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You are here: BAILII >> Databases >> England and Wales Court of Appeal (Civil Division) Decisions >> Matthews v East Suffolk Health Authority [2000] EWCA Civ 58 (25 February 2000)
URL: http://www.bailii.org/ew/cases/EWCA/Civ/2000/58.html
Cite as: [2000] EWCA Civ 58
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Case No: QBENF 98/1472/A2
IN THE SUPREME COURT OF JUDICATURE
COURT OF APPEAL (CIVIL DIVISION)
ON APPEAL FROM THE QUEEN'S BENCH DIVISION
(MR JUSTICE SCOTT BAKER)
Royal Courts of Justice
Strand, London, WC2A 2LL
Friday 25th February 2000
LORD JUSTICE HENRY
LORD JUSTICE ROBERT WALKER
and
MR JUSTICE ALLIOTT
- - - - - - - - - - - - - - - - - - - - -
BETH
LINDA MATTHEWS |
Appellant | |
- and - |
||
EAST SUFFOLK HEALTH AUTHORITY |
Respondent |
(Transcript of the Handed Down Judgment of
Smith Bernal Reporting Limited, 180 Fleet Street
London EC4A 2HD
Tel No: 0171 421 4040, Fax No: 0171 831 8838
Official Shorthand Writers to the Court)
- - - - - - - - - - - - - - - - - - - - -
C Purchas Esq, QC and Miss D Taylor
(instructed by Messrs Merricks, Ipswich for the Appellant)
R Owen Esq, QC and M Forde Esq
(instructed by Mills & Reeve, Cambridge for the Respondent)
- - - - - - - - - - - - - - - - - - - - -
As Approved by the Court
Crown Copyright ©
LORD JUSTICE HENRY:
1. This is an appeal against the dismissal on 31st July 1998 by Mr Justice Scott Baker of the action brought on behalf of Beth Matthews for medical negligence resulting in her sustaining serious brain damage at her birth on 4th August 1982. The action was brought against her general practitioner, the First Defendant, and the East Suffolk Health Authority, the Third Defendants, as being responsible for the acts and omissions of the staff at the hospital who attended Mrs Matthews at her confinement. This appeal relates solely to the actions and inactions of the Third Defendants (who I will refer to as "the hospital").
2. As it was not relevant to the issues at trial or the appeal, we do not know why this case was not tried until nearly 16 years after the event. The trial was therefore without the benefit of the recollection of witnesses to and protagonists in the events leading up to and after the birth. Instead the Court had to rely on the contemporaneous medical records and the analysis of those records by six expert medical witnesses. On the debit side those records are not complete; there were no nursing charts, no prescription charts, the X-rays are no longer in existence, and there were never any MRI scans. The Court had to do the best it could with the evidence available.
3. The background facts were these:
i) The appellant was born the elder of identical twins at Ipswich Hospital on 4th August 1982. As a result of the events at her birth, she now suffers from cerebral palsy and is severely disabled.
ii) Beth's mother was admitted to hospital on 3rd August 1982. Her contractions started at 6.30pm. The doctors who saw Mrs Matthews that evening and the midwife who attended to her did not diagnose that she was carrying twins. Twins were not diagnosed until 7.20am on 4th August when a compound presentation of feet and a head were observed at the mouth of the birth canal.
iii) The second stage of Mrs Matthews' labour began at 5.55am, and Beth was not born until 8.21am.
iv) At birth, Beth was suffering from mild asphyxia and needed immediate intubation for five minutes.
v) Nothing further of note occurred until 5th August 1982. Indeed, Beth appeared to be making good progress for a premature baby of 32 weeks gestation, as was shown by a blood gas reading taken at 9.15am on 5th August, which Dr Bamford, a consultant at the hospital, described as "very reassuring".
vi) At noon on 5th August Beth underwent what the clinical notes describe as "an episode of `collapse'". When offered a bottle by a nurse she took one suck and went pale. Her skin colour was mottled and she had poor peripheral perfusion.
vii) However, she appeared to make a good recovery as, ten minutes later the notes describe her as "a good colour, alert and active".
viii) A blood analysis taken at 1.00pm showed a normal white cell count, some acidosis and high urea.
ix) At 5.00pm Beth had a further attack in which she went pale and looked unwell. Her legs were mottled. Antibiotic treatment was started soon after this second attack.
x) The first signs of neurological distress were observed at 8.00pm. Beth became irritable with arching of her back and extensor tone in her arms and legs. She was noted to have dilated pupils and tense fontanelle.
xi) The full extent of Beth's injuries was not discovered until after her discharge. By 22 months she was recognised as having spastic quadriplegia.
