Mills v Lee & Ors

NEW SOUTH WALES COURT OF APPEAL

CITATION: Mills v Lee & Ors [2007] NSWCA 332

FILE NUMBER(S):
40701/06

HEARING DATE(S): 23 October 2007

JUDGMENT DATE: 26 November 2007

PARTIES:
Joshua Adam Mills by his tutor Leslie Mills
Effie Marjorie Lee and Philip George Lee Executors of the estate of the late Eric Bruce Lee
Dr P T Frost
Hospital Corporation Australia Pty Ltd t/as The Hills Private Hospital

JUDGMENT OF: Ipp JA Tobias JA Basten JA

LOWER COURT JURISDICTION: Supreme Court

LOWER COURT FILE NUMBER(S): SC 20176/02

LOWER COURT JUDICIAL OFFICER: Hislop J

LOWER COURT DATE OF DECISION: 6 October 2007

LOWER COURT MEDIUM NEUTRAL CITATION:
Mills v Lee & Ors [2006] NSWSC 1031

COUNSEL:
A: R S McIlwaine SC / M Eagle
R: A J Sullivan QC / J Downing

SOLICITORS:
A: Velleley & Associates, Sydney
R: Paul Tsaousidis, Sydney

CATCHWORDS:
NEGLIGENCE – Medical Practitioner – Whether breach of duty and causation
APPEAL AND NEW TRIAL – Interference with judge’s finding of fact – Findings based on expert evidence – Whether findings made by judge were open on the evidence at trial

LEGISLATION CITED:
N/A

CASES CITED:
N/A

DECISION:
Appeal dismissed with costs

JUDGMENT:

IN THE SUPREME COURT
OF NEW SOUTH WALES
COURT OF APPEAL

CA 40701/06
SC 20176/02
IPP JA
TOBIAS JA
BASTEN JA
Monday 26 November 2007

JOSHUA ADAM MILLS BY HIS TUTOR LESLIE MILLS v EFFIE MARJORIE LEE & PHILIP GEORGE LEE, EXECUTORS OF THE ESTATE OF THE LATE ERIC BRUCE LEE & ORS

