Mugweni v NHS London

Grace Mugweni was born on the 28^th March 1983. Very soon after her birth it was identified that she was a sick child. Some of her difficulties were subsequently identified as arising from CHARGE syndrome, which is congenital. But in consequence of tests undertaken at Guy’s Hospital in London in August 1983 the presence of an atrial septal secundum defect (“ASD”) was revealed. That is, putting it broadly, a malfunction consisting of a hole in the wall between the upper pumping chambers of the heart. There was also identified a patent ductus arteriosus (“PDA”). The ductus arteriosus is a blood vessel in the fetus which passes blood from the pulmonary artery direct to the aorta and which normally should be converted, but here was not, after birth.

It was decided that an immediate operation, in respect both of the ASD and of the PDA, was needed. That took place on 9^th August 1983. The experienced consultant cardio-thoracic surgeon in charge of the operation was Mr Yates, assisted by Dr Sayin. The attending consultant anaesthetist was Dr Hasbury. Others, such as a perfusionist, registrar, anaesthetic assistant and theatre nurses, would also, as the trial judge found, have been present. The operation necessarily involved a period of time when there was a cardio-pulmonary bypass.

There is no doubt that at some stage in the operation a tension pneumothorax (“PNT”) (air collecting in the pleural cavity) arose. There is no doubt that Grace suffered a cardiac arrest. The principal allegation, put shortly, was that Dr Hasbury, in breach of duty, failed to recognise the signs prior to the arrest and had he done so injury ultimately said to have accrued to Grace, in the form of damage to the watershed areas of the brain, would not have occurred. The respondent on the other hand said that the relevant injury had arisen as a result of the cardio-pulmonary bypass itself, without any negligence on the part of anyone.

Grace is now 27 years old. She is severely damaged. She suffers from spastic quadriplegia, epilepsy, hearing and visual loss, behavioural problems and significant cognitive impairment. Mr Block QC, appearing with Miss Ayling on behalf of the respondent, rightly paid tribute to the devoted, indeed heroic, love, care and attention that Grace’s mother has given her daughter throughout the years since the operation. The attendant responsibilities, anxieties and pressures on Mrs Mugweni are only too easy to imagine.

The claim form was issued on 11^th March 2009. The matter came on for trial before Langstaff J (who is, of course, very experienced in such cases). There was a 10 day hearing. By a detailed reserved judgment ([2011] EWHC 334(QB)) handed down on 23^rd February 2011 the judge found that a breach of duty on the part of Dr Hasbury had been made out: but that such breach had not, on the facts, been proved to be causative of any relevant damage. Accordingly he dismissed the claim.

Permission to appeal was granted by Dame Janet Smith DBE on 1^st June 2011. The respondent then sought to cross-appeal against the finding of breach of duty; and permission to cross-appeal was granted by Dame Janet Smith on 15^th September 2011.

There can be no doubt that this must have been an extremely difficult trial for all concerned: both in the presentation of the respective cases by the respective advocates and in the resolution of the issues by the trial judge.

First, there was the fact that the operation in question took place over 27 years ago. In the interim Dr Hasbury had died. So had Mr Yates. No evidence, as Mr Block emphasised, was available from them or from any of the others present: with one exception, who in the event, as the judge found, was unable to assist. Although a few records had survived – including, and importantly, Mr Yates’ own contemporaneously typed-up operating note – others, such as perfusion records, anaesthetic charts, ECG readings and so on, were no longer available. The death of Mr Yates and Dr Hasbury also meant that they were not able to explain in detail what the extant notes conveyed or to explain what their own practices (in 1983) for such an operation would have been.

Second, and in consequence, the various experts - covering no fewer than nine different disciplines – had to seek to reconstruct what may have happened by reference to events of long ago and in the light of a significant lack of primary evidence. The difficulties experienced were enhanced by what was agreed to be a fact: that the occurrence of a tension PNT giving rise to a cardiac arrest in a context such as the present was very rare. Indeed none of the distinguished experts appearing before the judge themselves had had personal experience of such an event. The judge observed in his introductory remarks:

“…most of the experts have struggled to understand why the brain damage which occurred should have happened in the circumstances in which it apparently did.”

