JACOB RIELY MCLENNAN an infant suing by his next friend YVONNE JOYCE MCLENNAN & ANOR -v- MCCALLUM & ANOR - [2007] WADC 67

JURISDICTION : DISTRICT COURT OF WESTERN AUSTRALIA
IN CIVIL

LOCATION: PERTH

CITATION: JACOB RIELY MCLENNAN an infant suing by his next friend YVONNE JOYCE MCLENNAN & ANOR -v- MCCALLUM & ANOR [2007] WADC 67

CORAM: WISBEY DCJ

HEARD: 6-10, 13-17 & 20-22 NOVEMBER 2006

DELIVERED : 9 MAY 2007

FILE NO/S: CIV 959 of 2003

BETWEEN: JACOB RIELY MCLENNAN an infant suing by his next friend YVONNE JOYCE MCLENNAN
First Plaintiff
YVONNE JOYCE MCLENNAN
Second Plaintiff
AND
KEITH ARNOLD MCCALLUM
First Defendant
THE MINISTER FOR HEALTH
Second Defendant

Catchwords:

Negligence - Breach of duty - Medical practitioner - Duty to warn of risks of natural delivery of breech presentation foetus - Nature of breech - Whether duty to deliver first plaintiff by caesarean section - Causation - First plaintiff born with cerebral palsy - Whether causal connection between manner of delivery and neurological condition of first plaintiff

Legislation:

Nil

Result:

Finding that no breach of duty by either defendant

Representation:

Counsel:

First Plaintiff                  :     Mr I Viner QC and Ms K L Hogan
Second Plaintiff             :     Mr I Viner QC and Ms K L Hogan
First Defendant              :     Mr K Martin QC and Mr J Thomson
Second Defendant         :     Ms C J Thatcher

Solicitors:

First Plaintiff                  :     Ilberys
Second Plaintiff             :     Ilberys
First Defendant              :     Clayton Utz
Second Defendant         :     State Solicitors Office

Case(s) referred to in judgment(s):

Bennett v Minister of Community Welfare (1992) 176 CLR 408
F v R (1983) 33 SASR 189
Jones v Dunkel (1959) 101 CLR 298
March v E & M H Stramare Pty Ltd (1991) 171 CLR 506
Rogers v Whitaker (1992) 175 CLR 479
Watt v Rama [1972] VR 353

WISBEY DCJ: Yvonne Joyce McLennan gave birth to the first plaintiff Jacob Riely McLennan on 15 May 1997 at the Kalgoorlie Regional Hospital, a medical facility operated by the second defendant. What ought to have been a joyous occasion was otherwise, as Jacob was born with severe encephalopathy (dyskinetic cerebral palsy) such that he is and will always be severely disabled. The controversy before the Court necessitates determining the primary cause of the debilitating condition, and whether it was the result of the negligence of either defendant. Whether it could have been avoided had appropriate steps been taken by either defendant in the management of Mrs McLennan immediately prior to and during Jacob's delivery.
The statement of claim alleges, and indeed it is common ground, that Mrs McLennan was, at the suggestion of the first defendant, admitted to the Kalgoorlie Regional Hospital on 14 May 1997 for induction and management during delivery, and that the first defendant, a specialist gynaecologist and obstetrician, was primarily responsible for her medical management.
The statement of claim alleges that the first defendant, the medical specialist supervising Mrs McLennan's labour, owed a duty to Jacob to exercise reasonable care and skill in the provision of advice and/or treatment given to Mrs McLennan. It is asserted that he breached that duty in that with the knowledge that the foetus presented as a double footling breech he:
(i)arranged for induction delivery of Jacob on 14 May 1997 without discussing with Mrs McLennan the attendant risks of that procedure being umbilical cord compression, head entrapment, and the inability to address such problems by caesarean section; and had she been so advised she would have elected to undergo caesarean delivery;
(ii)induced labour at about 1800 hours on 14 May 1997 without properly addressing the possibility of a rapid progression of labour, and of consequent complications;
(iii)utilised a labour catalyst (Prostin) when he knew or ought to have known that it would stimulate uterine contractions thereby increasing the likelihood of the risks referred to in par (i) eventuating, and the foetus suffering oxygen deprivation;
(iv)failed to give the relevant staff of the second defendant adequate instructions as to the monitoring of Mrs McLennan's condition during labour and the appropriate steps to be taken consequent upon the result of such monitoring.
(v)failed to advise Mrs McLennan before 0400 hours on 15 May 1997 of the necessity for the delivery to be effected by caesarean section.
It is alleged that the second defendant, having the responsibility for the provision of nursing and medical services at the Kalgoorlie Regional Hospital, owed a duty to Jacob to ensure that all reasonable skill and care was provided in respect of Mrs McLennan's accouchement; and was in breach of duty in that it:
(i)failed to report the result of CTG monitoring to the first defendant at any time prior to 0440 hours on 15 May 1997;
(ii)failed to advise the first defendant of the rupture of Mrs McLennan's membranes at 0315 hours on 15 May 1997, and/or the presence of stronger contractions at 0400 hours;
(iii)failed to continuously monitor labour electronically; and particularly after spontaneous rupture of the membranes;
(iv)failed to take any or any adequate steps to attempt to increase the foetal heart rate (which had fallen to about 90 beats per minute) between 0430 and 0500 hours, and to improve the blood flow.
An allegation that the second defendant was vicariously responsible for the negligence of the first defendant was abandoned, as was the second plaintiff's claim.
The statement of claim alleges that Jacob's debilitating condition was the result of a period of oxygen deprivation during labour that would not have occurred, alternatively would have been truncated and its consequence ameliorated, had he been delivered by caesarean section before 0400 hours on 15 May 1997 (par 34(a) of the statement of claim). Sub pars (b) to (e) do not take the matter further.
Resolution of this controversy is not assisted by the extraordinary delay between the events which give rise to the cause of action, and the date of hearing, particularly when it is necessary to retrospectively determine appropriate standards of medical care; and because Nurse Gilks, the midwife in charge of the delivery, died on 16 July 2002.