Judgment

IPP JA: I agree with Tobias JA.
TOBIAS JA: On the evening of 21 July 1983 the appellant was delivered by lower segment caesarean section at Westmead Hospital (Westmead) by Professor Trudinger. He was intubated and transferred to the Neonatal Intensive Care Unit where he developed respiratory distress syndrome which progressed to bronchopulmonary dysplasia (BPD) and periventricular leukoencephalopathy (PVLE). The latter involved damage to the periventricular white matter resulting in cerebral palsy with spastic quadriplegia and severe intellectual impairment.
The appellant’s mother, KM, was admitted to Westmead at approximately 11am on the day of his birth having been transferred from Baulkham Hills Private Hospital (the Hospital) where she had been last admitted on 24 June 1983 suffering episodes of intermittent vaginal bleeding. She remained in the hospital initially under the care of the second respondent, Dr Frost and, after 8 July 1983, under the late Dr Lee. Both doctors were general practitioners but for many years had conducted practices confined to obstetrics and gynaecology. Each was a recognised specialist in those areas of medicine. It was common ground that each of them owed a duty of care to KM and the appellant, which was that of a specialist obstetrician and gynaecologist.
In 2002 the appellant instituted proceedings in the Supreme Court against the Estate of Dr Lee (he having died prior to the commencement of proceedings), Dr Frost and the Hospital alleging negligence in the failure of each of them to properly treat KM prior to her transfer to Westmead and Dr Lee’s failure to transfer her prior to 21 July 1983.
The statement of claim (the Sixth Further Amended Statement of Claim dated 30 November 2005) alleged numerous particulars of negligence against all three respondents, not all of which have been pursued on the appeal.
The proceedings were heard by Hislop J over a period of some 20 days in November and December 2005. On 6 October 2006 his Honour delivered judgment in which he found in favour of the respondents and entered a verdict and judgment in their favour. The appellant appealed to this Court from his Honour’s decision but conceded during the course of the hearing that he could not succeed against Dr Frost or the Hospital and that the appeal should be dismissed with respect to those respondents. Furthermore, a number of the appeal grounds directed to Dr Lee were ultimately abandoned.
At the end of the day the appellant’s case was confined to the allegation that Dr Lee breached his duty of care to the appellant by failing at approximately 11pm on 20 July 1983 and/or at approximately 8am on 21 July 1983 to administer the broad spectrum antibiotic, Ampicillin, prophylactically to KM at which time she was allegedly exhibiting signs of intrauterine infection with the potential to develop into chorioamnionitis. At the very least, so it was alleged, had such antibiotics been administered in a timely fashion KM would not have developed, as she did, chorioamnionitis which was accepted as the primary trigger which led to the development by the appellant of respiratory distress syndrome.
Some preliminary findings of the primary judge
During the period KM was in the Hospital from 24 June 1983 she suffered episodes of intermittent vaginal bleeding. The hospital notes record intermittent bright [fresh] bleeding on a number of occasions and on others brownish mild loss [old blood]. The fresh blood was usually associated with intermittent contractions that were managed by bed rest, sedation and some tocolytic agents [drugs administered to stop contractions]. His Honour noted (at [15]) that KM’s pregnancy was high risk by reason of the potential for worsening bleeding and separation of the placenta. There was therefore a likely prospect that the appellant would be born prematurely. This was recognised by both Drs Frost and Lee in that the objective of their treatment was to prolong the period that the appellant remained in utero in order to reduce the dangers associated with prematurity.
His Honour found that the most likely source of KM’s bleeding was from behind the placenta where it joined the uterus. Normally in pregnancy a mucus plug forms at the entrance to the cervix providing a barrier between the uterus and the vagina. The vaginal bleeding evidenced that the cervical plug was no longer acting as an effective barrier. This gave rise to the potential for bacteria to ascend from the vagina through the cervix into the uterus.
Relevant to the issues ultimately argued on the appeal were the following findings of the primary judge which were not challenged:
(a)There was no record that KM received any antibiotic treatment either while in the Hospital or after her transfer to Westmead;
(b)At all times whilst KM was in the Hospital her membranes were intact and did not rupture until after her admission to Westmead;
(c)          A Westmead histopathology report dated 27 July 1983 stated that KM’s membranes revealed   acute chorioamnionitis. This condition was explained by his Honour as follows (at [26]):
“The chorion is the outermost of the two membranes that enclose the foetus. The amnion is the innermost membrane. These membranes fuse during pregnancy and form a fluid filled sac for the protection of the foetus. Chorioamnionitis is an inflammatory or infectious process which involves, inter alia, the chorion and amnion.”
(d)The dominant cause of the appellant’s PVLE and BPD was the chorioamnionitis established by the pathology findings reported on 27 July 1983;
(e)          In 1983 a clinical diagnosis of chorioamnionitis was usually based upon the presence of two or   more of the following symptoms:
·              Maternal fever (most clinicians required a temperature of 38° for more than four hours)
·              Maternal tachycardia
·              Foetal tachycardia
·              Uterine tenderness
·              Rupture of membranes
·              Foul odour of the amniotic fluid
·              Peripheral blood leukocytosis [excessive number of white cells]
(f)Although multiple cultures were taken from the appellant and KM at Westmead following his birth, none was positive for infection. They failed to demonstrate a known neonatal pathogen. No coliforms were seen or cultured from the appellant.
The appellant ultimately conceded that none of the symptoms referred to in subparagraph (d) above were present when Dr Lee examined KM at 11pm on 20 July and that, at most, only one of them, uterine tenderness, was present on the morning of 21 July at which time Dr Lee directed the transfer of KM to Westmead. In other words, it was not contended on the appeal that Dr Lee ought to have made a clinical diagnosis of chorioamnionitis at any time whilst KM was under his care. However, it was contended that he ought to have diagnosed an intrauterine infection or, at least, have suspected such an infection and therefore administered antibiotics. Whether or not there were signs which would have supported any such diagnosis or suspicion and/or whether a reasonably competent obstetrician would have responded in the circumstances by administering antibiotics formed the crux of the appeal.
The nature of the evidence at trial
The evidence at the trial comprised the clinical and nursing notes of the Hospital and, to a lesser extent, those of Westmead together with expert testimony from a number of specialist medical practitioners. In this respect the appellant qualified the specialist obstetricians/gynaecologists Dr McMaster-Fay, Dr Molloy and Professor Mackay. Each prepared reports and gave oral evidence. No evidence of a neonatologist was adduced in the appellant’s case.
The respondents qualified the specialist obstetricians/gynaecologists Drs Child, Lyneham and Hinde and, a neonatologist, Dr McPhee. Their reports were also tendered and, save for Dr Hinde who had died prior to the hearing, each was called to give oral evidence. Professor Trudinger, into whose care KM was admitted, was also called in the respondent’s case.
All the experts who gave evidence were extensively cross-examined. However, ultimately the primary judge preferred the evidence of the respondent’s experts to those of the appellant.
The first ground of appeal
Ground 1 of the Amended Notice of Appeal alleged that the primary judge erred in finding that there was no breach of duty in not transferring KM to Westmead in time. In his judgment his Honour referred to this allegation as a failure to refer KM to a tertiary medical institution (Westmead) in a timely manner when either Dr Frost or Dr Lee knew or ought to have known that KM was at risk of pre-term delivery.
His Honour dealt with this allegation in the following paragraphs of his judgment:
“48The [appellant] submitted, based particularly on the evidence of Drs McMaster-Fay, Molloy and Professor MacKay that KM should have been transferred to Westmead Hospital earlier than 21 July 1983, at least from 6 July 1983 onwards, because her pregnancy had reached a point where there was a very high risk that she could go into labour and deliver.
49It was recognised by [her] and [Dr Frost] that the [appellant]’s birth would probably be premature and that the neonatal intensive care facilities which existed at Westmead Hospital should be availed of in order to increase the [appellant]’s prospects of a favourable outcome. It was known that Westmead Hospital was 10 – 15 minutes from the hospital by road ambulance and that the birth process would take a number of hours to develop.
50Professor Trudinger, into whose care KM came when transferred to Westmead Hospital, gave evidence that labour would last 6 – 10 hours and the transfer should occur when the clinician was convinced the patient was in labour and that delivery was going to occur in the near future. It was a matter for the clinical judgment of the attending doctor to determine when the transfer should be made. Some competent doctors may have made the transfer earlier than it was made, others would have done as [Dr Lee] did.
