them. It also shows up the slender factual material on which some opinions were based. 115 Mr Roger Varley Clements, a clinician, notes that he was in considerable agreement with Professor Fisk's report (Blue (4)904). At Blue (4)922 he says that there are so many uncertainties concerning the Syntocinon regime because of the paucity of hospital records, that it is difficult to form a clear opinion concerning its use. "If a court were to find that Syntocinon was continued in excessive dosage beyond 12 noon then I would concede that this may well have contributed to Calandre's problem in that it may have deprived her of her metabolic reserve, setting up the conditions in which a period of severe near-total asphyxia would be more damaging than for a normal fetus. Only in that respect can I envisage any role for the Syntocinon in this case. I believe that if the Syntocinon alone were responsible for Calandre's damage, by several hours of hyperstimulation her brain damage would be of a different type. "On the balance of probabilities Calandre Simpson's injuries are due to repeated incompetent attempts at vaginal delivery; overdosage with Syntocinon, if it occurred, may perhaps have made her more vulnerable to that event." 116 The cross examination of Mr Clements went on for some time. The cross examiner was suggesting to Mr Clements that, for instance, Black (2) 311, having regard to the unexpectedly severe outcome from the application of forceps he should accept that there was a probability that there was a second force at work being hypertonic contractions of the uterus. Mr Clements said: "I don't think that's sufficient to make it a probability. It makes it a possibility but it doesn't make it a probability. Where counsel and I part company is the necessity to produce a second pathology to explain the outcome. "I don't find it necessary to have a second pathology, particularly in circumstances where if a softening up process on the baby were needed there is ample opportunity for that softening up in the four forceps attempts which led to the damaging attempt. I don't see the need for the separate pathology. All this conjecture about the dose of Syntocinon and what it might have done is really no more than that. "I would need to see some evidence that the baby showed signs of stress, of resources being exhausted, before I could say that was probable. Of course I allow that it is possible." 117 Mr Clements maintained his view that the failed forceps delivery was of itself a sufficient explanation for the outcome (Black (2) 314). However, at Black (2) 315 he did go as far as to say that because of the Syntocinon regime there was an increased risk of hypertonus. 118 The next to be called was Dr Janet Rennie who gave evidence at Black (2) 338 that she had a specialist interest in the diseases of the newborn, that is, babies from birth to one month of age and that she was actively involved in clinical practice in that area of medicine. Like Mr Clements, she practised in England. Dr Rennie, at Blue (3) 636 was of the opinion that the plaintiff's brain insult was acquired between 13.40 and 14.17 on 5 July and she suffered a period of hypoxia lasting for 20 minutes during this time, which began when the foetal heart rate fell. She said that if this period of hypoxia had been avoided or lasted for less than 10 minutes the plaintiff would have survived intact. 119 In examination in chief at Black (2) 355, Dr Rennie was asked about the significance of rotating the foetal head with Kiellands forceps and she said: "It would appear that it was the application of the Kiellands forceps which was temporarily associated with the bradycardia in Calandre's case. In general, removal of the blades of the forceps allows the bradycardia to recover but, clearly, this did not happen, either because this was the culmination of a sequence of attempts at operative delivery and previous applications had caused stress to the foetus, possibly a transient bradycardia which had recovered. … So it could be that there was repeated head compression and the final attempt at head compression caused a bradycardia which did not recover. Alternatively, the cord could have become compressed by the forceps blade because it lay alongside the head. … ".

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She said she had not seen such a case reported. However, she had experienced head compression from forceps producing bradycardia which did not recover, but as I understand it that was a case where she had given that as her opinion in litigation which had not yet concluded. 122 At 375 she agreed that she had had experience of cases from which the foetus had not recovered from excessive doses of Syntocinon. However at 376 the doctor said: "I do not feel that I need to have, as Professor Fisk, does, an additional reason for the bradycardia". 123 I now pass to the evidence of Dr Hinde. Dr Hinde gave a report that he considered that the plaintiff's injuries were probably the result of repeated attempts at forceps delivery. He thought that a more likely explanation than cord entanglement for lack of supporting evidence. He did not direct his mind specifically to the problems of Syntocinon but noted that the oxytocin regime can only be regarded as aggressive, even by 1970s standards (Blue (3) 596). He also noted at Blue (3) 605 that there was no unacceptable delay in the provision of an operating theatre by the hospital, the decision for caesarean section having been made about 1.55 pm and delivery achieved by 2.17 pm. In cross examination, Dr Hinde said at Black (6) 1450 that he was worried about the partogram and wondered whether it had been filled in upside down. He said at 1451 that this partogram was only introduced to the hospital some months beforehand "and I have found in going through obstetric histories in recent years that there is often confusion and incorrect entries by midwives." 124 At Black (7) 1656 and following, Dr Hinde was closely cross examined on vagal bradycardia and bradycardia where there was an hypoxic element at work as well. At 1656 Mr Brereton asked Dr Hinde: "Q. Distinct from bradycardia caused by hypoxia, … there is another form of bradycardia, is there not, in which the decelerations tend to mirror in reverse the contractions? A. Yes. Q. And that bradycardia is associated with pressure on the foetal head? A. Yes. Q. And so far as we understand it, that pressure on the foetal head stimulates the vagal nerve? A. Yes. Q. And the vagal nerve causes a neuronal transmitter chemical to be released which suppresses the foetal heart rate? A. Yes. Q. And that is a chemical which has a short half life? A. Yes. Q. And when the pressure on the head stimulating the vagal nerve is relieved, that type of bradycardia remits? A. Yes. Q. And that's called commonly vagal bradycardia? A. Yes. … ."