As the judge rightly said, it was not possible given the lapse of time to give “point accuracy” to supposed facts where the truth will fall within a range. His task, of course, was to assess whether the appellant had proved the case on the balance of probabilities on the evidence that was available. In this regard, it is only right to record that the judge’s view was that no adventitious advantage had been sought or gained by the appellant in not bringing the case earlier.

It has to be said that the judge’s task was not made easier by the way in which the issues which have loomed large on this appeal came to be formulated. In saying that, I intend no criticism of anyone in what was a formidably complex case and where counsel have clearly conducted matters with very great care.

In a nutshell, the original claim was to the effect that Dr Hasbury negligently failed to detect “the early signs of the developing” tension PNT and to arrange for the chest to be opened – thereby relieving the PNT – before the cardiac arrest: and that by the time the PNT was relieved, after the cardiac arrest, the appellant had suffered “such a prolonged period of cerebral hypo-perfusion” that she sustained permanent neurological damage.

In the event, the experts were agreed that a PNT was so rare in such a context that a reasonably skilled consultant anaesthetist could not be expected to have been alerted to signs of one. However, that did not ultimately signify: for a tamponade was, it was agreed, a recurrent risk in such a context and one to which an anaesthetist would need to be alert: and the signs for that would have broadly corresponded to those for a developing tension PNT.

On causation the appellant’s pleaded case was that the failure to note and treat promptly the PNT caused the hypoxic-ischaemic brain damage to occur. In the alternative an allegation was made during the trial by amended pleading that the respondent’s negligence “contributed in a more than negligible way to the hypoxic-ischaemic brain damage between the point when the impending circulatory and ventilatory failure should have been relieved until adequate perfusion to the watershed areas [of the brain] was restored.”

The Defence was to the effect that there was no negligence; that the appellant was closely monitored at all times; and that the cardiac arrest was sudden and unexpected. Causation was denied; and it was averred that the damage arising was not the result of the tension PNT but was all the result of pre-existing congenital disorder and congenital heart disease and of non-negligent consequences of the surgery necessary to treat the congenital heart disease.

Thus until trial the appellant’s case was that all the relevant damage (and subject to the agreed matters mentioned in paragraph 28 below) was caused by the alleged negligent oversight on the part of Dr Hasbury. The Defendant’s case was that it was all caused by the pre-existing condition of the appellant and by non-negligent consequences of the bypass surgery.

It was only at the opening of the trial, as we were told, that the further scenario (in due course reflected in the amended pleading) – and which has predominated in this appeal – was advanced on behalf of the appellant. That is, that there was, as it were, a “double-hit”: even if some damage was caused (non-negligently) by the bypass a material contribution was made to the overall damage to the brain by the PNT and subsequent cardiac arrest which would not have resulted had there been no negligence on the part of Dr Hasbury.

Very fairly, the respondent took no pleading point at trial. Nor was any adjournment sought. But, in what was already an extremely difficult and complex case, further difficulties and complexities were now added. For one thing, the experts from the various disciplines had not previously submitted reports to deal with this new theory. In consequence, they had not met before trial to discuss areas of agreement or disagreement on the point. For another thing, when they came to give evidence, the experts were having to give answers on this topic in a case which was still developing: moreover in the context of an operational procedure which had had an outcome not previously experienced by any of them.

The background facts are set out with care and detail in the judge’s judgment. That detail does not need to be replicated here. In essence the position was this.

That Grace was experiencing difficulties was noted by her mother soon after birth. Further, records that survive indicate that she was diagnosed with a heart murmur. On referral to Guy’s Hospital “left heart failure which is getting worse” was noted. The investigations in August 1983 then revealed the existence of an ASD and PDA.

The operation which it was decided should be undertaken took place soon after, on 9^th August 1983. The evidence was that ordinarily such an operation might be performed either neo-natally (when the baby was less than 28 days old) or when the child was around 4 or 5 years old. That it was decided to undertake the operation then was an indication of the perceived seriousness. No criticism is made of the decision to operate.

