Diamond v Simpson (No 3) - vardanega roberts solicitors
Diamond v Simpson (No 3) - vardanega roberts solicitors
Diamond v Simpson (No 3) - vardanega roberts solicitors
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
New South Wales Court of Appeal<br />
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
Last Updated: 17 December 2003<br />
NEW SOUTH WALES COURT OF APPEAL<br />
CITATION: <strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373<br />
FILE NUMBER(S):<br />
40962/01<br />
HEARING DATE(S): 18, 19, 20 February 2003; 18, 19 June 2003 [Contribution Claim]<br />
JUDGMENT DATE: 16/12/2003<br />
PARTIES:<br />
Robert <strong>Diamond</strong> (Appellant)<br />
Trustees of the Sisters of St Joseph (Respondent)<br />
JUDGMENT OF: Meagher JA Ipp JA Young CJ in Eq<br />
LOWER COURT JURISDICTION: Supreme Court - Common Law Division<br />
LOWER COURT FILE NUMBER(S): 12791/87<br />
LOWER COURT JUDICIAL OFFICER: Whealy J<br />
COUNSEL:<br />
P L G Brereton SC and I F Butcher (A)<br />
P Hall QC and S A Woods (R)<br />
SOLICITORS:<br />
Blake Dawson Waldron (A)<br />
Makinson & d'Apice (R)<br />
CATCHWORDS:<br />
NEGLIGENCE- Hospital- Defective birth case- Scientific evidence- Whether hospital and doctor contributed to defective birth.<br />
LEGISLATION CITED:<br />
Evidence Act 1995<br />
Law Reform (Miscellaneous Provisions) Act 1946, s 5<br />
Limitation Act 1969<br />
Supreme Court Act 1970, s 75A(5)<br />
DECISION:<br />
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
(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<br />
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<br />
amount of such amount if the same cannot be agreed; (4) Cross appeal dismissed with costs.<br />
JUDGMENT:<br />
IN THE SUPREME COURT<br />
OF NEW SOUTH WALES<br />
COURT OF APPEAL<br />
40962/01<br />
MEAGHER JA<br />
IPP JA<br />
YOUNG CJ in EQ<br />
Tuesday 16 December 2003<br />
ROBERT DIAMOND v CALANDRE SIMPSON AND TRUSTEES OF THE SISTERS OF ST JOSEPH (NO 3)<br />
CATCHWORDS<br />
NEGLIGENCE- Hospital- Defective birth case- Scientific evidence- Whether hospital and doctor contributed to defective birth.<br />
FACTS<br />
The plaintiff was born under circumstances from which she has suffered lifelong cerebral palsy. In a lengthy trial she was awarded<br />
damages of $14 million, reduced on appeal to $11 million. The doctor admitted negligence.<br />
The doctor sued the hospital for contribution. The trial judge found that the hospital had been negligent in administering to the<br />
plaintiff's mother an overdose of Syntocinon. However, he found that that negligence was not a cause of the plaintiff's damage. He<br />
accordingly found a verdict for the hospital.<br />
On appeal, the Court considered that the evidence provided by the hospital's partogram and the correct application of the principles of<br />
scientific evidence meant that the probabilities were that there was more than one cause of the plaintiff's injury and that both the<br />
doctor and the hospital's act of administering an overdose of Syntocinon contributed to the plaintiff's injury. In the circumstances, the<br />
doctor and the hospital should be equally liable for the plaintiff's damage.<br />
(1) Appeal allowed.<br />
ORDERS<br />
(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<br />
respect of orders made against the cross claimant in these proceedings.<br />
(3) Liberty to apply to a Master to certify the amount of such amount if the same cannot be agreed.<br />
(4) Cross appeal dismissed with costs.<br />
IN THE SUPREME COURT<br />
OF NEW SOUTH WALES<br />
COURT OF APPEAL<br />
40962/01<br />
MEAGHER JA<br />
IPP JA<br />
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
YOUNG CJ in EQ<br />
Tuesday 16 December 2003<br />
ROBERT DIAMOND v CALANDRE SIMPSON AND TRUSTEES OF THE SISTERS OF ST JOSEPH (NO 3)<br />
1 MEAGHER JA: I agree with Young CJ in Eq.<br />
2 IPP JA: I agree with Young CJ in Eq.<br />
Judgment<br />
3 YOUNG CJ in EQ: This is the second tranche of the appeals arising out of the birth of the first respondent ("the plaintiff"),<br />
Calandre <strong>Simpson</strong>, on 5 July 1979. The birth took place in a hospital operated by the second respondent ("the hospital"). The doctor<br />
in charge of the birth was the appellant ("the doctor").<br />
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.<br />
5 The trial of the plaintiff's action came on before Whealy J and lasted for 12 weeks of hearing.<br />
6 On the first day of the trial, the doctor admitted liability and the plaintiff thereupon discontinued against the hospital. His Honour<br />
then had to consider the question of the quantum of damages as against the doctor, and also had to consider a cross claim for<br />
contribution by the doctor against the hospital.<br />
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<br />
Honour found that the hospital was negligent, but that such negligence did not cause the plaintiff's damage. Accordingly, he<br />
dismissed the cross claim.<br />
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<br />
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.<br />
There was also a subsequent judgment on costs by the same panel; see [2003] NSWCA 78, delivered on 9 April 2003.<br />
9 The present appeal seeks to have the hospital contribute to the damages that have to be paid to the plaintiff by the doctor.<br />
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<br />
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<br />
suffered by the plaintiff. The doctor suggests that the hospital should contribute 50% of the amount ordered to be paid by the doctor.<br />
11 The hospital, in its notice of contention, challenges the finding of negligent conduct. It also says that because the doctor was<br />
grossly negligent, he is not entitled to contribution at all. There is also a cross appeal by the hospital on a procedural matter, relating<br />
to whether the trial judge should have given late leave to the doctor to amend his cross claim.<br />
12 It is convenient to consider the issues that arise on this appeal under the following heads:<br />
A. Glossary and List of Dramatis Personae;<br />
B. The Factual Background;<br />
C. Applicable Principles of Appellate Review;<br />
D. The Opposing Arguments on Appeal;<br />
E. Expert Evidence;<br />
F. Undisputed Relevant Facts;<br />
G. The Syntocinon Argument;<br />
H. The Medical Evidence;<br />
I. The Trial Judge's Findings;<br />
J. Problems with Multiple Causes;<br />
K. Resolution of the Issues;<br />
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
L. The <strong>No</strong>tice of Contention;<br />
M. Collateral Matters;<br />
N. The Result of the Appeal.<br />
O. The Orders to be made.<br />
A. Glossary and List of Dramatis Personae<br />
13 This glossary is not intended to be anything more than a list of brief (often over -simplified) definitions of medical terms used in<br />
these reasons.<br />
ACIDOSIS An acid condition of the blood.<br />
APGAR An index indicating colour, respiratory effort,<br />
muscle tone, heart rate and reflex irritability<br />
of a new born baby. APGAR is an acronym for Appearance, Pulse rate, Grimace, Activity (muscle tone) and Respiratory effort. The<br />
scale is 0 for very poor, 1 for problem and 2 for good.<br />
AUSCULTATION Examination by listening.<br />
BRADYCARDIA A slowing of the heart rate. In 1979 "normal"<br />
heart rate for a foetus was considered to be<br />
120-160 beats per minute (bpm).<br />
CORD COMPRESSION Occlusion of the umbilical cord.<br />
EPIDURAL Stimulant injection to control pain during<br />
child birth.<br />
HYPERSTIMULATION Over stimulation - 5 contractions or more in<br />
any ten minute period. However see [15] below.<br />
HYPERTONUS A form of hyperstimulation of the uterus<br />
manifested by a raised resting tone and elevation of contractions one into the other (coupling).<br />
HYPOSTIMULATION Under stimulation.<br />
HYPOTONUS Low pressure of bodily fluid.<br />
HYPOXIC See [12].<br />
INTERVILLOUS The placenta is an outer growth from the<br />
foetus which has hundreds of little finger<br />
processes called "villi" which are immersed<br />
in a bath of maternal blood. Thus there is<br />
always a barrier between the foetus and the<br />
mother. The placental space is referred to as<br />
"the intervillous space".<br />
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<strong>Diamond</strong> v <strong>Simpson</strong> (<strong>No</strong> 3) [2003] NSWCA 373 (16 December 2003)<br />
MECONIUM Dark excrement of a foetus.<br />
OXYTOCIN A hormone which stimulates contractions.<br />
NON TRIAL FORCEPS Forceps used outside the operating theatre.<br />
PARTOGRAM A hospital chart recording heart beats of<br />
mother and foetus and noting oxytocin dose<br />
and administration of other drugs.<br />
SYNTOCINON Synthetic oxytocin.<br />
TACHYCARDIA Fast heart rate.<br />
TACHYSYSTOLE A lot of contractions close together.<br />
TITRATION The method of mixing the solution and<br />
adjusting the dosage.<br />
VAGAL See [13].<br />
VILLAE See Intervillous.<br />
14 The terms "hypoxic" and "vagal" are vital ones in this case. The Gould Medical dictionary defines the term "hypoxic" as<br />
"Reduction in availability of oxygen to tissue due to a decrease in the partial pressure of oxygen in the arterial blood".<br />
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<br />
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<br />
short half life so that when the vagal stimulus is removed, the chemical dissipates and the heart rate recovers.<br />
16 In the present case, the injury was caused by unremitting bradycardia. The key question in this part of the case is whether that<br />
bradycardia had a solely vagal cause or whether there was an hypoxic cause as well and, if so, what was that hypoxic cause.<br />
17 It must be noted that Mr Brereton put that there was no particular magic in the classic definition of hyperstimulation noted in [11].<br />
Indeed virtually all the experts agreed that this is so. Even if contractions did not exceed 5 in 10 minutes there could still be<br />
occasioned depletion of foetal metabolic reserves.<br />
18 Three types of forceps are referred to in this case, Wrigleys, Neville Barnes and Kiellands. It is difficult to describe the differences<br />
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<br />
with virtually no handles: one cannot get much traction from them. Neville Barnes forceps are a standard pair of classical long<br />
forceps with a handle that one can lock and squeeze together. They cannot be used to rotate. Kiellands forceps are different in two<br />
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<br />
dangerous as they can squash the baby's head. See Dr Clements at Black Vol 1, 194 -5.<br />
19 Eight expert medical witnesses were called by the parties. The plaintiff called Mr Roger Clements, an obstetrician, Dr Janet<br />
Rennie, a neo-natal clinician, and Dr Frederick Hinde, a specialist gynaecologist. The doctor called Professor Nicholas Fisk, an<br />
English Professor of Obstetrics and Gynaecology, described by his Honour as a foetal physiologist, Dr Robert Lyneham, a consultant<br />
obstetrician and gynaecologist, Dr John Keogh, a specialist in obstetrics and gynaecology, and Dr John Pennington, obstetrician and<br />
gynaecologist. The hospital called Professor David Ellwood, Professor of Obstetrics and Gynaecology, another foetal physiologist.<br />
20 In summary, his Honour found the views of Mr Clements and Dr Rennie very compelling. He was very much persuaded by Dr<br />
Hinde. He preferred Professor Ellwood to Professor Fisk, and did not find much assistance in the evidence of Drs Lyneham, Keogh or<br />
Pennington. This is a matter to which I will return.<br />
21 The only other person who needs to be described at this stage is Geraldine Ranclaud, who was the midwife/nurse involved in the<br />
delivery of the plaintiff. Sister Ranclaud was an experienced nurse. She made a statement on 1 February 1988 about the matter, but<br />
unfortunately died in 1993. Her statement was tendered at the trial, but of course, there could be no cross examination on this<br />
statement.<br />
B. The Factual Background<br />
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22 The background facts can be shortly stated. Mrs Gail <strong>Simpson</strong>, whom I will call "the mother", was admitted to the hospital on the<br />
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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<br />
membranes and Syntocinon was administered to help induce labour. I will need to examine what occurred between 8.10 am and 1.30<br />
pm that day in more detail later. For the present, I am merely outlining the background.<br />
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.<br />
He tried five times to deliver the baby by forceps of three different types. During the final attempt with Kiellands forceps the doctor<br />
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<br />
heart beat reduced from about 140 beats per minute (bpm) to between 60 and 80 bpm.<br />
24 These attempts at forceps delivery took 15 to 20 minutes. After the last attempt, the mother was taken to the operating theatre<br />
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<br />
decision was made to take the mother into the operating theatre and the time of delivery.<br />
25 The plaintiff's condition at delivery was poor. Her APGAR was 10010 one minute after delivery.<br />
26 The plaintiff developed cerebral palsy. It is common ground that she suffered a terminal bradycardia for at least 15 minutes,<br />
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<br />
minutes and this is recognised as a situation where brain damage will most likely result.<br />
27 The plaintiff sued the doctor in these proceedings which she commenced on 3 April 1987, that is, almost eight years after the<br />
event.<br />
28 By cross claim filed on 27 February 1991 in what Whealy J, in a preliminary judgment, <strong>Simpson</strong> v <strong>Diamond</strong> [2001] NSWSC<br />
150, called "a bland pleading", the doctor sought contribution or indemnity from the hospital without disclosing much by way of<br />
particulars as to why the contribution was sought.<br />
29 In <strong>No</strong>vember 1999, the doctor's <strong>solicitors</strong> furnished the hospital's <strong>solicitors</strong> with a proposed amended cross claim. Discussions<br />
went on for some time about this. A formal amended cross claim document was provided by the doctor's <strong>solicitors</strong> on 20 July 2000.<br />
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<br />
prejudiced because of the death of Sister Ranclaud, Whealy J allowed the amended cross claim to be filed and it was filed on 27<br />
February 2001.<br />
30 In what I have described as a collateral issue, the hospital seeks to reverse that decision.<br />
31 The trial commenced before Whealy J and lasted three months. His Honour then reserved his judgment, and on 5 <strong>No</strong>vember 2001,<br />
found a verdict for the plaintiff against the doctor, but dismissed the doctor's cross claim for contribution.<br />
32 When considering his Honour's judgment I shall refer to paragraph numbers making this clear by the use of square brackets.<br />
33 His Honour found at [1403]:<br />
"I find that the plaintiff's injury was caused solely by Dr <strong>Diamond</strong>'s negligent use of forceps. This, coupled with the fact that the<br />
instrumental attempts were made in the labour ward, induced an unremitting bradycardia which continued until birth."<br />