The evidence

Yvonne Joyce McLennan

Mrs McLennan, a married woman born on 9 July 1963, was at the relevant time living in Kambalda, and had training and experience in caring for the disabled. She has given birth to three children, Zachary born 13 April 1995, Jacob born 15 May 1997, and Taylor born 31 August 1998.
Jacob was conceived in August 1996, and approximately 12 weeks into the pregnancy Mrs McLennan attended the Kambalda nursing post and was advised to consult a general practitioner. Consequently she consulted Dr Date and saw him monthly until 30 weeks into the term, and thereafter on a fortnightly basis. At about 35 weeks she noticed a lot of foetal movement, and when she attended Dr Date at 38 weeks he advised her that the foetus was in breech position, and referred her to the first defendant. At this stage she was suffering from what she described as "hay fever or a cold".
Mrs McLennan was reluctant to transfer to another practitioner but was advised by Dr Date that he did not undertake breech deliveries. Consequently she attended upon the first defendant at his consulting rooms on 7 May 1997, taking with her a referral letter from Dr Date which indicated the foetus was in a frank or footling breech position. Her husband also attended.
Mrs McLennan stated that the first defendant asked her if there was a smoker in the home. He performed both an external and internal ultrasound and commented that the foetus was male. Mrs McLennan indicated she observed from the ultrasound screen that the foetus was in an upright position, the head being under her rib cage, and the legs and feet being lower in the abdominal area. The legs were crossed "a bit like a Buddha". She stated that the first defendant advised that her cervix was two to three centimetres dilated. Following an unsuccessful attempt to carry out an external cephalic version the first defendant advised Mrs McLennan that she needed to be booked into the Kalgoorlie Regional Hospital for induction of labour using Prostaglandin gel (Prostin). As a consequence, and bearing a request note from the first defendant, she took steps to book in for the night of 14 May 1997. Mrs McLennan stated that following enquiry from her, the first defendant said that he only did caesarean sections in an emergency, and that women were made to have babies. She stated that there was no discussion about optional procedures or risks, and indicted to the Court that if she had been advised that the baby's health was at risk with a vaginal delivery, she would have elected to have a caesarean section. Her recollection was that her husband was with her during the entire consultation.
Mrs McLennan attended the Kalgoorlie Regional Hospital on 14 May 1997 as arranged, and was admitted at approximately 1700 hours. The first defendant saw her at about 1800 hours and following a physical examination arranged an ultrasound. Mrs McLennan stated the picture was not clear, but she could see that the baby's legs were crossed. She could only see the top of the legs and buttocks, which were much lower than previously. The first defendant also carried out an internal examination, and stated that there was approximately two to three centimetres dilation of the cervix. Having first requested the nurse to monitor contractions, he inserted Prostin and left, stating he would probably deliver the baby in the morning. During the course of monitoring the nurse commented that although the contractions were weak, they appeared to be getting more regular. At about 2100 hours Nurse Gilks came on duty.
Mrs McLennan stated that at approximately 0315 hours on 15 May 1997 her membranes ruptured and she summonsed Nurse Gilks who examined the fluid and commented that it was amniotic and clear. Nurse Gilks checked the contractions which were then three minutes apart, and the foetal heart beat. Nurse Gilks gave her a "papery blue towel" with which Mrs McLennan allegedly wiped up the fluid. Mrs McLennan being ambulant, then attempted to contact her husband. The contractions became more intense, and at her request Mrs McLennan was moved by Nurse Gilks to the labour ward at about 0400 hours. Mrs McLennan stated that she began walking around the labour ward because it helped her contractions. The contractions became more painful, and Nurse Gilks attended Mrs McLennan at about 0415 hours and suggested that she go to the toilet and empty her bladder as it might help. In the course of so doing Mrs McLennan felt something distend between her legs and observed that it was a baby's leg which was a "dark bluey‑grey" or "a horrible colour". She used the toilet alarm button to summons Nurse Gilks, was instructed to return to her bed, which she did unaided, and Nurse Gilks checked the foetal heart beat. Nurse Gilks left the room in a concerned state, returning after about five minutes and placed an oxygen mask on Mrs McLennan's face, and instructed her not to push. Shortly thereafter the first defendant arrived and assisted Nurse Gilks deliver Jacob, by releasing the shoulders and head.
Jacob was delivered at 0458 hours and Mrs McLennan stated that he was a dreadful blue/grey colour and not breathing. The first defendant, and a paediatrician Dr Jeffries‑Stokes, set about resuscitating him with oxygen. Dr Jeffries‑Stokes advised Mrs McLennan that Jacob was quite ill, was fitting, and required evacuation to Princess Margaret Hospital by Royal Flying Doctor Service.
In cross‑examination Mrs McLennan agreed that her third child Taylor who had a birth weight of 3205 grams was delivered vaginally by the first defendant notwithstanding that she was in breech; but claimed that she was not really given the option of a caesarean section. She confirmed that in respect of the birth of Jacob and Taylor she wanted the delivery to be as natural as possible and didn't want an epidural or episiotomy. She agreed that her first child Zachary's birth weight was 3100 grams whereas Jacob's weight was 2700 grams. She agreed that she smoked during her pregnancies but denied that she had ever stated that she had 10 cigarettes a day, claiming that was a maximum, and that there were days when she had considerably less, or none at all. Her smoking habits were consistent throughout the three pregnancies, and she claimed to have been unaware at any material time that there was any strong connection between smoking, and foetal compromise. Mrs McLennan stated that she was aware of the caesarean section procedure because Zachary had been in the transverse position prior to delivery and her medical advisers had explained the situation to her. She had also been to birthing classes and read a basic birth text.
When questioned about recordings concerning her smoking habit made by people such as a hospital nurse and the paediatric neurologist Dr Smith in his report of 22 October 2002, she suggested they must have misunderstood what she had said.
Mrs McLennan agreed that she had nasal symptoms about a month before Jacob's birth but denied they were akin to influenza, and could not recall her husband or Zachary having similar symptoms. She agreed that Zachary suffered from an illness affecting his hands, foot and mouth, some two to three months before Jacob's birth. She confirmed that her height was 170 centimetres. She accepted as correct the notation in the documentation recording that at one stage during delivery Taylor had a foetal heart rate of 50 for 10 minutes.
Mrs McLennan acknowledged that her statement made on 11 June 2001 (Exhibit 10.116) was intended to set out the circumstances relating to Jacob's birth, and confirmed that she had viewed hospital records prior to making that statement. She agreed that the indication in the statement that she had seen the first defendant on two occasions prior to her admission to hospital, was incorrect. She had used the term frank breech in her statement because of what she had been told. She stated that the ultrasound that she viewed at the hospital seemed to show the baby's buttocks and thigh area. She was adamant that although her statement did not so indicate, she had been responsible for mopping up the fluid when her membranes ruptured at the hospital. Her recollection was that Nurse Gilks performed a vaginal examination at around 0400 hours after her membranes ruptured. She was adamant that Nurse Gilks suggested she go to the toilet and that whilst on the toilet she observed a portion of a leg of a greyish‑blue colour protruding from her vagina, although neither fact is referred to in the statement.
Mrs McLennan was adamant that her husband was with her when she attended upon the first defendant on 7 May 1997, and that the appointment was of the order of 15‑20 minutes duration. Her recollection was that the first defendant carried out an internal and external ultrasound demonstrating to her the position of the foetus, and told her that it was male. He was critical of the fact that she smoked. She would not accept that the first defendant demonstrated various breech positions to her, or embarked upon any detailed discussion of the methods, advantages, disadvantages and risks associated with delivery. She recalled raising with the first defendant the issue of a caesarean section by asking whether she would require a C‑section which she agreed she did not want. The first defendant responded, critical of the term "C‑section", stating that he did caesarean sections, but only in an emergency.
Mrs McLennan claimed that her husband attended most of her consultations with Dr Date. She stated that when she was pregnant with Taylor she and her husband attended the first defendant on a few occasions; but she was able to distinguish those visits from that on 7 May 1997 because "with Taylor I'd already had a child that was breech and I believed I understood my options as well".
When cross‑examined by counsel for the second defendant Mrs McLennan agreed that she saw the first defendant shortly after admission and an ultrasound was only undertaken by him. Following admission, and before Nurse Gilks took over at about 2100 hours, she was monitored by a younger nurse, whose name she could not recall. By that stage the belt had been removed from her abdomen, which she thought occurred shortly after her husband left, it having been applied for approximately 1 to 2 hours. It seems that she walked around the ward from time to time and would have been observed by nursing staff. She had no recollection of being approached by a student midwife seeking permission to be present at the delivery. She stated that the first defendant and Nurse Gilks both performed a vaginal examination, that by Nurse Gilks occurring after Mrs McLennan had attempted to ring her husband. She recalled Nurse Gilks checking the foetal heart rate after her membranes ruptured, but she was vague as to the number of checks carried out, and timing. She agreed that the contractions never reached the stage where she required pain relief. She was definite that it was Nurse Gilks who suggested that she go to the toilet, and upon her return urged her not to push; and felt that more than 10 or 15 minutes would have elapsed between the time she left the toilet and Jacob's birth.