There was some dispute between the relevant experts as to the likely length of the operation, from its start to the end of the anaesthesia. The judge found that it would have taken around 4 to 4½ hours. He found that there would have been around 30 to 45 minutes of anaesthetic preparation, before draping. The surgeon would then have opened the chest, exposing the heart, and the PDA would have been ligated following which the ASD would have been closed with the heart stilled on bypass. It was and is well recognised that being on bypass carries particular risks: the heart would have been held in ventricular fibrillation, with circulation being maintained by a bypass machine. The judge resolved disputes between the relevant experts by finding that the period of bypass would here have lasted between 30 and 40 minutes.

Before and after the bypass, Grace would have had her lungs ventilated: this would have included use of a bag, connected by an Ayre’s T-piece to the ventilation tube, manually squeezed. The judge found that manual ventilation was likely at the point of coming off the bypass (and again just before transfer to the incubator and the equipment was disconnected). It was further found by the judge that there “was no reason for anyone to think that at that stage there was any compromise to the blood flow to the brain” – that is, at the stage just before she came off bypass.

After Grace had come off bypass, a period of time would have elapsed before she was to be placed in an incubator. In that time, the sternal opening would have been closed (the judge concluding that would have taken around 10 minutes) and then the chest closed: if that passed without incident, it would have taken, as found, no more than 20 minutes from completion of sternal closure to transfer to incubator (and thence to the intensive care unit).

In the words of the judge:

“At some point – as to exactly when this was between the time of closure of the sternum and finishing applying the dressings there is no evidence – Grace suffered a “cardiac arrest.””

The words “cardiac arrest” was of rather uncertain meaning. In this context they derive from Mr Yates’ typewritten note of the operation. Clearly this is an important document. It read in the relevant respects as follows:

“…..After venting all air from the heart and closing all incisions the heart regained sinus rhythm spontaneously on removing the fibrillation current. On discontinuing bypass the heart took over the circulation satisfactorily and post-op pressures revealed a right ventricular pressure of 35mmHg with no evidence of significant venous arterial Oxygen saturation step up across the right heart.

Having ascertained there was satisfactory haemostasis the pericardium was closed and the chest closed routinely with retrosternal and peri-cardial drains.

As the patient was being prepared to be moved to the incubator from the operating table cardiac arrest occurred and external cardiac massage was necessary.

The chest was re-opened under massage conditions and it was confirmed that there was no tamponade but the cause of the arrest was a right tension pneumothorax. The tension pneumothorax was relieved and a right pleural drain inserted by when the heart had regained normal sinus rhythm and a good circulatory status. At no time was there any significant period of circulatory arrest.

The chest was then re-closed routinely with retrosternal and pericardial drains.”

A hand-written note in the clinical records states in the relevant respects:

“Difficulty on coming off bypass because of R.sided pneumothorax + ET tube blocked with secretions (Patient arrested)…”

That note also records the need for isoprenaline (a drug which increases the rate of the heart beat and heart contractility).

The following day an ultra sound of the brain was taken, reported to be normal. Later, however, epileptiform fits were noted and the rate of growth of the brain flattened. Subsequent neuro-radiological testing indicated that the encephalopathy was caused by damage to the watershed, or border zone, areas of the brain. The judge put it in this way:

“20.

The encephalopathy indicated by the fits has been shown by neuro-radiological imaging to be caused by damage to the watershed (or "border zone") areas of the brain. These are the areas lying between the distribution of one cerebral artery and its peripheral vessels and the next. It is not difficult to understand that if blood flow to the brain drops for long enough, such that oxygenation of the tissues might be affected, these areas will be the first to be affected. An analogy thought by the experts to be useful is that of a garden sprinkler. The area of lawn between two sprinklers will be perfused so long as the water pressure is sufficient. If it drops, then the spread of water diminishes, and part of the lawn is parched and may die.”

The judge emphasised that this pattern of injury was to be distinguished from an acute hypoxic insult. He found that some of Grace’s current functional disabilities were a consequence of watershed brain damage “which classically is caused by under-perfusion of the brain”. It may be recalled, however, that it was common ground that Grace also suffered from a congenital syndrome called CHARGE syndrome. Very sensibly, the parties before trial agreed as to which elements of Grace’s functional difficulties were attributable to CHARGE and which were sustained peri-operatively: with an agreed proportion in terms of causation as to cognitive impairments and learning difficulties.