4. The judge's conclusions on the issues were set out in his judgment at page 34:
"1. The first defendant was at fault for not referring Mrs Matthews to resolve whether she had twins.
2. Had he done so, the probability is that her labour would have been managed not on the basis that there might be twins but that there were premature twins.
3. The third defendants are not at fault in the management of labour in any way other than allowing the second stage to continue for too long.
4. The plaintiff did not sustain any significant birth asphyxia, and accordingly the fault of allowing the second stage of labour to continue too long was not causative of the plaintiff's brain damage.
5. The plaintiff suffered from septicaemia caused by infection by streptococcus faecalis, probably when she was in the birth canal.
6. The septicaemia caused periventricular leucomalacia which is responsible for the plaintiff's brain damage.
7. No concurrent or contributory cause of the brain damage is established, the only candidate apart from birth asphyxia being some prenatal pathology.
8. The plaintiff's post-natal care was indisputably satisfactory until noon on 5th August 1982 and from 5.30pm on the same day when treatment by antibiotics was commenced.
9. It is not proved that if the plaintiff had been treated with antibiotics soon after 12.00 her brain damage would have been any less.
Accordingly, with considerable regret, and applying the law as I must, I am driven to the conclusion that Beth's claim for damages must fail.
10. The third defendants, their servants or agents, were in breach of a duty of care in failing to consider the possibility of infection at noon or soon after and had they done so immediately they would have treated the plaintiff with antibiotics."
5. The crucial factual dispute related to conclusion 9, which came into play as a result of the finding in negligence at conclusion 10. The question for the court was whether the plaintiff had proved that prompt treatment with antibiotics at 12.00 noon would have lessened or avoided the brain damage sustained by Beth.
6. The first question was what caused the brain damage. The background to this question was that, though the experts were generally agreed that septicaemia alone could have caused the brain damage (judgment (J) 11F), it would be surprising
"... for septicaemia to produce such a severe outcome unless there was a contributory cause." (J 12B)
So the experts sought for another contributory cause. Professor Wyatt and Dr Davies looked to birth asphyxia (albeit by different routes). The judge rejected their theories as being speculative. He agreed with Professor Wigglesworth and Dr Roberton that the infection itself could account for the damage suffered by Beth. He concluded:
"There is, in my judgment, no adequate evidence to find that Beth suffered asphyxia of any significance, ie that caused any brain damage or led to the results that either Dr Davies or Professor Wyatt suggested as a possibility.
There is no evidence to support either the theory of Dr Davies that birth asphyxia could make the brain more vulnerable to the subsequent septicaemia insult or the Professor Wyatt theory of damage to the blood/brain barrier. Neither is supported by any literature. Both are speculative. They did not impress any of the defendants' experts."
There was no appeal against those findings.
7. The immediate consequence of the judge's finding that septicaemia was the proven cause of the plaintiff's brain damage was that it became irrelevant that the twins were not diagnosed, and irrelevant that the second stage of labour took longer that it should have. The direct consequences of that is that the decks were cleared for the issue:
"Should antibiotics have been prescribed after the episode at 12 mid-day on 5th August 1982 and before they were, in fact, prescribed, following another episode five and a half hours later?"
The judge found that if the possibility of infection had been considered, antibiotics would have been given. That issue is further defined by the fact that there is no criticism of the care of the new born baby up until the episode at noon, nor any criticism of her treatment after 5.30pm that day when antibiotics were started.
8. Clearly, with antibiotics, the general rule is that the sooner they are given after the onset of septicaemia, the better. It was the plaintiff's case that antibiotics given after the episode at 12 noon would have caught the first signs of infection and prevented any permanent brain damage. The hospital met this case by the evidence of Professor Wigglesworth, a Professor of Perinatal Pathology at Hammersmith Hospital. He first identified, in his witness statement, periventricular leucomalacia (PVL) as the cause of the brain damage; brain damage which, if once sustained, would render it too late for antibiotics to save the situation.