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There was then cross examination to the effect that vagal bradycardia could be caused by application of forceps, but ordinarily, once the stimulus is relieved the bradycardia would remit. 125 However, at 1662 Dr Hinde said: "I don't accept that you have to have trauma to produce adverse effects as a result of forceps delivery. I believe that if you persist with forceps deliveries for long enough, a forceps delivery for long enough, and produce bradycardia as a result of the manipulation, then the foetus can remain hypoxic because of it. I don't accept that the sole method of injury to a foetus is a traumatic one. … Q. But if the forceps are applied, there is a drop in the foetal heart and they are removed promptly thereafter, you wouldn't expect a vagal mechanism alone to produce a bradycardia which lasts, a profound bradycardia which lasts for 18 minutes or more? A. In most cases no. Q. And that's because the neuronal transmitter, the chemical which causes the decrease in the foetal heart rate, would dissipate and the foetal heart recover? A. Yes, but this is the neuronal transmitter which has been produced as a result of the immediate application of the forceps. This, to me, does not consider the possibility that these repeated attempts have set up a mechanism within the brain which is causing the vagotonia to persist and hence bradycardia and hence deleterious effect on the foetus. (1663) Q. Is that speculation, doctor? A. It is based on the fact that on rare occasions where I have had a failed forceps there will be no trauma to the foetus, but you take the foetal heart rate when you decide to abandon it and go and do a caesarean section. The foetal heart rate may stay low or go up and down before such time as you can proceed to the caesarean section. Q. It may come back up? A. Yes, yes. I have said it may come back up but on other occasions the intervention seems to set in train a persisting bradycardia. Q. And that may be because as well as the vagal bradycardia, there has been some hypoxic element at work as well? A. Yes. Q. And indeed, if there were, that would make that result of a persisting bradycardia, much more physiologically understandable? A. Yes, under those circumstances." 126 At 1665 he continued in that line: "I believe that the multiple attempts at forceps, as opposed to pulls, can in fact set in train a vagotonic response that won't remit. If it doesn't remit then you get persisting bradycardia on top of any that may have existed in the first place."

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Mr Brereton continued his questioning: "What literature or studies, doctor, are you aware of that deal with a vagotonic response that does not remit? A. Simply experience that at times where failed forceps have occurred the foetal heart rate remains low with no demonstrable trauma in the subsequently delivered foetus. Q. I think we agreed a while ago that an explanation for that might be if there was a hypoxic cause as well, such as cord constriction? A. But I wouldn't say it was in every case. … (1666) Q. And as I think we discussed earlier, if there were some such hypoxic component that would make a profound unremitting bradycardia much more physiologically understandable than just a established vagotonic response? A. Yes. … Q. If the foetus's metabolic reserves are depleted then her, or his, vulnerability to a short period of bradycardia from which she might otherwise have recovered is increased? A. Yes." 127 At 1675, Mr Brereton asked: "And if hyperstimulation continues, and the placental villi continue not to be adequately replenished then there will be a progressive drain on the foetal reserves? A. Obviously if the foetus has a reduced supply of oxygen, then these things are set in train which will produce acidosis and reduction of reserves, yes. Q. Even before producing acidosis, the reserves can be depleted while the foetus's adjustive mechanisms are responding to the reduced oxygen supply? A. Yes, that intervenes between the two. Q. Ultimately once acidosis sets in, then the hyperstimulation can of itself ultimately produce a terminal profound bradycardia? A. If you have got a very acidotic baby that has been subjected to very frequent contractions, yes." 128 At 1679: "If there had been a reduction in foetal metabolic reserves but she was not yet acidotic, you would not necessarily expect to see decelerations indicative of foetal distress at that time, would you? A. This is essentially a theoretical concept, but my expectation would be if you have a baby which is in a situation of compromise, then they will respond poorly to intervention and my expectation would be that as soon as you started to do the forceps delivery, I would have the expectation that you would see an adverse effect on the foetal heart rate." 129 At page 1683, Mr Brereton asked Dr Hinde whether it is "highly probable that during her labour she was contracting at a greater frequency than permitted the placental villi supplying Calandre to be fully replenished?" "A. It's possible but it's not … it would not be my view on the balance of probabilities that that was so, but I can't exclude that possibility. Q. And if she was doing that, then the foetal reserves may well have been compromised? A. If she was doing it, yes. … Q. And if that pattern of hyperstimulation plus compromise of the foetal reserves were taking place, then that would make much more readily explicable the outcome so far as a profound period of bradycardia following the Kiellands forceps is concerned? A. If all those factors were operative, it follows that the foetus is less able to withstand manipulation in the second stage of labour to effect delivery. Q. And absent such a contributing cause as well as the manipulation with the forceps, we really don't have an acceptable physiological explanation for a period of bradycardia which exceeded 18 minutes, do we? A. We mightn't have a physiological explanation but it's well recognised in texts for example on cardiotocography that there are certain things which will cause a profound alteration in a foetal heart rate pattern in a foetus which has previously shown to be healthy. One of those things is cord prolapse. Another is abruption of the placenta and the third is intervention, once you attempt a breech delivery, once you attempt a forceps delivery. These things are recognised as being common causes of an abrupt change in the pattern of foetal heart rate and status of the foetus.