34 His Honour said at [1416] that he accepted on the evidence that there was never a real possibility that the mother had experienced<br />
continuous contractions during the hour prior to midday. This appears to be unassailable. His Honour continued at [1417] that he<br />
rejected the contention that the contraction frequency resulted in an interval between contractions of just under 60 seconds. He did so<br />
on the ground that the mother's evidence was to the contrary. However, as Mr Brereton submits, the mother's testimony on this issue<br />
was not likely to have been accurate. There was evidence that a mother in the position of Mrs <strong>Simpson</strong> would not have been in a<br />
position to make precise observations of the extent of her contractions, moreover, there would be a small difference in time between<br />
her experience of pain and the start and finish of each contraction.<br />
35 His Honour also rejected at [1418] and [1419] that the entries in the fluid balance chart could have supported the Syntocinon<br />
theory because observations of the various nurses and doctors did not disclose that they had observed signs which would have been<br />
quite apparent had the fluid been administered in the way the Syntocinon theory suggested.<br />
36 At [1423] his Honour remarked that it was obviously dangerous to attempt to reconstruct events by way of expert interpretation of<br />
hospital records. Particularly was this so where some of the records were ambiguous and Sister Ranclaud, the only person who might<br />
have been able properly to interpret them, had died before the trial. His Honour said that it was obvious that in many respects the<br />
hospital records did not provide a firm skeleton for reconstruction. His Honour said:<br />
"I remain unsatisfied and unpersuaded, despite the variations of approach, that there is any real probability that hyperstimulation<br />
occurred."<br />
37 Regarding the contribution claim, his Honour said at [1406]:<br />
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"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<br />
<strong>Simpson</strong>. This was, contrary to the doctor's instructions, at a rate 43% higher than the prescribed rate. The nursing staff was solely<br />
responsible for this breach of duty. Dr <strong>Diamond</strong> had no role in the administration of the excessive concentration."<br />
However, he said at [1450]:<br />
"Calandre was not harmed by Syntocinon. Until the end stage of the instrumental attempts, her heart rate remained within normal<br />
limits. There was no tachycardia preceding an onset of bradycardia. At the time the Kiellands forceps were employed, there occurred<br />
'the first real sign of foetal distress'. The recovery of the heart rate following the drop during the Neville Barnes applications<br />
reinforced that this was so."<br />
He thus held that the negligence of the hospital with respect to the dose of Syntocinon was not a cause of the plaintiff's damage and so<br />
dismissed the cross claim.<br />
38 As I have said, the vital question in the current appeal is whether the terminal bradycardia was solely a result of the vagal<br />
interference caused by the use of forceps. The appellant doctor says it is necessary to find another, an hypoxic cause, as well [see<br />
Glossary for definition]. Principally this is because he says normally a vagal interference with blood supply lasts only for a very short<br />
period. The significance of the short period is that no lasting harm befalls the foetus as, when normal conditions are resumed, it<br />
quickly recovers. The doctor says that the hypoxic cause is the hospital's negligence in administering an excessive dose of Syntocinon<br />
which produced hyperstimulation and so used up the foetus' metabolic reserves. The hospital denies that there is a need for a second<br />
cause in addition to the vagal cause and, further, denies that the excessive dose of Syntocinon was an additional cause of the terminal<br />
bradycardia.<br />
39 The hospital denies that it is necessary to find a second, an hypoxic cause, but further says that if one has to be found it is to be<br />
found in the occlusion of the cord by forceps. Both counsel told us that his Honour did not so find.<br />
C. Applicable Principles of Appellate Review<br />
40 Mr Hall commenced his supplementary submissions with a quotation from the judgment of Isaacs J in Dearman v Dearman<br />
(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<br />
given in the first instance." He then emphasized with reference to high authority the advantage that the trial judge has. He cited<br />
extensively from the judgment of Kirby J in State Rail Authority v Earthline Constructions Pty Ltd (1999) 73 ALJR 306, 330<br />
[90-1].<br />
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<br />
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<br />
weight to, the trial judge's advantages.<br />
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<br />
evidence of expert witnesses occupying over 1,500 pages of transcript, the learned trial judge was at a considerable advantage, and<br />
this Court should not disturb his findings of fact unless they were not available on the evidence.<br />
43 He then went on to say:<br />
"The principle applies to expert witnesses in the same way that it applies to lay witnesses. The trial judge has the advantage of having<br />
seen the experts presenting their opinions, and their manner of dealing with competing opinions and propositions put in cross -<br />
examination.<br />
"In particular, where the opinion expressed by an expert is based upon their experience, and where that experience forms a legitimate<br />
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:<br />
X & Y v Pal (1991) 23 NSWLR 26, 34.<br />
"It is also submitted that where the issue under appeal is the issue of causation, an appellate court would be cautious in subjecting the<br />
learned trial judge's reasons to meticulous scrutiny in the search of error: the conclusion as to causation is one that is 'often reached<br />
intuitively': Chappel v Hart (1998) 195 CLR 232, 290 [148]."<br />
44 Mr Brereton submits that:<br />
Page 7 of 31<br />
"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<br />
position of advantage if that finding is founded on substantially on an assessment of credibility, based to a significant extent on<br />
observations of demeanour (see Devries v Australian National Railways Commission (1993) 177 CLR 472, 479 (Brennan,<br />
Gaudron and McHugh JJ), 480 (Deane and Dawson JJ)), the rationale which underlies that approach is that the trial judge is<br />
acknowledged to enjoy a position of advantage, vis -a-vis an appellate court, in assessing demeanour. Demeanour did not play a<br />
significant role in the trial judge's resolution of those factual issues which remain in dispute on the appeal. The argument turns on<br />
objective facts and inferences, and the use and analysis of expert evidence, not the acceptance of one witness over another on<br />
demeanour."<br />
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45 Mr Brereton then says that it is very necessary to make a distinction between findings of primary fact and inferences to be drawn<br />
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<br />
that inhibitions put on appellate courts in cases such as Abalos v Australian Postal Commission (1990) 171 CLR 167, 178-9 do not<br />
concern the present appeal. This is the case, as was Warren v Coombes (1979) 142 CLR 531, 541, where it is clear that:<br />
"Where the question is whether particular inference should be drawn from proved facts the appellate court has the right and duty to<br />
decide the question for itself."<br />
However he says, by way of backup submissions that:<br />
"In any event, a trial judge's finding of fact, even when based on demeanour, are open to be reviewed on appeal on the footing that<br />
there is too fragile a basis for them." State Rail Authority v Earthline Constructions Pty Ltd.<br />
46 Mr Brereton puts that, as Viscount Simonds said in Benmax v Austin Motor Co Ltd [1955] AC 370, 373 "it may often be<br />
difficult to say what is a simple fact and what is inference from fact." In the present case he says that the distinction between<br />
simple/primary facts and inferred facts is unhelpful. He puts that by reason of the hospital's own inadequate record keeping, almost all<br />
of the critical facts in this case depend on inferences and many of what should be "simple facts" require expert opinion.<br />
47 Mr Brereton puts that, essentially, the only simple facts are:<br />
(1) What dosage of Syntocinon was given?<br />
(2) What was the uterine response;<br />
(3) What was the foetal heart rate at various times.<br />
However even here, because of inadequate records there has to be inference on these matters also.<br />
48 As counsel reminded us, the High Court has recently considered the matter again in Fox v Percy (2003) 77 ALJR 989 and in<br />
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<br />
unnecessary to consider whether "the judicial authority about disturbing evidence on the basis of assessments of credibility applies, or<br />
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<br />
decision at trial is the acceptability of the witness's opinion, the extent of his or her experience in the speciality and whether one<br />
expert's conclusion is more acceptable and logical than that of another expert." His Honour noted that there were differing views on<br />
that question and referred in a footnote to Ahmedi v Ahmedi (1991) 23 NSWLR 288, 291, the Earthline Constructions case at 321<br />
[68] and referred also to Watts v Rake (1960) 108 CLR 158, 162-3.<br />
49 However, Mr Brereton says that most significant is paragraph 42 of the judgment of Kirby J at p 1111, where his Honour notes<br />
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<br />
there were multiple causes, because all the plaintiff had to show was that the defendant's conduct was a cause, not necessarily the<br />
cause, of her injury.<br />
50 Mr Brereton points out that in the Earthline case, the High Court did allow the appeal even though the trial judge had been<br />
heavily swayed by his impression of a witness on giving evidence, by taking regard to other evidence at the trial.<br />
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.<br />
This is because almost all the findings made by the judge were of inferred facts. Moreover, with minor exceptions, there were no<br />
problems as to credibility.<br />
D. The Opposing Arguments on Appeal<br />
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<br />
by two concurrent causes, one of them hypoxic rather than by one vagal cause only.<br />
53 He further says that the trial judge erred in taking the view that he could give greater weight to the observations (or non -<br />
observations) of the clinicians than to the evidence of the scientists.<br />
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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<br />
on the evidence and his decision was well within the range.<br />
55 The heart of the case for contribution between the doctor and the hospital is whether the latter's negligence in administering an<br />
overdose of Syntocinon to the plaintiff's mother was a contributing cause of the plaintiff's injury.<br />
56 The learned trial judge found that the hospital was negligent in relation to the dosage of Syntocinon (see [1406]). However, his<br />
Honour held that that was not a contributing cause of the injury.<br />
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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<br />
injuries. The excessive Syntocinon regime produced such a level of contractions in Mrs <strong>Simpson</strong> that the reduced opportunity for<br />
replenishment of the placental villae between contractions resulted in the depletion of Calandre's foetal metabolic reserves, such that<br />
her ability to withstand the stresses of labour, including instrumentation, was impaired and compromised, with the consequence that,<br />
when otherwise she would have recovered from the forceps episode without permanent damage, she was unable to do so ("the<br />
Syntocinon theory").<br />
58 Mr Brereton puts it that a compelling reason for this conclusion is that the failed forceps were an insufficient explanation for the<br />
catastrophic outcome, unless some other, hypoxic, mechanism were also at work. This was the opinion, in particular, of the two foetal<br />
physiologists, Professors Fisk (for the appellant) and Ellwood (for the hospital). Although finding Professor Ellwood's approach to be<br />
"both reasonable and convincing", his Honour (contrary to both Professor Ellwood and Professor Fisk) did not accept that it was<br />
necessary to find an hypoxic explanation as well as a vagal bradycardia. Rather, his Honour accepted the evidence of the clinicians<br />
(Mr Clements and Dr Hinde), that it was not necessary to look for a second pathology. In so doing, his Honour apparently took the<br />
view that the clinicians Dr Hinde and Mr Clements "knew what they have seen", and were not concerned with the "niceties of<br />
precision" which troubled the foetal physiologists. This approach did not do justice to the scientific evidence. His Honour did not<br />
analyse the expert evidence - scientific and clinical - with the rigour required. His Honour should have concluded that the result was<br />
not explicable in the absence of a second pathology.<br />
59 These are the basic contentions. There were, of course, arguments on the details. These are considered when matters of detail are<br />
discussed in these reasons.<br />
E. Expert Evidence<br />
60 The solution to the very awkward problems presented to the Court in this case lies in the proper interpretation of the expert<br />
evidence and analysis of records compiled at the time of the plaintiff's birth.<br />
61 There is no doubt as to the eminence and qualification of all the experts who gave evidence in this case. However their evidence<br />
was not entirely consistent. In particular, there was tension between the clinicians and the scientists which I have already noted and<br />
will discuss in the appropriate part of these reasons.<br />
62 It must be remembered that "the parties have invoked the decision of a judicial tribunal and not an oracular pronouncement by an<br />
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<br />
expert evidence. Where expert evidence is contradictory, the Court resolves the conflict applying "logic and commonsense to the best<br />
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]<br />
2 Qd R 472, 474.<br />
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<br />
judge is not entitled merely to pick the most impressive of the expert witnesses put before him or her.<br />
64 It must be remembered further that, whilst under the Evidence Act 1995 it is admissible for experts to give evidence of opinion<br />
close to the ultimate issue, the closer they approach the ultimate issue the more careful judicial scrutiny should be: R v GK (2001) 53<br />
NSWLR 317, 326; Adler v ASIC (2003) 46 ACSR 504, 633.<br />
65 In Makita (Australia) Pty Ltd v Sprowles (2001) 52 NSWLR 705 at 729 and following, Heydon JA, when a member of this<br />
Court, gave detailed guidance as to the way in which courts should approach expert evidence. He said [59] at p 729, with respect to<br />
the expert in that case, Professor Morton:<br />
"a prime duty of experts in giving opinion evidence [is] to furnish the trier of fact with criteria enabling evaluation of the validity of<br />