Geoffrey Norman McLennan

Mr McLennan gave evidence of his support of his wife during the pregnancy, including attending with her upon Dr Date, particularly at the consultation when Dr Date indicated that he was having trouble detecting a heart beat and concluded that the foetus was in a breech position. Mr McLennan stated that he was with his wife at the consultation with the first defendant on 7 May 1997, his main function apparently being to care for their two year old son Zachary. He recalled the first defendant performing an ultrasound and endeavouring to turn the foetus. He stated that the first defendant had a "general chat" with his wife "that's all I remember". The first defendant said that there was plenty of room in the uterus and the baby might right itself. As they sat at the first defendant's desk Mrs McLennan asked whether she would have to have a C‑section and the first defendant responded "I don't do C‑sections, I do caesareans but you won't have to worry about that because women are made to have babies." The first defendant directed Mrs McLennan to go and book into the Kalgoorlie Regional Hospital. Mr McLennan stated that the consultation lasted 20 to 30 minutes.
Mr McLennan drove his wife to hospital on 14 May 1997 and stated that shortly after admission the first defendant arrived, viewed the ultrasound, and commented that he would use inducing gel. Mr McLennan professed being unaware of health risks to the foetus by reason of smoking by a pregnant woman and I felt was less than frank when discussing his wife's smoking habits. He was adamant that he had only attended the first defendant's rooms on one occasion, and denied that the hospital booking was made by phone. He agreed that it was his wife's desire to give birth naturally if possible. He could only recall one nurse attending upon his wife in hospital.
Generally I did not regard his evidence as convincing.

Ronald William Date

Dr Date, Mrs McLennan's general practitioner, produced in evidence his antenatal records dealing with eight consultations from 30 October 1996 to 1 May 1987 (Exhibit 10.2). He also identified pathology and ultrasound records relating to the period of the pregnancy. He confirmed that the record for 22 April 1997 indicated that Mrs McLennan presented on that date with an upper respiratory tract infection, which he described as a presentation of symptoms consistent with a mild flu like illness. He stated that it did not require any specific treatment, and was not of concern to him in respect of the pregnancy. The record contained a presentation sketch on 7 April 1997 which showed a cephalic presentation; one on 22 April 1997 showing the foetus with the buttocks presenting, which he described as a frank breech; and that on 1 May 1997 showing the foetus with the feet presenting, which he described as a footling breech. He stated that the consultation on 22 April 1997 was a routine consultation, and Mrs McLennan did not comment about any excess movement of the foetus.

In cross‑examination he agreed that his presentation sketch made 1 May 1997 demonstrated the foetus in a transverse lie position rather than as a footling breech. He confirmed that it was his practice to warn pregnant women of the adverse consequences of smoking. He agreed that by letter dated 7 May 1997 the first defendant advised him that the foetal position was an extended breech. He stated that on 15 May 1997 he received a telephone call at about 0440 hours, and proceeded forthwith to the hospital arriving about 10 minutes later. At that stage Jacob had been delivered. He confirmed that he had made a note in the integrated progress notes (Exhibit 10.51) which inter alia recorded "15.5.97 approx 2/24 0430‑0830 assisted with resus of above". The notation 0430 was his estimate of when he arrived at the hospital, but on reflection he thought it was probably erroneous.

Sven Harald Thonell

Dr Thonell, a paediatric radiologist, is the director of diagnostic imaging at Princess Margaret Hospital, having worked in that area for approximately 25 years. He explained that in new‑borns it was possible to carry out cranial or brain ultrasound through portals such as the fontanelle or a very thin bone on the side of the head, making it possible to see most of the brain. Normally it was possible to perform ultrasound scans of the baby's brain in the first few months, enabling the detection of such conditions as haemorrhage, brain swelling, and structural abnormality. He stated that CT scanning is no longer undertaken since it may cause brain damage in the new‑born, a fact that was not appreciated in 1997. A CT scan demonstrates the absorption of various parts of the brain.
Dealing with a situation where a baby's brain was denied oxygen, Dr Thonell stated that early changes wouldn't be observable on a CT scan, but would be picked up after several hours, thus identifying areas where there was brain swelling and reduced attenuation in the parts of the brain that had been ischaemic. Maximum swelling of the brain would occur between two to three days of the triggering event, and then begin to settle. If swelling was observed, all it was possible to say was that it had occurred within the previous three days. Dr Thonell stated:
"If we see swelling we can only say that it occurred within the last sort of three days. Obviously if its gross swelling it would have to take more time than if its only mild swelling, or it may have taken even longer because the swelling may be settling so its very difficult to time it."
He stated that the swelling would have disappeared if the initiating event occurred some weeks before the scanning.
Dr Thonell identified the ultrasound and CT reports which demonstrated:
(i)The cranial ultrasound performed at 1130 hours on 16 May 1997 indicated appearance in keeping with a moderate generalised oedema. There was a suggestion of luxury perfusion (increased blood flow) consistent with prior infarction.
(ii)The cranial ultrasound performed on 20 May 1997 at 1620 hours showed a generalised increased ecogenicity and that the oedema appeared to have settled to some extent. The appearance demonstrated on CT probably corresponded to blood brain barrier damage due to ischaemic change.
(iii)The CT scan carried out on 20 May 1997 at 1130 hours suggested widespread changes through both hemispheres suggestive of areas of cerebral oedema or infarction.
In his report dated 23 May 2002 Dr Thonell stated inter alia:
"The ultrasound showed signs of generalised oedema (swelling) of the brain but no ultrasound evidence of haemorrhage. The doppler study of the internal carotid and anterior cerebral arteries showed a low resistive index which, considered in association with other factors such as low apgar score at birth, degree of metabolic acidosis, onset of spontaneous respiration etc, carries a poor prognosis.
The resistive index is measure of the relationship between the maximum systolic and end‑diastolic velocities of arterial blood to the brain. In Master McLennan's case the end‑diastolic velocity was relatively high (twice the expected norm for a term infant) giving rise to a reduced relative velocity of blood flow or low resistive index. This would suggest an increased perfusion of the brain found after an episode of hypoxia (lack of oxygen to the brain) sometimes called 'luxury perfusion'.
The CT showed several areas of low attenuation (darker on CT) and poor differentiation between the white and grey matter indicating oedema or swelling of the brain as on the earlier ultrasound and/or areas of brain infarction. In addition to this there were areas within the central parts of the brain or basal ganglia which showed an increased blood perfusion and 'contrast enhancement' ie intravenous administered contrast passing through the blood/brain barrier into areas damaged by hypoxia (lack of oxygen). This sort of damage is most often associated with a sudden severe hypoxic event.
Oedema or swelling of the brain becomes maximal only 2‑3 days after an hypoxic event and usually settles thereafter."
Dr Thonell concluded that the likelihood was that the changes seen were referable to an event or events either shortly before, during, or immediately after birth.
In evidence‑in‑chief Dr Thonell expanded on the observations appearing in the ultrasound and CT reports, and the comments in his written report. He stated that the ultrasound and CT scan investigations did not indicate an hypoxic event as early as 34‑36 weeks into the pregnancy because if there had been such an event it would have resulted in brain atrophy, which was not identified. He indicated that it would require a quite severe and sudden injury to the brain to result in the observable damage to the basal ganglia. There was no radiological sign of earlier brain damage.
Damage to the basal ganglia was usually associated with a sudden and profound insult to the brain from ischaemia or hypovolaemia. Following infarction and the brain being starved of oxygen supply whether due to hypoxia or hypovolaemia there was an increased blood flow to the deprived area (luxury perfusion).
In cross‑examination Dr Thonell agreed that it was not possible to determine the cause of the pathology simply by looking at the results of ultrasound and CT scanning. He agreed that he had said in his report that the cerebral damage observed was most often associated with a sudden severe hypoxic event, rather than that it was caused by a sudden severe hypoxic event, because causation was outside his area of expertise. He agreed that there were many factors involved in causing damage to the brain.