The judge made these findings:

“26.

In the foetus, this process would require around 30 minutes of damaging hypo-perfusion, following an hour of non-damaging hypoxia. On this, all the medical experts (and in particular, Drs. Rennie, Miles and Professor Mitchell) were agreed on paper. During the hour, described by some as a "priming period", the resistance of the brain to injury is slowly and gradually overcome. A neonate and infant (as with older people) generally has the capacity to auto-regulate blood flow to the brain. Thus, if pressure of supply to the brain (arterial pressure) (on which flow and hence perfusion centrally depends, assuming that the resistance of the brain blood vessels is constant, though the evidence was that it also depends on volume and the extent to which oxygen is carried by the blood at the time) drops, the blood vessels in the brain will dilate, so that a flow of an equivalent amount of oxygenated blood to provide the necessary nutrients for brain function is maintained. Volume is increased with slower flow; and resistance is also reduced, maintaining sufficient oxygenation. Similarly, if pressure increases (as, in an adult, where there is significant physical exertion) the blood vessels will constrict, to the reverse effect. The automatic response is not simply to pressure. An increase in the concentration of carbon dioxide in the blood, for instance, will also cause dilation of the blood vessels, to increase cerebral flow.

27.

The postulated half hour is that during which the damage occurs. Once a cell is damaged, it will die. In addition to the brain's capacity more generally to auto-regulate blood supply, the cells will have reserves of nutrient, but in the absence of sufficiency of supply this is only some, though little, further defence.

28.

Critically for the present case, the existence of watershed damage on its own shows there has not been an acute anoxia, as in the case of a damaging cardiac arrest. In such a case, the deep grey matter of the brain and basal ganglia would be affected. Here, they were not. Accordingly, however deep and long there may have been under-perfusion of Grace's brain, from whichever cause, the damage was not caused by her cardiac arrest. This does not exclude the lack of flow during cardiac arrest and resuscitation contributing to the damage, by adding to a process of hypoxic-ischaemic damage which was established at the time, at least if Dr. James' third meaning of "cardiac arrest" is accepted -though possibly in respect of his first or second too - since a lack of flow is by definition less than low flow for the time it persists. However, any decision whether there has probably been such damage must be heavily influenced by the surgeon's own words "At no time was there any significant period of circulatory arrest" and the observation that once the pneumothorax was relieved by re-opening the chest the heart "regained normal circulatory rhythm and a good circulatory status", both of which argue against it. Further, Dr. Rosenbloom (whose evidence on this I accept) told me that watershed damage is not progressive in extent even where hypoxic-ischaemia persists, unless the ischaemia worsens. To return to the analogy of the garden sprinkler: if low pressure causes the spray to fall short of an area, it will still perfuse the lawn within the area the spray still covers, and the reduced flow will not widen the belt of damaged lawn unless the pressure drops further, to the extent that the formerly (slightly) wet areas become dry.”

The judge then went on to emphasise that Grace was already a sick child, and not typical of those to whom the general parameters of an hour priming time and 30 minutes damaging period might apply. He found that her condition was “unusually serious” of its type.

The judge went on to hold that Grace, a sick and atypical child, suffered brain damage as a result of hypo-perfusion of the brain and did not suffer acute consequences from her cardiac arrest. He further held that it was certain that she suffered a tension PNT. Having reviewed the evidence, his conclusion – which is not open to challenge – was that the tension PNT was the most probable cause of the cardiac arrest and potentially could, if it lasted long enough, have caused hypoxic-ischaemic brain damage.

It was agreed between the expert anaesthetist witnesses that there were 5 stages to a tension PNT (1) entry of air into the pleural cavity from a damaged lung (2) increased pressure as more air was forced in (3) the air would compress the affected lung, would displace the heart to the contralateral side and would compress the other (contralateral) lung as well, thereby compromising circulation and pulmonary ventilation (a helpful diagram was in the Bundles to illustrate this) (4) the compromise would cause a fall in oxygen saturation in the blood, a rise in expired carbon dioxide tension, an increase in heart rate followed by a fall, a fall in cardiac output and a reduction in oxygen supply to brain and other organs (including heart). This would lead to (5) cardiac arrest.