the expert's conclusions."<br />
66 He pointed out that that view had been accepted by a large number of judicial and academic writers. His Honour then continued at<br />
731 [64]:<br />
"The basal principle is that what an expert gives is an opinion based on facts. Because of that, the expert must either prove by<br />
admissible means the facts on which the opinion is based, or state explicitly the assumptions as to fact on which the opinion is based.<br />
If other admissible evidence establishes that the matters assumed are 'sufficiently like' the matters established 'to render the opinion of<br />
the expert of any value', even though they may not correspond 'with complete precision' the opinion will be admissible and material;<br />
see generally Paric v John Holland Constructions Pty Ltd [1984] 2 NSWLR 505, 509-510; Paric v John Holland<br />
(Constructions) Pty Ltd (1985) 59 ALJR 844, 846."<br />
At 733, after discussing a series of other cases his Honour said that there was underlying a number of observations in the leading<br />
cases "that the trier of fact must arrive at an independent assessment of the opinions and their value, and that this cannot be done<br />
unless their basis is explained."<br />
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67 The problem arises in the instant case because, if I can over-simplify the position for a moment, the key question was whether a<br />
second cause of terminal bradycardia was required. On this point, the expert evidence of Professors Fisk and Ellwood was that a<br />
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second, an hypoxic, cause was necessary (they thought of different hypoxic causes but that is bye the bye). Mr Brereton says that<br />
merely because the evidence of the clinicians showed that they had seen some cases where there had not been an obvious second<br />
cause or a second cause which they had been able to discern was no reason for putting aside the expert opinions of Professors Fisk<br />
and Ellwood.<br />
68 Mr Brereton says that the present is a classic case of mere ipse dixit of experts preferred by the trial judge. For instance he notes<br />
that Mr Clements could only identify one or two cases with which he had been concerned, declining to discuss others on the basis of<br />
confidentiality. Thus there could be little opportunity to test his evidence. Indeed the so -called clinical experience was more within<br />
Mr Clements' medico-legal theorizing.<br />
69 Dr Rennie also relied only on one actual case from her medico -legal practice. I will set out her evidence in detail later in these<br />
reasons.<br />
70 Again, Dr Hinde relied on his clinical experience. At Black 1684 Mr Brereton asked him:<br />
"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?<br />
A. It is just experience that you see this happening."<br />
At Black 1685, Dr Hinde said:<br />
"A. Well, if the foetal heart remains low there has to be a continuing vagal action."<br />
Mr Brereton asked:<br />
"Q. But what causes it?<br />
A. Well, as I have said, I am basing what I say on practical observations, rather than theoretical concepts.<br />
Q. And so far as we know at this stage there is no scientific analysis which explains that?<br />
A. Because fortunately there are very few cases like this.<br />
Q. Would you agree that there is no scientific explanation which explains a continued sustained vagal bradycardia?<br />
A. There is no scientific explanation because it would be extremely difficult to do a study which, under the circumstances of what we<br />
are discussing addressed this question."<br />
71 The impression I obtained from these passages is that Dr Hinde was relying on his own experience rather than objective<br />
experience from literature.<br />
72 Mr Brereton submits that the opinion of Dr Hinde that forceps alone can lead to sustained bradycardia is based purely and simply<br />
on an observation of forceps being followed by bradycardia in rare cases in the past. This involves the unstated and unproven<br />
assumption that in those cases, there was a causal connection; and, therefore, the supposition that there could have been such a<br />
connection in the plaintiff's case. However, neither Dr Hinde nor the hospital has put forward any factual matters at all which would<br />
allow evaluation of the opinion about causation in those earlier cases, or as to how conclusion could be drawn from them applicable<br />
to the plaintiff's case. While in some cases a temporal association may be sufficient to permit a causal relationship to be inferred, the<br />
evidence of the foetal physiologists means that this is not such a case.<br />
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<br />
Makita v Sprowles (supra).<br />
74 There is a lot of force in this submission.<br />
75 His Honour seems to have considered that there was some dichotomy between "scientific certainty" expected from the perspective<br />
of a foetal physiologist and the observations of the clinician "who knows what he has seen"; see [1448].<br />
76 I agree with the submission of Mr Brereton in this regard:<br />
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"This does not do justice to the role of scientific evidence. Here, two eminent foetal physiologists - one on each side of the record -<br />
agreed that a second pathology was necessary to explain the outcome. It was not enough to discount that to find that clinicians, not<br />
even able to describe particular cases on which their professional opinion depended, thought otherwise.<br />
This was no question of 'searching for scientific certitude'; two scientists on opposing sides said that the outcome was not possible<br />
without a second pathology, and his Honour should have so found. In a field of specialised knowledge (foetal physiology), the<br />
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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<br />
should not have been put aside without compelling reasons. The evidence of the decisions - Mr Clements and Dr Hinde - did not<br />
provide such a basis."<br />
F. Undisputed Relevant Facts<br />
77 The following is based on the doctor's submissions (Orange 3 et seq), adjusted by reference to the hospital's submissions (Orange<br />
125 et seq).<br />
(1) Mrs <strong>Simpson</strong> arrived at the hospital on 4 July 1979 at 8.30 pm for the purposes of a planned induction of labour. She was taken to<br />
the labour award at about 8.10 am on 5 July 1979, when Dr <strong>Diamond</strong> performed an artificial rupture of membranes, and gave<br />
instructions to commence Syntocinon to help induce labour.<br />
(2) Dr <strong>Diamond</strong>'s protocol for Syntocinon was 10 units of Syntocinon in 1000 mls of fluid, commencing at 20 drops per minute<br />
(dpm) and increasing by 10 dpm every 15 minutes or half hour until a maximum of 60 dpm was reached. However, the evidence<br />
shows 10 units of Syntocinon was added to 700 mls of fluid, a substantially stronger concentration than the doctor prescribed.<br />
Calculations given to us indicate that the overdose was 43% at 9.30 am -9.45 am, but was only 2% from 11.30 am.<br />
(3) The Syntocinon drip was commenced at 9.30 am at a rate of 20 dpm. At 10 am it was increased to 30 dpm and at 10.30 am to 40<br />
dpm (equivalent to 56 dpm of a 10 unit in 1000 mls solution). The doctor's submission said that this was almost the maximum<br />
permissible rate of administration: this was not put in issue in the hospital's submissions.<br />
(4) At 10.30 am Mrs <strong>Simpson</strong> went into labour.<br />
(5) At 11 am, the rate of administration of the Syntocinon was decreased to 30 dpm at which rate it continued until 12 noon.<br />
(6) The foetal heart rate (FHR) was checked periodically using a Pinnards stethoscope. When recorded, it was within normal limits.<br />
There was no record of any observation of the FHR in the hospital notes after 12.45 pm.<br />
(7) The doctor (who had gone to a nearby hospital at Randwick for a surgical list) was called to the hospital, informed of the progress<br />
of the labour, and arrived in the labour ward to see Mrs <strong>Simpson</strong> at 1.30 pm. Mrs <strong>Simpson</strong> was then in pain. The doctor was informed<br />
by nursing staff that there were no abnormalities and that the FHR was normal.<br />
(8) The doctor performed a vaginal examination.<br />
(9) From the nursing staff's assessment using the Pinnards stethoscope, the foetal heart rate appeared to be in the normal range. The<br />
doctor re -checked the position of the head, then attempted delivery with Neville Barnes forceps. This too was not successful. The<br />
doctor performed an episiotomy, and made a second attempt with the Neville Barnes forceps.<br />
(10) At about the time of the second attempt with the Neville Barnes, a doppler was applied to assist FHR monitoring. Following the<br />
second attempt with Neville Barnes, the FHR was heard on the doppler to drop to 100 bpm, but it recovered quickly.<br />
(11) As no descent had been achieved, the doctor decided to use the Kiellands forceps because he felt that he may have made an error<br />
in diagnosing presentation, and that the baby's head may have been in an occipito -posterior (OP) position (rather than, as he had<br />
thought, occipito -anterior (OA)). The doctor applied the Kiellands forceps, rotated the foetus, and applied traction.<br />
(12) During the attempt with the Kiellands forceps, the foetal heart rate was heard to fall to between 60 and 80 bpm where it then<br />
remained. The doctor re-rotated the foetal head, back to the original position. There had been a total of five attempts with forceps to<br />
deliver the baby, over 15 to 20 minutes, without any descent having been achieved. The doctor then decided to proceed to Caesarean<br />
section.<br />
(13) After taking Mrs <strong>Simpson</strong> to an operating theatre, calling an anaesthetist, and preparing for the operation, the Caesarean section<br />
commenced at 2.15 pm. Present during the operation were Dr Williams (anaesthetist), Dr Hakim (assistant surgeon) and Dr Van Vliet<br />
(neo-natologist).<br />
(14) Calandre was delivered in a poor condition at 2.17 pm.<br />
Page 11 of 31<br />
(15) The anterior lip of Mrs <strong>Simpson</strong>'s cervix was later discovered to be missing. [The significance of this is, as the Judge said at<br />
[1375] that this probably occurred during the forceps applications].<br />
(16) At birth, Calandre's glucose level was normal. However, a foetus might have its metabolic reserves depleted or exhausted, but<br />
still have at birth a normal glucose level. The absence of a need for excessive doses of glucose for the first day or so is not a perfect<br />
test and is no more than "an observation in some cases". (See Red Volume 3, 501). It is inconclusive.<br />
(17) <strong>No</strong> meconium staining was observed. The absence of meconium staining is inconclusive as to whether there has been a depletion<br />
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or exhaustion of foetal metabolic reserves.<br />
G. The Syntocinon Argument<br />
78 The doctor's principal argument as ultimately formulated was that it was necessary to find a second cause, an hypoxic cause over<br />
and above any damage caused by the negligent use of forceps. Indeed, there was evidence particularly from Professors Fisk and<br />
Ellwood that it was necessary to find an hypoxic explanation as well as a vagal bradycardia. However, his Honour rejected this view.<br />
79 The doctor says that that second cause is to be found in hyperstimulation of the mother by the hospital administering Syntocinon in<br />
a dose of 10 units in 700 mls in lieu of 1000 mls thus initially increasing the dose by 43%.<br />
80 The effect was, so the argument ran, that hyperstimulation so used the foetus' metabolic reserves that when the forceps caused<br />
bradycardia there were insufficient reserves to recover as would normally happen if there was abuse of a foetus by forceps.<br />
81 The argument was boosted by evidence that more than one of the eminent medical experts said they did not know of any case<br />
where there was unremitting bradycardia brought about by non -hypoxic causes alone.<br />
82 However, there was also substantial evidence from clinicians that they had observed cases where one vagal cause might suffice.<br />
83 His Honour completely rejected the Syntocinon theory. Mr Brereton says that his Honour was in error in doing so. Mr Brereton<br />
says that properly considered the expert evidence of Professors Fisk and Ellwood must have been accepted and was not, when<br />
properly analysed, affected by the view of the clinicians.<br />
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<br />
hypoxic explanation was necessary Professor Elwood's view that that explanation was to be found through the forceps impinging on<br />
or occluding the umbilical cord was to be preferred. However, his Honour did not so find, indeed I believe eventually this was<br />
common ground.<br />
85 The argument was that hyperstimulation brought about by administering Syntocinon in 700 mls in lieu of 1000 mls so used up the<br />
foetus' metabolic reserves that it was unable to replenish when there was vagal bradycardia caused by the last pull of the forceps.<br />
86 At [1414] the learned Judge said that the excess dose of Syntocinon "was clearly capable of producing hyperstimulation as<br />
defined. The question is: 'did it'?"<br />
87 A crucial piece of evidence in this case is the partogram kept by the hospital staff to record the progress of labour.<br />
88 The partogram is printed to record a number of different matters including the Foetal Heart Rate (FHR) and Contraction<br />
Frequency and Duration. It is basically on squared paper with numerals on the left hand side, sometimes adjacent to the lines between<br />
squares and sometimes, as is the case of Contraction Frequency and Duration amidships between the dividing lines.<br />
89 Vertical lines map out the time scale in quarter hour periods for FHR and half hour periods for Contraction Frequency and<br />
Duration.<br />
Page 12 of 31<br />
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<br />
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<br />
the evidence the possibility of that occurring is extremely remote. Mr Hall did not seriously contest this. It is probable that the crosses<br />
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<br />
accurate.<br />
91 The part of the partogram that is of particular importance is contained in Appendix 1. That part shows the "contract frequency and<br />
duration" and the "oxytocic dose".<br />
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<br />
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<br />
reduced to 30 dpm. Dosage at 30 dpm continued until 12 noon.<br />
93 Mr Brereton submitted that the hospital's administration of Syntocinon, contrary to the doctor's instructions, at a rate 43% higher<br />
than the prescribed rate, occurred during the period from 11.00 am to midday. This submission is borne out by the partogram.<br />
94 The partogram is capable of being of even greater significance in regard to the frequency of contractions during the critical period<br />
between 11.00 am and midday.<br />
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<br />
partogram indicates that, between 11.00 am and midday on the day in question, Mrs <strong>Simpson</strong> experienced continuous contractions, or<br />
