Evans v Birmingham & the Black Country Strategic Health Authority

At the conclusion of the argument we announced that we had decided to dismiss this appeal and that our reasons for doing so would be given later. These are my reasons.

The appellant was born at the Birmingham Maternity Hospital on the 14^th September 1990 at 00.24 hours. Dr Barry, who was the Senior House Officer in Neonatology at the hospital at the time remembered the birth. He described the appellant as “by far the “flattest” baby at delivery that I was ever called to resuscitate.” Unhappily, she now suffers from choreo-athetoid cerebral palsy and is seriously handicapped. She brought this claim for damages on the basis that the respondents, by their servants or agents, were negligent in the management of her birth; and that negligence caused the cerebral insult which has resulted in her disabilities. The respondents denied both negligence and causation. The District Judge ordered a trial of the preliminary issues of breach of duty and causation. This was heard by HH Judge Oliver-Jones QC in Birmingham in November 2006. In his judgment of the 8^th February 2007, the judge found the respondents to have been in breach of duty in one respect (which was essentially admitted at the hearing) but held that that breach of duty had not caused or materially contributed to the appellant’s condition. The appellant appeals simply on the basis that the judge’s conclusion as to causation is unsustainable on the evidence in view of the breach of duty which had so clearly been established.

Before going into the detailed arguments, it may be helpful just to set out an overview of the factual background so as to put the issues in context. Labour was extremely prolonged. The appellant’s mother was admitted to hospital at about 10.00hrs on the 12^th September 1990 with irregular contractions which had begun at 03.00hrs. Although she was therefore in the early stage of labour, what was described as the “active phase” did not begin until almost 24 hours later on the 13^th September 1990. A vaginal examination was carried out at 13.15hrs on the 13^th September at which time the cervix was recorded as 6cm dilated. The appellant’s mother was then transferred to the Delivery Suite. At 14.27hrs an artificial rupture of the membranes was performed, a foetal scalp electrode applied, and a vaginal examination was carried out by the midwife who recorded the cervix as being either 7-8cm or 8cm dilated.

At 16.45hrs the appellant’s mother was seen by the Senior Registrar, Dr Payne, and the Registrar, Dr Kilby. The latter was to manage the labour thereafter. It would appear that he saw the appellant’s mother again at 17.55 hours at which time the cervix was still only 8cm dilated. He concluded that there had been a secondary arrest, and the decision was then taken to augment labour artificially by using the drug Syntocinon. Further dilation to 10 cm was achieved by 21.15hrs. By then Dr Kilby had concluded that the probability was that delivery would have to be by caesarean section, as, despite strong contractions, labour was progressing very slowly. As a result an epidural was sited at 20.20hrs.

Despite the fact that there had been such slow progress, particularly in relation to the appellant’s head, Dr Kilby took the decision to allow labour to continue to see whether or not a vaginal delivery was still possible. Dr Kilby did not see the appellant’s mother again until 23.25hrs. At that stage he decided to obtain a foetal blood sample for analysis. He had decided, as his notes make clear, that if the sample showed a satisfactory pH reading (a matter to which I will return later) he would carry out a trial of forceps in the theatre; otherwise he would proceed immediately to a caesarean section. He discussed this decision with Dr Payne, who approved.

The foetal blood sample reading showed a pH level of 7.278 which was accepted by all the witnesses as being normal in the sense that it did not indicate acidosis and therefore a risk of hypoxia. Between 23.40hrs and 23.55hrs the appellant’s mother was being prepared for theatre, including a top-up of the epidural anaesthetic. During that period the foetal heart monitor showed that the appellant was developing tachycardia with variable or late decelerations, which has been described as complicated tachycardia. The appellant’s mother was transferred to theatre at 24.00hrs. The procedures in theatre appear to have commenced at 00.10hrs or thereabouts. The operation note records the foetal heart rate at 155 to 160 per minute. The note reads “attempted application of Kiellands forceps; not able easily to apply the blades. Trial abandoned.” In evidence, however, Dr Kilby said that he only inserted one blade of the forceps but was not able to obtain a satisfactory position. The note continues “on removal of blades (reduced): FHR “(foetal heart rate) “80 to 70min”.