51Drs Hinde, Lyneham and Child were of the opinion that KM had been referred in a timely manner to Westmead Hospital. [Dr Frost] acknowledged he would have made the transfer during the course of 20 July 1983. Dr McPhee, the paediatrician, considered the transfer should have been made earlier but acknowledged that what had occurred was common practice in the 1980’s and 1990’s and that the timing in this case had not caused any problems.”
The appellant relied solely upon his written submissions with respect to this ground and it was not elaborated upon in oral argument. However, many of the submissions made on behalf of the appellant with respect to this ground were related to the allegation, which was extensively dealt with in oral argument, that the clinical signs on the evening of 20 July were such as to indicate that KM had an infection and that antibiotics should then have been administered which would have resulted in a better outcome with respect to the appellant. Those submissions are more appropriately dealt with under the other grounds of appeal that were pressed.
So far as Ground 1 is concerned, the primary complaint of the appellant was that the primary judge did not have sufficient regard to Dr McPhee’s evidence called on behalf of the respondents that KM should have been transferred to Westmead at an earlier point of time because of recurrent antepartum haemorrhaging. Although it was acknowledged that his Honour had referred (at [51]) to the opinion of Dr McPhee that the transfer should have been made earlier, it was submitted that there had been no consideration of the reasons advanced by him in support of that view.
Reliance was therefore placed upon Dr McPhee’s evidence to the effect that on 30 June 2003 preparations were being made for the delivery of the appellant by caesarean section and, had that occurred, transfer to a neonatal intensive care unit immediately following delivery was essential. As the Hospital did not have such a unit, KM should have been transferred to Westmead prior to delivery. The difficulty with this submission based on this part of Dr McPhee’s evidence is that the possibility of delivery by caesarean section was obviously abandoned at that time. The point Dr McPhee sought to make was that in relation to a very premature baby (being only 26 weeks as at 30 June 1983), delivery by caesarean section should only take place in a tertiary institution such as Westmead where there was a neonatal intensive care unit to which the newborn could be transferred without delay. Of course, that is exactly what occurred when Dr Lee transferred KM to Westmead on the morning of 21 July.
The appellant also submitted that Dr McPhee had opined that it was imprudent to keep a woman with recurrent antepartum haemorrhage at a peripheral centre such as the Hospital, although he acknowledged that in 1983 that was common practice at least in South Australia. However, Dr McPhee also acknowledged that he was not an obstetrician and was speaking only as a perinatologist. Although transfer to a hospital like Westmead would be optimal, in 1983 it was quite common for mothers with problems similar to those of KM to reside at secondary level centres such as the Hospital pending a crisis that justified a transfer to a tertiary institution. In my opinion it was clearly open to his Honour to accept that that was so and it is apparent from his findings in [51] of his judgment that he did.
Similar evidence was given by Dr McPhee in relation to incidents of loss of bright blood which occurred on 11, 12 and 13 July. To the extent to which delivery was imminent, KM should, according to Dr McPhee, have been transferred to a tertiary institution such as Westmead where there was an intensive neonatal care unit. Again he emphasised that that was his view as a neonatal paediatrician. Further, as Dr McPhee himself noted, KM had been experiencing slight to moderate blood loss and irregular contractions for three weeks during which time she had not gone into labour. In these circumstances, even though it was a high-risk pregnancy, it was a matter for the clinical judgment of the obstetrician as to whether to rush in and deliver the baby.
When taken through the nursing notes in respect of day and evening of 20 July, Dr McPhee’s response to the assertion that what was then occurring was just another example of why KM should have been transferred to Westmead earlier was as follows:
“A. As I keep saying, I think that that’s the prudent thing to do and certainly from my clinical practice that’s appropriate. One could argue, in retrospect, that in fact it was a fine piece of clinical judgment over the preceding three and a half weeks, because she didn’t progress, there was no evidence of foetal distress and she got that extra three and a half weeks in a peripheral hospital perhaps, perhaps closer to her family and of greater clinical comfort to her.
Again, I’m speaking as a perinatal neonatologist and it’s I who has to get up at 5 o’clock in the morning and pick up these babies, so I’d much rather them (sic) in my hospital than someone else’s. But I do think it’s more than just my convenience. It’s prudent clinical practice and more and more I think this sort of case is now cared for in a tertiary centre and less and less is it cared for in a secondary centre.
I think there is general agreement amongst the perinatal community that this probably isn’t a prudent course of action. But I would like to stress that one could argue that what’s happened up until now that – well, it certainly hasn’t caused any problem and has actually, perhaps by luck, reflected good clinical judgment.”
In re-examination the following exchange occurred:
“Q.         Doctor, several times you have said that in respect of my friend’s questions about transferring from Baulkham Hills to a tertiary unit, the neonatologist point of view is that is what you would do. Those answers were given in the context of a possibility of delivery of the baby, weren’t they?
A.           Yes.
Q.           Why is it from a neonatologist point of view, where there is a likelihood or a possibility of imminent delivery, you would regard the transfer of the tertiary unit being desirable?
A.           Because the transfer to a tertiary unit means that the baby is inborn. That means that my team and myself look after the baby from the moment of delivery. We don’t have to rely, perhaps, on the resuscitation of that baby by the paediatrician, who rarely looks after very tiny babies, and the initial care of the baby is in a peripheral sense. There are many studies that show that outborn prems have – the outcome of outborn prems, that is prems born out of tertiary structures, are not as good as those inborn.”
Dr McPhee also clarified in re-examination his statement that recurrent antepartum haemorrhaging was indicative of a high-risk pregnancy. In so doing he made it clear that recurrent antepartum haemorrhage, whether or not there was infection, could have adverse neonatal or maternal morbidity outcomes in that it could potentially result in an obstetric catastrophe. In other words, the high risk associated with recurrent antepartum haemorrhaging was not the potential for infection but the potential for a massive haemorrhage which, if it occurred, could have an adverse outcome with respect to the baby as well as the mother.
It follows in my opinion that when examined in context, there was no necessity for the primary judge to refer in detail to the evidence of Dr McPhee on which reliance is now placed and that his summary of that evidence in [51] of his judgment was more than adequate. In any event, given the qualification emphasised by Dr McPhee that the question of transfer from a secondary to a tertiary institution was a matter for the clinical judgment of the treating obstetrician, it was clearly open to the primary judge to accept the evidence of the respondent’s expert obstetricians on this issue in preference to the views of the similarly qualified experts called by the appellant. No error on his Honour’s part has been demonstrated.
Finally, reference should be made to paras 29 and 30 of the report of Professor Trudinger dated 28 November 2005 who was the admitting obstetrician on 21 July 1983 at a time when he was Senior Lecturer in Obstetrics and Gynaecology at the University of Sydney at Westmead. He said:
“29.The clinical records indicate to me that [KM] was managed for antepartum haemorrhage and threatened premature labour during the period of time she was admitted to Baulkham Hills Private Hospital. Had she been transferred into my care at Westmead Hospital at any time earlier than she was in fact transferred, or had she been admitted to Westmead Hospital under my care from the outset, instead of Baulkham Hills Private Hospital, her overall management would have been essentially the same in that I would have followed a conservative path seeking to prolong the pregnancy and gain foetal maturity. This conservative plan requires monitoring foetal condition to ensure welfare. Unless there was change in foetal or maternal condition, I would await the onset of spontaneous labour and then effect delivery, which is what occurred in this case.
30.During the period June-July 1983, [KM’s] pregnancy progressed from 25 to 30 weeks. In 1983, the perinatal mortality of a baby born at this gestation ranged from 50% to 15% and there was a significant risk of long term major handicaps including such outcomes as cerebral palsy, blindness, epileptic seizures and deafness which might occur in 25% to 50% of the survivors at the earlier part of this gestational age range. It is for this reason that I would have pursued a conservative management plan seeking to prolong the pregnancy as far as possible unless there was evidence of risk and lack of welfare in the foetus or mother (for example material blood loss, hypertension, infection). On the 21st July I thought [KM] was in early labour and delivery was inevitable.”