contractions of 60 seconds each, every two minute period. Mr Brereton submitted, on the other hand, that, during that time, the<br />
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partogram indicates that Mrs <strong>Simpson</strong> experienced contractions of 60 seconds every one to two minutes.<br />
96 I have pointed out that the classic definition of hyperstimulation is five contractions or more in a ten minute period (subject to the<br />
comment in [17] above). The likelihood of hyperstimulation occurring increases as the frequency of contractions within this period<br />
increases.<br />
97 Thus, if Mrs <strong>Simpson</strong> experienced 60 second contractions every one to two minutes in the one hour period from 11.00 am to<br />
midday, that would be powerful evidence of hyperstimulation (as the contractions were then likely to have exceeded five contractions<br />
in every ten minute period over this time).<br />
98 The proposition that contractions occurred for 60 seconds every minute (advanced by Mr Hall) would mean that there would have<br />
been continuous contractions, that is, there would have been no break whatever between contractions. There was evidence that<br />
continuous contractions with no interval between would have been contrary to foetal life. This appears to have been accepted by his<br />
Honour. The partogram does not support such a construction and I would reject it.<br />
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<br />
to 3.00 pm (see Appendix 1).<br />
100 The numbers "1" to "6-10" in the "Contraction Frequency & Duration" section represent time periods measured in minutes .<br />
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<br />
to 10 minutes.<br />
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<br />
the number "5" are to be filled in when the patient has contractions every five to six minutes.<br />
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<br />
five to six minutes between 10.30 am to 11.00 am, Mrs <strong>Simpson</strong> was experiencing contractions that endured for 20 seconds each.<br />
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<br />
patient has contractions every four to five minutes, those to the right of the number "3" when the patient has contractions every three<br />
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<br />
right of the number "1" when the patient has contractions every one to two minutes.<br />
104 Thus, the number "60", where it appears in two places between the 11 am and 12 midday columns, indicates that, every one to<br />
two minutes, from 11 to 11.30 am and from 11.30 am to 12 midday, Mrs <strong>Simpson</strong> was experiencing contractions of 60 seconds each.<br />
105 Further, the number "60", where it appears between the 12 midday and 1.00 pm columns, indicates that, every two to three<br />
minutes from 12 midday to 12.30 pm, Mrs <strong>Simpson</strong> was experiencing contractions of 60 seconds each.<br />
106 In other words, I consider that the natural meaning of the partogram supports Mr Brereton's submissions. The partogram is<br />
compelling evidence that for an hour, from 11.00 am to midday, Mrs <strong>Simpson</strong> experienced contractions of 60 seconds every 1 to 2<br />
minutes. Contractions at such a rate are readily capable of causing hyperstimulation.<br />
107 Mrs <strong>Simpson</strong> testified that, in the period between 11.00 am to midday, she was experiencing contractions of a minute on and a<br />
minute off. Whealy J accepted her evidence on this issue. His Honour dealt with the conflict between her evidence and the partogram<br />
by observing, "the entries in the partogram may have been a simple error later corrected".<br />
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<br />
finding that the partogram contained an error was his Honour's preference for the oral testimony of Mrs <strong>Simpson</strong>. But, as I have<br />
noted, the accuracy of Mrs <strong>Simpson</strong>'s evidence on this issue was inherently suspect as she would have found it extremely difficult to<br />
make precise observations of the duration of her contractions and, in any event, there would have been a small difference in time<br />
between her experience of pain and the start and finish of each contraction.<br />
109 The partogram is evidence emanating from the hospital itself. It is the hospital's own document. It falls to the hospital to establish<br />
that it is inaccurate.<br />
110 The hospital, however, led no evidence to the effect that the partogram was likely to be inaccurate in regard to the duration and<br />
frequency of contractions over the relevant period, it led no evidence rebutting the natural meaning of the partogram and it led no<br />
evidence suggesting that the partogram contained an error. Moreover, the partogram contains no inherent improbabilities or<br />
contradictions in regard to this issue.<br />
111 In the circumstances, I consider that his Honour erred in rejecting the natural meaning of the partogram and in failing to find that,<br />
during the period 11.00 am to midday, 60 second contractions took place every one to two minutes.<br />
H. The Medical Evidence<br />
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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<br />
review the evidence of the doctors in the order in which they were called to give evidence.<br />
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<br />
indicate that there is more than one passage which was read to us three times in the course of the five day appeal hearing.<br />
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<br />
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<br />
shows up the slender factual material on which some opinions were based.<br />
115 Mr Roger Varley Clements, a clinician, notes that he was in considerable agreement with Professor Fisk's report (Blue (4)904).<br />
At Blue (4)922 he says that there are so many uncertainties concerning the Syntocinon regime because of the paucity of hospital<br />
records, that it is difficult to form a clear opinion concerning its use.<br />
"If a court were to find that Syntocinon was continued in excessive dosage beyond 12 noon then I would concede that this may well<br />
have contributed to Calandre's problem in that it may have deprived her of her metabolic reserve, setting up the conditions in which a<br />
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<br />
the Syntocinon in this case. I believe that if the Syntocinon alone were responsible for Calandre's damage, by several hours of<br />
hyperstimulation her brain damage would be of a different type.<br />
"On the balance of probabilities Calandre <strong>Simpson</strong>'s injuries are due to repeated incompetent attempts at vaginal delivery; overdosage<br />
with Syntocinon, if it occurred, may perhaps have made her more vulnerable to that event."<br />
116 The cross examination of Mr Clements went on for some time. The cross examiner was suggesting to Mr Clements that, for<br />
instance, Black (2) 311, having regard to the unexpectedly severe outcome from the application of forceps he should accept that there<br />
was a probability that there was a second force at work being hypertonic contractions of the uterus. Mr Clements said:<br />
"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<br />
part company is the necessity to produce a second pathology to explain the outcome.<br />
"I don't find it necessary to have a second pathology, particularly in circumstances where if a softening up process on the baby were<br />
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<br />
need for the separate pathology. All this conjecture about the dose of Syntocinon and what it might have done is really no more than<br />
that.<br />
"I would need to see some evidence that the baby showed signs of stress, of resources being exhausted, before I could say that was<br />
probable. Of course I allow that it is possible."<br />
117 Mr Clements maintained his view that the failed forceps delivery was of itself a sufficient explanation for the outcome (Black (2)<br />
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<br />
hypertonus.<br />
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<br />
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<br />
medicine. Like Mr Clements, she practised in England. Dr Rennie, at Blue (3) 636 was of the opinion that the plaintiff's brain insult<br />
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<br />
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<br />
plaintiff would have survived intact.<br />
119 In examination in chief at Black (2) 355, Dr Rennie was asked about the significance of rotating the foetal head with Kiellands<br />
forceps and she said:<br />
"It would appear that it was the application of the Kiellands forceps which was temporarily associated with the bradycardia in<br />
Calandre's case. In general, removal of the blades of the forceps allows the bradycardia to recover but, clearly, this did not happen,<br />
either because this was the culmination of a sequence of attempts at operative delivery and previous applications had caused stress to<br />
the foetus, possibly a transient bradycardia which had recovered. ... So it could be that there was repeated head compression and the<br />
final attempt at head compression caused a bradycardia which did not recover. Alternatively, the cord could have become compressed<br />
by the forceps blade because it lay alongside the head. ... ".<br />
At 357 she added:<br />
"If the cord is compressed and bruised, then it could become a permanent reduction but the precise mechanism of this bradycardia, I<br />
suspect, will never be known. We can but speculate as to the possible mechanisms."<br />
120 At 367, in cross examination, Dr Rennie was asked:<br />
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"Q. So is this the position: that excessive Syntocinon can of itself produce a severe and total hypoxic insult?<br />
A. If the foetus is stressed to the point of collapsing solely and only as a result of Syntocinon, that is possible, but one would<br />
anticipate prior changes in the foetal circulation.<br />
...<br />
Q. What causes the collapse is a lack of oxygen supply to the foetus, isn't it?<br />
A. The foetus has got to the stage where there is absolutely no reserve left and the entire circulation collapses.<br />
Q. And excessive Syntocinon, without the help of forceps, can of itself produce a result equivalent to what has been seen in<br />
Calandre's case, can't it?<br />
A. It can, but it would be very exceptional to observe normal foetal heart rate patterns in the run up to this collapse."<br />
121 At 371 the doctor admitted that it is rare to see a forceps delivery which produces a bradycardia which does not recover.<br />
"It is so rare that I'm unable to comment on whether or not that would be associated with physical trauma."<br />
She said she had not seen such a case reported. However, she had experienced head compression from forceps producing bradycardia<br />
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<br />
concluded.<br />
122 At 375 she agreed that she had had experience of cases from which the foetus had not recovered from excessive doses of<br />
Syntocinon. However at 376 the doctor said:<br />
"I do not feel that I need to have, as Professor Fisk, does, an additional reason for the bradycardia".<br />
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<br />
result of repeated attempts at forceps delivery. He thought that a more likely explanation than cord entanglement for lack of<br />
supporting evidence. He did not direct his mind specifically to the problems of Syntocinon but noted that the oxytocin regime can<br />
only be regarded as aggressive, even by 1970s standards (Blue (3) 596). He also noted at Blue (3) 605 that there was no unacceptable<br />
delay in the provision of an operating theatre by the hospital, the decision for caesarean section having been made about 1.55 pm and<br />
delivery achieved by 2.17 pm. In cross examination, Dr Hinde said at Black (6) 1450 that he was worried about the partogram and<br />
wondered whether it had been filled in upside down. He said at 1451 that this partogram was only introduced to the hospital some<br />
months beforehand "and I have found in going through obstetric histories in recent years that there is often confusion and incorrect<br />
entries by midwives."<br />
124 At Black (7) 1656 and following, Dr Hinde was closely cross examined on vagal bradycardia and bradycardia where there was an<br />
hypoxic element at work as well. At 1656 Mr Brereton asked Dr Hinde:<br />
"Q. Distinct from bradycardia caused by hypoxia, ... there is another form of bradycardia, is there not, in which the decelerations tend<br />
to mirror in reverse the contractions?<br />
A. Yes.<br />
Q. And that bradycardia is associated with pressure on the foetal head?<br />
A. Yes.<br />
Q. And so far as we understand it, that pressure on the foetal head stimulates the vagal nerve?<br />
A. Yes.<br />
Q. And the vagal nerve causes a neuronal transmitter chemical to be released which suppresses the foetal heart rate?<br />
A. Yes.<br />
Q. And that is a chemical which has a short half life?<br />
A. Yes.<br />
Q. And when the pressure on the head stimulating the vagal nerve is relieved, that type of bradycardia remits?<br />
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A. Yes.<br />
Q. And that's called commonly vagal bradycardia?<br />
A. Yes.<br />
... ."<br />
There was then cross examination to the effect that vagal bradycardia could be caused by application of forceps, but ordinarily, once<br />
the stimulus is relieved the bradycardia would remit.<br />
125 However, at 1662 Dr Hinde said:<br />
"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<br />
forceps deliveries for long enough, a forceps delivery for long enough, and produce bradycardia as a result of the manipulation, then<br />
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.<br />
...<br />
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<br />
vagal mechanism alone to produce a bradycardia which lasts, a profound bradycardia which lasts for 18 minutes or more?<br />
A. In most cases no.<br />
Q. And that's because the neuronal transmitter, the chemical which causes the decrease in the foetal heart rate, would dissipate and the<br />
foetal heart recover?<br />
A. Yes, but this is the neuronal transmitter which has been produced as a result of the immediate application of the forceps. This, to<br />
me, does not consider the possibility that these repeated attempts have set up a mechanism within the brain which is causing the<br />
vagotonia to persist and hence bradycardia and hence deleterious effect on the foetus.<br />
(1663) Q. Is that speculation, doctor?<br />
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<br />
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<br />
down before such time as you can proceed to the caesarean section.<br />
Q. It may come back up?<br />
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.<br />
Q. And that may be because as well as the vagal bradycardia, there has been some hypoxic element at work as well?<br />
A. Yes.<br />
Q. And indeed, if there were, that would make that result of a persisting bradycardia, much more physiologically understandable?<br />
A. Yes, under those circumstances."<br />
126 At 1665 he continued in that line:<br />
"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<br />
doesn't remit then you get persisting bradycardia on top of any that may have existed in the first place."<br />