9. It seems to me noteworthy that, though PVL was ultimately accepted by all experts as being the cause of the brain damage manifested at 8.00pm, only Professor Wigglesworth and Dr Roberton identified it in their witness statements. Professor Wigglesworth said:
"The episode of collapse at 27 hours age [ie 12 noon] associated with an attempt at bottle feeding and marked by pallor, skin mottling and poor circulation was related to the recognition of an infection with streptococcus faecalis. This was treated by antibiotics and signs of cerebral irritation with dilated pupils and tense fontanelle developed some eight hours later [ie 8.00pm]. There was clearly significant sepsis due to strep faecalis, an organism that may well have been acquired during passage through the birth canal. A pre-term infant who suffers an infection of this type is at risk of developing haemorrhagic or ischaemic damage to the brain, quite apart from the possibility of meningitis. A likely sequence would be a bleed into the ventricles followed, at a later stage, by a ischaemic damage to the cerebral white matter, periventricular leucomalacia (PVL) ...
I think it is most likely that the episode of collapse at 27 hours would have triggered haemorrhagic and/or ischaemic brain damage, as mentioned above, that became manifest in the form of cerebral irritation with extensor arching of the back some eight hours later. The eight hour delay is about the time one might expect to elapse between onset of brain damage and appearance of signs. The reason for this delay is that it takes some hours for a spreading haemorrhage or increasing brain oedema due to ischaemia to reach the stage where physical signs develop. I consider it unlikely that the administration of antibiotics soon after 12.00 on 5.8.82 would have had an significant influence on this course of events as the brain damage would already have been initiated."
PVL was ischaemic brain damage.
10. Dr Roberton, though clearly puzzled by the severity of Beth's long term neurological deficit, commented that
"In recent years the literature has shown a consistent and striking association between PVL, the subsequent cerebral palsy of the sort suffered by Beth Matthews and infection in the neo-natal period"
11. His evidence turned on the destructive mechanisms of PVL, and whether PVL induced brain damage occurred before the time when antibiotics would have been given. Here, as the judge remarked, it was common ground (and he found as a fact) that the brain damage suffered was PVL. He accurately described its operation:
"PVL caused by septicaemia is the consequence of oedema in the peri-ventricular cells caused in turn by cytokines produced as the body reacts to toxins produced by the bacteria. The effect of the oedema is to impede the blood supply to the cells so that eventually they die. The process is not a gradual or continuous one. It is not a case (and there was a graphic description in the evidence) of the bacteria or their by-products `nibbling away' at the brain. The damage is caused at the point at which the circulation to the peri-ventricular cells is finally compromised. This point was described by Professor Wigglesworth as a watershed. Once you have gone past it the damage is rapid and irreversible. The fact, as Professor Wigglesworth said, that the infection builds up slowly does not mean that the damage builds up slowly. What keeps the brain cells alive is the blood supply: when it stops they die." (J30 - 31)
12. The hospital's case, accepted by the judge, was that once the damage had been done by the PVL, it was too late for antibiotics to retrieve the situation. The judge was to find that that brain damage occurred at 12.00 noon.
13. The next question of fact was when were the first signs of brain damage manifested. Professor Wigglesworth focused on the signs of neurological illness at 8.00pm on 5th August 1982 (see the Supplementary Core Bundle pp 137 and 155). He identified the acute neurological signs then occurring (the arching of the back, the extensor tone in the limbs, dilated pupils and a tense fontanelle) and emphasised that one had to work backwards from there to establish the time of brain damage.
14. The significance of working backwards was that in what happened at 8.00pm there was a fixed point, namely that what was seen was the evidence of PVL-caused brain damage that had actually occurred. The judge found this as a fact (J30B) and also said that it was common ground. Mr Purchas QC for the plaintiff accepted that it was common ground that the first signs of neurological illness were at 8.00pm - indeed he opened his cross-examination of Professor Wigglesworth with such an acknowledgement - but did not accept that that was a manifestation of brain damage which had already occurred. This is because it was the plaintiff's case that it is possible for babies who suffer from neurological signs such as were exhibited at 8.00pm to make a complete recovery. That is a point to which I shall return.