Paul Bernard Colditz

Professor Colditz is the professor of perinatal medicine at the University of Queensland, and is the director of the Perinatal Research Centre at the Royal Brisbane Women's Hospital. He is well qualified, and actively involved in foetal and neonatal clinical care and research, having a special interest in brain development and damage in the foetus and new‑born. He was a member of a medical experts body chaired by Professor McLennan which produced the 1999 International Consensus Statement or the "template for defining causal relation between acute intrapartum events and cerebral palsy" the purpose of which was to synthesise the available evidence from a broad range of disciplines on that subject. He stated the exercise highlighted the fact that intrapartum events were uncommon causes of cerebral palsy.
In dealing with some of the matters in the statement he pointed out that metabolic acidosis in the blood was the product of a shortage of oxygen to body tissues. Base excess which is zero for a normal person, determines the severity of the metabolic acidosis, ‑12 or greater being of consequence, a foetus being unable to survive at ‑30. He stated that dyskinetic cerebral palsy, which was not a common type of cerebral palsy, would only result from injury to basal ganglia. A foetus existed at a mean oxygen saturation of 50 per cent, as distinct from an oxygen saturation level close to 100 per cent on birth, and was well accustomed to living in an hypoxic environment. Hypoxia alone was unlikely to damage the foetus. Brain damage resulted from a complete lack of oxygen to the brain tissue, which would occur if the blood flow failed. In such a case there was hypoxic ischaemic encephalopathy.
In his report of 7 August 2006 Professor Colditz summarised what he regarded as the relevant clinical details. He readily accepted that the International Consensus Statement, which he noted had wide acceptance, was a useful synthesis of available evidence relevant in establishing whether in a particular case intrapartum events may have been the cause of cerebral palsy, particularly because in the majority of cases of cerebral palsy the condition did not have its origin in the events of labour.
Dealing specifically with the essential criteria required by the Consensus Statement, as applicable to this case, he noted that at about 0914 hours the base excess was ‑12 confirming the presence of severe metabolic acidosis. He noted that Jacob's heart rate was depressed late in labour, and shortly before birth could not be detected (drawing the inference that it was absent or at best extremely low). It was severely bradycardic at 60 beats per minute immediately after birth. He regarded this as evidence of severe cardiac depression, most likely explainable on the basis of a severe acidosis being present. He inferred that the metabolic acidosis level at birth was most likely in the range ‑12 to ‑25. There was a good cardiac response to resuscitation, suggesting that the metabolic acidosis level would be correcting over the four hours from the time of birth until the recording of the first blood gas with a base excess of ‑12. He was confident that there was early moderate to severe neonatal encephalopathy and cerebral palsy of the spastic quadriplegic or dyskinetic type.
Professor Colditz agreed that cerebral palsy was more commonly encountered in a situation where there was a growth restricted foetus, although the vast majority of growth restricted babies did not have it. He appears initially to have taken the view that Jacob was programmed to be a small baby and did not have late or asymmetric growth restriction. He acknowledged that the risk of cerebral palsy was higher for a foetus in breech presentation, however the vast majority of those in breech presentation did not develop that condition. Professor Colditz was not of the view that Jacob had congenital defects having an association with his condition, and discounted possible intrapartum infection as relevant to any metabolic causes. He expressed the opinion that there was no evidence of asymmetric growth restriction. He considered that there was a single hypoxic event sufficient to cause sudden severe hypoxia on the basis that:
"Following a period of labour in which foetal heart rate was normal at all times, membranes ruptured with a poorly engaged footling breech presentation. This is a high risk situation for either umbilical cord prolapse or for cord compression…cord prolapse was sought and found not to be present at that time. There was no CTG in place and neither was one put in place and hence there was only intermittent observation and recording of the foetal heart rate…the foetal heart rate was normal until shortly before the time of delivery. At that time there was a sustained and serious degree of foetal bradycardia. Immediately prior to birth the foetal heart rate was absent (or at least could not be obtained)…In the context of a footling breech presentation with ruptured membranes, the sequence of events surely suggests that a 'sentinel event' had occurred, namely in the form of cord compression…Whilst in my view the hypoxia and resultant bradycardia was present for at least 25 minutes and possibly for up to almost 1 hour, even if it were present for only 17 minutes (a possibility presented in the questions below) then this is sufficient to cause the injury observed in the brain of the plaintiff, namely extensive damage to the cortex but most importantly involvement of the basal ganglia as well.
…there is a narrow window between injury and death. Characteristically the brain is able to withstand 15 minutes of total hypoxia without injury. By about 20 minutes, the basal ganglia are damaged. By 25 minutes, the cortex is extensively damaged and by 30 minutes the foetus does not survive. Of course these times are approximate but there is good evidence of the progression of injury to death in this manner."
In his supplementary report of 6 November 2006 Professor Colditz addressed specifically the issues of growth restriction and foetal or maternal infection to which he made reference in his evidence, describing each as an unlikely contributor to Jacob's condition.
In the course of his evidence Professor Colditz explained and confirmed the contents of his reports.
In the context of addressing the issue as to whether the foetus had been in footling breech presentation Professor Colditz confirmed that he was not an obstetrician but had literally taken a look at some of the notes and made his own interpretation to reach the conclusion that it was a footling breech. He was particularly influenced by the first defendant's drawing.
Professor Colditz stated that dyskinetic cerebral palsy only occurred when there was basal ganglia injury.
In addressing the use of Prostin, Professor Colditz stated that it was a standard way of inducing labour, but because there was a great difference in sensitivity between females it was the practice to monitor by CTG for some period of time around the insertion of Prostin.
Professor Colditz stated that the Apgar scores indicated that following birth Jacob's brain remained fairly depressed. Referring to the seizures that were observed subsequent to birth, he stated that seizures occurred in a situation where the brain was under severe metabolic stress, and in this case there was no explanation other than Jacob had a severe hypoxic ischaemic episode to the brain. He referred to the creatinine reading which he stated was indicative of kidney damage from an acute insult and very characteristic of hypoxic ischaemic injury. Radiological evidence of basal ganglia injury was confirmatory of a severe hypoxic ischaemic injury.
Professor Colditz appears to confirm the views of Dr Thonell that the ultrasound and CT scans were indicative of a very severe acute cerebral stress at around the time of birth.
Professor Colditz stated that a baby with congenital abnormality was more likely to have some form of brain maldevelopment than otherwise. He stated that the bilateral hip dysplasia and scoliosis occurred post‑birth as a consequence of cerebral palsy, and were not congenital abnormalities; and that undescended testes, if such there was, constituted a minor form of congenital abnormality.
Dealing specifically with asymmetrical growth restriction, Professor Colditz stated that if there was a normal growth trajectory, the length, head circumference and weight would be normal. If there was a period of foetal under‑nutrition, adverse environment, or chronic foetal hypoxia, the first foetal response was to drop weight significantly. If the stress continued then length was affected, and head circumference was the last to be affected. He stated that asymmetric growth was where there was a difference between the expected head dimension and weight, and his preliminary conclusion had been that Jacob was a symmetrically small baby. He discounted a dysmorphic condition (abnormal development) which might affect the brain and result in cerebral palsy, because there was no evidence of dysmorphism of the brain.
Professor Colditz referred to the definition in the Consensus Statement of a singleton hypoxic event, and when asked what that event was in the case of Jacob replied:
"I don't think we know what the singleton hypoxic event was. We know that a number of things didn't happen. The uterus didn't rupture. We also noted that the foetus was apparently, from all the observations, doing quite well. Subsequently it suddenly had bradycardia that was sustained and resulted in a severe compromise at the time of birth, so I think it may come back to semantics. I mean perhaps I could best crystallise things by saying I think I'm taking a common sense approach whereas Professor McLennan is taking a hanging off the words as a specific example of things that may cause a singleton event."
When asked to summarise his common sense approach he stated:
"That is the sequence of observations from early in labour suggesting that the foetus is not compromised, normal foetal heart rates then for no particular reason, but that is not uncommon as the onset of signs of foetal compromise manifest as bradycardia, and finally, the severe depression of the baby when born shortly after."
In cross‑examination Professor Colditz agreed with the statement made in his report that an intrapartum event was an uncommon cause of cerebral palsy. He was referred to the report of the paediatric neurologist, Dr Peter Walsh (Exhibit 10.91) who reported:
"It is therefore likely that the injury to Jacob's brain occurred within a day or two of birth rather than several weeks before birth. It is possible, however, that he suffered some adverse events during the pregnancy, for example, the neonatal viral infection which may have predisposed him to be particularly susceptible or sensitive to a relatively mild degree of hypoxia at birth. I have made this suggestion because there appears to be considerable incongruity between the apparently relatively benign progress of the labour and the severe neurological outcome."
and agreed that it was a possibility, but that it didn't explain the acute cerebral oedema, and the events on the early CT scan imaging. He also stated that he did not agree with Dr Walsh's assessment that there was "a relatively benign labour". When pressed concerning the acute event, he repeated that he could not identify the event, which was not an uncommon situation.
Professor Colditz appeared to shift ground and was prepared to agree with Professor McLennan that in Jacobs case there had been severe growth restriction (below the 10^th percentile), but disagreed that it meant that there was a tenfold increase in risk, stating that the literature suggested an increased risk of somewhere between 1.6 to sixfold. He also pointed out that the risk factor did not explain the clinical indicia at birth. His view was that the key determinant of asymmetry was a comparison of weight with head circumference, not weight with length, and he concluded that there was a symmetrical growth restriction which started early in pregnancy. He did not agree that there was significant data suggesting increased vulnerability from infection, and thereby cerebral palsy outcome, in small growth babies, but accepted that there was good evidence that infection can damage the foetal brain.
Dealing with his inferential reasoning that there had been a singleton hypoxic event, Professor Colditz referred in particular to what he described as foetal bradycardia, no foetal heart rate detectable immediately prior to birth, and a heart rate of 60 one minute after birth, commenting that:
"I mean that can only occur in the context of there having been a preceding severe hypoxic episode, lasting long enough to cause severe acidosis".
He agreed that the notation that a foetal heart rate could not be heard immediately prior to birth, did not necessarily indicate that it was absent. Referring to Professor Stanley's work, he agreed with her conclusions that there was a link between growth restriction and cerebral palsy – it was a risk factor. He agreed with Professor McLennan's statement that over the last 40 years there had been no drop in the rate of cerebral palsy, which was still at the rate of about 2 to 2.5 per thousand live births.