As the judge stated, if the evidence was right that 30 minutes of damaging hypoxic-ischaemia was needed for watershed damage to occur then that would give insufficient time for the developing tension PNT to have caused it: because of his findings that the closing process of the operation – from sternal closure to transfer to incubator – would have taken no more than around 20 minutes and that the subsequent cardiac arrest was to be excluded. That, indeed, was essentially the respondent’s case: the respondent further arguing, of course, that the watershed damage was caused by Grace being on cardio-pulmonary bypass (all experts agreeing that there generally is significantly increased neurological morbidity when children have been on bypass). The appellant’s riposte was to the effect that no medical literature supported a link between a cardio-pulmonary bypass and watershed damage. Nor did the extant records reveal any observed drop in perfusion during the bypass.

It was said that certain potential signs where there is a developing tension PNT may be present. But the judge found that, by reference to 1983 practice and in the circumstances of an operation of this kind, there would have been no negligence in a reasonably competent anaesthetist not spotting “any or all” of such signs. However, there were – as found – monitors both of arterial and of venous pressures. The judge assessed the evidence and found that a developing tension PNT would increase central venous pressure and reduce arterial pressure. The judge concluded:

“On balance…it is likely…that at some stage before cardiac arrest Grace’s arterial pressure would have gradually risen before falling abruptly; and that her central venous pressure would have risen…”

The crucial question then was as to when this would have happened. The relevant expert called by the appellant (Professor Hatch) thought that a drop in arterial pressure would be a “late sign” and the rise in venous pressure should be noticeable “at least before the cardiac arrest”: at that stage the signs were there for an anaesthetist requiring intervention. Dr James, called by the respondent, said that blood pressure changes happen late in the case of PNTs (as the judge accepted) and that there would only be dramatic change in the pressures just before the cardiac arrest. He further said that fall in arterial pressure and rise in venous pressure would be late signs. The judge said that generally he accepted the evidence of Dr James in preference to that of Professor Hatch where they conflicted. The judge further noted, however, that while a tension PNT was not to be anticipated, tamponade – in effect, an accumulation of blood compressing the heart – was well known as an ever present risk in operations of this kind. The signs would have been similar to that of a developing tension PNT. The judge said this in paragraph 63 of his judgment:

“It is likely that one or other or more of the operating team would have been alert to signs that it might be happening. If there had been such signs, for any appreciable length of time prior to arrest, they would probably have been spotted, and action taken to remedy a supposed tamponade (pneumothorax would at most be a secondary differential diagnosis, because of its comparative rarity).”

In the event, the judge’s findings on breach were these:

“65.

Thus, on this point, I have to reconcile the fact that the pneumothorax developed within (at the very most) 25 minutes to the stage of arrest, probably gradually from a small leak, yet did so to the point of causing cardiac arrest, with the probable physiology (making due allowance for biological variability of response, as Paige recorded) which envisages increasing venous pressure and dropping arterial pressure as tension must have mounted within the chest, and with the view that it is unlikely that the monitor readings were clearly out of the ordinary until late in the process. Dr. James in evidence envisaged the readings might have required action for between 90 seconds to 2 minutes, at a time when it is not unreasonable to think that attention might have been elsewhere – lines disconnected, or being disconnected; baby prepared for moving to the incubator; hand ventilation distracting the anaesthetist. This is possible, and if so it might be asking too much of a clinician in that situation to have been aware of the sudden fall in arterial pressure and rise in central venous pressure presaging collapse, especially since it would not be clear if actual monitors were there to read at the time. However, I think it more likely that (reconciling these considerations) there was a slightly longer period of time within which a monitor was likely to have been displaying readings which vigilance should have indicated showed a need for urgent investigation. Putting a time on this is undoubtedly to select a figure which is wrong, and conveys a spurious accuracy if taken too precisely. However, I cannot think that the readings would have invited action for as long as 5 minutes. Before that any alterations in pressures would have been gradual, would not have indicated a tamponade to reasonably vigilant observers (and I cannot accept that all of the potential observers failed to be in this category), and the observable pressures must have been missed by Dr. Hasbury as the person centrally responsible when the attention of others was elsewhere, though briefly, in the period immediately leading up to transfer. It may have been that his manual ventilation (following machine ventilation) was that which very suddenly produced an additional surge of air into the chest which upset the broad equilibrium of pressures of which Dr. James spoke, to tip the pneumothorax from an insidious development to a potentially catastrophic one. I cannot easily accept, however, that the pressures would have been detectably worrying for as short a period as Dr. James suggested. The likely range is 2 – 3 minutes, though there can be no point precision about this.”