All the expert witnesses agreed that this lowered heart rate indicated that the appellant had suffered a serious hypoxic event. The bradycardia persisted throughout the procedure. In the operation note Dr Kilby described thick meconium staining behind the head with the umbilical cord round the neck. The judge concluded that the reduction in foetal heart rate occurred between 0.10hrs and 0.15hrs and that the period of profound hypoxia was at least 13 minutes. That was calculated by adding to the period of hypoxia during the procedure a further period after birth and before intubation of the appellant had been successfully achieved, which was, on the evidence, anything between 3 and a quarter minutes and 6 minutes on the basis of the extant notes.

There were essentially two allegations made by the appellant. First, it was said that she should have been delivered at or before 21.30hrs on the 13^th September 1990 or at the very least by 23.35. Had she been delivered by then, there is no reason to believe that she would have suffered any brain damage. Second, when Syntocinon was administered, it was administered at too high a dose. The result was that the uterus was over simulated, causing excessive contractions. It was agreed that the maximum number of contractions per ten minutes period should have been five. For significant periods the records show that the appellant’s mother was experiencing contractions at five to six or six per ten minute period. The consequence, it was said, was that the appellant was subjected to stress as a result of those contractions which resulted in what was described as her foetal reserves being depleted, that is she was progressively less able to cope with the labour process. Accordingly whatever it was that resulted in the ultimate hypoxic event, that loss of foetal reserve made a material contribution at the very least to her inability to cope with that event or events.

The judge rejected the first basis upon which the appellant put her case. There is no appeal against that decision. As far as the second is concerned, Dr Kilby frankly admitted that he failed to appreciate that the appellant’s mother was experiencing excess contractions, and that he should have at least reduced the rate at which Syntocinon was being administered. The respondents accordingly formally admitted a breach of duty in failing to notice shortly after 21.00hrs that the Syntocinon should have been turned down. The judge concluded, however, as I have indicated in the first paragraph, that the excess contractions neither caused nor contributed to the ultimate hypoxic event which caused the damage to the appellant’s brain.

Mr Redfern, QC on behalf of the appellant, submits that the facts in this case should have driven the judge inexorably to the conclusion that at the very least the excess contractions made a material contribution to that hypoxic event. Syntocinon is an artificial hormone which replicates the effect of the natural hormone, oxytocin, in stimulating the wall of the uterus so as to produce contractions. We were referred to the data sheet relating to Syntocinon. In dealing with dose administration, this states that in the event of uterine hyperactivity and/or foetal distress, the infusion must be discontinued immediately. The consequence of hyperactivity is that it may cause foetal distress, asphyxia and death. He submitted that there was no controversy about this. All the experts agreed that the effect of excess contractions would be to subject the appellant to the stress of more numerous and frequent contractions than should have been the case. The inevitable consequence, Mr Redfern submitted was that by 23.35hrs on the 13^th September, the appellant was at the end of her ability to cope with the stress of labour. That can be shown by the fact that after the taking of the foetal blood sample, which he accepts was entirely normal, the appellant went into distress which manifested itself in sustained complicated tachycardia which, according to the literature, accepted again by all the experts, is associated with acidosis, that is a pH level equal to or less than 7.25. It follows, he submits, that by the time the appellant was subjected to the trial of forceps the appellant was already in a seriously compromised condition. The judge, he submits, failed to recognise or adequately deal with what he describes at the inevitable logic of this argument.

The judge gave a detailed and careful judgment. He set out the history of the labour in substantially greater detail than I have done above. That was necessary in order to enable him to deal with the allegation of negligence which he rejected. In relation to the issue which is under appeal, the important parts of his judgment are those which deal with the evidence of the expert witnesses. These were Mr Johnson and Dr Rosenbloom, an obstetrician and a paediatric neurologist respectively on behalf of the appellant, and Mr Porter and Dr Thomas, again an obstetrician and a paediatric neurologist respectively, for the respondents. The judge expressed his relevant conclusions in the following terms:

“95.