When cross‑examined by counsel for the second defendant Professor Colditz agreed that his conclusion that there had been a bradycardiac event relied inter alia on the integrated progress notes that there was a drop in the foetal heart rate to 90 which was not picking up after contractions, and that no foetal heart beat was detected immediately prior to delivery. He accepted that the partogram suggested a normal foetal heart rate at about 0425 hours, and that it was reasonable to conclude that the foetal heart rate was probably within normal range prior to 0425. He accepted that the foetal heart rates recorded on the partogram were supplemented by others on the integrated progress notes, so that there were recordings at times other than as shown on the partogram, and noted it would be normal to record on the partogram once labour commenced. He agreed that the normal base line heart rate for a foetus was between 110 and 160 beats per minute, and the fact that it fell outside the normal range did not necessarily mean that damage had then occurred.
In re‑examination Professor Colditz said:
"Cerebral palsy can be caused by many different things but in this particular case we have what is to my mind an inexorable logical sequence of events that is limitation of oxygen supply to the foetus that is through the umbilical cord that resulting in foetal bradycardia severe depression at birth, very low Apgar scores, the need for resuscitation, very slow response to resuscitation referable oedema documented in the early ultrasound changes the acidosis etc. So I think the limitation of oxygen, in this case, available to the foetus via the cord is really a very critical event. It is the thing that's set in chain this sequence of events."