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… (1684) Q. So that leaves us with an inadequate explanation for how pressure on the foetal head alone could cause not just a bradycardia, which it clearly can, but one which lasts for 18 minutes or more? A. I believe that if you set this mechanism in train then sometimes the vagotonia doesn't remit and although there may be an oxygen supply coming to the foetus, the foetus is incapable of distributing it satisfactorily to protect its central nervous system. Q. And I think you have accepted that there is nothing in the literature to support the theory of a vagotonia that doesn't remit? A. It is just experience that you see this happening. Q. And I think you have accepted in our discussion that your experience in which you have seen that happening may be because there is an association between the manipulation and some hypoxic contributing factor? A. Obviously if a foetus is hypoxic for some other reason it will withstand manipulation less well and hence be more likely to remain bradycardic. Q. And such an explanation provides an understandable mechanism by which the outcome in this case, or of the sort that is seen in this case, could happen whereas the idea of an exclusively vagal cause does not? A. No, I don't think you can reject the concept that manipulation producing a vagal cause, a vagal cause for this can be excluded. On the other hand, you have got a foetus which at the start of the labour was perfectly well and hence less likely to respond to the things that you have mentioned. Q. If the vagal mechanism is pressure on the head stimulating a nerve, producing a neuronal transmitter which has a short half life, then how, once the pressure which stimulates the nerve is removed, could the vagal mechanism continue to produce a bradycardia? (1685) A. You are right in what you are saying, that the pressure produces the release of a chemical transmitter, but if in this prolonged episode a further mechanism comes into play, maintaining vagal action, then the question of the short half life of a chemical transmitter doesn't enter into it if it is still being released. Q. What further mechanism could come into place to maintain vagal action? A. What further mechanism is, I think, the fact that you have attempted these multiple manipulations which … are recognised to cause a prolonged and severe change in foetal heart rate pattern in an otherwise previously healthy foetus. It is one of the things that can produce this. Q. You were saying that perhaps some other mechanism could come into play to maintain the vagal stimulation. What I am asking is what could that other mechanism, once the pressure is relieved to maintain the vagal stimulation, be? A. I think the very fact that the baby has undergone all these manipulations and as a result doesn't respond, doesn't recover, in the normal way. Q. That doesn't really provide an explanation for a continued vagal stimulation, does it? A. Well, if the foetal heart remains low there has to be a continuing vagal action." 130 Professor Fisk said that there was clear evidence of hyperstimulation and (Blue (4) 833): "In my opinion, Calandre's apparently rapid decompensation and oxygen deprivation in response to the forceps attempts cannot be explained entirely by her failed forceps delivery. Mrs Simpson received a Syntocinon infusion to induce labour that appears to have been given in both an excessive concentration, and at an excessive infusion rate. There was evidence of uterine hyperstimulation which, in my opinion, was a direct result of the Syntocinon over-dosage. In my opinion her rapid decompensation at around the time of the attempted forceps delivery is more probably than not explained by hyperstimulation. This either reduced her reserve to cope with the stresses of the failed forceps delivery, and/or lead to a tonic contraction which acutely and substantially compromised her oxygen supply." 131 Professor Fisk is also an English doctor, a Professor of Obstetrics and Gynaecology. There was a long cross examination of Professor Fisk, but he did not move from the position he had taken in his report. 132 Dr Lyneham in his report at Blue (3) 673 said it was "highly likely that there was hyperstimulation of the uterus". He noted that "some degree of foetal hypoxia is a feature of normal labour. With each uterine contraction blood flow in the intervillous space in the placenta is impaired and the oxygen supply to the foetus is reduced. These changes are intermittent, and the healthy foetus recovers well between contractions. Hyperstimulation of the uterus, such as that which may be caused by excessive administration of Syntocinon producing prolonged tonic contractions without episodes of relaxation during which placental blood flow can return to normal, can be associated with hypoxia to the foetus." 133 At 680 he said that: "Considering the baby's condition at birth and afterwards, it is my opinion that it is more likely than not that [tonic uterine] contractions were present."

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The doctor continued later: "We know that hyperstimulation occurs in 61 per cent of women, according to the Satin study, of people who receive the sort of dose of Syntocinon that Mrs Simpson received. … 60 second contractions every two minutes that would, at the very least, be borderline hyperstimulation." 134 Dr Keogh is a staff specialist in obstetrics and gynaecology at Hornsby Hospital who lectures in those subjects at the University of Sydney. His view was that there was insufficient evidence to find that the doctor was negligent. His evidence does not really affect the present matter before the Court and we were referred to very little of his oral evidence or cross examination. 135 Dr John Pennington reported at Blue (2) 402 that in his view both the doctor and the hospital acted in accordance with proper professional standards and contemporary obstetric practices. In re-examination at Black (7) 1731, Mr Brereton put to Dr Pennington: "Q. It was put to you that a persistence of attempts with forceps could give rise to an unremitting bradycardia and you said that was true. When you answered that question, were you addressing your mind exclusively to a bradycardia caused by a vagal mechanism, or to some other situation? A. It doesn't matter in the sense that in the practical sense you have the bradycardia which may be due to vagal nerve stimulation but at that time there is no way that you know and nor, I submit, that you really care in the sense that in a practical sense you need to expedite the circumstances." 136 Finally, Professor Ellwood gave evidence for the hospital. Professor Ellwood is a Professor of Obstetrics and Gynaecology at the Canberra Clinical School, University of Sydney, at its Canberra Hospital branch. In his report at Blue (4) 889, Professor Ellwood said: "… in this case the rate of Syntocinon administration was at the limits of the accepted rate and this may have caused a degree of uterine hyperstimulation as indicated by a tachysystole. Nevertheless, this does not appear to have adversely affected the foetal heart rate … . [890] In conclusion, there is no objective evidence for an effect on foetal condition caused by uterine hyperstimulation either before midday when the partogram observations cease, or after that time and until the forceps delivery is attempted. In contrast, there is evidence of a foetal response to the Kiellands rotation, and the possibility of a prolonged bradycardia, which continued until delivery about 25 minutes later." 137 At Black (7) 1591, Mr Brereton cross examined Professor Ellwood: "Q. Now, I think we discussed this morning but I think you agree that the midwife's targets should be to achieve with Syntocinon something in the order of three to four contractions in 10 minutes? A. I remember the discussion and I said that three to four, or four to five, I really wouldn't draw a distinction between that, and perhaps an optimal number is about four in 10. Q. Certainly if the contractions were between five and six in 10 minutes that would be hyperstimulation? A. That would be defined by some authors as tachysystole and that would be a rate of contraction above what I would consider to be optimal. Q. And that rate of contraction is sufficient to cause such embarrassment to the foetus as to result in ultimately a profound bradycardia and permanent brain damage? A. That depends on the condition of the foetus before the hyperstimulation begins and how long it goes on for. … Q. But if in an induced labour the foetus is subjected to an hour of contractions of between five and six in 10 minutes, it is quite consistent with your experience … during that period to see but subtle changes on the cardiotocograph? A. Yes, it certainly is in my clinical experience to see those CTG changes occurring. Q. Thereafter, even after the contractions remit a little from the five to six, to perhaps more normal limits, to see in the next hour or so some late decelerations? A. My own clinical experience would be to see the CTG recover and return to normal once the contraction pattern becomes more normal. Q. Can I suggest that it is within your experience, clinical or medico legal, that during the period after an hour of hyperstimulation, you might continue to see late decelerations? A. I can't recall seeing a period of hyperstimulation of that duration, once it has been corrected, to continue to cause CTG changes. … Q. And after some time of that, it is within your experience, isn't it, that from the hyperstimulation, followed by that period of late decelerations, one can then have a profound terminal bradycardia? A. The late decelerations reflect a degree of oxygen desaturation occurring with a contraction. Whether that then continues into acidemia and then the kind of terminal bradycardia you are describing, would depend on the ability of the foetus to withstand that oxygen desaturation, and whether or not the reason for the desaturation has been corrected. Q. And if the foetus's reserves have been sapped by the period of hyperstimulation, then a period of profound bradycardia can result? A. Yes, that's certainly possible." 