The significance of an excessive contraction rate is that there is less time between contractions for the foetus to recover from the compressive effects of each contraction. Thus it is argued that this will erode foetal reserve. Every contraction during any labour has the potential to erode foetal reserves. But, nonetheless most foetuses are able to cope with the effects of contractions. Between 19.50 hours and 23.35 hours – a period of three hours and forty-five minutes – the expert obstetrics witnesses (not withstanding some of the literature), would not have been critical of a total of 115 contractions [viz 5 contractions in every one of the twenty-three 10 minute periods]. There were an additional nine (maximum) contractions during the same period, caused by the Syntocinon infusion not being turned down. There was no evidence before me, particularly from the paediatric neurologists, to suggest this handful of additional contractions made any significant difference to Kathryn’s well-being. On the contrary at 23.38 hours the foetal blood sample showed that there had not been any erosion of foetal reserve. Had there been such erosion as I was invited to conclude there was, then the foetal pH would not, in my judgment have been as good as it was and as everyone agrees it was.

96.

Thus, in my judgment, it has not been established that on the balance of probabilities, the marginal improvement in foetal condition which would probably have derived from the turning down of the rate of infusion, would have prevented or reduced the damage which Kathryn sustained. All of the expert witnesses were very ambivalent about the mechanism and quantum of the erosion of the foetal reserves given the normal pH recorded 23.38 hours. I have already reviewed their evidence and I prefer the evidence of Mr Porter and Dr Thomas on this aspect of the case. Dr Thomas in particular was clear that the normal foetal pH was indicative of there having been no erosion to foetal reserves up to the time it was recorded. I accept this evidence. There was no evidence that contradicted this conclusion. On the contrary, Mr Johnston agreed that the additional dose of Syntocinon did not render the pH result less good than the result that would otherwise have obtained at 23.35hrs…, nor did it make a substantial difference to the foetal reserves…, and Dr Rosenbloom accepted that at 23.35hrs there would have been no more than the usual erosion of reserves which occurs in the second stage of labour.

97.

What was the cause of the damage which Kathryn suffered? There was insufficient time between 23.38 hours and the onset of profound bradycardia at or before 00.15hrs on the 14^th September for the foetal reserves to be depleted to such an extent so to cause brain damage; this was not in dispute. It follows, in my judgment, that something other than erosion of foetal reserves was responsible. The first sign of damaging hypoxia came, in my judgment, at the onset of profound bradycardia and not before. No one can be criticised by the fact that the period of the onset of profound bradycardia and resuscitation was, as I have already found as a fact, at least 13 minutes. The paediatric neurologists agreed that this period of hypoxia was sufficient to account for Kathryn’s brain damage whatever the state of foetal reserves had been at the time of the onset of bradycardia. Indeed, even if I were wrong in my finding of fact and the period was 12 minutes (and on any view it could not have been less than this) this too was sufficient time.

98.

In my judgment it was more likely than not that the damage was caused solely by the occlusion of the umbilical cord in association with the use of the Keilland’s forceps blade. This conclusion is supported by the following:

a.

Mr Porter’s evidence throughout, first appearing in his first report ….

b.

Mr Johnson’s agreement with Mr Porter’s opinion, as expressed in Mr Johnson’s written comments upon Mr Porter’s first report. Mr Johnson said, at this time, “I do agree with Mr Porter that the attempted and unsuccessful application of the anterior blade in some way caused the cord which had been previously compressed to become more occluded.” Both obstetric experts were willing to reach this conclusion not withstanding the absence of reference to such a mechanism in the literature.

c.

The very strong temporal link between the introduction of the forceps blade and the onset of profound and damaging bradycardia. To ignore this temporal link would, in my judgment, be wholly illogical.

d.

Dr Thomas’s evidence which I prefer that to Dr Rosenbloom. Dr Thomas eliminated, as I have done, any reason for the sudden fetal bradycardia other than “a sudden umbilical cord event”. In particular, and supported by the literature, he eliminated (on the basis of probability) the undoubted (agreed) period of complicated tachycardia between 23.40 hrs and 23.55hrs.”