15. The reason for working backwards is that the 8.00pm episode and the symptoms of cerebral irritation shown then are what Professor Wigglesworth described as "the first fact that we can get out" (21/40F) about when the brain damage occurred. He then dealt with the time lag between brain damage and the physical signs such as were manifested at 8.00pm. He distinguished between where the brain damage is massive, so that the brain is immediately destroyed where there is no gap, and "the sort of brain damage we are looking at there" (21/41F) where there is a lag. He distinguished a "catastrophic" event such as "an acute ruptured uterus" where the lag is as short as two to three hours, at one end of the scale, and at the other:
"The maximum I think is somewhere between the 12 and the 24 hour period. Probably 15, 16 hours would be rather late" (21/42D)
16. He then looked for such an event: "some sign that something may have gone wrong which would fit in with that time period", and concluded:
"I think the first obvious event is the collapse at 27 hours, 12 noon on day 2, that is eight hours before the signs of neurological damage became apparent. That would be the sort of mid-point average time that you might expect for the development of signs." (21/42F)
17. That evidence put the focus on what happened at 12 noon. Professor Wigglesworth dealt with this as follows:
"I picked that episode because it was a fairly striking change in behaviour, and ... in the sequence of events in development of any form of brain damage ... there is usually some recognisable clinical event at the time of onset when the damage actually happens" (21/61D)
18. In cross-examination it was put to him that what was observed at 12 noon were the early signs of septicaemia. The conclusion of Mr Purchas's cross-examination on this topic was:
"Q. And if these were the first clinical signs of septicaemia at 12 o'clock that day, then giving antibiotics intravenously could well have halted the progress of the septicaemia, could it not?
A. I accept that, yes.
Q. By halting the process [progress] of septicaemia would have made it probable that brain injury would not subsequently have occurred; do you agree?
A. I do not know. I think that time as being equally likely to be the time of the onset of the brain damage. That it was the initial, meaning the initial event, the collapse, that meant that the brain was being damaged, so I do not know. It may have done if, in fact, the [brain] damage occurred later than that, but we do not have very much time to play with, that is what I am trying to get at." (21/73)
He then agreed with the judge that there were three possibilities: first that the giving of antibiotics then might have made not a scrap of difference to brain damage; second that there might have been no brain damage at all if antibiotics were given very soon after 12 noon; third that there might have been some brain damage but less if antibiotics were given then.
19. In relation to those three possibilities, the judge accurately summarised the effect of that evidence:
"Professor Wigglesworth only assists the plaintiffs case on the assumption that the brain damage occurred at a time after the antibiotics would have been given, at say, 2.30pm. He cannot say precisely when it occurred."
Then he quotes Professor Wigglesworth's evidence on the time lag, and that part of his written statement were he considered it unlikely that the administration of antibiotics soon after noon would have altered events because the brain damage would already have been initiated.
20. The judge then summarised the plaintiff's case, with brief summaries of the evidence given by Professor Wyatt, Dr Davies, Professor Wigglesworth (whose evidence I have dealt with above), Professor Hall, Dr Roberton and Dr Kovar.
21. In summary, three paediatricians gave evidence that antibiotics given at noon would have prevented or reduced the brain damage suffered. Their difficulty was that that would only be true if the antibiotics preceded the brain damage. If the brain damage had already happened, the antibiotics would be too late. They also found it hard to accept that the symptoms described at 12 noon in relation to what the hospital records describe as the "episode of `collapse'" were serious enough to indicate brain damage then sustained, and considered that they could merely indicate the first sign of sepsis. This was Group D streptococcus faecalis, which is relatively benign and responds quickly to antibiotics. Witnesses also pointed to the improvement apparently achieved by antibiotics when they were administered at 5.30pm. Having summarised the plaintiff's case the judge summarised the hospital's primary case:
"As Mr Owen pointed out, whether an early administration of antibiotics would have made any difference turns on when the plaintiff's brain damage occurred. As Professor Kovar said in his evidence, this is something no-one can say with any certainty. The bottom line is: `We do not know'. Mr Owen's point is that if it is not possible to say when the damage occurred, then it is not possible to say whether the administration of antibiotics after the 12 o'clock episode would have had the effect contended for by the plaintiff; and the plaintiff will have failed to discharge the burden of proof.