William Boyd Molloy

Dr Molloy is a consultant gynaecologist and obstetrician practising in Sydney, although he ceased obstetrics in January 2000. His CV demonstrates that he has significant and varied experience in his discipline. During his 34 years of practice in obstetrics he had experience in the delivery of babies in breech presentation, being principally full breech, and rarely a footling breech. He stated that breech delivery was effected vaginally until a change in practice in the 70's and early 80's, particularly in the case of primigravid breeches, when it became accepted world‑wide that delivery should be by elective caesarean section. The principal requirement for caesarean delivery was because the largest part of the baby was the head, and coming last there was the risk of head entrapment.
Dr Molloy's reports, which he confirmed, were received in evidence (Exhibit 13.1‑13.5).
In his report dated 23 November 2004 Dr Molloy expressed the view that the foetus was presenting as a footling breech on 7 and 14 May 1997 and, as a consequence, the first defendant should have offered a caesarean section because of the associated risks. He recorded that a footling breech (foot presenting) as against a frank breech (buttocks presenting) had a higher risk of cord prolapse and ensuing complications. He expressed the view that the use of Prostin was inappropriate, but that seems to be based on the premise that there was a footling breech. Also that continuous monitoring was essential. He reported that it was normal practice in labour wards without a monitor, for the foetal heart rate to be checked every hour over a two to three minute period. It was his view that following spontaneous rupture of the membranes an examination should have been carried out to make sure there was no cord presentation, or that it was coming down between the foetus and the pelvic side wall; and the first defendant should have been contacted and requested to attend the hospital. Continuous monitoring should have taken place at this time. It would have been inappropriate for Mrs McLennan to be advised to attend the toilet. Once there was a foot prolapse, delivery should have been completed using a breech extraction technique. The report seems to indicate that Dr Molloy formed the view the first defendant took 15 minutes to attend the hospital after being contacted, and then a further 13 minutes to deliver Jacob.
In his report dated 8 February 2005 Dr Molloy basically agreed with the views expressed by Professor MacKay in his report dated 18 December 2004.
In his report of 26 April 2006 Dr Molloy dealt specifically with the sketches made by the first defendant on 7 and 14 May, concluding that each demonstrated a footling breech.
In his report of 20 July 2006 Dr Molloy addressed the situation that would have been applicable if the foetus was presenting as a flexed or complete breech and stated:
"Provided that Dr McCallum did not feel that the baby was large and the case that was known of her previous cephalic delivery, he may well have contemplated a vaginal delivery, but as I have stated to you, there is a footling breech present on this occasion and not a frank (complete) breech present. Nevertheless, he should have monitored this patient throughout labour."
He also stated that if it was a complete breech Mrs McLennan should have been induced in day time and monitored throughout labour.
In evidence Dr Molloy made it clear that the major risk of the breech delivery was head entrapment. He was firm in his evidence, as he was in his reports, that the first defendant's sketches indicated a footling breech which he defined as "usually where the feet are below the buttocks, or the leg itself is fully extended below the buttocks, leg or legs." He indicated that if the foetus was firmly in the pelvis as at 7 May it was unlikely to move thereafter. When asked to describe why, with a footling breech, the incidence of prolapsed cord and ensuing complications was a lot higher Dr Molloy said:
"Well, first of all the cord can slip down when the legs are out of the way and this can either do one of two things. First of all it can be a cord presentation which is an absolute acute emergency or secondly you can get cord compression if the cord slips down somewhat but not fully and therefore not palpable."
He stated that although it was possible to get a cord prolapse with a frank breech, it was less likely since the foetus formed a tighter fit within the pelvis.
Dr Molloy stated that on 14 May the first defendant should have organised to perform a caesarean section "the next day or so". He was against the use of Prostin on the basis that there was a possibility Mrs McLennan might go into strong labour very quickly, with possible adverse consequences, such as a ruptured uterus. He agreed that from the time that a foot prolapsed at 0430 hours until Jacob was delivered at 0457 or 0458 hours, there was insufficient time to have performed a caesarean section, which he considered would take at least 30 minutes and probably longer. Dr Molloy considered that Jacob was probably in an hypoxic state because of cord compression.
When addressing the Prostin manufacturer's recommendations, Dr Molloy seemed to be of the view, as was the first defendant, that a malpresentation essentially referred to a footling breech.
When asked to comment on Professor McLennan's opinion about the cause of cerebral palsy, Dr Molloy responded "Yes he has a number that he sprouts forth, yes", which suggests a lack of objectivity. In addressing his disputation with Professor McLennan he expressed the view that right up until the time Mrs McLennan was "induced" the foetus was perfectly well; the first time there was any indication to the contrary was about 0430; and thereafter until delivery there was a period of 28 minutes when all sorts of things could have gone wrong, and he believed did. Dr Molloy was also critical of the fact that a paediatrician was not summonsed at the same time as the first defendant, although I have some difficulty concluding in all the circumstances that it would have made any difference to the outcome.
In cross‑examination Dr Molloy expressed the view that a flexed or complete breech necessarily converted to a footling breech in the delivery process, which appears to be a somewhat extraordinary proposition. He was not aware of the Hannah randomised multicentre term breech trial. He agreed that his criticism of the use of Prostin was essentially based on his conclusion that it was a footling breech. He pointed out that it was necessary to be careful with the controlling of the dose, agreeing that it was widely used in 1997, and that "We have all used it but it's a two edge sword."
Referring to the fact that Mrs McLennan had previously given birth to a 3100 gram baby, Dr Molloy seemed prepared to accept that it was probably acceptable in her case to deliver a frank breech vaginally. He observed generally that:
"The largest thing coming through the pelvis is the baby's head which is the last thing, and let me tell you every obstetrician has got stuck with one, otherwise they haven't practised."
That statement, if correct, would seem to confirm that every obstetrician has had experience with breech delivery naturally. He stated that most obstetricians were nervous about delivering breeches other than by way of caesarean section "but that's now not then".
Dr Molloy's attention was drawn to guide line No 20 of the Royal College of Obstetricians and Gynaecologists entitled "The Management of Breech Presentation" a guide line published in the aftermath of the Hannah trial, and it was put to him that the commentary was completely inconsistent with any suggestion that a complete breech prior to the Hannah trial was to be treated in the same way as a footling breech, that is, dealt with only by caesarean section, and he appeared, albeit reluctantly, to accept that proposition.
It was put to Dr Molloy that his oral evidence was inconsistent with the statement in his report of 20 July 2006 that, provided the first defendant did not feel the foetus was large, he may well have contemplated a vaginal delivery; but he denied there had been a change in his position. After some prevarication, and with apparent reluctance, he accepted that if in fact in Mrs McLennan's case the foetus had been a complete breech, it would not have been inappropriate to proceed by way of vaginal delivery.
Dr Molloy agreed that the foetal heart rates of 120 recorded at 0315 hours, 132 recorded at 0330 hours, and 128 recorded at 0400 hours were within normal range, but stated that one did not know what was happening in between times, and the readings would have been taken when Mrs McLennan was not contracting. He agreed that the information available up until 0400 hours was indicative of a perfectly natural onset of labour, but stated that one did not know what was happening during contractions, and that there should have been continuous monitoring. When Professor McLennan's assertion that CTG monitoring had the potential to throw up a false positive return of 99.8 per cent was put to him, there appeared to be a reluctance to address the issue. He referred to the integrated progress note that at 0315 hours there was a spontaneous rupture of membranes with irregular moderate to mild contractions four to five minutes apart, and stated that it was an indication that Mrs McLennan was actually in labour at that time. He agreed that at the time the foetal heart rate dropped to 90 it was necessary to deliver Jacob as quickly as possible, but was reluctant to concede that in fact occurred.
During cross‑examination by counsel for the second defendant, Dr Molloy agreed that the process of labour was essentially divided into three stages; the first comprising the latent, active and transitional phase; the second when the patient was fully dilated; and the third from after the delivery of the baby until delivery of the placenta. In general terms the first stage was the longest and least painful; the second stage when the patient was fully dilated could be between 15 minutes to an hour; and the third stage from the delivery of the baby to the delivery of the placenta was something in the order of 5‑10 minutes.
Dr Molloy agreed his reports were based on two factual premise, the first being that on 14 May the foetus was a footling breech presentation, and the second being event timing. He agreed that with a footling presentation there was the risk of cord prolapse, or compression, which explained why the midwife had made the particular notation "no cord felt" in the vaginal examination following the spontaneous rupture of the membranes. The other risk area was head entrapment when (inter alia) part of the cord would be compressed with the head, although he accepted that it had not happened in this case. He agreed that there was probably going to be some compression of the cord with a vaginal breech delivery, but notwithstanding, the vast majority of breech presentations that were delivered vaginally were healthy normal babies. The problem with compression of a cord was when it occurred over a long period.
Dr Molloy also agreed that the time sequence of events was very important, and that there was some difficulty getting a clear impression of that from the integrated progress notes; with which I entirely agree. When his attention was directed to the summary of labour and delivery (Exhibit 10.36), he disputed the notation that labour commenced at 0400 hours, stating that it commenced at about 0315 hours when the membranes ruptured, although accepting that it depended on the frequency and strength of contractions. He agreed that the record "fully dilated at 0440 hours" appeared to have originally been noted "0540 hours". He also accepted that it was a reasonable proposition that the notation "fully dilated at 0440 hours" corresponding, as it did, with the integrated progress note that at 0440 hours the foetal heart rate was 90, and not picking up, indicated a time when examination took place, and demonstrated a need to contact the first defendant. He confirmed that once the foetal heart rate had been recorded as 90 and not picking up after contractions, the necessary focus of attention was to deliver Jacob as quickly as possible, and emphasised that unless a decision had been taken by 0315 hours to proceed to caesarean section, it was pointless thereafter to contemplate it. Essentially he seemed to take the position that a midwife only had the responsibility of notifying the specialist obstetrician of significant events such as the rupture of the membranes or adverse foetal heart beat recording, and not changes within the normal pattern of labour. He also agreed that the foetal heart rate was generally recorded by the midwife when the mother was not contracting.
In re‑examination, Dr Molloy stated that recordings on the partogram generally commenced when the patient was transferred to the labour ward.

