Lennie (A Child) v Royal Victoria Infirmary & Associated Hospitals NHS Trust

This is an appeal by the claimant from an order made by Judge Langan QC sitting as a High Court Judge in this City on the 11th March 2006, following the trial of this action, whereby he dismissed this claim against the defendants for damages for negligence. The claimant was born at the Royal Victoria Infirmary on the 16th March 1998 and has suffered from moderate to severe four limb dystonic spastic cerebral palsy with significant cognitive delay from the time of his birth. It was common ground that his mother suffered a placental abruption shortly before his birth, a process by which the placental attachment to the uterus is disrupted by haemorrhage. It was also common ground that the claimant's condition was caused by birth hypoxia secondary to placental abruption.

The crisis in the mother's condition was noted at 20.25 when the midwife on duty observed that the fetal heart-rate had descended to 90 beats per minute ("bpm") and was not recovering. A registrar, Dr. Wood, made two attempts at delivery at 20.45 by using a Kiellands forceps. Both of these attempts failed and it was common ground that if either had succeeded catastrophic damage would probably not have occurred. The judge said at paragraph 31 of his judgment that irrespective of any questions of fault or causation the outcome was a calamity. The question he had to determine was whether this calamity was caused by any negligence in the care the claimant and his mother received at the defendants’ hospital.

It was a curious features of this case that an allegation of negligence in relation to the attempt to achieve a forceps delivery surfaced for the first time just before the trial started. Dr. Wood had not previously been made the subject of criticism, and he then made a supplementary witness statement describing how he had acted 8 years earlier. During his evidence-in-chief he still did not know precisely what he was said to have done wrong, because leading counsel then acting for the claimant did not condescend to any details about this in his opening speech. In cross-examination it emerged for the first time that it was being said against Dr. Wood that his attempts failed because the baby's head was higher than he had thought it was. Alternatively, if the baby's head was at the level of the ischial spine as he thought, it was said it was negligent to attempt a forceps delivery with the baby's head at that level except in a real medical emergency. The judge held that this was a real medical emergency and this observation was not challenged on the appeal.

In the event the judge robustly rejected the "head too high" ground of challenge in favour of two possible explanations proffered by the defendants' expert witness, Professor Thornton. However, he went on to grant the claimant permission to appeal on this issue on the grounds that his conclusion depended on inferences to be drawn from findings of fact which were not, or not significantly, in dispute, and an appeal court might well draw different inferences from those facts.

The claimant's former advisors did not seek permission to appeal on any other ground. However, a new team of lawyers who were not concerned with the carriage of the claimant's case until after the trial obtained permission to amend the grounds of appeal by reinstating the three other issues on which the claimant failed at the trial. These related to decisions which the defendants' medical staff took, or failed to take, in relation to the level of dosage of syntocinon that was being used as a means of inducing the baby's birth. It was said in particular that the dosage should not have been increased and should probably have been reduced at about 17.48, and that after about 18.30 it should certainly have been reduced and preferably stopped altogether.

Although no case was identified in the medical literature of a syntocinon induced placental abruption occurring at a late stage of labour, it was being argued at the trial that it was the syntocinon level that probably caused the abruption. On the appeal the claimant's new advisors put their case on causation in a different way.

The forceps issue, although it arose at the end of the mother's labour, can conveniently be considered first since it can be dealt with quite quickly. Dr. Wood had come on duty at 20.00. He took over from Dr. Esen, who had had the medical care of the claimant's mother from the time that she was admitted to the labour ward at 09.00 that morning. This was her second child. She had had an uneventful pregnancy, and on 13th March, when the baby was 7 days overdue, she was booked to be admitted to hospital for induction of labour three days later.

Dr. Wood and Dr. Esen both shared her care with Dr. Bullen, a senior specialist registrar. At about 17.00 Dr. Esen had discussed his proposed care plan with both Dr. Bullen and Professor Davison, who was the consultant on duty. Professor Davison did not feature in the history thereafter. The judge found that all the defendants’ witnesses of fact were doing their best to recount what they observed and did that day, and that the claimant's mother was plainly an honest and reliable witness who also did her best to recall the events of the day.

Of the two expert witnesses Mr. Johnson (for the claimant) and Professor Thornton (for the defendants) the judge said that both were distinguished obstetricians, and that neither was more obviously a more impressive witness than the other.

As I have said the medical emergency started that evening at 20.25. At that time Ms Fellows, the midwife who came on duty at 20.00, observed from the cardio-tacograph (CTG) that the fetal heart-rate had descended to 90 bpm and was not recovering. The judge had earlier explained that a reading below 110 bpm signified bradycardia (a slow heartbeat) and was indicative of fetal distress. Ms Fellows moved the mother to her left side, administered facial oxygen and summoned the doctors.

The judge found that Dr. Bullen and Dr. Wood arrived between 20.30 and 20.36. They decided that they must immediately take active steps to deliver the baby. Dr. Bullen knew that the mother's first child had been a forceps delivery after the use of a ventouse had failed to effect delivery. At 20.40 they therefore decided to proceed straight to a forceps delivery. Dr. Wood used a Kiellands forceps. His contemporary note reads:

“Per abdomen 0/5.