138 At 1594, Mr Brereton put that the hyperstimulation can result in a profound terminal bradycardia due to a sapping of reserves. The Professor replied: "A. The hypothetical picture that you are painting, I would agree with if the period of uterine tachysystole was sustained and there was no signs of recovery and resumption of a normal pattern of uterine contractions. Q. And in that situation the profound terminal bradycardia can itself, in those circumstances in your experience, produce permanent brain damage or do damage to the basal ganglia? A. It can certainly cause severe foetal hypoxia and acidemia and the condition of newborn encephalopathy. It is getting outside my area of expertise to comment on the exact nature of the brain damage. … (1595) Q. From that discussion I take it you agree that hyperstimulation produced by excessive Syntocinon usage can of itself result in a severe hypoxic insult to the foetus? A. A period of uterine tachysystole, if sustained, can certainly lead to foetal hypoxia. Whether it does or whether it doesn't depends on the foetal reserve and the duration of the tachysystole." 139 There was considerable cross examination along the lines of that administered to the other medical experts as to the difference between vagal and hypoxic bradycardia. At 1606, Mr Brereton asked: … Is this the position then, that though there may well have been a vagal element to that final terminal bradycardia in Calandre Simpson, the duration which it must have had to explain her outcome, is such that in your opinion there must have been a hypoxic as well as a vagal cause? A. Yes, but I would qualify that by saying that the hypoxic cause, or the hypoxic element, could have been quite acute if it is related to cord occlusion. Q. Cord occlusion is one possibility that you posit so far as a hypoxic cause is concerned? A. Yes. (1607) Q. And another perfectly plausible possibility is that the foetal reserves had been sapped by a period of hyperstimulation? A. It is a possibility. I find it a less likely possibility because of the duration of the apparent period of uterine tachysystole, and in my clinical experience I would expect the foetus with normal reserve to have tolerated that period of hyperstimulation and to have recovered. … Q. One thing I guess is clear after the discussion we have had, that one thing we can now exclude following our discussion this afternoon, is the idea that vagal bradycardia alone, attributable to a series of five pulls with forceps, caused this terminal bradycardia? A. The evidence that we have to support your statement is of a foetal heart rate that was heard to decelerate and recover during the second attempt with the Neville Barnes forceps and that would suggest a normal vagal response and then recovery. Because we don't have a continuous heart rate recording throughout the whole episode, I would find it hard to completely agree with your statement. I think we do have the likely possibility of recurrent vagal stimulation with the recurrent attempted forceps delivery. Whether the accumulation of that vagal stimulation has contributed to the terminal bradycardia, I think it is possible. Q. It is not quite my question; not whether the accumulation contributed to it, but one thing we can say for certain is that vagal bradycardia alone, even the accumulation, cannot fully explain the bradycardia of 18 to 25 minutes which ensued? A. I would find it hard to accept that it was vagal alone. Q. And even allowing for the accumulation of five attempts on the probabilities in your opinion, there must have been a hypoxic cause as well? A. I think there must have been a contributing cause. By the term hypoxic cause I wouldn't necessarily mean that there was foetal hypoxia before the bradycardia occurred. I don't quite understand the mechanism of bradycardia that occurs with cord occlusion. It may well be more complex than simply reducing blood flow and reducing oxygen supply, but I certainly do accept the argument that there is likely to have been some additional mechanism other than vagal stimulation and if that involves the cord, then ultimately there is a component of that which is hypoxic. Q. And the alternative explanation for the cord is over-stimulation of the uterus and a sapping of the foetal reserves as a result? A. That is a possible explanation. … but I find the gap between the period of apparent tachysystole and the prolonged bradycardia difficult to explain if there was prolonged hypoxia throughout that whole period of time. …". 140 At p 1614, Mr Brereton asked: "Do you agree that although traction on the cord during rotation might cause temporary reduction in blood flow and foetal oxygenation you would expect to see a degree of recovery once that traction was released? A. In the hypothetical situation where a rotation has caused some cord compression, I wouldn't use the word traction, traction in itself I don't think would cause the bradycardia but where it has caused some compression and if that compression is completely reversed then I would expect to see recovery. The exception to that may be that if … there are already other factors that could lead to bradycardia such as vagal stimulation and the compression continues for a long enough period of time then the foetus may not be able to recover. There may be a combination then of hypoxia, vagal stimulation, the two things together, could lead to ongoing bradycardia. (1622) Q. … do I understand your position to be that if there were cord involvement in this case the probable scenario is that of partial occlusion resulting from cord tension from the rotating manoeuvre? A. I believe that's the most likely cause in this case. I can't completely exclude cord occlusion by the forcep blade impinging on a loop of cord … (1623) Q. What are you talking about, Professor, when you speak of the most likely version of cord involvement in this case being a partial occlusion due to rotation, what do you have in your mind in terms of percentage reduction in blood flow by that? A. Anywhere between nought and a hundred per cent. Q. Well a hundred per cent isn't partial? A. A hundred per cent is complete. I have no way of knowing. Q. And nought is no occlusion at all? A. That's why I answered with those two extremes. I have no way of knowing. The hypothetical situation we have reached is that is a mechanism whereby the cord is compressed during the rotation, I have no way of knowing what degree of compression has occurred, what degree of occlusion has occurred. (1626) Q. Professor, if I can approach it this way, yesterday I think we agreed that as well as the vagal mechanism for this bradycardia in Calandre's case, to last as long as it did and to have the profound effects which it did, there must have been a hypoxic mechanism at work also? A. Yes. Q. If that hypoxic mechanism was, as you posit, cord compression attributable to the rotational manoeuvre, what I am suggesting is that it is unlikely, not impossible but unlikely, that that manoeuvre and that that cord compression to have produced a sufficient drop or a sufficient level of foetal acidosis to sustain the bradycardia before it would have remitted from its vagal cause, before the vagal aspect would have remitted? A. I think you prefaced your question or you used early on in your question the word 'unlikely'; no, I don't believe it is unlikely. I think it's quite possible that the vagal mechanism could go on for sufficient time for the hypoxic mechanism to then continue to cause the bradycardia. Q. Are you suggesting that the vagal mechanism could continue for five to ten minutes? A. I am not applying the five to ten minutes time frame, what I said is I believe that the vagal mechanism could well operate for sufficient time for the hypoxic mechanism to cut in. If we are talking of a vagal mechanism that goes on for a few minutes, two, three, four minutes there could be sufficient cord occlusion to then have caused sufficient hypoxia for that mechanism to then take over. Q. Professor, it is unlikely in the extreme, isn't it, that the vagal mechanism would continue for four or five minutes after the forceps had been removed? A. No, it's not unlikely in the extreme. I have certainly seen bradycardias continue for that period of time. With respect I said two, three, or four, I didn't say five. Q. That's why I was asking about five. I can accept your two, three or four? A. I can't make a distinction between two, three, four or five in such a mechanism. I have seen vagal responses continue for quite a long period of time, up to ten minutes I have seen. Q. With no hypoxic component? A. Yes, with no hypoxic component. Q. You can be quite confident there was no hypoxic component in that? A. Yes, the baby was born with no abnormal blood gases."