Eric Vincent MacKay

Mr MacKay who is presently retired, save for "medico‑legal" work, has considerable experience and qualification in the field of obstetrics and gynaecology, and was the Professor of the Department of Obstetrics and Gynaecology at the University of Queensland from 1964 to 1989. His reports of 18 December 2004 and 25 August 2006 were received in evidence (Exhibit 14.1 and 14.2).
At the date of giving evidence Mr MacKay was 82 years old, and it follows that his practical obstetric skills had not been manifest for some time, his last practical obstetric involvement being in the early 1980's. His answers to questions concerning his ceasing to be a member of the Royal College of Australian and New Zealand Obstetricians and Gynaecologists were somewhat evasive. His present academic interest appears to be directed to medico‑legal issues.
In his report of 18 December 2004 he referred to the decision to carry out an induction, stating that as it represented an act of interference in the natural course of labour – ie, its onset and progression – the decision to carry it out should only be made on a cost benefit basis. Having recorded that he was not given any information as to why an induction was proposed, he concluded that it was contra‑indicated. He considered that the uterine activity evident at the end of the post Prostin CTG trace should have indicated the need to continue the trace, and to notify the first defendant. He reported that there were a number of reasons why an obstetrician should be cautious about vaginal delivery of a breech baby, the first being the risk of head entrapment, and the second and major problem being compression of the umbilical cord, usually because of its lower position or prolapse following rupture of the membranes, the incidence of prolapse being about 3 per cent of all breech presentations, and being significantly higher where the breech did not fill the lower uterine segment ‑ presentations other than extended (frank) type.
Proceeding on the basis that when Mrs McLennan was admitted to the ward on 14 May 1997 the foetal feet were presenting, Mr MacKay was of the view that there was a strong case for elective caesarean section.
Mr MacKay reported that the CTG showed significant uterine activity, with contractions finally about every two minutes, and he stated that in a case such as this where there was an ever present risk of major umbilical cord compression, intermittent foetal heart rate auscultation was not appropriate. He expressed the view that CTG monitoring if not then in operation, should have commenced when the membranes ruptured. Mr MacKay considered that when the foetal heart rate dropped to 90 it was virtually certain that it was caused by cord compression. He suggested that at that stage emergency aid should have been undertaken including the administering of a tocolytic drug to quieten the uterus (this presumably would have delayed delivery). It is clear from the report that Mr MacKay proceeded on the basis that the foetus was a footling breech.
In the annexure to his report, answering specific questions, Mr MacKay stated that if the breech was thought to be of the extended legs type, it was appropriate to suggest that a trial of labour was reasonable. He reported that if there was sufficient indication for induction of labour, there was sufficient indication for continuous monitoring of labour. He agreed that manual auscultation had been shown to be as effective as CTG monitoring in general, but because of the risk of cord complication in this particular case, periodic monitoring was not adequate. He reported that sustained bradycardia could only be tolerated by the foetus for 10‑15 minutes before risk of serious central nervous system damage. He considered that there was a hiatus in monitoring between 0400 and 0440 hours when bradycardia supervened, and where continuous monitoring could have provided an alert. He generally appears to have taken the view that there was excessive delay between foot protrusion and delivery, although he did not set out his reason for that conclusion.
Mr MacKay's report of 25 August 2006 makes it very clear that his mind was closed to any position other than that the foetus was in the footling breech presentation. He seems particularly to conclude that the use of Prostin resulted in hyper‑stimulation of the uterus, although that does not appear from the hospitals records to be correct. He agreed that statistically it had been shown that intermittent auscultation was in general equivalent to continuous monitoring in terms of morbidity outcome, but stated that was not applicable where there was an abnormal presentation.
In evidence, Mr MacKay confirmed the views in his two reports. He stated that Prostin was on balance the cause of the fairly rapid labour since it was known to have a relaxing effect on the cervix, and a stimulatory effect on the uterus. He stated that the CTG indicated that there were about six contractions in the last 13 minutes of the recording, which meant that they were two to two and a half minutes apart, and that one liked to see about a minute between contractions. He concluded that when the trace stopped the rate of contractions was still escalating.