There was nothing in the appellant’s written submissions on Ground 1 which indicated that in cross-examination Professor Trudinger recanted from those opinions. On that basis alone the appellant has not established that had KM been transferred to Westmead at an earlier point of time such as at 11pm on 20 July when she was seen by Dr Lee, her treatment on admission to that institution would have been any different to that undertaken by Professor Trudinger or that there would have been a different outcome with respect to the appellant than that which in fact occurred.
In these circumstances, the appellant has also failed to establish that any breach of duty by Dr Lee in not transferring KM to Westmead at an earlier point of time materially contributed to the appellant’s condition.
Grounds of Appeal 10-15 – Breach of Duty
The appellant’s oral submissions on the appeal were directed to Grounds of Appeal 10 to 15 which challenged the following findings of the primary judge:
”117There was no clinical evidence of chorioamnionitis or an intrauterine infection on the evening of 20 July 1983 or early on 21 July 1983. I accept the evidence that the clinical signs first manifested themselves on and after KM’s arrival at Westmead Hospital. I do not accept that KM’s presentation on the evening of 20 July 1983 should have alerted the first defendant, exercising reasonable care, to the possible presence of chorioamnionitis or intrauterine infection. It is only with the benefit of hindsight that such can be suggested, if at all.
118Even if the signs of chorioamnionitis or intrauterine infection appeared shortly before transfer to Westmead Hospital this would not have required action by the first defendant as the care of KM was being transferred to Westmead Hospital at that stage. It is not without significance that Professor Trudinger, into whose care KM was transferred, did not diagnose chorioamnionitis or treat KM for any infection.
119Furthermore even if the first defendant had concluded the plaintiff had chorioamnionitis on the evening of 20 July or morning of 21 July 1983 and did not administer antibiotics this would not constitute a breach of duty as it would be reasonable for him to proceed on the view held by many competent medical practitioners in 1983 that in the absence of ruptured membranes the administration of antibiotics would be ineffective.”
The thrust of those submissions was that his Honour had failed to deal with the evidence of the respondent’s own experts who, so it was submitted, had accepted that there were clinical signs present prior to 21 July 1983 that KM was suffering from chorioamnionitis or intrauterine infection which, in accordance with proper practice, mandated the administration of broad spectrum antibiotics.
Particular reliance was placed by the appellant in oral argument on the evidence of Dr Lyneham in his report of 23 April 2005 where, after noting the distinction between a histological diagnosis of chorioamnionitis (which can precede, rather than be caused by, pre-term labour) and a clinical diagnosis of chorioamnionitis, he expressed the view that in the present case chorioamnionitis became clinically apparent on 20 July 1983 and that by the time KM was transferred to Westmead “she did have clinical evidence of chorioamnionitis”.
Before dealing in detail with this evidence, the following matters need to be borne in mind. First, the ultimate proposition advanced by the appellant was that even though it was not possible for Dr Lee to have made a positive diagnosis of chorioamnionitis on the evening of 20 July 1983, nevertheless there was sufficient evidence or signs of infection as to justify treating that infection, be it fact or suspicion, by antibiotics which, had they been administered, would have prevented KM developing chorioamnionitis.
Second, for this purpose the appellant accepted the finding of the primary judge that in the absence of ruptured membranes the administration of antibiotics would be ineffective in terms of protecting the foetus which was already protected by the intact membranes that constituted a barrier to the movement of infection through to the uterus. Rather, the appellant sought to focus on the proposition that once KM was diagnosed with intrauterine infection or there were signs of such an infection, as was submitted to be the case as at 11pm on 20 July, the case for administration of broad spectrum antibiotics was made out not for the purposes of directly protecting the foetus but for the purpose of curing the mother of that infection which, if it continued, would progress to chorioamnionitis.
Third, the evidence of Dr McPhee, which on this point was unchallenged, was that perinatal infection/inflammation was strongly linked to PVLE with chorioamnionitis being associated with a particularly high risk. The mechanism by which PVLE was caused was thought to involve inflammatory mediators or cytokines released by the placenta and/or foetus in response to infection/inflammation. In particular, Dr McPhee in his report of 11 June 2004 had stated:
“Overall, our current understanding of PVLE is that the major contributory factors are an immature brain (mainly between 24-34 weeks gestation), focal ischemia/hypoperfusion, subsequent reperfusion injury due to reactive oxygen species, and inflammatory mediators released during feto-maternal infection. It should be emphasised that our understanding of PVLE is incomplete, and that very little was known about this pattern of brain injury in 1983 … With respect to the case of [the appellant] particular risk factors of PVLE included antepartum haemorrhage, preterm delivery (at 29 weeks), and feto-maternal inflammation, as evidenced by the presence of clinical and histological chorioamnionitis.”
Dr McPhee elaborated on this in a passage recorded by the primary judge at [124]:
“With respect to PVLE, the pathophysiologic process does not necessarily involve infection of the fetus, but simply exposure of the fetus to inflammatory mediators (or cytokines) produced within the infected/inflamed chorioamniotic tissues. Thus, detailed microbiologic investigation in such cases frequently fails to demonstrate the presence of invasive pathogens in the mother, placenta or baby. These observations have lead to the understanding such chorioamnionitis in the presence of ruptured membranes may reflect local infection with ‘low grade’ pathogens (eg anaerobic organisms), but that the deleterious effects on the fetus are mediated by the release of inflammatory mediators that cross into the fetal compartment and injury the immature brain.”
In his oral evidence in chief Dr McPhee was referred to the following passage in his report dated 11 June 2004:
“As discussed above their danger in this clinical scenario may relate to the distant toxic effects of the inflammatory mediators released from the infected/inflamed chorioamniotic tissues, rather than direct cerebral or pulmonary tissue infection.”
which he then explained in the following exchange cited by his Honour at [124]:
“Q.         Translating that to lay language, is the situation that chorioamnionitis was one where the foetus doesn’t get infected as such; is that right?
A.           Correct.
Q.           But what happens is that there is infection or inflamed tissues elsewhere and they release something called ‘inflammatory mediators’; is that right?
A.           Correct.
Q.           What are inflammatory mediators?
A.           Well, these are things that the body produces to help it fight the infection, for example. Some inflammatory mediators cause your temperature to go up which has an effect on the thalamus of the brain. Other mediators attract white blood cells into the area to help fight infection. And there are a huge range of these various molecules. And we are not sure exactly how they sit in balance, but there’s very good evidence that a number of them are particularly toxic to the periventricular area of the brain and, in fact, one can produce damage to the brain simply by exposing preterm brains to these molecules – not to the infection, but to the molecules. So I think of this as damage at a distance, if you like.”
Fourth, Dr McPhee’s statement in the same report that PVLE was associated epidemiologically with antepartum haemorrhage was based on articles published no earlier than 1996.
Fifth, although Dr McPhee accepted, given the strong epidemiological evidence in favour of chorioamnionitis as a causal factor in the pathogenesis of both PVLE and BPD, that in conjunction with the appellant’s prematurity, it was the dominant factor in his development of those conditions, he nevertheless acknowledged that PVLE could occur after recurrent antepartum haemorrhage without clinical chorioamnionitis and was occasionally seen after a relatively uneventful preterm course. Importantly, with respect to PVLE, the pathophysiologic process did not necessarily involve infection of the foetus but simply exposure of the foetus to inflammatory mediators (or cytokines) produced within the infected/inflamed chorioamnionitic tissues: see [36] above.
Sixth, Dr McPhee pointed out that much of the epidemiologic data was based on a histopathological rather than clinical diagnosis of chorioamnionitis and as such was founded upon retrospective analysis of potential contributory factors. Importantly he emphasised that his comments with respect to the relationship between chorioamnionitis and PVLE reflected the state of medical knowledge as at 2004/2005; in 1983 the pattern of injury which the appellant sustained and the understanding of its causation was “virtually unknown”. He thus emphasised that his analysis of the cause of the appellant’s neural injury was based on a retrospective analysis of available facts regarding the case. Accordingly, although he believed that KM’s chorioamnionitis as demonstrated on histopathologic examination of the placenta at Westmead was a likely factor in the genesis of the appellant’s neural injury, he did not believe that there was convincing evidence of this process at the time of the appellant’s birth. He thus agreed with Professor Trudinger’s comments regarding the absence of convincing clinical signs of a diagnosis of acute chorioamnionitis in the present case as KM did not have a temperature exceeding 38°C and did not have an offensive liquor odour. Although there was uterine tenderness and an evolving tachycardia, the history of antepartum and then intrapartum bleeding suggested abruption of the placenta as a far more plausible clinical diagnosis.
Finally, Dr McPhee noted that much of the evidence cited by Professor McKay and Dr McMaster-Fay in support of the use of intrapartum antibiotics in such a setting was based on studies conducted after 1983. He considered that in the case of KM and the appellant, it was important to note that no neonatal or maternal infections were seen at least prior to the admission of KM to Westmead. It is noteworthy that Dr McPhee concluded in these terms:
“Thus, unlike a retrospective analysis of a particular clinical course of action based on outcome, clinical care typically involves serial assessments of an evolving clinical situation, with a decision to intervene being based on the sum of risks and benefits attributable to various interrelated factors and treatments.”
It is also important in the context of the appellant’s challenge to the primary judge’s findings in [117]-[119] of his judgment to record the contents of the nursing or clinical notes on the evening of 20 July and the morning of 21 July. They are summarised in Dr Lyneham’s report as follows:
“20 July 1983
The Mother continued to have moderate bright serous loss with normal observations. The maternal pulse rate was 95/minute and the Mother was afebrile.
That evening the Mother developed more contractions associated with moderate bright vaginal bleeding. Dr Lee was contacted at 1750, 2200 and 2230. Sedation was administered without effect and Dr Lee advised he would come and see the Mother.
Dr Lee attended at 2300 and performed a speculum vaginal examination and found the cervix to be long, posterior and closed, so that the Mother’s contractions had not in fact resulted in any cervical changes. The Mother was now ‘complaining of frequent sweats’ but she was afebrile. During the day the Mother’s pulse rate was documented at 95/minute and the foetal heart rate was 148 and 142 bpm and the Mother was afebrile.
21 July 1983
The Mother had a bright vaginal loss at 0700 with regular contractions. She was nauseated++ and shaking but maternal observations were satisfactory, she had a pulse rate of 95/minute and a temperature of 36.8°C. The foetal heart rate was 132/minute. The Mother was seen by Dr Lee and her transfer to Westmead Hospital arranged. She was about 31 weeks by dates, 29 weeks by the 24 week ultrasound.”
With respect to the alleged signs of intrauterine infection, much was made by the appellant of the presumed fact that when Dr Lee attended KM at 2300 on the evening of 20 July she was complaining of “frequent sweats” although she was afebrile, that is, she was not feverish and did not have an elevated temperature. In fact, according to the hospital records at 9pm on 20 July her temperature was 36.8°C.
The appellant sought to make a great deal of Dr Lee’s knowledge at 11pm on 20 July that KM was complaining of frequent sweats, this being a sign, so it was contended, that she was suffering from intrauterine infection. Absent the sweating, there was nothing in the notes that would have indicated any clinical signs of such an infection. Certainly, none of the symptoms necessary for a diagnosis of chorioamnionitis were present at that time. Furthermore, neither KM’s pulse rate nor the foetal heart rate indicated either maternal or foetal tachycardia or distress.
Neither Dr McMaster-Fay nor Professor McKay made reference to KM’s frequent sweats on the night of 20 July. According to Dr Molloy, usually frequent sweats indicate that “there is probably an infection around”. In cross-examination Professor Trudinger accepted that sweating was one explanation of a human experiencing a high temperature but he rejected that that was the situation with KM, observing that the reference in the notes to KM sweating but being afebrile suggested to him that she was not pyretic (that is, she did not have a high temperature) so that that was not the explanation for the sweating.
Dr McPhee made an oblique reference to maternal sweating and nausea (albeit without fever) on the night preceding KM’s transfer to Westmead as perhaps an indication of evolving evidence of chorioamnionitis. However, in cross-examination he stated that the diagnosis of chorioamnionitis was only made “in retrospect”.