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He then found that the injury was caused solely by the doctor's negligent use of forceps. 149 His Honour then further considered the Syntocinon argument at [1424]. He said: "There are further reasons which support and confirm my belief that there was no hyperstimulation in this case and no depletion of the foetal reserves consequent upon the excessive dose of Syntocinon. These are, first, the conviction that Dr Diamond's negligent acts were plainly sufficient of themselves to have occasioned Calandre's injuries without the need to resort to an additional or contributory cause. This conviction, in turn, is based upon the acceptance of the hospital's argument that there is, notwithstanding the rarity of the situation, an acceptable and well understood mechanism involved in the plaintiff's injury; and the rejection of the first defendant's argument that the injury in inexplicable or unlikely without the existence of a contributory cause. 150 Mr Brereton in my view rightly submitted that [1424] poses the wrong question. The real question was whether the hospital's actions also had causal consequences to the plaintiff. 151 The Judge continued at [1425]: "Secondly, there is my satisfaction with the proposition advanced on the hospital's behalf that, despite the poor record keeping involved, there was adequate monitoring by the nursing staff of the baby's foetal heart and that there was, throughout the entire period, no abnormality detected. This, in turn, persuades me that the nursing staff's acceptance of normality was entirely justified. I am also satisfied that Dr Diamond was entitled to be satisfied, based on his own observations, that the FHR and contraction patterns were normal. These matters provide additional reasons negating the presence of any depletion of the foetal metabolic reserves. There is further support in the expert opinions of Dr Rennie, Dr Hinde and Mr Clements. Although the first defendant's case adverted to a possibility that there may have been present a depletion of foetal reserves but that this may not have been detectable or in fact detected especially between 1240 and 1350, I am not persuaded that this is so." 152 With respect these statements do not fairly reflect the evidence as a whole. The hospital records, particularly the partogram, do show matters of concern. Further, the support of the evidence of Drs Rennie and Hinde and Mr Clements really does not lead to any strong view against the Syntocinon argument. 153 Whealy J continued at [1426]: " Dr Diamond's negligence "The starting point is Dr Diamond's admission of liability. It must not be overlooked that, although the issues in the cross-claim have made it necessary to identify precisely the negligence involved, the plain fact is that the negligent 'manner, timing and circumstances of use of forceps' have been admitted." 154 Again Mr Brereton correctly says that the learned judge misdirected himself. In proceedings for contribution, there is no warrant for starting the fact finding exercise from the doctor's admission of negligence. The vital question is the consequence of the hospital's negligence. 155 The learned judge then spent some time discussing why in his view the doctor's actions must have been negligent. He then continued at [1434]: "A circumstance then occurred that was important. The Doppler was applied probably about the time of the second pull with the Neville Barnes although it may have happened a little earlier. It appears that, following the second Neville Barnes application, there was a drop in the foetal heart. But this recovered immediately. This fact is important for two reasons: first, it shows, for the first time, an adverse reaction to the instrumental attempts. Secondly, the recovery of the heart rate almost immediately points very strongly against any suggestion of depletion of foetal reserves. This was the point made with considerable effect by Dr Hinde whose evidence in this regard I found compelling. He had said that if there had been embarrassment of the foetus over the preceding two or three hours as a consequence of hyperstimulation, there would have been a fall in the foetal heart rate as soon as the forceps were used, rather than only after the third or fourth attempt at forceps delivery (T 2694 lines 38-55; see also T 2874 lines 10-15 and 45; T 2875 line 5; T 3037 lines 5-15). This was the 'side step' to which Dr Hinde had made reference in his evidence. To my mind it was a compelling observation. If there were this substantial depletion of metabolic reserves within the foetus, why was its displeasure not shown as soon as the instrumental attempts commenced? In my opinion, this was a telling point against the Syntocinon argument." 156 This critical finding which is a foundation of the hospital's case needs to be closely examined. 157 The only evidence that there was not "a fall in the foetal heart rate as soon as the forceps were used" is that of the partogram which showed a constant foetal heart rate of 140 bpm. As have stated, there is evidence that such a constant heart rate was highly improbable and the likely purpose of recording a constant foetal heart rate of 140 bpm was to indicate that it fell within the normal range of 120 bpm to 160 bpm. This is consistent with Dr Hinde's comment during cross examination at Black (7) 1520-1 that he did not believe that the foetal heart rate would have remained at 140 bpm until after the third or fourth attempts to deliver the baby by use of forceps. 158 In my view there is a significant weakness in the evidence that there was in fact a constant foetal heart rate of 140 bpm and that there was no fall in the foetal heart rate as soon as the forceps were used. 159 Accordingly, in my view the force of the point which Whealy J regarded as "telling" against "the Syntocinon argument" is very much diminished. 160 I agree with Mr Brereton that when one realizes this the force of the point being made is very much diminished. 