Cervix fully dilated.

Right occipital transverse at spines.

Easy application of blades (anterior) wandering/posterior direct.

No rotation of head, although blades rotated x 2.”

By the time both attempts at forceps delivery had failed (because the blades slipped from the baby's head both times) the fetal heart-rate had gone down to 80 bpm. A reading of 50 bpm was recorded when the mother arrived at the theatre. When the baby was born in poor condition at 21.03 it became apparent that a placental abruption had occurred.

In his written and oral evidence Dr. Wood said that he had decided to use a Kiellands forceps due to the position of the head which required rotation. He thought it would be feasible to deliver the baby vaginally because the baby's head was low enough and the mother's pelvis was adequate for this purpose. The judge explained how the blades of the forceps are placed on the narrowest part of the baby's skull, around the lower part of the cheek and on the side of the chin. When they are properly applied the handles of the forceps will be parallel with each other. Forceps must be used with caution, without exerting undue pressure on the head.

Dr. Wood said that when the forceps were in place he would introduce a finger to check exactly where they were in relation to the baby's head. He would then push the baby's head up about 0.25 centimetres in the direction of the mother's head before rotating the blades. His aim was to rotate the head through a 90 degree angle, but on each occasion the blades had slipped around the baby's head and rotation was not achieved. He said he had performed 130 to 150 forceps deliveries, 100 of these by the time of the incident with which this court is concerned, and the blades had slipped on only two other occasions: on one of these he had succeeded at a second attempt.

In his examination-in-chief he said that he felt that the baby's head was sufficiently low down in the pelvis for a forceps delivery to be attempted. In cross-examination he denied that delivery had failed because the head was in fact higher than he thought.

There were three pieces of evidence which placed the baby's head at the level of the ischial spine, and one which placed it even lower. The first three consisted of a note of a vaginal examination made by Dr. Esen at 19.30, Dr. Wood's own note, and Dr. Wood's evidence at the trial. The fourth, Dr. Wood's note "Per abdomen 0/5" placed the head 3 centimetres below the spines. The judge considered that this was probably a mistake, but there was no evidence at all to support Dr. Johnson's last minute theory that the head had been too high above the spines, and the accuracy of Dr. Esen's note was not challenged on cross-examination. The judge said he could see no reason why he should reject Dr. Wood's evidence that the handles of the forceps were parallel when he tried to rotate the head, and Mr. Johnson had accepted that his theory could not be right if this evidence was accepted.

The judge was also unimpressed by the way in which this criticism of Dr. Wood had crystallized. Mr. Johnson was an acknowledged expert and teacher in the use of the forceps. While acknowledging its value he regarded it as the most dangerous tool in obstetrics. The way in which he had thought of the "head too high" theory two or three days before the trial was unconvincing.

The judge considered the two possible explanations proffered by Professor Thornton were far more likely. The first was that this child was bigger than his older brother and constituted a tight fit in his mother's pelvis and he was therefore more resistant to rotation. The second was that Dr. Wood unfortunately selected forceps which had a larger than usual separation of the tips. This possibility was mentioned in one of the textbooks produced in evidence at the trial.

Unlike Mr. Johnson's theory neither of these theories involved the rejection of all the evidence about the level of the baby's head. The judge ended this part of his judgment by saying that while it was impossible to say definitively why forceps delivery had failed, it was to a high degree improbable that this failure was attributable to the position of the head being still above the ischial spines.

On the appeal Miss Gumbel QC, who appeared for the claimant in this court, did not seek to challenge the Judge's rejection of the “head too high” case. Instead she sought to advance a new argument, to the effect that the failure to affect a satisfactory forceps delivery called for an explanation and the judge was entitled to infer that Dr. Wood had been negligent in the absence of a satisfactory explanation. She referred in this context to the evidence that Mr. Johnson had never experienced this mishap except in his very early days. Professor Thornton had never had this experience himself. Dr. Bullen had only found the blades slipping once when he was trying to deliver a premature baby, although he said that even in experienced hands there was an accepted failure rate, and apart from one occasion, when neither the blades nor the head had rotated, Dr. Wood had only had this mishap once before when he had succeeded at a second attempt.

This revised way of putting the claimant's case ran into the following formidable difficulties:

The second of these points, about the size of the forceps, admits of no further elaboration. As to the first, Miss Gumbel sought to explain to us that Professor Thornton's theory was inconsistent with Dr. Wood's description of how he put his fingers in and pushed the baby's head up. But this point, if a good one, should have been put to Professor Thornton at the trial and not raised for the first time on an appeal.

It is noteworthy that Professor Thornton said in his evidence-in-chief that a slipping forceps was an unusual but a well-recognised occurrence. He knew that other people had experienced this happening, and that was one of the reasons why people were taught to check that this head had indeed rotated just in case the forceps had slipped over the head. Dr. Bullen gave a similar explanation.