Mr Brereton continued his questioning:<br />
"What literature or studies, doctor, are you aware of that deal with a vagotonic response that does not remit?<br />
A. Simply experience that at times where failed forceps have occurred the foetal heart rate remains low with no demonstrable trauma<br />
in the subsequently delivered foetus.<br />
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?<br />
A. But I wouldn't say it was in every case.<br />
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...<br />
(1666) Q. And as I think we discussed earlier, if there were some such hypoxic component that would make a profound unremitting<br />
bradycardia much more physiologically understandable than just a established vagotonic response?<br />
A. Yes.<br />
...<br />
Q. If the foetus's metabolic reserves are depleted then her, or his, vulnerability to a short period of bradycardia from which she might<br />
otherwise have recovered is increased?<br />
A. Yes."<br />
127 At 1675, Mr Brereton asked:<br />
"And if hyperstimulation continues, and the placental villi continue not to be adequately replenished then there will be a progressive<br />
drain on the foetal reserves?<br />
A. Obviously if the foetus has a reduced supply of oxygen, then these things are set in train which will produce acidosis and reduction<br />
of reserves, yes.<br />
Q. Even before producing acidosis, the reserves can be depleted while the foetus's adjustive mechanisms are responding to the<br />
reduced oxygen supply?<br />
A. Yes, that intervenes between the two.<br />
Q. Ultimately once acidosis sets in, then the hyperstimulation can of itself ultimately produce a terminal profound bradycardia?<br />
A. If you have got a very acidotic baby that has been subjected to very frequent contractions, yes."<br />
128 At 1679:<br />
"If there had been a reduction in foetal metabolic reserves but she was not yet acidotic, you would not necessarily expect to see<br />
decelerations indicative of foetal distress at that time, would you?<br />
A. This is essentially a theoretical concept, but my expectation would be if you have a baby which is in a situation of compromise,<br />
then they will respond poorly to intervention and my expectation would be that as soon as you started to do the forceps delivery, I<br />
would have the expectation that you would see an adverse effect on the foetal heart rate."<br />
129 At page 1683, Mr Brereton asked Dr Hinde whether it is "highly probable that during her labour she was contracting at a greater<br />
frequency than permitted the placental villi supplying Calandre to be fully replenished?"<br />
"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<br />
possibility.<br />
Q. And if she was doing that, then the foetal reserves may well have been compromised?<br />
A. If she was doing it, yes.<br />
...<br />
Q. And if that pattern of hyperstimulation plus compromise of the foetal reserves were taking place, then that would make much more<br />
readily explicable the outcome so far as a profound period of bradycardia following the Kiellands forceps is concerned?<br />
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<br />
effect delivery.<br />
Q. And absent such a contributing cause as well as the manipulation with the forceps, we really don't have an acceptable<br />
physiological explanation for a period of bradycardia which exceeded 18 minutes, do we?<br />
Page 17 of 31<br />
A. We mightn't have a physiological explanation but it's well recognised in texts for example on cardiotocography that there are<br />
certain things which will cause a profound alteration in a foetal heart rate pattern in a foetus which has previously shown to be<br />
healthy. One of those things is cord prolapse. Another is abruption of the placenta and the third is intervention, once you attempt a<br />
breech delivery, once you attempt a forceps delivery. These things are recognised as being common causes of an abrupt change in the<br />
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pattern of foetal heart rate and status of the foetus.<br />
...<br />
(1684) Q. So that leaves us with an inadequate explanation for how pressure on the foetal head alone could cause not just a<br />
bradycardia, which it clearly can, but one which lasts for 18 minutes or more?<br />
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<br />
supply coming to the foetus, the foetus is incapable of distributing it satisfactorily to protect its central nervous system.<br />
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?<br />
A. It is just experience that you see this happening.<br />
Q. And I think you have accepted in our discussion that your experience in which you have seen that happening may be because there<br />
is an association between the manipulation and some hypoxic contributing factor?<br />
A. Obviously if a foetus is hypoxic for some other reason it will withstand manipulation less well and hence be more likely to remain<br />
bradycardic.<br />
Q. And such an explanation provides an understandable mechanism by which the outcome in this case, or of the sort that is seen in<br />
this case, could happen whereas the idea of an exclusively vagal cause does not?<br />
A. <strong>No</strong>, I don't think you can reject the concept that manipulation producing a vagal cause, a vagal cause for this can be excluded. On<br />
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<br />
that you have mentioned.<br />
Q. If the vagal mechanism is pressure on the head stimulating a nerve, producing a neuronal transmitter which has a short half life,<br />
then how, once the pressure which stimulates the nerve is removed, could the vagal mechanism continue to produce a bradycardia?<br />
(1685) A. You are right in what you are saying, that the pressure produces the release of a chemical transmitter, but if in this<br />
prolonged episode a further mechanism comes into play, maintaining vagal action, then the question of the short half life of a<br />
chemical transmitter doesn't enter into it if it is still being released.<br />
Q. What further mechanism could come into place to maintain vagal action?<br />
A. What further mechanism is, I think, the fact that you have attempted these multiple manipulations which ... are recognised to cause<br />
a prolonged and severe change in foetal heart rate pattern in an otherwise previously healthy foetus. It is one of the things that can<br />
produce this.<br />
Q. You were saying that perhaps some other mechanism could come into play to maintain the vagal stimulation. What I am asking is<br />
what could that other mechanism, once the pressure is relieved to maintain the vagal stimulation, be?<br />
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<br />
normal way.<br />
Q. That doesn't really provide an explanation for a continued vagal stimulation, does it?<br />
A. Well, if the foetal heart remains low there has to be a continuing vagal action."<br />
130 Professor Fisk said that there was clear evidence of hyperstimulation and (Blue (4) 833):<br />
"In my opinion, Calandre's apparently rapid decompensation and oxygen deprivation in response to the forceps attempts cannot be<br />
explained entirely by her failed forceps delivery. Mrs <strong>Simpson</strong> received a Syntocinon infusion to induce labour that appears to have<br />
been given in both an excessive concentration, and at an excessive infusion rate. There was evidence of uterine hyperstimulation<br />
which, in my opinion, was a direct result of the Syntocinon over -dosage. In my opinion her rapid decompensation at around the time<br />
of the attempted forceps delivery is more probably than not explained by hyperstimulation. This either reduced her reserve to cope<br />
with the stresses of the failed forceps delivery, and/or lead to a tonic contraction which acutely and substantially compromised her<br />
oxygen supply."<br />
131 Professor Fisk is also an English doctor, a Professor of Obstetrics and Gynaecology. There was a long cross examination of<br />
Professor Fisk, but he did not move from the position he had taken in his report.<br />
Page 18 of 31<br />
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<br />
"some degree of foetal hypoxia is a feature of normal labour. With each uterine contraction blood flow in the intervillous space in the<br />
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placenta is impaired and the oxygen supply to the foetus is reduced. These changes are intermittent, and the healthy foetus recovers<br />
well between contractions. Hyperstimulation of the uterus, such as that which may be caused by excessive administration of<br />
Syntocinon producing prolonged tonic contractions without episodes of relaxation during which placental blood flow can return to<br />
normal, can be associated with hypoxia to the foetus."<br />
133 At 680 he said that:<br />
"Considering the baby's condition at birth and afterwards, it is my opinion that it is more likely than not that [tonic uterine]<br />
contractions were present."<br />
Dr Lyneham is a Consultant Obstetrician and Gynaecologist with special interest in reproductive endocrinology. At Black (4) 856 -7<br />
Mr Brereton in chief asked Dr Lyneham, to assume the correctness of Mrs <strong>Simpson</strong>'s evidence that her contractions were one minute<br />
on and one minute off in connection with possible hyperstimulation. The doctor said:<br />
"To an extent, I guess, it lessens the evidence, if by hyperstimulation one means contractions coming more frequently than every two<br />
minutes, but the assessment of contractions by someone in labour, although it can be done with reasonable accuracy, the definition of<br />
hyperstimulation doesn't enjoy such precision, and clearly if the contractions were coming every one minute and 50 seconds rather<br />
than two minutes, by definition that's hyperstimulation but the physiological effect may or may not be all that much different."<br />
The doctor continued later:<br />
"We know that hyperstimulation occurs in 61 per cent of women, according to the Satin study, of people who receive the sort of dose<br />
of Syntocinon that Mrs <strong>Simpson</strong> received. ... 60 second contractions every two minutes that would, at the very least, be borderline<br />
hyperstimulation."<br />
134 Dr Keogh is a staff specialist in obstetrics and gynaecology at Hornsby Hospital who lectures in those subjects at the University<br />
of Sydney. His view was that there was insufficient evidence to find that the doctor was negligent. His evidence does not really affect<br />
the present matter before the Court and we were referred to very little of his oral evidence or cross examination.<br />
135 Dr John Pennington reported at Blue (2) 402 that in his view both the doctor and the hospital acted in accordance with proper<br />
professional standards and contemporary obstetric practices. In re -examination at Black (7) 1731, Mr Brereton put to Dr Pennington:<br />
"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<br />
true. When you answered that question, were you addressing your mind exclusively to a bradycardia caused by a vagal mechanism, or<br />
to some other situation?<br />
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<br />
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<br />
expedite the circumstances."<br />
136 Finally, Professor Ellwood gave evidence for the hospital. Professor Ellwood is a Professor of Obstetrics and Gynaecology at the<br />
Canberra Clinical School, University of Sydney, at its Canberra Hospital branch. In his report at Blue (4) 889, Professor Ellwood<br />
said:<br />
"... in this case the rate of Syntocinon administration was at the limits of the accepted rate and this may have caused a degree of<br />
uterine hyperstimulation as indicated by a tachysystole. Nevertheless, this does not appear to have adversely affected the foetal heart<br />
rate ... .<br />
[890] In conclusion, there is no objective evidence for an effect on foetal condition caused by uterine hyperstimulation either before<br />
midday when the partogram observations cease, or after that time and until the forceps delivery is attempted.<br />
In contrast, there is evidence of a foetal response to the Kiellands rotation, and the possibility of a prolonged bradycardia, which<br />
continued until delivery about 25 minutes later."<br />
137 At Black (7) 1591, Mr Brereton cross examined Professor Ellwood:<br />
"Q. <strong>No</strong>w, I think we discussed this morning but I think you agree that the midwife's targets should be to achieve with Syntocinon<br />
something in the order of three to four contractions in 10 minutes?<br />
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<br />
perhaps an optimal number is about four in 10.<br />
Q. Certainly if the contractions were between five and six in 10 minutes that would be hyperstimulation?<br />
Page 19 of 31<br />
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<br />
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optimal.<br />
Q. And that rate of contraction is sufficient to cause such embarrassment to the foetus as to result in ultimately a profound<br />
bradycardia and permanent brain damage?<br />
A. That depends on the condition of the foetus before the hyperstimulation begins and how long it goes on for.<br />
...<br />
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<br />
consistent with your experience ... during that period to see but subtle changes on the cardiotocograph?<br />
A. Yes, it certainly is in my clinical experience to see those CTG changes occurring.<br />
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<br />
some late decelerations?<br />
A. My own clinical experience would be to see the CTG recover and return to normal once the contraction pattern becomes more<br />
normal.<br />
Q. Can I suggest that it is within your experience, clinical or medico legal, that during the period after an hour of hyperstimulation,<br />
you might continue to see late decelerations?<br />
A. I can't recall seeing a period of hyperstimulation of that duration, once it has been corrected, to continue to cause CTG changes.<br />
...<br />
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<br />
decelerations, one can then have a profound terminal bradycardia?<br />
A. The late decelerations reflect a degree of oxygen desaturation occurring with a contraction. Whether that then continues into<br />
acidemia and then the kind of terminal bradycardia you are describing, would depend on the ability of the foetus to withstand that<br />
oxygen desaturation, and whether or not the reason for the desaturation has been corrected.<br />
Q. And if the foetus's reserves have been sapped by the period of hyperstimulation, then a period of profound bradycardia can result?<br />
A. Yes, that's certainly possible."<br />
138 At 1594, Mr Brereton put that the hyperstimulation can result in a profound terminal bradycardia due to a sapping of reserves.<br />
The Professor replied:<br />
"A. The hypothetical picture that you are painting, I would agree with if the period of uterine tachysystole was sustained and there<br />
was no signs of recovery and resumption of a normal pattern of uterine contractions.<br />
Q. And in that situation the profound terminal bradycardia can itself, in those circumstances in your experience, produce permanent<br />
brain damage or do damage to the basal ganglia?<br />
A. It can certainly cause severe foetal hypoxia and acidemia and the condition of newborn encephalopathy. It is getting outside my<br />
area of expertise to comment on the exact nature of the brain damage.<br />
...<br />
Page 20 of 31<br />