Mason CJ in March v E & M H Stramare Pty Ltd (1991) 171 CLR 506 said at 509:
"In philosophy and science, the concept of causation has been developed in the context of explaining phenomena by reference to the relationship between conditions and occurrences. In law, on the other hand, problems of causation arise in the context of ascertaining or apportioning legal responsibility for a given occurrence."
Mason CJ, Deane and Toohey JJ stated in Bennett v Minister of Community Welfare (1992) 176 CLR 408 at 412‑413:
"In the realm of negligence, causation is essentially a question of fact, to be resolved as a matter of common sense. In resolving that question, the 'but for' test, applied as a negative criterion of causation, has an important role to play but it is not a comprehensive and exclusive test of causation; value judgments and policy considerations necessarily intrude."
It is accepted that Jacob was born with severe encephalopathy, and the question is what was its cause.
Dr Thonell stated that where a baby's brain was denied oxygen it would manifest in brain swelling and reduced attenuation in parts of the brain that had been ischaemic. Maximum swelling would occur between 2 to 3 days of the triggering event and then begin to resolve. If swelling was observed radiologically all that could be said is that it had occurred within 2 or 3 days of its identification. His interpretation was that the cranial ultrasound performed on 16 May 1997 indicated moderate generalised oedema. The cranial ultrasound performed on 20 May 1997 suggested some resolution. The CT scan carried out on 20 May 1997 indicated widespread changes suggestive of area of cerebral oedema or infarction. He considered that scanning demonstrated increased blood perfusion in the basal ganglia most often associated with a sudden severe hypoxic event. The likelihood was that the changes observed radiologically were referable to an event or events either shortly before, during or immediately after birth, and that it would require a severe and sudden injury to the brain to result in the observable damage to the basal ganglia.
Professor Colditz, a participant and contributor to the 1999 International Consensus Statement, confirmed the view expressed in the statement that acute intrapartum events were an uncommon cause of cerebral palsy. A foetus was well accustomed to living in an hypoxic environment and hypoxia alone was unlikely to damage the foetal brain. Brain damage resulted from a complete lack of oxygen to the brain tissue which would result if the blood flow failed, possibly resulting in hypoxic ischaemic encephalopathy. He agreed that cerebral palsy was more commonly encountered in a growth restricted foetus, although the vast majority of growth restricted babies did not develop cerebral palsy. Growth restriction was a risk factor. Also, that the risk of cerebral palsy was higher for a foetus in breech presentation, although again the vast majority of those in breech did not develop that condition. At trial he resiled from the position he had earlier taken, and agreed that Jacob was growth restricted (below the 10^th percentile) and that intrauterine growth restriction was a risk factor for cerebral palsy which he put at between 1.6 to sixfold. His view was that the radiological evidence of basal ganglia injury was confirmatory of a severe hypoxic ischaemic injury. He conceded that he didn't not know what the singleton hypoxic event was causing the condition because the uterus had not ruptured and the foetus was from all observations doing quite well until there was sudden and sustained bradycardia "for no particular reason". He then inferred that there had been an hypoxic event namely cord compression notwithstanding that he was unable to identify it or its timing. He accepted that the hospital records indicated that the foetal heart rate was normal up until 0425 hours on 15 May 1997.
Dr Molloy considered that Jacob was probably in an hypoxic state because of cord compression. Compression was deleterious when it occurred over a long period of time.
Mr MacKay considered that it was virtually certain that the drop in the foetal heart rate was caused by cord compression or possibly hyperstimulation. He agreed that Jacob, being a small baby, would pose no problem negotiating the birth canal. He drew the inference that there was cord compression from the fact that in his view there was no other logical explanation for the fall in the foetal heart rate.
The first defendant's evidence was that there had not been any head entrapment or cord prolapse or entanglement, and no clinical indication of cord compression. He arranged an ultrasound following admission and ascertained that there were no cord problems at that time.
Profession MacLennan stated that considerable research into cerebral palsy had led to the presently held the view that only 1 per cent of babies born with the condition were thought to have been compromised by an acute de novo primary asphyxial event in labour. Over the 38 years since he commenced practice the incidence of cerebral palsy in term births had not changed notwithstanding the dramatic escalation in the rate of caesarean sections before labour, more efficient surgical methods, a dramatic increase in electronic foetal monitoring, and better neonatal resuscitation. He considered that Jacob's birth rate was around the third percentile, and that he had asymmetrical growth restriction. Professor MacLennan referred to the report of Dr Ian Walpole commenting on very deep hand and feet creases which was possibly indicative of an unsound intrauterine environment. The consensus of current scientific evidence was that the neuropathology of cerebral palsy was established silently during pregnancy, and that signs of foetal neurological compromise often did not appear until the stresses of labour. His view was that the risk of cerebral palsy was approximately tenfold in term babies under the 10^th percentile in weight for gestational age. One third of babies born with cerebral palsy had an inflammatory response syndrome. A foetal heart rate of 90 was not indicative of total hypoxia and was present in approximately one third of all second stage labours. He accepted that in a small number of cases neuropathology could begin and become established in a healthy foetus following an acute hypoxic event intrapartum. His conclusion was that Jacob was already chronically stressed with resultant intrauterine growth restriction and reduced reserves, and experienced further stress in a rapid labour and assisted breach delivery. There was no theoretical explanation why an intact healthy foetal brain would have become acutely and severely ischaemic or hypoxic during what was a short labour, and it was more likely that the neuropathology of the cerebral palsy was already established before labour. He stated that it was impossible for a radiologist to differentiate between late peri‑natal neurological compromise and that in a growth retarded foetus where final and irreversible neuropathology was established only in the last 2 hours before delivery. Professor MacLennan stated that it was unusual to get cord compression in a normal labour unless the cord was tightly around the foetal neck or fell down and got compressed by the presenting part above it. Research had demonstrated that intrauterine growth restriction was a major risk for cerebral palsy. He would not accept that there was acute de novo hypoxia between 0440 hours and 0457 hours, stating that Jacob was very severely growth restricted (23 per cent down on his weight) indicative of the fact that he had been chronically comprised for weeks. He was not a healthy baby going into labour.
Dr Renou referred to Jacob's birth weight stating that he was born in a very poor condition with gross central nervous system dysfunction which was unlikely to be the consequence of the quick and uncomplicated labour. He thought that the CTG trace suggested an abnormal response to the normal stresses of early labour in a baby who already had severe central nervous system dysfunction.
Dr Walsh, a paediatric neurologist, speculated that Jacob may have suffered some adverse events during pregnancy which could have made him particularly sensitive to a mild degree of hypoxia at birth; apparently being troubled by the incongruity between the benign labour and the neurological outcome. He felt that the EEGs were consistent with hypoxic ischaemic encephalopathy.
Another paediatric neurologist Dr Lindsay Smith reported on 22 October 2002 (Exhibit 10.93) that:
"The major thrust as I indicated in my report of the Monday the 2^nd of September 2002 on page 4 first paragraph is whether or not Jacob was abnormal prior to delivery or not. I posed this question to mother directly during the consultation in relation to the unexplained, presumed to be drug reaction to sodium malproate, coma at the age of 3 years. The alternative explanation for this is that he has an inborn error of metabolism that falls in to the mitochondrial group and that the ability of the brain to withstand the stresses and strains of both delivery and of other post natal events is severely compromised leading to a decrease in function. This does not obviate the fact that such stresses and strains did occur and if it is reasonable that he had a pre‑existing condition then certainly the mode of delivery would have exacerbated his present level of disability. I strongly recommend that the specific question be directed to his treating physician Dr Avihu Boneh, Metabolic Physician, Genetics Health, Royal Children's Hospital, Flemington Road, Parkville, in relation to the question of the underlying diagnosis and the likelihood that this young man had a pre‑existing abnormality.
The evidence is silent as to any metabolic enquiry.
Dr Ian Walpole a consultant geneticist reported on 4 November 1997 (Exhibit 10.16) inter alia that:
"Findings of note were multiple pressure dimples on bony prominences, and it was difficult to extend the fingers of both hands, right more than left. The transverse palmar creases were extremely deep and I believe would be indicative of intrauterine fisting…
I think that in light of the nature of clinical signs present at birth the intrauterine foetal condition had not been sound, as reflected in the poor response to birth stress, the very deep hand and foot creases which may be attributed to long standing clenching and the subcutaneous dimples as seen in hypokineses."
Considerable attention was directed during the trial to the Consensus Statement and the factors which it requires to be established before it can be asserted that cerebral palsy is the result of an acute intrapartum hypoxic event. Clearly the Statement is looking at causation from a scientific rather than legal perspective. The Court's task is to determine whether "as a matter of common sense" on the balance of probabilities Jacob's condition can be attributed to an acute intrapartum hypoxic event. The Consensus Statement is significant however in that it is an acknowledgment by a substantial international body of medical expertise in this area that cerebral palsy is rarely the consequence of an acute intrapartum hypoxic event. Also that intrauterine growth restriction appears to have a reasonable association with the condition (it is a risk factor). Further that there is doubt as to the efficacy of electronic foetal monitoring.
It is axiomatic that the burden of proof is on the first plaintiff to establish on the balance of probabilities that the condition of cerebral palsy was caused by an event during labour. ("a period of oxygen deprivation" – par 34 of statement of claim.)
The evidence of Nurses Jones, Freeman and the first defendant, and the integrated progress notes and partogram, demonstrate that there was no rupture of the uterus, placental abruption, head entrapment, or cord entanglement or prolapse; and there was a rapid labour and delivery.
The first defendant did not identify any clinical evidence of cord compression, and having regard to the speed of the delivery, if such there was, it would have been of short duration and would not have been expected to have resulted in brain damage.
Professor MacLennan stated that it was unusual to get cord compression in a normal labour unless the cord was tightly around the foetal neck, or fell down and got compressed by the presenting part above it. There is no evidence of such occurrence.
The experts who support the proposition that there was cord compression resulting in hypoxia and subsequent brain damage, appear to draw that inference from the fact that they believe there was a footling breech presentation; the drop in foetal heart rate with none detectable immediately prior to birth; the subsequent radiological imaging; and an inability to ascribe any other cause.
As against that there was an apparently benign labour, and I am satisfied that Jacob was asymmetrically growth restricted, indicative of an unsound intrauterine environment, which is a risk factor having an association with cerebral palsy. That raises the possibility that the drop in the foetal heart rate was part of the clinical reaction of a chronically compromised foetus to the normal stresses of labour.
Bearing in mind that Jacob's heart rate was 60 immediately following delivery, I have difficulty accepting that his heart was not functioning as he was delivered.
Dr Thonell attributed the radiological evidence of brain damage to an event or events either shortly before, during, or immediately after birth. The evidence establishes that Jacob did not make any real respiration effort for approximately 8 minutes after birth which was not explored during evidence but would seem to be an extremely relevant factor in this respect.
The evidence also establishes that an acute intrapartum hypoxic event is a relatively rare cause of the condition.
In Jones v Dunkel (1959) 101 CLR 298 when discussing the civil burden of proof Dixon CJ said at p 304:
"In an action of negligence for death or personal injuries the plaintiff must fail unless he offers evidence supporting some positive inference implying negligence and it must be an inference which arises as an affirmative conclusion from the circumstances proved in evidence and one which they establish to the reasonable satisfaction of a judicial mind. It is true that 'you need only circumstances raising a more probable inference in favour of what is alleged'. But 'they must do more than give rise to conflicting inferences of equal degree of probability so that the choice between them is mere matter of conjecture'. These phrases are taken from an unreported judgment of this Court in Bradshaw v McEwans Pty Ltd which is referred to in Holloway v McFeeters, by Williams, Webb and Taylor JJ. The passage continues: 'All that is necessary is that according to the course of common experience the more probable inference from the circumstances that sufficiently appear by evidence or admission, left unexplained, should be that the injury arose from the defendant's negligence. By more probable is meant no more than that upon a balance of probabilities such an inference might reasonably be considered to have some greater degree of likelihood.' But the law which this passage attempts to explain does not authorise a court to choose between guesses, where the possibilities are not unlimited, on the ground that one guess seems more likely than another or the others. The facts proved must form a reasonable basis for a definite conclusion affirmatively drawn of the truth of which the tribunal of fact may reasonably be satisfied."
That is equally applicable to proof of causation, bearing in mind of course that "causation is essentially a question of fact to be resolved as a matter of common sense".
At the end of the day identification of the cause of Jacob's condition is having regard to the totality of the evidence a "mere matter of conjecture". I am not satisfied that it arose out of any particular event in labour.
Having regard to my findings generally it is not necessary to address the contribution issue.
The first plaintiff's claim against each defendant is dismissed.