There would no doubt have been a much fuller answer if the claimant's case at trial had been advanced along the lines suggested by Miss Gumbel. Instead, the claimant's closing written submissions at the trial presented to the judge, Mr. Johnson's "head too high" explanation, Professor Thornton's true explanation and a fourth possibility called "God knows why", with no suggestion that if the defendants could not provide a reasonable explanation negligence should be filed against them. In these circumstances it is not in my judgment open to the claimant to put forward this new case on the appeal, because evidence was not adduced to meet it at the trial. This part of the appeal therefore fails.

I turn now to the allegations that relate to the syntocinon level. Syntocinon is an oxytocin infusion administered intravenously by drip for the purpose of inducing or enhancing the mother's labour. The aim is to establish a pattern of contractions similar to that of normal labour. Dr. Esen's plan when he examined the mother at 10,00 on the morning of 26th March was to start administering the drug within 2 hours if by that time there was not a satisfactory pattern of contractions. A helpful chart included within the judgment shows how the drug was first administered at a rate of 1.2 millilitres per hour, and the dose was then increased in stages to level of 7.2 millilitres per hour at 14.22. The evidence showed it was then held level at that rate until it was increased to 9.6 millilitres per hour at 17.48. This event marks the first of the two points of challenge in this part of the case.

The number of contractions and their strength were measured by palpating the mother's abdomen. "3:10" means 3 contractions every 10 minutes and so on. The chart records "3:10 varying in strength" at 12.30 and thereafter 4 contractions every 10 minutes up to 16.30. The dilatation of the cervix increased from 4 centimetres at 10.00 to 8 centimetres ascertained at the vaginal examination at 17.30. At 16.30 the head was still 4 centimetres above the level of ischial spines.

Nothing of note had happened up to the time when Dr. Esen reviewed the mother's progress at 16.50. He noted that the CTG occasionally showed "early deceleration" on which nothing turns, and that there was rather slow progress in the mother's labour. He decided that he would conduct a vaginal examination and take a fetal blood sample from the baby's skull to ascertain whether the fetus had become acidotic as the PH of its blood was lowered. Before taking either of these steps he would discuss his plan with the senior registrar, and in the event both Dr. Bullen and Professor Davison approved what he was doing.

There was some confusion over the timing of some of the contemporary notes, but by the end of the trial it appeared to be generally accepted that Dr. Esen took the fetal blood sample at about 17.29 and performed his vaginal examination while the sample was being tested. The report came back at 17.33. At 17.48 the syntocinon level was increased to 9.6 millilitres per hour.

For the purpose of taking the fetal blood sample the mother had to be placed on her left side with her left leg drawn up to her chest as far as possible and her right foot in a stirrup. At the same time the doctor would be washing and scrubbing and the patient had to be covered with sterile drapes. After considering the results of the vaginal examination and the fetal blood sample report, Dr. Esen decided to increase the syntocinon rate to 9.6 millilitres per hour. His note shows he intended to discuss the case with Professor Davison in 2 hours’ time.

The PH reading of the blood sample was satisfactory, but the dilatation of the cervix still measured only 8 centimetres and the baby's head was still 3 centimetres above the level of the ischial spines. He noted that the CTG was "Much better now." It was agreed he was mistaken when he noted the position of the fetus as "occipito-anterior" which would have been a favourable position for delivery. The fetus was eventually in a right occipito transfer position, which could not have been reached if Dr. Esen's note had recorded the position correctly.

The judge found that notes apparently made by Miss Waterston, the midwife on duty between 17.35 and 17.45, must in fact have recorded the position after the syntocinon dose was increased at 17.48, being a time which she noted on the CTG trace. After recording the increased dose Miss Waterston noted that the contractions were very painful and there was a discussion about the need for painkilling relief. A note ascribed to 17.45, but in fact made rather later on the Judge's findings, showed that the contractions were now too powerful and close together and the mother was not now coping well. They discussed analgesia or an epidural injection. A note ascribed to 17.50 shows that an epidural injection was decided upon, and at 18.10 a test dose of epidural injection was delivered.

The reason why the judge reached his conclusion about the timing of the various notes was that the pain and contractions were more likely to follow the stimulus of an increased dose as opposed to a static dose. Mr. Johnson said that Dr. Esen's decision to increase the syntocinon dose at this stage evidenced a substandard level of care, an expression he equated with negligence. He attached significance in this context to the deep late deceleration to 80 bpm that was noted on the CTG at 17.20. Although the contraction rate evidenced slow progress in labour, itself an indication for increasing the syntocinon, Mr. Johnson considered that an increased baseline on the CTG, which appeared very clearly on the CTG trace when 17.00 and 17.50, represented a contraindication. He was doubtful of the value to be attributed to a fetal blood sample taken when syntocinon was being administered, and he placed great weight on the mistake made by Dr. Esen over the position of the fetus.

He said that any finding other than an occipito-anterior position represented positional disproportion, and in such an event "you don't crank up the contractions." An irresistible force (the contractions) would be meeting an irresistible object (the uterus), and increasing the contractions involved the risk of rupturing the uterus. He said there was no virtue in forcing a baby out too quickly. He considered that Dr. Esen had made a negligent error and that this error was critical to his analysis of this part of the case. If the position of the fetus had been correctly identified as occipito-posterior, a decision to increase the syntocinon would not have been acceptable.