It is the third defendant's primary case that it is not possible on the balance of probabilities to establish when the brain damage occurred. In my judgment it is critical in approaching this issue to have some understanding of the process by which the septicaemia leads to brain damage." (J29 - 30)
22. The judge then went on to consider the mechanisms of PVL in the detailed passage already quoted. He dealt with the lag period and then said:
"There is usually, said Professor Wigglesworth, a recognisable event when the damage actually happened. In this case 12 o'clock was a fairly striking change of behaviour. With the manifestation of neurological signs eight hours later it would fit comfortably within the Professor's normal time gap of two to fifteen hours. Dr [sic] Wigglesworth's expertise is pathology. No other expert in this case has similar expertise. I find his evidence, on the question of whether any earlier administration of antibiotics would have made a difference, compelling. In his experience the brain damage is likely all to have occurred on the single occasion; sometimes not, but that would be the exception rather than the rule." (J31 - 32)
He then made five findings of fact; I have numbered them for convenience sake:
"(i) I accept Professor Wigglesworth's evidence that the damage to the brain is usually marked by a change in clinical condition. There is usually a recognised clinical event at the time of onset.
(ii) I find on balance of probabilities that the neurological signs observed at 8.00pm cannot be attributed to the episode that occurred at about 5.00pm. It was not of sufficient seriousness to have caused such symptoms after an interval of three hours.
(iii) The only other change in clinical condition recorded in the medical notes is the collapse at 12.00. Its timing is consistent with it marking the brain damage that gave the signs of cerebral malfunction eight hours later.
(iv) I accept the analysis of Professor Wigglesworth and conclude that the episode at 12 o'clock marked the point at which the brain damage occurred.
(v) Whether I am right or wrong about that I cannot be satisfied on the balance of probabilities that the evidence establishes the occurrence of any brain damage at a later time (ie whether the initial brain damage or any other further brain damage).
In the end I have had to choose on this issue between the evidence of Dr [sic] Wigglesworth as I have analysed it above, and the broad proposition that the longer a baby is exposed to infection the greater the likelihood of an adverse outcome. Nowhere has the broad proposition been supported by a logical analysis of what was actually happening to Beth. On the other hand, Professor Wigglesworth's analysis was subject to close scrutiny and in my judgment withstood it. Accordingly, I find that the earlier administration of antibiotics would not on balance of probabilities have made a material difference."
He then set out his conclusions which I quoted earlier in this judgment.
23. The first difficulty the plaintiff faces is that this is an appeal purely on questions of fact. It is a fundamental challenge to the factual conclusions the judge reached. It is not, as I understand it, said that there was no evidence on which he could reach the conclusion he did, but it is said that he plainly reached the wrong conclusion. It is also said that that conclusion was against the weight of the evidence - but then again weight is pre-eminently for the trial judge. And, apart from the fact that many if not most of his factual findings have been challenged, there has been no criticism of the trial judge in his handling of the case. His reasons for finding as he did are entirely transparent. He heard evidence from six distinguished expert witnesses, and reached a clear and logical conclusion. I do not understand it to be said that he misunderstood that evidence. The case is that it is plain he simply got it wrong.
24. The basic principles applying to appeals on questions of fact are clear. The duty of the Court is to rehear the case - to reconsider it on the basis of the materials before the trial judge. Such reconsideration should give realistic recognition to the advantages given to the trial judge. The most obvious of those advantages - that is having seen and heard the witnesses give evidence in a case where credibility is in issue - might at first glance seem not to arise in a case such as this where all the live evidence was from expert witnesses. But there are still real advantages to be drawn from having heard the evidence, and heard the challenges: advantages that it is hard or impossible to equal by study of the transcript. And here another factor comes into play. The judge heard those witnesses on more issues than were canvassed in this appeal. Therefore he heard their evidence over a wider field, which again is an advantage we cannot enjoy. For instance, in rejecting Professor Wyatt's and Dr Davies's separate theories as to another contributory cause of infection, the judge described them as "speculative".
25. In Wilsher -v- Essex Area Health Authority [1988] 1 AC 1074 at 1091, Lord Bridge said:
"Where expert witnesses are radically at issue about complex technical questions within their own field and are examined and cross-examined at length about their conflicting theories, I believe that the judge's advantage is seeing them and hearing them is scarcely less important than when he has to resolve some conflict of primary fact between lay witnesses in purely mundane matters."