The judge went on to hold, that given the “ever-present risk” of tamponade, a reasonably careful anaesthetist should have detected the signs shortly (measured in seconds, not minutes) after they became detectable. He found Dr Hasbury in breach of duty accordingly.

The judge made the following relevant and important findings by reference to the breach of duty as found:

The judge then went on to consider, at length and under a different heading, what was the probable cause of the injury which in fact occurred. He reviewed the expert evidence. He noted that Dr Rennie – the expert neonatologist called by the respondent – modified her general view that normally (based on cases of foetal injury) an hour of non-damaging hypoxia would precede the 30 minute period of damaging hypoxia sufficient to cause watershed damage. She thought that it could sometimes be very considerably shorter than one hour. Dr Rennie did so on the footing that “autoregulation” – which would generally need to be “overcome” in the ordinary situation – had probably already been significantly impaired: just because Grace was already a sick and impaired child prior to the surgery and was over 4 months old at the time of the surgery. Reliance was placed on an article by Barkovich (1999) in support of her explanation. The general position ultimately advanced by Dr Rennie on this aspect came to be called “the maturation shift” at trial.

The judge reviewed the evidence, and supporting medical literature, and analysed it in detail. It was noted that there were, in fact, some (limited) reported examples of watershed injury arising in babies after bypass procedures: although the judge found that did not provide “unequivocal support” for Dr Rennie’s proposition. The judge, at all events, accepted Dr Rennie’s theory of maturation shift and also Dr Rennie’s evidence that Grace’s auto-regulation was so compromised by her existing condition that the time on bypass would have been capable of being sufficient to permit the injury which occurred. He proceeded to reject the appellant’s argument that the bypass procedure should be discounted as a cause of low perfusion.

The judge went on to reject a further submission of Dr Powers QC, on behalf of the appellant, to the effect that the 30 minute or so period was not an absolute or a given; and that the depth, rather than the duration, of the low perfusion might count more. The judge rejected that as not consistent with the evidence. He then held that there had been a period of 30 minutes or so of significant hypoxic-ischeamia occurring during the bypass and which caused the brain damage.

The judge expressed these conclusions:

“101.

Making all due allowance for margin, a period of 30 minutes is far removed from the time I have found available in this case. Despite many attendant uncertainties, the best picture is one of a maximum time of 25 minutes, within which the hypoxia would have had to arise, followed by a period around resuscitation and restoration of circulation, which I accept from the typed surgical note would have been short. Within that 25 minutes, I have already held it unlikely that there was any significant hypotension (so as to be detectable) until some 2-3 minutes before the arrest. The hypotension would have developed only gradually before that, given the likely size of the leak. The resultant period is on any view so far removed from 30 minutes as for reliance on that figure to preclude it. I have no better figure to adopt. Accordingly, I do not think it probable that the hypoperfusion injury to Grace's brain was caused by the pneumothorax. Put simply, there was not enough time for this to have happened.

102.

When allied to the evidence that there was no demonstrable acute consequence from the cardiac arrest, there is no evidence that that arrest caused any further damage – the case in respect of "breach causation" assumes that it did, as a natural continuation of an hypoxic process which was already underway. Given my conclusion that there was insufficient time for such a process to occur in connection with the pneumothorax, it must follow that there is no evidence of any process which was ongoing to which the short period of loss of cerebral flow occurring during cardiac arrest could have made a contribution.”