(1595) Q. From that discussion I take it you agree that hyperstimulation produced by excessive Syntocinon usage can of itself result<br />
in a severe hypoxic insult to the foetus?<br />
A. A period of uterine tachysystole, if sustained, can certainly lead to foetal hypoxia. Whether it does or whether it doesn't depends on<br />
the foetal reserve and the duration of the tachysystole."<br />
139 There was considerable cross examination along the lines of that administered to the other medical experts as to the difference<br />
between vagal and hypoxic bradycardia. At 1606, Mr Brereton asked:<br />
... Is this the position then, that though there may well have been a vagal element to that final terminal bradycardia in Calandre<br />
<strong>Simpson</strong>, the duration which it must have had to explain her outcome, is such that in your opinion there must have been a hypoxic as<br />
well as a vagal cause?<br />
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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<br />
to cord occlusion.<br />
Q. Cord occlusion is one possibility that you posit so far as a hypoxic cause is concerned?<br />
A. Yes.<br />
(1607) Q. And another perfectly plausible possibility is that the foetal reserves had been sapped by a period of hyperstimulation?<br />
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<br />
clinical experience I would expect the foetus with normal reserve to have tolerated that period of hyperstimulation and to have<br />
recovered.<br />
...<br />
Q. One thing I guess is clear after the discussion we have had, that one thing we can now exclude following our discussion this<br />
afternoon, is the idea that vagal bradycardia alone, attributable to a series of five pulls with forceps, caused this terminal bradycardia?<br />
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<br />
second attempt with the Neville Barnes forceps and that would suggest a normal vagal response and then recovery. Because we don't<br />
have a continuous heart rate recording throughout the whole episode, I would find it hard to completely agree with your statement. I<br />
think we do have the likely possibility of recurrent vagal stimulation with the recurrent attempted forceps delivery. Whether the<br />
accumulation of that vagal stimulation has contributed to the terminal bradycardia, I think it is possible.<br />
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<br />
bradycardia alone, even the accumulation, cannot fully explain the bradycardia of 18 to 25 minutes which ensued?<br />
A. I would find it hard to accept that it was vagal alone.<br />
Q. And even allowing for the accumulation of five attempts on the probabilities in your opinion, there must have been a hypoxic<br />
cause as well?<br />
A. I think there must have been a contributing cause. By the term hypoxic cause I wouldn't necessarily mean that there was foetal<br />
hypoxia before the bradycardia occurred. I don't quite understand the mechanism of bradycardia that occurs with cord occlusion. It<br />
may well be more complex than simply reducing blood flow and reducing oxygen supply, but I certainly do accept the argument that<br />
there is likely to have been some additional mechanism other than vagal stimulation and if that involves the cord, then ultimately<br />
there is a component of that which is hypoxic.<br />
Q. And the alternative explanation for the cord is over-stimulation of the uterus and a sapping of the foetal reserves as a result?<br />
A. That is a possible explanation. ... but I find the gap between the period of apparent tachysystole and the prolonged bradycardia<br />
difficult to explain if there was prolonged hypoxia throughout that whole period of time. ...".<br />
140 At p 1614, Mr Brereton asked:<br />
"Do you agree that although traction on the cord during rotation might cause temporary reduction in blood flow and foetal<br />
oxygenation you would expect to see a degree of recovery once that traction was released?<br />
Page 21 of 31<br />
A. In the hypothetical situation where a rotation has caused some cord compression, I wouldn't use the word traction, traction in itself<br />
I don't think would cause the bradycardia but where it has caused some compression and if that compression is completely reversed<br />
then I would expect to see recovery.<br />
The exception to that may be that if ... there are already other factors that could lead to bradycardia such as vagal stimulation and the<br />
compression continues for a long enough period of time then the foetus may not be able to recover. There may be a combination then<br />
of hypoxia, vagal stimulation, the two things together, could lead to ongoing bradycardia.<br />
(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<br />
occlusion resulting from cord tension from the rotating manoeuvre?<br />
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<br />
of cord ...<br />
(1623) Q. What are you talking about, Professor, when you speak of the most likely version of cord involvement in this case being a<br />
partial occlusion due to rotation, what do you have in your mind in terms of percentage reduction in blood flow by that?<br />
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A. Anywhere between nought and a hundred per cent.<br />
Q. Well a hundred per cent isn't partial?<br />
A. A hundred per cent is complete. I have no way of knowing.<br />
Q. And nought is no occlusion at all?<br />
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<br />
mechanism whereby the cord is compressed during the rotation, I have no way of knowing what degree of compression has occurred,<br />
what degree of occlusion has occurred.<br />
(1626) Q. Professor, if I can approach it this way, yesterday I think we agreed that as well as the vagal mechanism for this<br />
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<br />
mechanism at work also?<br />
A. Yes.<br />
Q. If that hypoxic mechanism was, as you posit, cord compression attributable to the rotational manoeuvre, what I am suggesting is<br />
that it is unlikely, not impossible but unlikely, that that manoeuvre and that that cord compression to have produced a sufficient drop<br />
or a sufficient level of foetal acidosis to sustain the bradycardia before it would have remitted from its vagal cause, before the vagal<br />
aspect would have remitted?<br />
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<br />
think it's quite possible that the vagal mechanism could go on for sufficient time for the hypoxic mechanism to then continue to cause<br />
the bradycardia.<br />
Q. Are you suggesting that the vagal mechanism could continue for five to ten minutes?<br />
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<br />
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,<br />
four minutes there could be sufficient cord occlusion to then have caused sufficient hypoxia for that mechanism to then take over.<br />
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<br />
had been removed?<br />
A. <strong>No</strong>, it's not unlikely in the extreme. I have certainly seen bradycardias continue for that period of time. With respect I said two,<br />
three, or four, I didn't say five.<br />
Q. That's why I was asking about five. I can accept your two, three or four?<br />
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<br />
long period of time, up to ten minutes I have seen.<br />
Q. With no hypoxic component?<br />
A. Yes, with no hypoxic component.<br />
Q. You can be quite confident there was no hypoxic component in that?<br />
A. Yes, the baby was born with no abnormal blood gases."<br />
Page 22 of 31<br />
I believe I have set out enough of the cross examination to give the flavour of Professor Ellwood's evidence. I will merely set out one<br />
more piece of evidence at Black (7) 1631 as to how far a woman who had been anaesthetised with an epidural anaesthetic might be<br />
aware of her contractions. Professor Ellwood said:<br />
"I think whether we have a complete or a partial epidural anaesthetic it would interfere with a woman's perception of the duration of<br />
her contractions."<br />
141 The only other medical evidence I need refer to is what is known as the Satin study. There were two studies by Dr Satin and<br />
others on high versus low dose oxytocin, one printed in July 1992 printed in Blue (2) 408 and the other in August 1993, Blue (3) 512.<br />
142 Mr Brereton pointed out that the dose of Syntocinon administered to the plaintiff's mother was faster and harder than any of the<br />
regimes that were there studied.<br />
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143 The first Satin study considers that a conservative definition of hyperstimulation is contractions of two minutes duration or<br />
greater or six or more contractions in ten minutes.<br />
144 The Satin studies generally note that there are potential advantages if a high dose of oxytocin is administered, but that such doses<br />
are associated with the undesirable side effect of hyperstimulation.<br />
I. The Trial Judge's Findings<br />
145 The learned trial judge carefully examined the medical evidence from approximately para [1170] onwards.<br />
146 I will examine what his Honour found in more detail shortly. However, it can be summarized by saying that his Honour generally<br />
preferred the observations of clinicians to the scientific theories of foetal physiologists. See particularly [1441] -[1442] set out below.<br />
147 At [1289] his Honour correctly noted that it was important for him as a tribunal of fact to keep steadily in mind that he needed to<br />
reach a level of "actual persuasion" in reaching factual conclusions. He cited Seltsam Pty Ltd v McGuiness (2000) 49 NSWLR 262,<br />
284, para [136].<br />
148 At [1402] his Honour turned to the final evaluation of the Syntocinon argument. He said:<br />
"I am neither persuaded nor satisfied that hyperstimulation occurred. To the extent that any degree of hyperstimulation may have<br />
occurred, I am not satisfied that any damage was occasioned to Calandre or that her foetal reserves were diminished or affected in any<br />
way whatsoever. Indeed, I am positively persuaded that there was no abnormality in the FHR associated with hyperstimulation and<br />
that Calandre, as a foetus, did not suffer any depletion of foetal metabolic reserves prior to Dr <strong>Diamond</strong>'s arrival at the hospital."<br />
He then found that the injury was caused solely by the doctor's negligent use of forceps.<br />
149 His Honour then further considered the Syntocinon argument at [1424]. He said:<br />
"There are further reasons which support and confirm my belief that there was no hyperstimulation in this case and no depletion of<br />
the foetal reserves consequent upon the excessive dose of Syntocinon. These are, first, the conviction that Dr <strong>Diamond</strong>'s negligent<br />
acts were plainly sufficient of themselves to have occasioned Calandre's injuries without the need to resort to an additional or<br />
contributory cause. This conviction, in turn, is based upon the acceptance of the hospital's argument that there is, notwithstanding the<br />
rarity of the situation, an acceptable and well understood mechanism involved in the plaintiff's injury; and the rejection of the first<br />
defendant's argument that the injury in inexplicable or unlikely without the existence of a contributory cause.<br />
150 Mr Brereton in my view rightly submitted that [1424] poses the wrong question. The real question was whether the hospital's<br />
actions also had causal consequences to the plaintiff.<br />
151 The Judge continued at [1425]:<br />
"Secondly, there is my satisfaction with the proposition advanced on the hospital's behalf that, despite the poor record keeping<br />
involved, there was adequate monitoring by the nursing staff of the baby's foetal heart and that there was, throughout the entire<br />
period, no abnormality detected. This, in turn, persuades me that the nursing staff's acceptance of normality was entirely justified. I<br />
am also satisfied that Dr <strong>Diamond</strong> was entitled to be satisfied, based on his own observations, that the FHR and contraction patterns<br />
were normal. These matters provide additional reasons negating the presence of any depletion of the foetal metabolic reserves. There<br />
is further support in the expert opinions of Dr Rennie, Dr Hinde and Mr Clements. Although the first defendant's case adverted to a<br />
possibility that there may have been present a depletion of foetal reserves but that this may not have been detectable or in fact<br />
detected especially between 1240 and 1350, I am not persuaded that this is so."<br />
152 With respect these statements do not fairly reflect the evidence as a whole. The hospital records, particularly the partogram, do<br />
show matters of concern. Further, the support of the evidence of Drs Rennie and Hinde and Mr Clements really does not lead to any<br />
strong view against the Syntocinon argument.<br />
153 Whealy J continued at [1426]:<br />
"Dr <strong>Diamond</strong>'s negligence<br />
Page 23 of 31<br />
"The starting point is Dr <strong>Diamond</strong>'s admission of liability. It must not be overlooked that, although the issues in the cross -claim have<br />
made it necessary to identify precisely the negligence involved, the plain fact is that the negligent 'manner, timing and circumstances<br />
of use of forceps' have been admitted."<br />
154 Again Mr Brereton correctly says that the learned judge misdirected himself. In proceedings for contribution, there is no warrant<br />
for starting the fact finding exercise from the doctor's admission of negligence. The vital question is the consequence of the hospital's<br />
negligence.<br />
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155 The learned judge then spent some time discussing why in his view the doctor's actions must have been negligent. He then<br />
continued at [1434]:<br />
"A circumstance then occurred that was important. The Doppler was applied probably about the time of the second pull with the<br />
Neville Barnes although it may have happened a little earlier. It appears that, following the second Neville Barnes application, there<br />
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,<br />
an adverse reaction to the instrumental attempts. Secondly, the recovery of the heart rate almost immediately points very strongly<br />
against any suggestion of depletion of foetal reserves. This was the point made with considerable effect by Dr Hinde whose evidence<br />
in this regard I found compelling. He had said that if there had been embarrassment of the foetus over the preceding two or three<br />
hours as a consequence of hyperstimulation, there would have been a fall in the foetal heart rate as soon as the forceps were used,<br />
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<br />
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<br />
compelling observation. If there were this substantial depletion of metabolic reserves within the foetus, why was its displeasure not<br />
shown as soon as the instrumental attempts commenced? In my opinion, this was a telling point against the Syntocinon argument."<br />
156 This critical finding which is a foundation of the hospital's case needs to be closely examined.<br />
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<br />
which showed a constant foetal heart rate of 140 bpm. As have stated, there is evidence that such a constant heart rate was highly<br />
improbable and the likely purpose of recording a constant foetal heart rate of 140 bpm was to indicate that it fell within the normal<br />