Dr Lyneham opined that there was no evidence of any intrauterine infection until KM developed a slight fever and tachycardia on the day that she was transferred to Westmead. However, he was of the opinion that “in retrospect”, the “frequent sweats and pulse rate of 95/minute at 2300 the night before” were probably the very first indications, but that these were not enough to warrant transfer of KM at midnight. Once that clinical evidence became available on the morning of 21 July, Dr Lee transferred KM to Westmead without delay.
Furthermore, when asked whether the usual practice in 1983 would be to prescribe antibiotics to an expectant mother with antepartum haemorrhage who was complaining of frequent sweats, Dr Lyneham responded:
“I think it would be unusual to give antibiotics purely for sweat[s]. You would want to have a bit more of an idea to know what was going on.”
Dr Child was cross-examined as to the significance of frequent sweats with respect to KM in the following exchange:
“Q.         Now frequent sweats would indicate to you, wouldn’t it, that there was something going on that was abnormal in the clinical situation we have here?
A.           Yes.
Q.           Afebrile would indicate that there was no fever?
A.           Yes.
Q.           But that wouldn’t diminish, would it, the fact that there was the ongoing patient still complaining of frequent sweats?
A.           Yes.
Q.           That would be an abnormality which would need to be considered?
A.           Observed, yes.
Q.           Well, more than just observed, because that’s one of the things which you say in your report of 30 November would be a maternal symptom upon which the usual practice would no longer be followed, but antibiotics would be prescribed. Do you agree with that?
A.           I’m trying to read three things at once. I mean, my interpretation of this in the notes is that Dr Lee, very intelligently, thought that the moment for transferring the patient was getting close and he transferred the patient the next day. So he was worried about it, he took that action, rather than prescribing antiobiotics which is not appropriate.
…
Q.           Wouldn’t a competent clinician, with the complaint of frequent sweats, as recorded in the notes, prescribe antibiotics?
A.           No.
Q.           Why not?
Q.           Well, purely on the basis of sweats, it’s not an indication for antibiotic. The most likely thing is that the patient’s getting a flu. They can still get a flu even though they’re in hospital.
…
Q.           If there was no recorded fever or maternal tachycardia and there was no record of maternal symptoms such as sweating, then, in those circumstances, antibiotics would not be prescribed?
A.           Yes.
Q.           But if there was sweating, won’t you agree that antibiotics should be administered?
A.           No, purely on the basis of sweating, no, I wouldn’t.
Q.           Would you agree that the cause of the sweating ought to be investigated?
A.           Yes, and it could be due to blood loss.
…
Q.           It could also be due to infection, couldn’t it?
A.           Yes.
…
Q.           Could I ask you this: In 1983 there were freely available antibiotics to treat infection generally?
A.           Yes.
Q,           And suitable antibiotics – that’s broad spectrum antibiotics – would have been the appropriate antibiotics to use if the clinician suspected infection and decided to administer antibiotics against the background of complaint of frequent sweating at 11 o’clock?
A.           Yes
Q.           Now I understand you won’t agree with the proposition that, in those circumstances, antibiotics should have been administered?
A.           I wouldn’t personally have administered antibiotics in those circumstances, no.
Q.           But you would, wouldn’t you, have wanted to determine the reason for the frequent sweating?
A.           Yes, yes.
…
Q.           Indeed, if you wanted to exclude infection, what simpler form of investigation would you have used?
A.           Taking the temperature.
Q.           That’s all?
A.           Yes.
Q.           Just simply taking the temperature?
A.           Taking it regularly, yes.
Q.           Well why wouldn’t you order a full blood count?
A.           Well, I’d need more to go on than just a sensation of sweating.
Q.           But that would indicate to a competent clinician that there was something wrong; is that right?
A.           Not necessarily, no. A lot of people sweat for various reasons, without it meaning that something’s wrong.”
Criticism of his Honour’s finding was also founded upon the concession of Dr Child in cross-examination that it was likely that KM was suffering from intrauterine infection prior to admission to Westmead “for a short period of time” or “for an hour or so”. However, that evidence did not amount to a concession on the part of Dr Child that either on the evening of 20 July or in the early morning of 21 July KM’s symptoms were such as to warrant an actual diagnosis of intrauterine infection. Furthermore, Dr Child made it clear that even if in 1983 he was highly suspicious that a patient had an intrauterine infection but that delivery was not to take place for at least three to four hours (as would have been the case with KM on the evening of 20 July), he would not have administered antibiotics to treat that infection where, as was the case with KM, the patient’s membranes were intact.