26. This truth was reaffirmed by their Lordships in Pickford -v- ICI [1998] 1 WLR 1189 at 1200 - 1201 where the contrast was drawn between the trial judge's advantage in having seen and heard the medical experts when "... all the Court of Appeal had before them was the printed evidence". A difficulty the judge had to face (perhaps - we know not - contributed to by the fact that these events had taken place so long before) was that there were so many uncertainties.
27. The judge accepted Professor Wigglesworth's evidence that the episode at 12 noon was when the brain damage occurred. But he also emphasised that whether he was right or wrong on that score, he could not be satisfied on the balance of probabilities that there was evidence establishing the onset of brain damage any later.
28. Neither the Notice of Appeal nor the appellant's skeleton argument advances any positive case on when the brain damage occurred, yet for the antibiotics to have any chance of success, the appellant has to show that the brain damage had not occurred when the antibiotics should have been used - 12.00 noon.
29. Mr Owen demonstrated that the paediatric experts were unable to say when the brain damage occurred. He made this good from the transcript:
"It seems likely that the bacteria were multiplying in the bloodstream over this period and were causing further abnormalities of the circulation, and in retrospect the perfusion to the brain, the blood supply to the brain was being progressively impaired, in my view, although this is a matter of speculation ultimately." (Wyatt - 20/40D - F).
"Q. ... of course what we do not know is how advanced the infection was when we arrive at 12 o'clock that morning. All we have in reality is the first sign of neurological problems noted at 8.30 but referring to the previous half hour, that is from 8 o'clock that evening when we have the signs of cerebral irritation, but we do not have any hard and fast way of knowing how long that process has been going on, do we?
A. No, we can just speculate because we do not know, no." (Davies - 21/18C in cross-examination)
"I can't say when the battle was lost." (Hall - 21/88E)
"Precisely when she went over the cliff, I don't know." (Roberton - 22/93D)
"I think the bottom line is that I do not know. ... I do not think we really know when the train actually left the station here." (Kovar - 22/152C & F)
Mr Owen's conclusion was:
"To state the obvious, if the appellant cannot establish on the balance of probabilities when such damage occurred, then she cannot establish that the administration of antibiotics after the 12.00 episode would have had the effect contended for, namely prevention or reduction of the brain damage."
30. That was the conclusion accepted by the judge: see the quotation from his judgment at paragraph 21.
31. Next, the appellants mount an attack on the qualifications of Professor Wigglesworth. The complaint is that as a pathologist, and not claiming to be an expert in the clinical course of infectious diseases in living patients, his evidence should be in some way downgraded.
32. Needless to say this point was aired before the judge, who did not find it necessary to deal specifically with it. He was in the best position to judge the value of Professor Wigglesworth's contribution. It can fairly be said that the PVL point was first taken by him, in his witness statement, and by trial had universal acceptance (within the boundaries previously indicated). He is, as his CV shows, a paediatric pathologist of considerable distinction, and his expertise is relevant to the nature and timing of the injury to the brain, and his contribution recognised by his fellows experts - see Wyatt 20/113 - 114;
"I have great respect for Professor Wigglesworth, who is an international authority on perinatal pathology."
Davies 21/14D - F:
"... There are experts on brain pathology with more experience of this than I.
...
Q. One of those experts ... being Professor Wigglesworth?
A. Yes."
and 21/18E:
"I have a great respect for Professor Wigglesworth's opinion."
and Hall at 22/6B, in context of expressing a doubt as to whether brain damage could occur at 12.00 without there being a "total collapse":
"I would not dream of disagreeing with Professor Wigglesworth's enormous knowledge of the subject."
33. The line of argument put forward by Professor Wigglesworth was logical, transparent and, as the judge remarked, stood up to the criticism made of it. And essentially Dr Roberton supported him. He agreed with the PVL mechanism, he agreed with the time lag between the events being triggered and the clinical symptoms occurring, but disagreed with the phrase "catastrophic collapse" to describe 12.00 noon (22/64 - 65). I am not clear that Professor Wigglesworth ever used that expression. At 21/79C - G he is clearly distinguishing catastrophic cases from the "episode of `collapse'" referred to in the hospital records.