Finally, Mr. Johnson said that this was evidently a busy day at the hospital. The midwives were often calling for medical assistance and a doctor was not available to answer every call. The prevailing circumstances were conducive to care being delivered below the appropriate level.

The judge rejected Mr. Johnson's analysis. On the final point Dr. Esen had discussed his decision in principle with the two senior doctors at 17.00 and he obtained a fetal blood sample and carried out a vaginal examination before increasing the syntocinon dose. Any surrounding circumstances were therefore irrelevant.

The judge said that the progress of labour could fairly be regarded as slow and that Mr. Johnson had conceded this. The achievement of further progress through an increase in the syntocinon dose was therefore indicated unless there were indications to the contrary. Possible contra-indications were the fetal heart-rate and what was said to be an indication of hyperstimulation on the CTG trace.

As to the former the CTG trace had shown a rapid recovery after the deceleration at 17.20, and the judge accepted Professor Thornton's evidence that that single deceleration was not such as to give cause for concern.

As to the raised baseline the judge said it was impossible to say whether this showed hyperstimulation or was caused by the mother being moved at about this time. The latter explanation seemed more probable because the baseline went down after 17.50 notwithstanding the stimulation created by the increased dose of syntocinon. The judge said on the evidence that it was impossible to identify in 1998 an optimum rate of contraction on which all obstetricians would agree. Professor Thornton said that five contractions every ten minutes was the desired rate and Mr. Johnson said he could "live with that."

Although the mother's contractions hit that rate at times, they were not running consistently at that level. Rather, they were just below the level which at least some obstetricians would regard as desirable. It could not therefore be negligent to increase the syntocinon rate so long as the other indications were favourable, as indeed they were.

The rate of progress in labour could reasonably be regarded as slow and the fetal blood sample showed that the fetus was healthy. In this context the judge explained why he preferred Professor Thornton's explanation of a textbook reference on which Mr. Johnson relied.

Finally, the judge rejected the suggestion that Dr. Esen had been negligent in erroneously noting the position of the fetus. This had never been put to him in cross-examination, and although Mr. Johnson ended by saying that this error was crucial to his analysis this did not emerge at the trial until after all the factual witnesses had left the witness box. On this issue the judge found Professor Thornton's opinion more convincing. It was not critical at that time to be precise about identifying the position of the fetus. Dr. Esen had been justified in conducting an examination that was minimally invasive. It was easy in those circumstances to make the simple error of mistaking one fontanelle for another. The judge added that even if he was wrong about this Mr. Johnson's assertion was far too weak to represent a peg on which the court could make a finding adverse to the defendants.

Miss Gumbel conceded that her case on this appeal was stronger in relation to the events that followed the period of bradycardia at 18.25 than it was in relation to the decision to increase syntocinon which was implemented at 17.48. This is understandable. When he directed the increase from 7.2 to 9.6 Dr. Esen followed the Royal Victoria Infirmary Delivery Suite Guidelines 1997, which told him that the majority of women should achieve adequate uterine activity by a dose of 7.2 millilitre per hour, but there was provision to go higher so long as any decision to increase beyond that level was taken in conjunction with the first on-call special registrar, as indeed happened in this case. It is noteworthy that counsel who had acted for the claimant at the trial did not seek permission to appeal against the judge's rejection of this part of his case, although this may have been due to the difficulties they faced on causation.

The first of the two grounds of appeal in relation to the decision to increase the dose to 9.6 was not seriously argued at the hearing of the appeal. This was understandable, because in my judgment the judge was perfectly entitled to place the greatest reliance on the midwife's note on the CTG as an accurate record at the time of the increase, as indeed Miss Waterston, the midwife in question, encouraged them to do. In any event, whether the moment the increase took effect was at 17.48 or 15 minutes earlier was of little material relevance.

The second ground of appeal suggested that the judge's finding that it was not negligent to increase the dose was a finding that was wrong and against the weight of the evidence. It was said that he had failed to take into account the argument in respect of a presentational disproportion, and had also failed to take into account the history of the mother's previous delivery. The judge had however considered the relevant evidence with very great care and preferred the evidence of Professor Thornton on the issues in dispute.

We did not see the witnesses and the impression an expert witness makes in the witness box gives a trial judge an advantage which is denied to an appellate judge, who must resist the temptation to re-try the case on the transcripts. As I have already observed, Dr. Esen was never given the opportunity of commenting on Mr. Johnson's belief, not shared by Professor Thornton nor accepted by the judge, that the increased use of syntocinon was not acceptable if the position of the fetus at 17.33 had been correctly ascertained as occipito-posterior.

As to the history of the mother's previous delivery Mr. Hart QC, who appeared for the defendants both at the trial and at the appeal, observed in his skeleton argument that this point had never been relied upon in the court below for the very good reason that the mother's previous delivery was by Neville Barnes forceps. These are used for delivery of babies in the occipito-anterior position, which Mr. Johnson did not regard as involving positional disproportion. Miss Gumbel understandably did not press this point on the hearing of the appeal. In my judgment there are no grounds for interfering with the judge's carefully expressed conclusion that it was not negligent to increase the dose to 9.6 at 17.48.