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<br />
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<br />
of forceps.<br />
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<br />
there was no fall in the foetal heart rate as soon as the forceps were used.<br />
159 Accordingly, in my view the force of the point which Whealy J regarded as "telling" against "the Syntocinon argument" is very<br />
much diminished.<br />
160 I agree with Mr Brereton that when one realizes this the force of the point being made is very much diminished.<br />
161 I should now briefly deal with the Judge's assessment of the expert medical witnesses which commences at [1437]. His Honour<br />
noted that the argument advanced by Professor Fisk, Dr Lyneham and Dr Keogh was that failed forceps attempts on their own were<br />
insufficient to explain the outcome, whereas Mr Clements and Dr Rennie and Dr Hinde took the opposite view with Professor<br />
Ellwood noting that an additional hypoxic element was necessary. His Honour said at [1440]:<br />
"In relation to the circumstances of this case, I am quite satisfied that the views expressed by the experts called on behalf of the<br />
hospital are correct. The views expressed by Mr Clements and Dr Rennie were very compelling. They were views derived from their<br />
own experience applied to the very unusual circumstances of the forceps applications and attempts in this case. Mr Clements was<br />
branded as an advocate in the first defendant's submissions. I did not find him to be so. I thought his evidence was carefully<br />
considered and well-balanced. Moreover, he brought to bear considerable experience and a high degree of intellectual rigour.<br />
Although Mr Brereton was critical in a number of respects in relation to the views of Mr Clements and Dr Hinde, a careful<br />
consideration of their evidence leads me to the conclusion that their evidence supports entirely the hospital's case.<br />
[1441] Dr Hinde, in particular, brought to bear on the issue, a lifelong breadth of clinical experience. ... In most cases it was his<br />
observation that bradycardia would remit. But in some it did not. He also stated, that there were occasions where, although no signs of<br />
external trauma were noticeable on the foetus, the manipulation had induced a quite marked bradycardia and hypoxia in the foetus.<br />
[1442] Mr Brereton SC endeavoured to confound Dr Hinde with the literature. ... <strong>No</strong>twithstanding this, he repeated that, based on his<br />
clinical experience, on rare occasions in circumstances where there had been a failed forceps ...the intervention appeared to have set<br />
up a persisting bradycardia.<br />
[1443] I was very much persuaded by the evidence of Dr Hinde. ... Mr Brereton did not seek to brand Dr Hinde as an advocate.<br />
Rather, he suggested that his views were outweighed by the evidence of the foetal physiologists.<br />
Page 24 of 31<br />
[1444] Professors Fisk and Ellwood were the two foetal physiologists called to address the issue. I prefer Professor Ellwood's views<br />
to those expressed by Professor Fisk. Although I gained considerable assistance from Professor Fisk's excellent report, I cannot say<br />
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 -<br />
examination would, I think, convince the reader that he was not prepared to make the most reasonable of concessions even when it<br />
was plainly the case that such a concession was called for.<br />
[1445] On the other hand, I found Professor Ellwood's approach to be both reasonable and convincing. It is true that he believed it<br />
was necessary to find a hypoxic element as well as the presence of vagal bradycardia. To that extent, he differed from Mr Clements<br />
and Dr Hinde. As a foetal physiologist, he was no doubt searching for scientific certitude. To the extent that a hypoxic element was<br />
necessary, he had no difficulty in accepting that it may well have arisen from the forceps impinging on or occluding the cord. ... It<br />
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was perfectly possible, indeed quite likely, that, during the instrumental attempts, a hypoxic element was set in force in addition to the<br />
bradycardia caused by the forceps applications.<br />
[1446] Importantly, Professor Ellwood said he had no difficulty with the proposition that there were two concepts operating at the<br />
same time but both related to the forceps use.<br />
[1448] In my opinion, Professor Ellwood and Dr Hinde were really describing the same thing. From the perspective of the foetal<br />
physiologist however, there was a need to be satisfied, as I have said, with a degree of scientific certitude. The experienced clinician<br />
is not necessarily as concerned with such niceties of precision. He knows what he has seen. Dr Hinde as an experienced obstetrician<br />
simply based his observations on his lifelong professional experience. He did not seek scientific certitude he simply knew as a matter<br />
of experience that failed forceps were sufficient to explain the mechanism. Dr Rennie had observed the same thing in clinical<br />
situations. She said, quite sensibly that the precise mechanism might never be known."<br />
162 Mr Brereton strongly criticises that method of approaching the problem. He says that the doctor is suing for contribution. He is<br />
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<br />
plaintiff. The scientific evidence, both by Professor Fisk and by Professor Ellwood, complete with reasons, was that one needs a<br />
second and hypoxic cause for the terminal bradycardia which caused the plaintiff's problems. The clinicians said that they had not<br />
always observed this. That, however, was no answer to the scientific evidence.<br />
163 As Mr Brereton put it in his closing address:<br />
"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<br />
second cause.' They don't deny the possibility of a second cause."<br />
164 He thus puts that the doctor had established that a second cause was necessary.<br />
165 The only two possible second causes were hyperstimulation and cord occlusion. There was acceptable evidence of<br />
hyperstimulation, particularly that provided by the partogram. On the other hand, the evidence about cord impingement doesn't begin<br />
to approach that sort of level and never gets beyond the level of a speculative possibility. Accordingly, Mr Brereton argues, the appeal<br />
must be allowed and the hospital ordered to contribute to the damages which the doctor has to pay to the plaintiff.<br />
166 For reasons which I will go into more fully in section M, that argument has a great deal of appeal.<br />
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<br />
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<br />
experience and knows what he's seen. The basis for Dr Hinde's view was not supported.<br />
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.<br />
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<br />
reasons are made out.<br />
J. Problems with Multiple Causes<br />
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<br />
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<br />
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<br />
contribution, the inquiry must go further.<br />
171 Mr Brereton commenced his submissions on this point by reference to Burrows v The March Gas & Coke Company (1870)<br />
LR 5 Ex 67 (Full Bench of Exchequer) and (1872) LR 7 Ex 96 (Exchequer Chamber). The facts were that a gas company contracted<br />
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<br />
under the contract into the plaintiff's shop where an employee of the gasfitter went into the shop carrying a lighted candle and an<br />
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<br />
behalf of the gasfitter's employee in carrying a lighted candle. The plaintiff sued the gas company alone and recovered a verdict. The<br />
defendant gas company was not relieved by the negligence of the gasfitter's employee. However, the court ventured the view that the<br />
gasfitter would also have been found liable to the plaintiff.<br />
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<br />
was a pillion passenger on Kerwood's motor cycle. Kerwood did not know the road and the parties had agreed that Avery, who was<br />
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<br />
off the road, Avery braked, Kerwood collided with Avery and the plaintiff was injured. Avery was held liable to the plaintiff.<br />
173 Another motor bike case, very similar to Sharp v Avery, is Smith v Harris [1939] 3 All ER 960.<br />
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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<br />
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<br />
lights. Shortly before 3 am The Koursk got out of position and was observed heading for The Clan Chisholm which hard -a-ported but<br />
did not reverse her engines. There was then a collision between The Koursk and The Clan Chisholm, and within about a minute there<br />
was a second collision between The Clan Chisholm and The Itria which sank. The Itria then sued The Clan Chisholm and The<br />
Koursk. The court held that The Clan Chisholm and The Koursk were not joint tortfeasors, they were concurrent tortfeasors, and each<br />
was liable to The Itria.<br />
175 In each of these cases, the court did not consider that the negligence of the third party involved was a novus actus interveniens,<br />
but rather that the parties were concurrent tortfeasors.<br />
176 In Bonnington Castings Ltd v Wardlaw [1956] AC 613, 621, Lord Reid said:<br />
"I cannot agree that the question is: which was the most probable source of the respondent's disease, the dust from the pneumatic<br />
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<br />
real question is whether the dust from the swing grinders materially contributed to the disease."<br />
177 In the case of concurrent tortfeasors, each is liable to the plaintiff and under the provisions of s 5 of the Law Reform<br />
Miscellaneous Provisions Act 1946, each is liable to make contribution to the other as each is a person who would, if sued, have<br />
been liable to the plaintiff.<br />
178 I will need to return to this in section K.<br />
K. Resolution of the Issues<br />
179 There are three major matters to consider, viz:<br />
A. Is it more likely than not that more than a vagal cause brought about the plaintiff's injury?<br />
B. Was that additional or contributory cause more likely than not to be brought about by the overdose of Syntocinon?<br />
C. If an additional or contributory cause is to be sought, is that cause more likely than not to be cord occlusion or impingement?<br />
180 In my view the answers to these questions are A. Yes; B. Yes; C. <strong>No</strong>. I will give my reasons.<br />
181 A. As Mr Brereton has submitted, the outcome and events are much better explained by two concurrent events, one of them<br />
hypoxic than by one vagal cause only.<br />
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<br />
scientists. I have already set out [1448] of the judgment where his Honour contrasted the scientist who required a great degree of<br />
scientific certitude with the experienced clinician of lifelong experience who knows what he has seen.<br />
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<br />
not give enough emphasis to evaluating the scientific evidence. He permitted himself to do that because he made the error of<br />
accepting that because clinicians did not always observe phenomenon X in connection with happening Y, even though the scientific<br />
evidence points strongly to this being the case, one can find as a fact that phenomenon X was not essential in happening Y.<br />
184 I have probably spent sufficient time discussing the problem. The bottom line is that the scientists said that a second hypoxic<br />
cause is to be expected for this event. The only contrary position was from clinicians who said that they had not always observed such<br />
a second cause. This, however, does not negate the expert evidence. The judge should have accepted it and held that it was more<br />
likely than not that a second hypoxic cause was present.<br />
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<br />
a second, hypoxic cause of the terminal bradycardia was present.<br />
186 B. Does the evidence show that that hypoxic cause was more likely than not the excessive dose of Syntocinon?<br />
187 Mr Hall says that the "specific facts" that the appellant bore the onus of establishing and was required to establish included:<br />
(a) Administration of the Syntocinon solution (in terms of volume and concentration) without regard for uterine contraction and not<br />
titrated against them.<br />
(b) Administration of the Syntocinon solution in a manner that produced hyperstimulation of the maternal uterus.<br />
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(c) The continuation of hyperstimulation at a level and over a period of time sufficient to give rise to an abnormal pattern of uterine<br />
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contractions.<br />
(d) The continuation of an abnormal pattern of uterine contractions over a period of time such as to produce foetal distress with<br />
abnormality in foetal heart rate.<br />
(e) That foetal distress consequent upon an abnormal contraction pattern resulted in a depletion of foetal metabolic reserves rendering<br />
the foetus vulnerable to hypoxia by non-trial forceps attempts.<br />
188 Whilst this may be correct in a technical sense, the matter is not so black and white in the circumstances of this case as the<br />
records, which were under the hospital's control, were not in the best of state.<br />
189 The evidence discloses that there was an overdose of Syntocinon. It shows that such an overdose probably will bring on<br />
hyperstimulation. The partogram evidence shows to my mind that there was hyperstimulation. The evidence of other hypoxic causes<br />
is merely speculative (see below). Thus, on the balance of probabilities, the second, hypoxic, cause was the overdose of Syntocinon.<br />
190 C. Mr Brereton says that if the Court comes to the conclusion that there was an hypoxic cause it is for the defendant to show that<br />
that cause was cord impingement. He says that it is clear that in such circumstances the evidentiary onus passes to the defendant:<br />
Watts v Rake (supra) at 159-160; Purkess v Crittenden (1965) 114 CLR 164, 168 and Shorey v P T Limited (supra).<br />
191 What Mr Brereton puts is correct. However there is no real need to delve into these matters. As I have said:<br />
(1) The partogram evidence is strong.<br />
(2) The contrary evidence (ie the evidence of the clinicians and the staff) is weak.<br />
(3) The scientific evidence is that one needs to find an hypoxic cause.<br />
(4) The Syntocinon theory provides that cause.<br />
(5) The partogram supports it.<br />
(6) The evidence on the only other possible hypoxic cause, cord occlusion is weak.<br />
(7) Thus, on the balance of probabilities the hospital's negligence in administering an overdose of Syntocinon was a cause of the<br />
injury.<br />
192 In my view we must uphold these submissions. The doctor, being in loco plaintiff is entitled to say to the hospital as the plaintiff<br />
would have said:<br />
"You have been negligent in the administration of Syntocinon as found by the Judge. <strong>No</strong>t only was the dosage higher than the<br />