As I noted in [31] above, particular reliance was placed by the appellant upon Dr Lyneham’s statement in his report of 23 April 2005 that chorioamnionitis became clinically apparent on 20 July 1983 and that at the time she was transferred to Westmead there was clinical evidence of that condition.
On the other hand, in the same report Dr Lyneham expressed agreement with Dr McMaster-Fay that KM probably had “sub-clinical chorioamnionitis” at some time prior to the appellant’s birth. However, he also said that there was no clinical evidence until just prior to her transfer to Westmead. Dr Lyneham further opined that even if KM had been transferred to Westmead at about 11am on 21 July with clinical evidence of chorioamnionitis, antibiotic treatment would not have commenced (consistent with contemporaneous proper professional standards) and that KM’s management would have been similar and the outcome the same as in fact occurred.
In a further report dated 25 October 2005 Dr Lyneham expressed the following reservation with respect to the statement in his previous reports that there was clinical evidence of chorioamnionitis when KM was transferred to Westmead. He said:
“…I note that as [KM] did not look unwell, her fever was mild and she did not have an offensive vaginal loss in the presence of ruptured membranes, Professor Trudinger did not make a diagnosis of chorioamnionitis. As he was of the view that there was no clinical chorioamnionitis, he did not give [KM] a dose of antibiotics when the baby was born, and [KM]’s temperature settled shortly after the baby was born without antibiotics having been administered. Although on retrospective analysis the clinical features that I discussed in my initial report could be linked to the diagnosis of chorioamnionitis made on histological examination of the placenta, such a diagnosis would not have been made on the basis of examining [KM] at the time of her transfer to Westmead Hospital.”
In cross-examination, when asked whether KM had clinical chorioamnionitis prior to her transfer to Westmead, he responded:
“that a retrospective analysis of her symptoms would be consistent with that but the clinical picture was just becoming clear at that time.”
Dr Lyneham further stated that on the night of 20 July there were some clinical manifestations which in retrospect were the first manifestations of the developing chorioamnionitis but which were not necessarily diagnosable at that time. When the statement in his report of 23 April 2005 that “the chorioamnionitis became clinically apparent on 20 July 1983” was put to him, he responded
“Yes, these were the first, at 11pm, these were the first manifestations of what, in my view, became more apparent as the clinical chorioamnionitis, that was 11pm on the 20th.
Q.           So at 11pm on the 20th this lady was showing signs which would indicate to a competent clinician that the pregnancy was infected?
A.           No, not necessarily.
Q.           Well, Doctor, chorioamnionitis is, as we have already discussed, an infection of the pregnancy, isn’t it?
A.           Maybe.
Q.           On your view there are clinical signs that there was chorioamnionitis.
A.           That view was made, or that opinion was put on the basis of my assessment of the notes. I didn’t have the advantage of assessing the patient, so I had to provide an opinion based on the notes, but I would defer to a competent clinician who is assessing the situation at the time.”
When it was suggested to Dr Lyneham that at 11pm on 20 July it would be his view that broad spectrum antibiotics should have been administered, his response was: “not on the basis of the clinical picture that was present at 11pm”. The following further exchange then took place:
“Q.         On 20 July, it is your view, as you have said, from reading the clinical notes that chorioamnionitis was clinically apparent?
A.           That is my view on a retrospective analysis, not being there assessing the patient at the time.
Q.           Which means that there was a very high risk that the unborn child could be infected, is that right?
Q.           The clinical picture in my view that presented on the evening of the 20th was consistent with chorioamnionitis but not necessarily diagnostic of chorioamnionitis.
Q.           So in those circumstances, a competent clinician, knowing what a great risk chorioamnionitis was to an unborn infant, would treat the mother with antibiotics?
A.           No.
Q.           You would just leave it?
A.           You wait and see how things assess, how things unfolded.
Q.           I suggest to you, doctor, that a competent clinician, once there were clinical signs consistent with chorioamnionitis, would treat the mother with broad spectrum antibiotics?
A.           No, quite emphatically that was not the clinical practice in 1983.
Q.           By that do you meant it wasn’t your clinical practice?
A.           The role of antibiotics was in clear-cut clinical chorioamnionitis. You would need to be confident about the diagnosis.
Q.           Is the answer to my question that a competent clinician faced with clinical signs consistent chorioamnionitis would administer broad spectrum antibiotics? Does that not conform with what your practice would have been in 1983?
A.           It would depend on the clinical picture that we have to cope with. The clinical picture could be consistent with chorioamnionitis but by the next day there is no evidence of chorioamnionitis, or the clinical picture could be consistent with very early chorioamnionitis and by the next day it is apparent. Retrospectively, one can say, in my view, that the picture late on the evening of the 20th was the very first manifestations of the disease as it unfolded but that is knowing how the clinical processes did unfold.
Q.           That is the very reason why at the first indication of signs consistent with clinical chorioamnionitis a competent clinician would treat with antibiotics?
A.           No, in my view it is quite the opposite. That is the very reason you wouldn’t give antibiotics until you were confident of the diagnosis.
Q.           If you treat the signs when they first arise then the outcome is likely to be wholly different, isn’t it?
A.           There was no evidence of that then and perhaps not even now.”
The appellant submitted that the error revealed by the first sentence of [117] of his Honour’s judgment was that the finding in question was made by him without dealing with the evidence that was to the contrary of that finding such as that of Dr Lyneham, Dr McPhee and Dr Molloy. I have already referred to the evidence of Dr Lyneham which, in my view, supported the primary judge’s finding. Dr Lyneham made it perfectly clear that his view that chorioamnionitis was clinically apparent on the evening of 20th July was based on a retrospective analysis of what ultimately occurred.
So far as Dr McPhee’s evidence was concerned, he referred in his report of 11 June 2004 to there being “evolving evidence of chorioamnionitis” on the morning of 21 July which may have extended over the preceding night. Importantly, Dr McPhee in the same report continued in these terms:
“The only potential criticism that could be raised in relation to this episode of the care would be the failure to prescribe antibiotics in the presence of signs of chorioamnionitis. Whilst I suspect that some would advocate such a course of action, I believe the most important step is to expedite delivery, and so remove the infected/inflamed chorioamnionitic material. This is perhaps supported by the observation that [KM]’s fever subsequently subsided without recourse to antibiotic therapy. Overall therefore, I can find no criticism with this period of care, though this matter would benefit from expert obstetric opinion.”
In cross-examination when it was put to him that he had stated in his report of 11 June 2004 that there was evidence on the night of the 20th of chorioamnionitis, Dr McPhee responded:
“Yes, that’s correct. I’d like to qualify that as a retrospective thing. I think mothers who have antepartum haemorrhage often have a little bit of sweating and nausea but there was certainly none of the traditional or hard features of chorioamnionitis.”
Dr Molloy in his report of 28 November 2005, having considered a full blood count report from Westmead dated 21 July 1983 after KM’s admission to that hospital, opined that the result of that full blood count indicated that there was infection present at the time that the blood was taken and that it would have been there for at least two to three days beforehand and maybe longer. However, as his Honour noted (at [109]), Dr Molloy was unable to find any support for that opinion in the literature and agreed that it was speculation on his part.
Further, in cross-examination of Dr Molloy the following exchange occurred:
“Q.         You would agree, would you not, that until, at the earliest, very shortly prior to the transfer of [KM] to Westmead on the morning of 21 July, no self-respecting clinical obstetrician could have made a diagnosis on the pattern of symptoms presented of chorioamnionitis?
A.           Well, it could well have been a subclinical infection. When she had an offensive odour back on 6 July, she could have been developing it, and that’s why I say antibiotics should have been given, to try to head this infection off at the pass, so to speak.
Q.           You would agree that no obstetrician could reasonably have made a diagnosis of chorioamnionitis prior to, at the earliest, a short time prior to the transfer of [KM] to Westmead on 21 July?
A.           It would have been diagnosed certainly that evening before.
Q.           And not before that, wouldn’t it?
A.           As such. As true chorioamnionitis. But there could have been a subclinical infection, otherwise she couldn’t have gone on, in that short time, the 24 hours, to have very acute chorioamnionitis, which was diagnosed, and reported on, on the pathology of the placenta.
Q.           That is just what acute chorioamnionitis means, isn’t it? It is a disease of sudden or rapid onset?
A.           Yes, but there have to be some preliminaries to it. Infection has to be in there somewhere and then multiply and develop.