The other disputed issue related to the standards of medical care following a prolonged period of bradycardia at 18.25. The judge said that this was a short matter over which he had experienced greater difficulty, and it was with some hesitation that he concluded that negligence had not been established. At about 18.00 the mother was lying on her left side in anticipation of the epidural injection. The fetal heart-rate was about 155 bpm and there were 4 or 5 contractions every 10 minutes. The judge found that a test dose had been administered by injection at 18.10 and the main dose at 18.20. The baseline fetal heart-rate was now 140 to 150 bpm.

At about 18.25 the period of bradycardia started and for about 3 minutes the fetal heart-rate fell to a level at or below 80 bpm. However, there was then a recovery to a baseline of about 130 bpm 4 to 5 minutes after the bradycardia started. The baseline then increased to 150 bpm and a note "CTG improving" was made during this period.

Miss Waterston was immediately alert to the significance of the bradycardia. She told the medical staff immediately, although no doctor was immediately available. In the event Dr. Esen arrived at, I think, 18.40 after dealing with another patient, and when he reviewed the situation everything was back to normal in his view.

At the centre of this issue is the question of the appropriate response to the prolonged bradycardia which started at 18.25. Mr. Johnson said it should have been treated as evidence of fetal distress and that the administration of syntocinon should have been immediately turned off or reduced. Professor Thornton said the proper approach was to summon a doctor, as in fact happened, and that the decision not to take any steps in relation to the syntocinon level was defensible.

I have already described how the allegation about the forceps delivery surfaced for the first time just before the trial, and the alleged significance of Dr. Esen's mistake over the position of the fetus at 17.30 emerged even later, after the factual evidence had been concluded. In relation to the standard of care at and after 18.28 Mr. Johnson's opinion had fluctuated. In his first report prepared in February 2001 he made no criticism of the standard of care at this time. A revised report prepared in September 2003 contained a single sentence to the effect that not to switch off the syntocinon at that time represented substandard care.

The judge referred, in my judgment wrongly, to a letter written in March 2005 when Mr. Johnson said that the hospital staff reacted appropriately to the episode of fetal distress at 18.28. I say that this was wrong because in this letter he was referring to the actions of the midwife.

In December 2005 Mr. Johnson developed his September 2003 criticism, and this played a prominent part in the trial. In making his criticisms Mr. Johnson relied particularly on a passage in a medical textbook to the effect that the manufacturers did not recommend the use of syntocinon if there was any evidence of fetal distress. In practical terms this recommendation embraced any abnormality of the fetal heart-rate, "If such an abnormality occurs during syntocinon infusion the infusion should be stopped immediately."

Professor Thornton said that this advice should not be regarded as universally prescriptive. When it was put to him that the syntocinon should have been stopped at 18.40 when the contractions began to increase he said “no”, for four reasons:

The judge found this approach convincing. It was true that the situation between 18.25 and 18.28 was such as to give rise to real concern, and it was unfortunate that the hospital's medical staff could not have responded more rapidly. However, he believed that this was a diversion because the issue was the same at 18.40 or 18.45 as it had been ten minutes earlier.

He said that the fetal blood sample was a recent one. On the second issue he recorded Mr. Johnson's evidence to the effect that fetal bradycardia frequently followed an epidural injection, but its incidence could reasonably be attributed to the epidural only if there was a fall in blood pressure, which did not occur in this case. However, the judge said it was common ground that the proper response to bradycardia following an epidural was to place the mother on her left side and await recovery. This was done and the desired result achieved in this case. He said there were no other signposts indicating that syntocinon should be stopped. Given the fact that the mother had been moved on to her left side after the epidural, the judge said that the likelihood was that the state of the CTG at about 18.28 was attributable to this movement.

On this part of the case Miss Gumbel criticised the judge for placing reliance on the fetal sample taken at about 17.30 as reliable evidence of the condition of the fetus one hour later following a period of bradycardia up to 3 minutes long. She also criticized the judge for his reasoning when he found that the bradycardia had probably been caused by the epidural injection at 18.20, and that in the circumstances Dr. Esen was entitled to make no change to his care plan for the patient when he saw her at 18.40.

As to the first of these points Professor Thornton had been very clear about the value of the sample taken at 17.30 as an indication for the future. He gave these answers to questions:

“Q. All this blood sample could show is whether or not at the time the sample was taken the fetus was not acidotic?

A. No, it can tell us quite a bit more than that yes. No, we have the - we know the level of the PH so we know whether it was on the borderline of acidotic or not abnormal at all.

Q. Well that is just what I put to you?

A.

We know the base excess, so we have in the present case a result that is not even remotely borderline, an absolutely normal result which tells us something about the fetus at that time, and unless major changes occur is likely to be telling us something about the fetus in the future.”

His evidence was also to the effect that the taking of a new fetal sample could not have rendered any useful evidence until about 40 minutes after the syntocinon had been stopped and the fetal heart-rate had been restored to normal.