161 I should now briefly deal with the Judge's assessment of the expert medical witnesses which commences at [1437]. His Honour noted that the argument advanced by Professor Fisk, Dr Lyneham and Dr Keogh was that failed forceps attempts on their own were insufficient to explain the outcome, whereas Mr Clements and Dr Rennie and Dr Hinde took the opposite view with Professor Ellwood noting that an additional hypoxic element was necessary. His Honour said at [1440]: "In relation to the circumstances of this case, I am quite satisfied that the views expressed by the experts called on behalf of the hospital are correct. The views expressed by Mr Clements and Dr Rennie were very compelling. They were views derived from their own experience applied to the very unusual circumstances of the forceps applications and attempts in this case. Mr Clements was branded as an advocate in the first defendant's submissions. I did not find him to be so. I thought his evidence was carefully considered and well-balanced. Moreover, he brought to bear considerable experience and a high degree of intellectual rigour. Although Mr Brereton was critical in a number of respects in relation to the views of Mr Clements and Dr Hinde, a careful consideration of their evidence leads me to the conclusion that their evidence supports entirely the hospital's case. [1441] Dr Hinde, in particular, brought to bear on the issue, a lifelong breadth of clinical experience. … In most cases it was his observation that bradycardia would remit. But in some it did not. He also stated, that there were occasions where, although no signs of external trauma were noticeable on the foetus, the manipulation had induced a quite marked bradycardia and hypoxia in the foetus. [1442] Mr Brereton SC endeavoured to confound Dr Hinde with the literature. … Notwithstanding this, he repeated that, based on his clinical experience, on rare occasions in circumstances where there had been a failed forceps …the intervention appeared to have set up a persisting bradycardia. [1443] I was very much persuaded by the evidence of Dr Hinde. … Mr Brereton did not seek to brand Dr Hinde as an advocate. Rather, he suggested that his views were outweighed by the evidence of the foetal physiologists. [1444] Professors Fisk and Ellwood were the two foetal physiologists called to address the issue. I prefer Professor Ellwood's views to those expressed by Professor Fisk. Although I gained considerable assistance from Professor Fisk's excellent report, I cannot say the same for his evidence. It was he, of all the expert witnesses, that I would brand as obdurate. A reading of his extensive cross-examination would, I think, convince the reader that he was not prepared to make the most reasonable of concessions even when it was plainly the case that such a concession was called for. [1445] On the other hand, I found Professor Ellwood's approach to be both reasonable and convincing. It is true that he believed it was necessary to find a hypoxic element as well as the presence of vagal bradycardia. To that extent, he differed from Mr Clements and Dr Hinde. As a foetal physiologist, he was no doubt searching for scientific certitude. To the extent that a hypoxic element was necessary, he had no difficulty in accepting that it may well have arisen from the forceps impinging on or occluding the cord. … It was perfectly possible, indeed quite likely, that, during the instrumental attempts, a hypoxic element was set in force in addition to the bradycardia caused by the forceps applications. [1446] Importantly, Professor Ellwood said he had no difficulty with the proposition that there were two concepts operating at the same time but both related to the forceps use. [1448] In my opinion, Professor Ellwood and Dr Hinde were really describing the same thing. From the perspective of the foetal physiologist however, there was a need to be satisfied, as I have said, with a degree of scientific certitude. The experienced clinician is not necessarily as concerned with such niceties of precision. He knows what he has seen. Dr Hinde as an experienced obstetrician simply based his observations on his lifelong professional experience. He did not seek scientific certitude he simply knew as a matter of experience that failed forceps were sufficient to explain the mechanism. Dr Rennie had observed the same thing in clinical situations. She said, quite sensibly that the precise mechanism might never be known." 162 Mr Brereton strongly criticises that method of approaching the problem. He says that the doctor is suing for contribution. He is thus in the same plight as a plaintiff who is showing by the necessary standard of proof that the hospital would have been liable to the plaintiff. The scientific evidence, both by Professor Fisk and by Professor Ellwood, complete with reasons, was that one needs a second and hypoxic cause for the terminal bradycardia which caused the plaintiff's problems. The clinicians said that they had not always observed this. That, however, was no answer to the scientific evidence. 163 As Mr Brereton put it in his closing address: "The evidence of the clinicians does not exclude a second cause in any event. What they said is 'we don't find the need to look for a second cause.' They don't deny the possibility of a second cause." 164 He thus puts that the doctor had established that a second cause was necessary. 165 The only two possible second causes were hyperstimulation and cord occlusion. There was acceptable evidence of hyperstimulation, particularly that provided by the partogram. On the other hand, the evidence about cord impingement doesn't begin to approach that sort of level and never gets beyond the level of a speculative possibility. Accordingly, Mr Brereton argues, the appeal must be allowed and the hospital ordered to contribute to the damages which the doctor has to pay to the plaintiff. 166 For reasons which I will go into more fully in section M, that argument has a great deal of appeal. 167 Mr Brereton further says that the trial judge did not follow the course laid down in the Makita case. He did not look to the facts which underlay Dr Hinde's opinions. The Judge fell into the error of simply accepting the opinion saying, that the expert has a lot of experience and knows what he's seen. The basis for Dr Hinde's view was not supported. 168 The same comment in Mr Brereton's view could be made about Mr Clement's evidence and to a lesser extent that of Dr Rennie. 169 In my view, for the reasons which are set out in the following parts of this judgment, Mr Brereton's attacks on the trial judge's reasons are made out.