prescribed rates, it was administered in such a way that it was received more rapidly than it should have been. Both the starting dose<br />
and increments are important in the association between aggressive Syntocinon regimes and possible hyperstimulation. Mrs <strong>Simpson</strong><br />
(as the Judge found) "was not a candidate for a high dose of Syntocinon". The plaintiff was injured. The dosage of Syntocinon<br />
administered by the hospital was prima facie capable of causing hyperstimulation; therefore Syntocinon was prima facie capable of<br />
causing the injury. Therefore the evidentiary onus is on the hospital, to show that the excessive dose of Syntocinon did not cause the<br />
injury."<br />
193 As I have already noted, although the Judge wavers towards cord occlusion in [1445] -[1447] of the judgment, he did not find<br />
cord impingement. One would have expected that had he wished to make such a finding, he would have made it explicitly.<br />
194 Mr Hall put that none of the experts ruled out the possibility of cord impingement or occlusion as the additional hypoxic element<br />
if one were required. He says that Dr Pennington initially opined cord entanglement as the most likely explanation for the failed<br />
forceps delivery and foetal distress. Professor Fisk acknowledged the possibility. Even Dr <strong>Diamond</strong> noted that the cord was tightly<br />
wrapped around the plaintiff's body or neck.<br />
195 As I have already noted, Professor Ellwood at Black (7) 1606 noted that cord occlusion is one possibility for the hypoxic cause.<br />
196 Mr Brereton submits that in the light of Professor Ellwood's cross examination, particularly the passages at Black (7) 1622 -3<br />
which I have set out above, the evidence of Professor Ellwood as to cord occlusion does not rise above speculation. I agree.<br />
197 Having given reasons on the major points, I should give brief mention to other matters highlighted in Mr Brereton's submissions.<br />
198 Mr Brereton called attention to four submissions which were really red herrings. These were:<br />
(a) That the Syntocinon theory was a revised theory which had to be altered to fit the evidence.<br />
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(b) That the doctor's submissions rely on the hospital's experts and not his own.<br />
(c) That the doctor was grossly negligent.<br />
(d) That, as the trial judge found, there was "no evidence" that the contraction frequency was something higher than one every two<br />
minutes, leading to the rejection of the possibility that there was a greater contraction frequency.<br />
199 As to these even if (a) and (b) are correct in fact, I agree that they are irrelevant.<br />
200 As to (c), whilst this may be an issue on the cross claim, it has no relevance as to whether there were concurrent causes of the<br />
plaintiff's injury.<br />
201 As to (d), the partogram evidence to which I have already referred shows its error.<br />
L. The <strong>No</strong>tice of Contention<br />
202 The notice of contention raised the point that his Honour's finding could be justified on other grounds. There were various<br />
matters raised in the notice which is set out on Red (3) 726, the basal submission is that his Honour erred in failing to find that the<br />
cross claimant's conduct amounted to gross negligence constituting a novus actus interveniens.<br />
203 The problem is that ordinarily a plaintiff who is injured must seek to mitigate her damage and if, as a result of seeking medical<br />
treatment for an injury, the injury is in fact made much worse, then that can be laid at the feet of the defendant. However, if the<br />
treatment obtained is so completely outside the bounds of what any reputable medical practitioner might do ( Lawrie v Meggitt<br />
(1974) 11 SASR 5, 8), then:<br />
"It is proper to regard the exacerbation of the plaintiff's condition as resulting solely from the grossly negligent medical treatment or<br />
advice, and the fact that the plaintiff acted reasonably in seeking and accepting the treatment or in following the advice will not make<br />
the original tortfeasor liable for that exacerbation."<br />
(Mahony v J Kruschich (Demolitions) Pty Ltd (1985) 156 CLR 522, 530).<br />
Mr Hall also relied on March v E & M H Stramare Pty Ltd (1991) 171 CLR 596, 517.<br />
204 Mr Hall submitted that in this case the negligence of the hospital was not itself a direct or indirect contributing cause of the<br />
intervening conduct of the doctor and he referred to Medlin v State Government Insurance Commission (1995) 182 CLR 1, 6. He<br />
put that the damage caused to the plaintiff by the gross negligence of the doctor was too remote from any conduct of the hospital and<br />
such a gross act of negligence and the resultant catastrophic injury to the plaintiff was not a foreseeable consequence of the conduct<br />
of the hospital.<br />
205 As his Honour said at [1457], it was unnecessary for him to consider this issue in the light of the fact that he has found against the<br />
doctor in relation to all the allegations made against the hospital.<br />
206 Mr Brereton's basic reply was, as he says at Orange (2) 250:<br />
"The defence of novus actus interveniens was not made out: the case is not one to which it applies, because it is one of concurrent,<br />
and not supervening, causes."<br />
However, as a fallback position, Mr Brereton puts that in any event the doctor's treatment did not have the requisite quality of<br />
gratuitous aggravation which might exonerate the original tortfeasor.<br />
207 I have already analysed the relevant cases and in my view Mr Brereton's submission is correct.<br />
208 Even if this were incorrect, I would agree with the submission at Orange (2) 255 that there was never any hint of any<br />
contemporary criticism of the doctor's management of the case by medical, nursing or administrative staff of the hospital, nor of any<br />
other investigatory procedure of substandard practice. Accordingly, in my view the point made by the notice of contention fails.<br />
M. Collateral Matters<br />
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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<br />
of the cross claim shortly before the trial commenced. I have already outlined the way in which the cross claim for contribution came<br />
to be presented and amended. Mr Hall says that the cross claim as originally filed simply repeated the allegations made by the<br />
plaintiff against the hospital, and that there was no allegation that any treatment provided by hospital staff themselves was in any way<br />
deficient. There was no hint of this until 1999 and the cross claim was not formally amended until 2 March 2001. The hospital<br />
contends that the death of Sister Ranclaud irremediably prejudiced the hospital's ability to answer the allegations made in the<br />
amended cross claim. The hospital acknowledges the difficulty of appealing against a discretionary judgment, but notes that when the<br />
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appellate court is convinced that the trial judge's discretion has miscarried resulting in an injustice, it is the appellate court's duty to<br />
intervene: Cohen v McWilliam (1995) 38 NSWLR 476, 492 and Tzouvelis v Victorian Railway Commissioners [1968] VR 112,<br />
139-140.<br />
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<br />
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<br />
deprived of an opportunity to adduce evidence on the relevant issues: FF Seeley <strong>No</strong>minees Pty Ltd v El Ar Initiations (UK) Ltd<br />
(<strong>No</strong> 2) (1990) 55 SASR 314, 315. Whealy J erred in determining that Sister Ranclaud's death did not substantially prejudice the<br />
hospital. He was under a misapprehension of fact that there were other hospital staff who would be available to assist in the hospital's<br />
defence, and indeed, applied the wrong principle, comparing the prejudice to the doctor and the prejudice to the hospital. He was also<br />
under the misapprehension that there was no greater prejudice to the hospital as a result of the application having been made in 2001<br />
or 1999 that if it had been made immediately after Sister Ranclaud's death in 1993. Indeed, it is put there was additional prejudice<br />
because in the intervening eight year period between Sister Ranclaud's death and the application to amend, the hospital continued to<br />
suffer the type of "presumptive prejudice" described by McHugh J in Brisbane South Regional Health Authority v Taylor (1996)<br />
186 CLR 541, 551, arising from the further deterioration in recollection and ability to recognise the significance of the relationship<br />
between events.<br />
211 Mr Brereton's riposte was that it was inappropriate to argue by analogy with the approach to extensions of time under the<br />
Limitation Act 1969 that the amendment should not have been permitted because of prejudice occasioned by Sister Ranclaud's death.<br />
This was not an application for an extension of time and no limitation question was involved. Prejudice resulting from declining<br />
memories and loss of witnesses does not count against an amendment which does not involve any extension of the limitation period.<br />
Surely it could never be argued that there could be no amendment at any time after Sister Ranclaud died, because she could have died<br />
at any time after the original cross claim was filed.<br />
212 In any event, Mr Brereton says, that the Judge's conclusion that the hospital was far from going into battle defenceless and<br />
unarmed was correct. The Judge was entitled to conclude, as he did, that the hospital should be in the position to adduce relevant<br />
evidence from other witnesses, tender the statement of Sister Ranclaud, and adduce expert evidence.<br />
213 Mr Brereton also points out that although the action was commenced many years previously, there was no exchange of expert<br />
reports on liability issues until 1998. So the first time the parties started exchanging experts' reports on liability was that year. The<br />
cross claim was mooted in 1999, and there was absolutely no reaction until 26 February 2001.<br />
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<br />
for his judgment. I cannot see any appealable error in the approach taken by his Honour, and indeed, there is something in what Mr<br />
Brereton says that the cross appellant's submissions do confuse principles to be applied in cases of amendments after limitation<br />
periods with cases of simple amendment. Accordingly, the cross appeal should be dismissed.<br />
N. The Result of the Appeal<br />
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<br />
seeing how they reacted under cross examination.<br />
216 However, when one analyses the situation more closely, the real decision to be made is somewhat different.<br />
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217 It may be that I have quoted more of the transcript than was, strictly speaking, warranted. However, I consider it necessary to do<br />
so in order to get the full flavour of the evidence of the various medical experts.<br />
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<br />
defendant's negligence could have been the cause of the plaintiff's injury. The Judge accepted that there was an excessive dose of<br />
Syntocinon. The scientists, on both sides, markedly Professor Fisk and Professor Ellwood have said that they would expect to find a<br />
second hypoxic cause for a continuing bradycardia.<br />
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<br />
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<br />
Honour seemed to suggest that there was some dichotomy in the view of the scientist on the one hand, and the practical man and<br />
woman dealing with situations on the ground who are not worried so much about theoretical causes. His Honour seemed to suggest<br />
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,<br />
applying common sense, one prefers the practice as witnessed by the practitioner to the theory of the scientist.<br />
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<br />
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<br />
have observed a second cause, does not negate the scientific opinion.<br />
221 Once that is accepted, and once it is accepted that, as I have indicated earlier, the learned trial judge excluded the middle when<br />
finding that the Syntocinon theory could not have any grounds, one is left with the situation where the quasi plaintiff has shown that<br />
the overdose of Syntocinon could well have caused the injury. The evidentiary onus then shifts to the defendant. The evidence as to<br />
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the hypoxic factor being the occlusion of the cord is not sufficiently supported by the evidence. Accordingly, the cross claimant must<br />
succeed.<br />
222 The cross claimant claims 50% contribution. He does that mainly on the basis that by analogy with the principle quality is equity,<br />
so where there is little material to distinguish between the contributions the same applies at common law. Mr Hall was aghast at this<br />
suggestion and submitted that if the hospital was found liable the doctor's negligence was far more than the hospital's negligence.<br />
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<br />
just and equitable having regard to the extent of the responsibility for the damage. However, that learned author also points out that<br />
apart from cases such as Sinclair v William Arnott Pty Ltd (<strong>No</strong> 2) (1963) 64 SR (NSW) 88, 96, where one tortfeasor owes a higher<br />
duty than the other, the percentage of contribution has been dealt with broadly and upon common sense principles, picking up words<br />
from The Volute [1922] 1 AC 129, 144, a contributory negligence case.<br />
224 In Broken Hill Pty Co Ltd v Duffy (1943) 16 ALJ 374, 376, Latham CJ, with whom Rich, Starke, McKiernan and Williams JJ<br />
agreed, said:<br />
"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<br />
reason why the rule contained in s 1 of the Maritime Conventions Act, 1911 (Imp), that where it is impossible to assign the precise<br />
degree of fault the responsibility shall be apportioned equally should not be applied to the similar provision of the Wrongs Act (SA)."<br />
225 The present case is one where despite the great bulk of evidence presented, the responsibility for the plaintiff's injuries is in this<br />
position.<br />
226 Accordingly, the apportionment should be 50/50.<br />
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<br />
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<br />
doctor was ordered to pay the plaintiff. The cross appeal should be dismissed with costs.<br />
O. The Orders to be Made<br />
228 The formal orders of the Court are thus:<br />
(1) Appeal allowed;<br />
(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<br />
respect of orders made against the cross claimant in these proceedings.<br />
(3) Liberty to apply to a Master to certify the amount of such amount if the same cannot be agreed.<br />
(4) Cross appeal dismissed with costs.<br />
TIME 8.00 9.00 10.00 11.00 12 MD 1.00 2.00 3.00<br />
HOURS 0 1 2 3 4 5 6 7<br />
CONTRACTION 1 6060<br />
FREQUENCY<br />
&<br />
DURATION<br />
OXYTOCIC<br />
DOSE<br />
2 60<br />
3<br />
4<br />
5 20<br />
6-10<br />
APPENDIX 1 - SECTION OF PARTOGRAM<br />
10 10 10 1010<br />
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************************<br />
LAST UPDATED: 16/12/2003<br />
20 30 40 3030<br />
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