The second point needs more thorough consideration. Mr. Johnson's evidence was to the effect that if the bradycardia had indeed been caused by the epidural injection one would expect to see evidence of a drop in mother's blood pressure, but the blood pressure reading was in fact normal.

Professor Thornton's evidence on this point was to this effect, I quote:

“It is generally believed that these transient bradycardias that occur after epidurals are caused by... low blood pressure in the mother. However, it is also well recognised that sometimes that low blood pressure is not detected by the doctors or midwives looking after the patient... unless the patient has a sort of intra-arterial catheter measuring their... blood pressure continuously. It is only measured... every 5 minutes. So it is perfectly possible, and I think likely in fact, that there was a drop in maternal blood pressure which caused that bradycardia... I am as near certain as I can be of anything the fact that it was not detected does not rule it out.”

I observe that in fact the blood pressure was only being taken every 15 minutes and that there was no reading between 18.15 and 18.30.

When Professor Thornton was reminded of the note which read "Turned onto left lateral side. BP 120/60" and it was put to him that this was an absolutely normal reading, he said:

“It depends a little bit whether that blood pressure was taken after that left lateral. If it was then of course the turning her has done the trick which it was intended to do of getting her blood pressure back to normal. That blood pressure is indeed normal.”

He summed up his evidence on this point at the end of his next answer:

“All the evidence was that this was a completely healthy fetus immediately prior to that single prolonged deceleration which immediately followed an epidural top up. They turned her onto her side, her blood pressure was adequate and the fetal heart rate recovered at that point, when Dr. Esen came back to see her, to normal.”

I would add that when Miss Waterston, the midwife who made the note about the blood pressure, was in the witness box Mr. Redfern QC, who then acted for the claimant, put to her as a question, adopting this as what in fact happened:

"Turned onto left lateral - then you take the blood pressure."

The judge dealt with this part of the evidence in a somewhat confusing way in an otherwise admirably careful judgment. To explain what I mean I must read from paragraphs 63, 66 and 67 of his judgment:

“[63] Professor Thornton's evidence was to the effect that he did not regard the last sentence [of the textbook passage put to him] as universally prescriptive .”

You take every case on its own.

“It was put to Dr. Thornton that at any rate by 18.40 when the rate of contractions began to increase and Dr. Esen had not yet arrived, the syntocinon should have been stopped. He disagreed, for reasons which were helpfully summarised in Mr. Hart's written submissions at the end of the hearing:

'(i) the doctor's knew the baby was in excellent condition [from the fetal blood sample at 17.33];

(ii)

bradycardia following epidural is common;

(iii)

so long as the bradycardia returns to normal it was reasonable to continue the syntocinon;

(iv)

the bradycardia did return to normal.'

[66] I have to say that I found Professor Thornton's approach convincing. I accept it, but not without scrutiny of each of its stages. As to (i), I simply underline the fact that the fetal blood sample was a recent one, taken within the hour which proceeded the bradycardia. I shall have to deal somewhat longer on (ii). It is accepted by Mr. Johnson that fetal bradycardia does frequently follow upon epidural, but he points out that the bradycardia could reasonably be attributed to the epidural only if it were combined with a fall in the mother's blood pressure Mrs. Lennie's blood pressure was recorded between 18.20 and 18.30, but there is nothing to suggest that the reading (120/60) was other than normal. It is, I think, common ground that the proper response to bradycardia following epidural is to place the mother on her left side and await a recovery. This is what occurred here, the fetal heart-rate did recover and so Professor Thornton's points (iii) and (iv) are made good. That cannot, however, be an end of the matter: because, even if each stage of his reasoning process thus far is unimpeachable, there may have been other signposts pointing to the need to discontinue the syntocinon.

[67] I do not think that there were any such signposts. Given the movement of Mrs. Lennie which was involved in the administration of the epidural, the likelihood is that the state of the tocograph around 18.28 was attributable to such movement. Anything that happened thereafter was, as I understood Mr. Johnson's evidence, confirmatory of an error already made rather than the provision of a warning belatedly to correct that error.”

Miss Gumbel argued that the judge's reasons for his conclusion that the bradycardia was caused by the epidural did not make sense, and that he cannot properly have understood the evidence on this issue.

Given the care and thoroughness that the judge displayed throughout this long judgment, which was replete with technical issues, this would be a surprising result to reach. However, I do not consider that we have to be driven to that conclusion. After all, the judge went out of his way to say the normal blood pressure reading was recorded between 18.20 and 18.30. He need not have said this if he believed that the blood pressure reading was taken before the onset of bradycardia at 18.25.

Against a background in which the judge said he found Professor Thornton's approach convincing, I interpret the reference "between 18.20 and 18.30" as meaning that the judge was alive to the possibility that the normal blood pressure reading (which is in fact ascribed to 18.30 in the chart) was taken after the bradycardia and after the mother was turned.

This was consistent with the convincing picture that Professor Thornton painted and one the judge was willing to accept. The fact that the fetal heart-rate was back at its normal baseline by the time Dr. Esen arrived at 18.40, coupled with the fact that the proved administration of an epidural injection at 18.20 provided a ready explanation for the transient period of bradycardia at 18.25, furnished a wholly credible scenario which the judge was willing to accept.