34. Dr Roberton supported his broad analysis. He said he "wouldn't quibble" with the time lag and accepted the general case that antibiotics at or after 12.00 would have been too late:
"At one very simplistic level, my Lord, I have to say I do not think it would have made any difference, for the reasons I am in great difficulty about stating precisely what and when the insult was that has damaged Beth's brain. And I think saying that saving - well, it would not be five hours, it would be considerably less than five hours because a decision would not be made until they have all the tests back and thought about it, perhaps 1 o'clock half past one. But saving three or four hours then, I think, just on first principles of analysis of what is wrong with Beth now, is unlikely to have influenced the outcome. If we look at the mechanism of sepsis induced PVL, the stimuli that caused the damage in Beth's brain must have occurred some time before that illness at 8 o'clock, when she was neurologically abnormal. Precisely when she went over that cliff, I do not know. It is very difficult to work out from the notes. And, of course, we know the stimulus to her going over, as it were, the brain being damaged, is not necessarily the active bacteria in the bloodstream; it is the chemicals produced by the body's response to the bacteria and by the bacteria - and those would go on circulating for some time after the bacterial growth had been inhibited by the anti-biotics. So it does not follow that just because you started antibiotics at mid-day, say, that that would have prevented brain damaging factors from circulating from some time between then and five o'clock, six o'clock, seven o'clock.
Q. Or eight o'clock, when we have the first positive evidence?
A. Eight o'clock when we have the first positive evidence." (22/92 - 93)
Professor Wigglesworth's expert evidence was clearly admissible and relevant. The weight to be given to it was a matter for the judge. He gave it great weight. He was entitled to do so.
35. Next it is submitted on behalf of the appellant that Professor Wigglesworth's evidence was inconsistent, and so should not have been relied on.
36. The transcript shows that the Professor was an extremely open witness. He was not defensive, and prepared to admit alternative possibilities as possibilities. He did not parade uncertainty as certainty. He accepted that he did not and could not know precisely when brain damage occurred and carefully explained his route to his conclusion. He accepted that you could suffer brain damage without neurological signs, and vice versa. He accepted that the time lag between the damage occurring and the visible signs that damage had occurred might, in the case of a new-born baby be as little as four hours. He accepted all those matters, yet held fast to his conclusion. The judge was quite entitled to conclude that those matters did not reflect adversely on his credibility, or the credibility of his thesis.
37. A running theme through the evidence was the lack of fixed points. At the end of the day, the signs of brain damage at 8.00pm are probably the only fixed point (though Mr Purchas would not accept that). Beyond that, what there is is either legitimate inference or illegitimate conjecture. The line between the two is sometimes difficult to draw. As Lord Hope said in Pickford -v- ICI Plc (above) at 1200A:
"As Lord Thankerton observed in Watt -v- Thomas [1947] AC 484, 487 the question of burden of proof as a determining factor does not arise at the end of the case except insofar as the court is ultimately unable to come to a definite conclusion on the evidence, or some part of it, and the question arises as to which party has to suffer from this. From time to time cases arise which are of that exceptional character. They include cases which depend on the assessment of complex and disputed medical evidence, where the court finds itself in difficulty in reaching a decision as to which side of the argument is the more acceptable. I think that this was such a case, and that the judge was justified in reminding himself where the onus lay as he examined the evidence."
The judge by his finding that the brain damage had occurred at 12.00 noon clearly regarded that as legitimate inference. By a parity of reasoning it seems to me that had he preferred the evidence of Professor Wyatt and Dr Davies, that treatment with antibiotics at noon would probably have resulted in the consequences or some of the consequences of brain damage being avoided, he could equally have treated that conclusion as legitimate inference. I am persuaded that the judge was entitled to make the factual finding that the brain damage was sustained at 12.00 noon.
38. But even if I were wrong in that, the burden of proof was on the appellant to show that prompt application of antibiotics at noon or soon thereafter would, on the balance of probability, have avoided or quantifiably reduced the injuries caused by the brain damage. In my judgment that has not been proven.
39. Accordingly, with regret as to the outcome, I feel bound to dismiss this appeal.
LORD JUSTICE ROBERT WALKER:
40. I agree.
MR JUSTICE ALLIOTT:
41. I also agree.