Q.           Even in the diagnosis of acute chorioamnionitis, the clinical diagnosis that is, as Creasy and Resnik pointed out, at this time, in 1984, reasonable clinicians were still in debate amongst themselves as to whether you should administer the antibiotics intrapartum or postpartum, weren’t they?
A.           They probably were in discussion. It all depends what they were doing about it clinically.
Q.           You know that, at least, there were reasonable obstetricians in Australia in 1983 who held the view that, even in the diagnosis of acute chorioamnionitis, and that is a clinical diagnosis, administration of any antibiotic therapy should await birth of the child?
A.           Well, there may have been some that held that theory but, if you had a diagnosis the evening before of chorioamnionitis, why weren’t antibiotics given, and why wasn’t the patient immediately transferred to Westmead?”
It should be noted that Dr Molloy’s reference that on the evening of 20 July there could have been a subclinical infection, is a concession that at that time the signs of an infection were subclinical and not clinical: in other words, they were at that time not clinically apparent. Furthermore, his last answer in the above exchange assumes that on the evening of 20 July a diagnosis of chorioamnionitis could have been made, an assumption that was never proven and, in fact, conceded as not being proven by the appellant given that there were none of the symptoms on the evening of 20 July accepted by the appellant as necessary before any such diagnosis could be made: see [10(d)] above.
The respondents submitted that in light of the foregoing evidence his Honour’s finding at [117] of there being “no clinical evidence of chorioamnionitis or an intrauterine infection” on the evening of 20 July or early on 21 July should be taken as a finding that the requirements for a clinical diagnosis of each of those conditions were not present. That was clearly the case in relation to chorioamnionitis and, on the evidence it was clearly open to his Honour to come to that same view with respect to intrauterine infection.
Given that KM was at all material times afebrile, that her temperature was normal or within a point of normal and that there was no evidence of maternal or foetal tachycardia, the only sign of possible infection was KM’s complaints of slight nausea and frequent sweats – the first was explained by the sedative drugs which were administered to her and the second could be the subject of any number of explanations of which infection was only one. However, the evidence indicated that although sweating in conjunction with a high temperature would be indicative of an infection, sweating in circumstances where KM was not pyretic and was afebrile was not consistent with her being infected. As Professor Trudinger observed, the position would be different if there was a haematogenous spread of infection to the uterus but that was not relevant to the present case where an intrauterine infection could not impact upon the uterus whilst the membranes were intact.
In my view it has not been demonstrated that it was not open to the primary judge to come to the finding he did in the first sentence of [117] of his judgment. Furthermore, no relevant error has been demonstrated with respect to his Honour’s findings in the last two sentences of that paragraph that KM’s presentation on the evening of 20 July should have alerted Dr Lee, exercising reasonable care, to the possible presence of chorioamnionitis or intrauterine infection and that it was only with the benefit of hindsight that such could be suggested.
The evidence to which I have referred also provides voluminous support for his Honour’s finding at [119] that in the absence of ruptured membranes, it would be reasonable for Dr Lee not to have administered antibiotics but, as he did, to have KM transferred to Westmead for further investigation and treatment. Without going into the evidence in detail as it was not the subject of serious challenge, it established that in the absence of ruptured membranes, the administration of antibiotics at a time when it might have been necessary for KM to be delivered of her baby by caesarean section would be contra-indicated and, in any event, would have made no difference to the ultimate outcome.
Accordingly, in my opinion the appellant has not made good his case that even if there were clinical signs of infection on the evening of 20 July or on the morning of 21 July, Dr Lee was in breach of his duty of care by failing to then administer antibiotics to KM.
Grounds of Appeal 16-22 – Causation
I turn now to the issue of causation. I have already referred to the evidence of Dr McPhee as to the pathopsychologic process that resulted in the appellant sustaining PVLE and BPD. The primary judge noted (at [121]) that it had been submitted by the respondents that even if KM had been treated with antibiotics at any time during her stay at the Hospital, it would have made no difference to the outcome for the appellant. He then observed (at [122]) that the only neonatologist to give evidence at the hearing was Dr McPhee, summarising his evidence at [123]-[124] (which I have recorded at [34]-[36] above, that chorioamnionitis was not a condition whereby the foetus becomes infected but, rather, where there is an infection or inflammation of the tissues causing inflammatory mediators to be released naturally by the body to help it fight the infection of which a number were particularly toxic to the periventricular area of the pre-term brain of the foetus when exposed not to the infection, but to the released molecules.
His Honour (at [125]) then noted the following conclusions of Dr McPhee:
“125 Dr McPhee concluded:
(a)… evidence for a role of infection and inflammation in a range of perinatal and preterm neonatal conditions has generated much interest in the use of perinatal antibiotics to avert these problems. To date however, apart from the use of intrapartum antibiotics to prevent group B streptococcal infection in the newborn, and antibiotics in the presence of preterm rupture of the membranes, the results of these strategies have been generally disappointing.
(b)… the use of broad spectrum antibiotics in the setting of preterm labour with intact membranes, based on a potential causal role of infection in the genesis of preterm labour, has been shown to be of no benefit, and possibly of some harm.
(c)I do not believe that there is any evidence that antibiotics at this time [i.e. on 6 July 1983], or even later when there was threatened preterm labour associated with antepartum bleeding, would have influenced the outcome.
(d)… given that there was no evidence of bacterial infection in Joshua, any discussion as to the potential of intrapartum antibiotics to have prevented same seems illogical.
(e)I do not believe … that there is any evidence to suggest that the use of pre- or intrapartum antibiotics in this case would have favourably influenced the outcome.
(f)Q. … And ‘generally disappointing’, does that mean that those studies reflect the fact that there is no evidence that outcomes are improved in the absence of ruptured membranes?
A.           In - other than with group B strep, yes.
Q.           Other than with group B strep?
A.           Yes. So the use of antibiotics in the presence of preterm labour with intact membranes produces no benefit to the newborn.”
That these conclusions applied in 1983 was established in the following exchange with Dr McPhee:
“Q. Doctor, you have indicated in your report, as a result of studies which have been done, that administration of antibiotics in the presence of intact membranes, apart from the group B strep situation, is now known to be of no benefit. Was that situation, to your understanding thought to be any different in 1983?
A. Not to my knowledge, no.”
The appellant placed much reliance on the evidence of Dr McMaster-Fay. In his report dated 27 November 2005 he opined that KM’s full blood count taken on her admission to Westmead on 21 July revealed that she had fulminating chorioamnionitis at that time which had been present “for a considerable length of time” and that there were strong indications that intrauterine infection had been present at least two weeks prior to 21 July. He therefore was of the view that early administration of broad-spectrum antibiotics would have treated that infection and prevented the appellant from becoming infected in utero and thus would have prevented his spastic cerebral palsy.
Dr McMaster-Fay was cross-examined upon a 2002 study relating to the intrapartum administration of antibiotics when a diagnosis of intra-amniotic infection had been made. The following exchange took place:
“Q.         And what they went on to conclude was there was not enough evidence from the trials to show which antibiotic is best, or whether it should be given before or after the baby is born?
A.           Correct.
Q.           So, in other words, even as at 2002, after much greater research into the matter, the state of knowledge on this particular point wasn’t much advanced by what Dr Gibbs was espousing in 1980, was it?
A.           Correct.
Q.           And it was, in other words, that, as at the time – assuming that a diagnosis of chorioamnionitis had been made – it was still an open question as to whether it was best to administer antibiotics at all; is that right?
A.           Yes.
Q.           And, secondly, it was still an open question, if they were administered, what type of antibiotics should be administered?
A.           Yes.
Q.           And, thirdly, it was still an open question, if it was decided to administer them and what time they were, as to when they should be administered?
A.           Yes.
Q.           And, fourthly, in respect of when they should be administered, it was still an open question whether it should be, on the one hand, whilst the baby was still in the uterus or whether the administration should commence after delivery?
A.           Yes.
Q.           And there were, in respect of each of those open questions, in 1983 in Australia, there were respectable practitioners of repute of the belief that one or the other of the two alternatives was the proper and reasonable one to adopt?
A.           Yes.”