Despite the attractive logic of Mr Redfern's submissions these clear findings by the judge make it extremely difficult for him to make good the argument that the judge came to a conclusion which he was not entitled to come to on the evidence. Although Mr Redfern did not shrink from saying that the judge’s preference for the evidence of Mr Porter and Dr Thomas was not reasoned, that is demonstrably incorrect. The judge considered that Mr Johnson’s evidence had not been “thought through” and gave clear examples from his evidence to support that conclusion. He considered that Mr Porter’s evidence had on the other hand been consistent throughout. And, in particular in relation to the critical question of whether or not the application of the anterior blade of the forceps in some way caused the cord to become more compressed or occluded, Mr Johnson expressly agreed this in his evidence as recorded in paragraph 98.d of the judgment. As far as Dr Rosenbloom was concerned, the judge was clearly concerned about the extent to which his evidence had been qualified and modified, in particular between the first and second parts of the hearing. The judge considered that Dr Rosenbloom had difficulty in reconciling his original views with the obstetric evidence ultimately given at the trial. There is, it seems to me, no justification accordingly for calling into question the judge’s assessment of the witnesses.

There are, however, three aspects of Mr Redfern’s detailed criticism of the Judge’s judgment which have some force. The first relates to paragraph 95 of the judgment, which I have set out above. The judge appears to have taken the view that the evidence showed only nine extra contractions beyond what would have been acceptable. Mr Redfern correctly points out that this fails to take into account a period of at least 40 minutes in which it is impossible to tell how many contractions occurred because that period was not recorded clearly. The judge considered that it was not safe to assume that there were excessive contractions within what he described as the “unknown” period. To the extent that this is not reasoned, Mr Redfern’s criticism is valid. But it does not meet the ultimate point made by the judge which is that, on the evidence before him, had there been significant erosion of foetal reserves, the foetal pH would not have been as good as it was, as he expressly says at the end of paragraph 95. This reflected what Dr Rosenbloom had himself said in oral evidence when he agreed that the foetal blood sample obtained at 23.38hrs was “as good a sample as one would expect at the second stage and that therefore it is unlikely that there had been unusual erosion of foetal reserve prior to 23.35hrs on 13^th September.” That was the critical point; and the judge’s finding was accordingly amply justified on the evidence.

Mr Redfern further submits that the judge nowhere grappled with the fact that there was clear evidence of foetal distress after the taking of the foetal blood sample at 23.35hrs. In fact, the judge dealt with it in paragraph 98. d. of his judgment. The judge there set out matters which supported his conclusion that the damage was caused solely by occlusion of the umbilical cord, and by reference to the expert evidence which he had preferred. He may have dealt with it shortly, but it cannot be said that he did not take it into account. Although he does not set it out in the judgment, this conclusion by Dr Thomas should be put in the context of the evidence of Mr Porter, which the judge accepted. Mr Porter considered that the tachycardia was to be explained either by a reaction to the taking of the foetal blood sample, or the result of the appellant’s mother being turned on her side, prepared for theatre, and having the epidural topped up. The fact that the judge did not deal in any more detail with this issue does not in my view in any way undermine his conclusion.

Mr Redfern further criticises the judge for his failure to appreciate that Dr Thomas’ evidence was not as clear cut as the judge expressed it in his judgment. We have been taken to passages in the cross-examination which suggest that he placed the onset of bradycardia before the time noted by Dr Kilby as the time the anterior blade of the forceps was applied, let alone withdrawn. This is in one sense correct, but depends for its validity on the notes as to time being exact. The real question was what could have caused the ultimate hypoxia. As to that his evidence was unequivocal. He rejected the argument of Dr Rosenbloom that there was too little time over the period of bradycardia to produce the level of hypoxia if the pH had been normal immediately before the bradycardia. The judge accurately encapsulated his evidence in the quotation in paragraph 98.d. That was entirely consistent with the other evidence about the way in which the heart rate collapsed.

At the end of the day, the appellant could only succeed if Mr Redfern had persuaded us that the judge was not entitled, on the material before him, to accept the evidence of Mr Porter and Dr Thomas. For the reasons that I have given above, that was an impossible task. Sympathy for the appellant and those who help and support her is not enough to entitle this court to interfere with the conclusions of the judge who has seen and evaluated the witnesses and has given full and clear reasons for the decision to which he has come.