If I were justified in believing that the judge had in indeed misunderstood the evidence, then I accept that reliance on the fetal sample alone might not have justified Dr. Esen's lack of concern at 18.40, even though no point was ever made at the trial about the possible unreliability of that piece of evidence, except on the grounds (which the judge had already rejected) that the administration of syntocinon in itself rendered such evidence suspect, and the later challenge that a new sample really needed to be taken following the bradycardia.

In the circumstances I interpret the judgment as showing that the judge indeed accepted every part of Professor Thornton's thesis. Notwithstanding the judge's approach, Miss Gumbel argued that Professor Thornton's evidence did not properly address the risk that Dr. Esen had to assess. On his state of knowledge at 18.40, she said it was not established that bradycardia had in fact been caused by the epidural and he was taking an unwarrantable risk that the fetus was suffering unexplained distress to which the proper response should have been to turn off the syntocinon until there was greater clarity about the cause of the bradycardia. The evidence from the fetal sample taken at 17.30 could not, she said, provide reassurance about the state of the fetus at 18.30.

I share the judge's view that this was the most difficult aspect of the case, but Miss Gumbel's excellent arguments have not persuaded me that he was wrong. Clinicians have to make difficult judgments in these cases, and since the case as advanced before us was never put in this way to Dr. Esen I am not persuaded that it would be appropriate to reverse the judge's findings on these grounds.

Finally, I turn to the part of the case which was concerned with causation. The evidence on causation developed at the trial along the following lines. One leading textbook says that the aetiology of placental abruption, which occurs in about 1 percent of pregnancies, remains an enigma. Apart from cases involving direct trauma to the uterus, the cause is obscure. Abdominal trauma, uterine decompression and prolonged rupture of a membrane were identified as possible causes.

Another leading textbook said that although numerous factors have been suggested to play a causal role, a "unifying etiologic concept" was still lacking. The best way of explaining the diversity of the associated factors that have been described was to ascribe it to an underlying disease of the deciduous and uterine blood vessels. On this approach placental abruption might be viewed as the final dramatic expression of a long-standing pregnancy disorder. Eight factors that were suggested as playing a role ranged from cocaine abuse and cigarette smoking on the one hand to maternal hypertension, trauma and inferior venal canal compression on the other.

Although neither expert was able to identify any association between syntocinon and placental abruption in their pre-trial reports, at the trial interest was centred on an extract from an undated ABPI compendium which related to syntocinon produced by Novartis:

“Over dosage

The fatal dose of syntocinon has not been established. Symptoms and consequences of over dosage are mentioned under 'side effects.' In addition, as a result of uterine over-stimulation placental abruption and/or anabiotic fluid embolism have been reported side effects. When oxytocin is used by intravenous injection for the induction or enhancement of labour its administration at too high a dosage results in uterine over-stimulation which may cause fetal distress, asphyxia and death.”

The 1999/2000 edition of the same publication contains similar passages. Mr. Johnson was of the opinion in his original report that it was more likely than not that if the syntocinon had been turned down at 17.00 the dysfunctional uterine activity would have settled down and the mother would have gone on to achieve full dilation. The process might have taken a little longer, but in the absence of any dysfunctional uterine activity he thought it improbable that there would have been any significant fetal distress.

He believed the defendants to be wrong in denying the abruption was caused by syntocinon. An abruption was not always a rapidly precipitous event. They could indeed evolve over a finite period which might be a matter of hours. He would not say that this abruption was particularly foreseeable. He agreed that gradual changes on a CTG did not mean that the abruption was foreseeable. At the time he wrote his reports he accepted that the defendants were on strong ground when they said there was nothing in the literature to indicate that syntocinon caused a placental abruption, but in the present case there was a clear association.

Professor Thornton responded quite briefly to the question whether the use of oxytocin in general, either on normal or raised dosage, associated with a placental abruption. He gave an unequivocal answer “no”. He said there was no reference to oxytocin in this context, either in the oxytocin data sheets or in the relevant chapters of large textbooks.

It was common ground at the trial that placental abruption was an uncommon phenomenon and an extremely rare occurrence in labour.

Mr. Johnson told the judge that from 17.48 onwards the mother received an excessive amount of syntocinon. This caused uterine hyperstimulation which was compatible with the cause of the abruption. The cause must either be that or something unknown. The warning on Novartis drug sheets of a temporal connection between increase in syntocinon and the occurrence of abruption pointed to the former.

Professor Thornton, in contrast, said that he had never previously come across the suggestion that hyperstimulation caused a placental abruption. Placental abruption meant the separation of the placenta, and he could not see a mechanism. Squeezing the uterus meant that the baby was pushed around. Syntocinon was used in 20 to 30 percent of labour. Although not unheard of, placental abruption was very rare in labour. The fact that data sheets stated that abruption had occurred when syntocinon had been administered did not mean that causation could be inferred. The textbooks did not mention it, and this was the first time he had heard the suggestion.