In cross-examination Dr McMaster-Fay also conceded that in 1983 as well as 2005 it was very difficult to make a clinical diagnosis of chorioamnionitis and that even if there was a suspicion of that condition, “you can just be wrong”. The witness asserted that there were two journal articles which referred to the administration of antibiotics before a clinical diagnosis of chorioamnionitis had been made. However, when pressed, he acknowledged that neither “talked about, in any shape or form, administering antibiotics …prior to the making of a diagnosis of chorioamnionitis”.
After acknowledging that not only had he not seen any academic article which suggested that antibiotics should be administered where there was only a suspicion of chorioamnionitis but also that he would have no “joy” in getting published an article which so suggested, the following exchange resulted:
“Q.         Because the indiscriminate use of antibiotics, as we said yesterday, is something which has a considerable public risk, isn’t it?
A.           It was perceived as such in those days; indiscriminate use.
Q.           For one thing, there was concern about the confusing effects of giving antibiotics to the mother, as they might compromise the testing of cultures on the baby; isn’t that right?
A.           Yes.
Q.           And they might, therefore, confuse the selection of the appropriate antibiotics for treatment of the baby?”
A.           Yes.
His Honour also referred (at [128]) to Dr McMaster-Fay’s acceptance that the only clinical situation in which antibiotics had been shown to reduce the incidence of chorioamnionitis was where there was pre-term rupture of the membranes. However, Professor McKay’s evidence referred to by his Honour was that chorioamnionitis could be beneficially treated by the use of antibiotics even where the membranes were intact thus giving rise to the submission by the appellant that harm to him could have been avoided if the initial infection (referred to on the appeal as an intrauterine infection) had been cured by the administration of antibiotics before chorioamnionitis had developed.
The difficulty with this submission, as his Honour pointed out at [132], was that given the unchallenged evidence of Dr McPhee on this point, for the appellant to succeed on the issue of causation required him to establish on the balance of probabilities that antibiotics should have been administered to KM at a time before the inflammatory mediators or cytokines had been released by that infection. Once those mediators had been released, the administration of antibiotics would have had no effect for although they may have reduced or eliminated the infection, they would have had no effect on the already released inflammatory mediators or cytokines, the toxic elements of which would have already impacted upon the periventricular area of the immature brain of the foetus eventually resulting in the neural damage which the appellant sustained.
His Honour held [at 133] that the evidence did not establish on the balance of probabilities when the cytokines were released. If they had been released before antibiotics were administered to KM at 11pm on 20 July (the earliest time suggested) then there was no evidence that the subsequent administration of antibiotics would have arrested the process which had already commenced. In the absence, therefore, of evidence to support a finding that the cytokines had not been released prior to when the antibiotics would have eliminated any intrauterine infection, the necessary causative link upon which the appellant’s case ultimately depended had not been established. Accordingly, at [135] the primary judge concluded that not only was the cause of the chorioamnionitis not known but also the appellant had not established that antibiotics that, he alleged, ought to have been administered to KM would have arrested in time the organism that was causative of that infection.
Finally, I refer to Dr Lyneham’s report of 18 June 2004 where he said:
“There is no way that Dr Lee, or anybody else, could have had knowledge or understanding of any link between chorioamnionitis and brain damage. Nor is there any treatment that Dr Lee could have instituted which would have influenced the sequence of events.”
Again, in the same report Dr Lyneham stated that there was in 1983 absolutely no knowledge amongst obstetricians that there was any link between the neurological outcome of an infant and chorioamnionitis, either symptomatic or asymptomatic.
Conclusion
The respondents’ ultimate submission was that in the light of the evidence to which I have referred, there could be no error in the primary judge’s finding that it was the reasonable view of competent obstetricians in 1983 that in the absence of ruptured membranes, the administration of antibiotics would be ineffective in combating or preventing chorioamnionitis. Furthermore, given that the relevant duty of care of Dr Lee in the present case was to the appellant and not KM, and as it was the reasonable view in 1983 of competent obstetricians that intact membranes acted as an effective barrier in protecting the foetus from ascending, as distinct from the haematogenous spread of, infection, his Honour should have found that Dr Lee did not breach his duty of care to the appellant in not commencing antibiotic therapy prior to KM’s transfer to Westmead. In other words, so it was submitted, according to the state of medical knowledge in 1983, Dr Lee could not reasonably have foreseen that if he did not administer antibiotics to KM whilst her membranes were intact, that the appellant was likely to suffer the harm that he did.
In my opinion these submissions should be accepted given my analysis of the evidence. It was amply open to the primary judge to prefer the evidence of the respondents’ medical witnesses and, in particular, that of Dr McPhee, the sole neonatologist to be called. In so doing, his Honour’s conclusions that there was no breach of duty on the part of Dr Lee and that in any even the appellant had not discharged the onus of establishing causation, were amply justified and in no way redolent of error.
I acknowledge that this is indeed a hard case in that the appellant has suffered a terrible injury which naturally evokes a highly sympathetic response. But that sad fact cannot justify a finding against Dr Lee in the absence of proof of negligence on his part. The primary judge found there was none and in my respectful opinion he was correct in so finding. The inevitable outcome of the appeal in those circumstances is that it should be dismissed with costs.
BASTEN JA: I agree with Tobias JA.

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LAST UPDATED: 28 November 2007

[2007] NSWCA 332

26 November 2007

Key Legal Topics

Areas of Law

Negligence & Tort

Evidence

Civil Procedure

Legal Concepts

Appeal

Breach

Causation

Duty of Care

Expert Evidence

Negligence