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J. Problems with Multiple Causes 170 I have already referred to the discussion in Shorey v P T Limited (supra) as to how courts can be misdirected by seeking a single cause in a case where there may well be multiple causes for the plaintiff's injury. Of course, all the plaintiff has to do is to show that the actions or inactions of a person whom she is suing is a cause of her injury. However, where one has to look at questions of contribution, the inquiry must go further. 171 Mr Brereton commenced his submissions on this point by reference to Burrows v The March Gas & Coke Company (1870) LR 5 Ex 67 (Full Bench of Exchequer) and (1872) LR 7 Ex 96 (Exchequer Chamber). The facts were that a gas company contracted to supply the plaintiff with the proper service pipe to convey gas from the main to his premises. Gas escaped from the pipe laid down under the contract into the plaintiff's shop where an employee of the gasfitter went into the shop carrying a lighted candle and an explosion took place. The jury found that the escape of gas was occasioned by a defect in the pipe, but that there was negligence on behalf of the gasfitter's employee in carrying a lighted candle. The plaintiff sued the gas company alone and recovered a verdict. The defendant gas company was not relieved by the negligence of the gasfitter's employee. However, the court ventured the view that the gasfitter would also have been found liable to the plaintiff. 172 Mr Brereton then refers to the decision of the English Court of Appeal in Sharp v Avery [1938] 4 All ER 85. There the plaintiff was a pillion passenger on Kerwood's motor cycle. Kerwood did not know the road and the parties had agreed that Avery, who was also driving a motor cycle, would take the lead and would act as pilot. Avery failed to take a bend in the road, Kerwood followed him off the road, Avery braked, Kerwood collided with Avery and the plaintiff was injured. Avery was held liable to the plaintiff. 173 Another motor bike case, very similar to Sharp v Avery, is Smith v Harris [1939] 3 All ER 960. 174 The classic case in this area is The Koursk [1924] P 140. In that case there was a convoy of five vessels in the Mediterranean in the closing years of World War I. The five vessels were under escort, and for security reasons, had to adopt a zig zag course without lights. Shortly before 3 am The Koursk got out of position and was observed heading for The Clan Chisholm which hard-a-ported but did not reverse her engines. There was then a collision between The Koursk and The Clan Chisholm, and within about a minute there was a second collision between The Clan Chisholm and The Itria which sank. The Itria then sued The Clan Chisholm and The Koursk. The court held that The Clan Chisholm and The Koursk were not joint tortfeasors, they were concurrent tortfeasors, and each was liable to The Itria. 175 In each of these cases, the court did not consider that the negligence of the third party involved was a novus actus interveniens, but rather that the parties were concurrent tortfeasors. 176 In Bonnington Castings Ltd v Wardlaw [1956] AC 613, 621, Lord Reid said: "I cannot agree that the question is: which was the most probable source of the respondent's disease, the dust from the pneumatic hammers or the dust from the swing grinders? It appears to me that the source of his disease was the dust from both sources, and the real question is whether the dust from the swing grinders materially contributed to the disease." 177 In the case of concurrent tortfeasors, each is liable to the plaintiff and under the provisions of s 5 of the Law Reform Miscellaneous Provisions Act 1946, each is liable to make contribution to the other as each is a person who would, if sued, have been liable to the plaintiff. 178 I will need to return to this in section K.

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C. If an additional or contributory cause is to be sought, is that cause more likely than not to be cord occlusion or impingement? 180 In my view the answers to these questions are A. Yes; B. Yes; C. No. I will give my reasons. 181 A. As Mr Brereton has submitted, the outcome and events are much better explained by two concurrent events, one of them hypoxic than by one vagal cause only. 182 As has been pointed out, his Honour's view is in the ultimate based on his preference for the evidence of the clinicians over the scientists. I have already set out [1448] of the judgment where his Honour contrasted the scientist who required a great degree of scientific certitude with the experienced clinician of lifelong experience who knows what he has seen. 183 I noted in section E the approach that needs to be taken to expert evidence. In my view, with respect, the learned trial judge did not give enough emphasis to evaluating the scientific evidence. He permitted himself to do that because he made the error of accepting that because clinicians did not always observe phenomenon X in connection with happening Y, even though the scientific evidence points strongly to this being the case, one can find as a fact that phenomenon X was not essential in happening Y. 184 I have probably spent sufficient time discussing the problem. The bottom line is that the scientists said that a second hypoxic cause is to be expected for this event. The only contrary position was from clinicians who said that they had not always observed such a second cause. This, however, does not negate the expert evidence. The judge should have accepted it and held that it was more likely than not that a second hypoxic cause was present. 185 In my view, the scientific evidence as I have reviewed it, led overwhelmingly to the conclusion that it is more likely than not that a second, hypoxic cause of the terminal bradycardia was present. 186 B. Does the evidence show that that hypoxic cause was more likely than not the excessive dose of Syntocinon? 187 Mr Hall says that the "specific facts" that the appellant bore the onus of establishing and was required to establish included:

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"You have been negligent in the administration of Syntocinon as found by the Judge. Not only was the dosage higher than the prescribed rates, it was administered in such a way that it was received more rapidly than it should have been. Both the starting dose and increments are important in the association between aggressive Syntocinon regimes and possible hyperstimulation. Mrs Simpson (as the Judge found) "was not a candidate for a high dose of Syntocinon". The plaintiff was injured. The dosage of Syntocinon administered by the hospital was prima facie capable of causing hyperstimulation; therefore Syntocinon was prima facie capable of causing the injury. Therefore the evidentiary onus is on the hospital, to show that the excessive dose of Syntocinon did not cause the injury." 193 As I have already noted, although the Judge wavers towards cord occlusion in [1445]-[1447] of the judgment, he did not find cord impingement. One would have expected that had he wished to make such a finding, he would have made it explicitly. 194 Mr Hall put that none of the experts ruled out the possibility of cord impingement or occlusion as the additional hypoxic element if one were required. He says that Dr Pennington initially opined cord entanglement as the most likely explanation for the failed forceps delivery and foetal distress. Professor Fisk acknowledged the possibility. Even Dr Diamond noted that the cord was tightly wrapped around the plaintiff's body or neck. 195 As I have already noted, Professor Ellwood at Black (7) 1606 noted that cord occlusion is one possibility for the hypoxic cause. 196 Mr Brereton submits that in the light of Professor Ellwood's cross examination, particularly the passages at Black (7) 1622-3 which I have set out above, the evidence of Professor Ellwood as to cord occlusion does not rise above speculation. I agree. 197 Having given reasons on the major points, I should give brief mention to other matters highlighted in Mr Brereton's submissions. 198 Mr Brereton called attention to four submissions which were really red herrings. These were:

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M. Collateral Matters 209 What I have listed as collateral matters is really the notice of cross appeal that his Honour was in error in allowing an amendment of the cross claim shortly before the trial commenced. I have already outlined the way in which the cross claim for contribution came to be presented and amended. Mr Hall says that the cross claim as originally filed simply repeated the allegations made by the plaintiff against the hospital, and that there was no allegation that any treatment provided by hospital staff themselves was in any way deficient. There was no hint of this until 1999 and the cross claim was not formally amended until 2 March 2001. The hospital contends that the death of Sister Ranclaud irremediably prejudiced the hospital's ability to answer the allegations made in the amended cross claim. The hospital acknowledges the difficulty of appealing against a discretionary judgment, but notes that when the appellate court is convinced that the trial judge's discretion has miscarried resulting in an injustice, it is the appellate court's duty to intervene: Cohen v McWilliam (1995) 38 NSWLR 476, 492 and Tzouvelis v Victorian Railway Commissioners [1968] VR 112, 139-140. 210 Mr Hall says that where there is injustice to the other party that cannot be remedied by an order for costs or the attachment of terms for the grant of leave, leave to amend ought to be refused. It is sufficient basis for refusing leave if the opposing party has been deprived of an opportunity to adduce evidence on the relevant issues: FF Seeley Nominees Pty Ltd v El Ar Initiations (UK) Ltd (No 2) (1990) 55 SASR 314, 315. Whealy J erred in determining that Sister Ranclaud's death did not substantially prejudice the hospital. He was under a misapprehension of fact that there were other hospital staff who would be available to assist in the hospital's defence, and indeed, applied the wrong principle, comparing the prejudice to the doctor and the prejudice to the hospital. He was also under the misapprehension that there was no greater prejudice to the hospital as a result of the application having been made in 2001 or 1999 that if it had been made immediately after Sister Ranclaud's death in 1993. Indeed, it is put there was additional prejudice because in the intervening eight year period between Sister Ranclaud's death and the application to amend, the hospital continued to suffer the type of "presumptive prejudice" described by McHugh J in Brisbane South Regional Health Authority v Taylor (1996) 186 CLR 541, 551, arising from the further deterioration in recollection and ability to recognise the significance of the relationship between events. 211 Mr Brereton's riposte was that it was inappropriate to argue by analogy with the approach to extensions of time under the Limitation Act 1969 that the amendment should not have been permitted because of prejudice occasioned by Sister Ranclaud's death. This was not an application for an extension of time and no limitation question was involved. Prejudice resulting from declining memories and loss of witnesses does not count against an amendment which does not involve any extension of the limitation period. Surely it could never be argued that there could be no amendment at any time after Sister Ranclaud died, because she could have died at any time after the original cross claim was filed. 212 In any event, Mr Brereton says, that the Judge's conclusion that the hospital was far from going into battle defenceless and unarmed was correct. The Judge was entitled to conclude, as he did, that the hospital should be in the position to adduce relevant evidence from other witnesses, tender the statement of Sister Ranclaud, and adduce expert evidence. 213 Mr Brereton also points out that although the action was commenced many years previously, there was no exchange of expert reports on liability issues until 1998. So the first time the parties started exchanging experts' reports on liability was that year. The cross claim was mooted in 1999, and there was absolutely no reaction until 26 February 2001. 214 In my view the discretion as to whether to allow an amendment was properly exercised by the learned trial judge. It was a matter for his judgment. I cannot see any appealable error in the approach taken by his Honour, and indeed, there is something in what Mr Brereton says that the cross appellant's submissions do confuse principles to be applied in cases of amendments after limitation periods with cases of simple amendment. Accordingly, the cross appeal should be dismissed.

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N. The Result of the Appeal 215 At first blush, this is an appeal on a question of fact where the trial judge had the opportunity of examining the witnesses and seeing how they reacted under cross examination. 216 However, when one analyses the situation more closely, the real decision to be made is somewhat different. 217 It may be that I have quoted more of the transcript than was, strictly speaking, warranted. However, I consider it necessary to do so in order to get the full flavour of the evidence of the various medical experts. 218 The doctor in the cross claim for contribution stands in the position of the plaintiff. All the plaintiff has to show is that the defendant's negligence could have been the cause of the plaintiff's injury. The Judge accepted that there was an excessive dose of Syntocinon. The scientists, on both sides, markedly Professor Fisk and Professor Ellwood have said that they would expect to find a second hypoxic cause for a continuing bradycardia. 219 I agree with Mr Brereton's submissions that the mere fact that the clinicians say they have not observed that in every case or that they have observed situations where they could not see a second cause, does not seem to me to take the matter any further. Yet his Honour seemed to suggest that there was some dichotomy in the view of the scientist on the one hand, and the practical man and woman dealing with situations on the ground who are not worried so much about theoretical causes. His Honour seemed to suggest that a scientist looks for certainty, whereas the practitioner looks for clinical results and tended to look at the matter as if to say, well, applying common sense, one prefers the practice as witnessed by the practitioner to the theory of the scientist. 220 However, that is not the way one looks at expert evidence at all. If there is undisputed scientific evidence that in order for a certain consequence to occur, there needs to be both a vagal and an hypoxic cause, the mere fact that a person in practice may not have observed a second cause, does not negate the scientific opinion. 221 Once that is accepted, and once it is accepted that, as I have indicated earlier, the learned trial judge excluded the middle when finding that the Syntocinon theory could not have any grounds, one is left with the situation where the quasi plaintiff has shown that the overdose of Syntocinon could well have caused the injury. The evidentiary onus then shifts to the defendant. The evidence as to the hypoxic factor being the occlusion of the cord is not sufficiently supported by the evidence. Accordingly, the cross claimant must succeed. 222 The cross claimant claims 50% contribution. He does that mainly on the basis that by analogy with the principle quality is equity, so where there is little material to distinguish between the contributions the same applies at common law. Mr Hall was aghast at this suggestion and submitted that if the hospital was found liable the doctor's negligence was far more than the hospital's negligence. 223 As Fleming on Torts 9th ed (LBC, Sydney, 1998) notes at p 297, the statutory mandate is that the contribution is to be what is just and equitable having regard to the extent of the responsibility for the damage. However, that learned author also points out that apart from cases such as Sinclair v William Arnott Pty Ltd (No 2) (1963) 64 SR (NSW) 88, 96, where one tortfeasor owes a higher duty than the other, the percentage of contribution has been dealt with broadly and upon common sense principles, picking up words from The Volute [1922] 1 AC 129, 144, a contributory negligence case. 224 In Broken Hill Pty Co Ltd v Duffy (1943) 16 ALJ 374, 376, Latham CJ, with whom Rich, Starke, McKiernan and Williams JJ agreed, said: "It was very difficult to say that either party was more responsible than the other for the accident, and, that being so, there was no reason why the rule contained in s 1 of the Maritime Conventions Act, 1911 (Imp), that where it is impossible to assign the precise degree of fault the responsibility shall be apportioned equally should not be applied to the similar provision of the Wrongs Act (SA)." 225 The present case is one where despite the great bulk of evidence presented, the responsibility for the plaintiff's injuries is in this position. 226 Accordingly, the apportionment should be 50/50. 227 Accordingly, in my view, the order of the Court should be that the appeal is allowed with costs, the order of the trial judge on the doctor's cross claim set aside and in lieu there be an order that the hospital contribute one-half of the damages and costs that the doctor was ordered to pay the plaintiff. The cross appeal should be dismissed with costs.