The judge accepted Professor Thornton's approach. He said if causation had been relevant he would not have found it established. Hyperstimulation had been defined as involving excess pressure and/or excessively long and/or frequent contractions. This was not a hyperstimulation case. Like Professor Thornton, the judge could not discern any significant changes from the CTG trace, particularly when regard was had to the accepted limitations of this form of monitoring, except for one transient 10 minute period from 18.40 onwards when contractions were occurring at the rate of 5 or 6 in each ten minute period. After that, the contractions returned to an acceptable rate.

The judge noted that none of the recognised textbook authorities had considered uterine stimulation as the possible cause of placental abruption, and the data sheets simply stated that an abruption was recorded without giving further details. There was not enough evidence to enable him to find either that hyperstimulation might lead to a placental abruption, or that it did in this case. Mr. Johnson's reliance on a temporal relationship was coming close to a "post hoc propter hoc" line of argument.

The judge ended this part of his judgment by discounting the value of some evidence that arrived after the formal taking of evidence had been concluded, in the form of a letter from the drug company which published the data sheets. The judge said that even if the evidence was admissible it added nothing. He also said that the fact that in some cases an increase in risk caused by negligence could be treated as proving a causal link could not carry the day in a case like this.

On the appeal Miss Gumbel sought to put her client's case on causation in a quite different way from the way it was put at the trial. She accepted that the placental abruption occurred at or before 20.20 for a reason which could not be ascribed to the defendants’ negligence, but she argued that if the syntocinon had been stopped at 17.48, or alternatively between about 18.30 and 18.40, on the balance of probabilities the baby would have been safely born by 20.20 either by a normal delivery, or if it was thought inadequate progress had been made in labour and it was felt that the cervix was not dilated properly, by caesarean section performed before that time.

In advancing her case that this argument was open to her on appeal she took us to the original pleadings. In paragraph (e) of the particulars of negligence complaint was made that the defendants

"failed to turn down or switch off syntocinon at 17.00 hours to allow labour to progress at a time when the cervix was 6 centimetres dilated and full dilatation would have been affected in an hour or so."

The following further information was later given:

“Had syntocinon been withdrawn uterine activity would have settled down. It is highly unlikely that a multigravida patient who has previously given birth to a nine pound infant, and who in the present pregnancy has reached seven centimetres dilatation, is going to stop contracting. The probability is that she would have proceeded to full dilatation without syntocinon with a more coordinate uterine activity and there would have been no damage to the baby. If in fact there had been no further progress in dilatation the decision would have been taken to carry out a caesarean section on the grounds of fetal distress, as indeed was the case.

When the defendants averred in their defence that it was highly unlikely that full dilatation would have been achieved without syntocinon, and certainly not within an hour or so of 17.00, Mr. Johnson commented in a letter dated 1st March 2005:

“I would say that the probability is that the labour would have progressed uneventfully had they turned the syntocinon off. Mrs. Lennie had already given birth to a baby weighing 9 pounds, however it was not the purpose of obstetric practice to use syntocinon in a multigravida patient to force a big baby out. If in fact the labour does not progress despite reasonable uterine contractions then they could and should have done a caesarean section.”

In his first report dated 20th February 2001 Mr. Johnson said that without the syntocinon the progress to full dilatation may have taken a little longer. In his evidence at the trial he said:

“It is not the purpose of obstetrics to squeeze a baby out like toothpaste. Labour takes a certain amount of time and unless there is fetal distress or anything else it does not matter if it takes six hours or ten hours really.”

There is no hint in these answers of a positive case being put forward to the effect that on the balance of probabilities this baby would have been born by one means or another before 20.20 if the syntocinon had been stopped. This way of putting the case was never canvassed at the trial and the defendants were never given the opportunity of adducing evidence to meet it. It is not in my judgment open to us to allow the claimant to change her causation case at this stage of the proceedings, and then to ask for a retrial so that she can put her case in a different way. In any event, such evidence as there is suggests that if syntocinon had been stopped at 17.48, or at 18.25 or 18.40, it would have taken longer to deliver the baby than in fact was the case.

Anybody who has been concerned with this history cannot but have the deepest sympathy for Mrs. Lennie and her family for what happened in 1998. However, for these reasons, I am satisfied that none of the grounds of appeal succeed and this appeal must be dismissed.

I would repeat, this is a case where one must feel the greatest sympathy for the claimant and his family, but for all the reasons given by Lord Justice Brooke I agree that this appeal must be dismissed.

This is, as we can all see, a very distressing case. It is, as the judge said, a calamity. The cause of Sontino's cerebral palsy was the placental abruption to which Lord Justice Brooke has referred. It is not now suggested that the placental abruption was itself caused by negligence on the part of the doctors or anyone at the hospital. On the judge's findings of fact it was thus a tragic accident. As my Lords have said, one can only have the greatest sympathy for both Sontino and his mother. However, the question we have to answer is whether the judge reached the wrong conclusion. For the reasons given by Lord Justice Brooke I agree that the answer to that question is that he did not.

I, therefore, agree that however sympathetic we are to Sontino and his mother we have no alternative but to dismiss the appeal.