In the final paragraph of his judgment, the judge repeated that his conclusion was, with regard to the brain injury suffered by Grace, that it was not realistically possible to have been caused by an undetected PNT. He said this in closing in paragraph 104:

“In the end, I concluded that although the Defendant's explanation was fragile, it was on the evidence realistically possible for the injury as suffered by Grace to have been a non-negligent consequence of surgery, and not realistically possible for it to have been caused by an undetected pneumothorax. Since I concluded that the pneumothorax (or, at least, cause for re-opening the chest as with suspected tamponade) should with the exercise of proper care have been detected, I have to ask further whether this and the cardiac arrest would probably have added to the damage. There is no evidence sufficient for me to make this finding. In conclusion, therefore, I find for the Defendant and dismiss the claim.”

Four grounds were advanced before us on behalf of the appellant in seeking to show that the judge was wrong in his conclusion.

The first ground was that the judge erred in concluding that there was no evidence that the period of hypo-perfusion caused by the breach of duty in failing to diagnose the PNT added to the watershed damage. In this regard we were referred (as had been the judge) to the decision of the Court of Appeal in Bailey v Ministry of Defence & Anor [2008] EWCA Civ 383; [2009] 1 WLR 1052. There, in the context of a medical negligence case, Waller LJ (with whom Sedley LJ and Smith LJ agreed) summarised the relevant principle in this way at paragraph 46 of his judgment:

“46.

In my view one cannot draw a distinction between medical negligence cases and others. I would summarise the position in relation to cumulative cause cases as follows. If the evidence demonstrates on a balance of probabilities that the injury would have occurred as a result of the non-tortious cause or causes in any event, the claimant will have failed to establish that the tortious cause contributed. Hotson exemplifies such a situation. If the evidence demonstrates that 'but for' the contribution of the tortious cause the injury would probably not have occurred, the claimant will (obviously) have discharged the burden. In a case where medical science cannot establish the probability that 'but for' an act of negligence the injury would not have happened but can establish that the contribution of the negligent cause was more than negligible, the 'but for' test is modified, and the claimant will succeed.”

It was accepted by all counsel before us that that accurately states the law. The appellant’s position overall is that the only proper conclusion which could have been reached on the evidence was that Grace’s watershed brain damage was materially contributed to by the Defendant’s negligence in failing to diagnose the developing tension PNT.

The second ground was that the judge failed to take into account the fact that the appellant would have continued to suffer a period of profound hypoperfusion after the cardiac arrest.

The third ground (developed in oral argument by Mr Jones on behalf of the appellant) was that the judge erred in concluding that the tension PNT could not have been detected with the exercise of reasonable skill and care until 2 to 3 minutes prior to the cardiac arrest.

The fourth ground (also developed in oral argument by Mr Jones) was to the effect that the judge had found a 9 to 10 minute period of potentially damaging hypo-perfusion but failed to realise that during that period the appellant’s blood pressure would (on the evidence) have had to have been half of normal: which Dr Hasbury should have noted.

Overall, therefore, the appellant’s grounds are entirely as to the judge’s evaluation of the evidence and as to his factual conclusions. Dr Powers did, however, very fairly – and rightly – accept that the judge was entitled to express, as he did, a general preference for the evidence of Dr James, (paediatric anaesthesia) Dr Rennie (neonatology) and Dr Rosenbloom (paediatric neurology), called by the respondent at trial, over their counterparts called by the appellant.

I will deal with each of the Grounds advanced in turn.

Dr Powers initially submitted that the judge’s conclusions on causation in paragraph 104 of his judgment were illogical and inconsistent with what he had earlier said in paragraph 73 of his judgment. There he had said:

“73.

If, despite this, the period of low perfusion was such that Grace's injury did occur in this much shorter timescale, the negligence would have resulted in a loss of a couple of minutes of what (on this hypothesis) would have been a short period rapidly causing damage. Since a cardiac arrest in such circumstances involves lower perfusion still than the loss of flow which precipitates it, it is likely that it contributed to the damage to an extent which was not insignificant. It would however not be causative of any greater damage than this. At most, therefore, the negligence would have contributed some 3 minutes of a potential 9 – 10 minutes of damaging hypo-perfusion. This is however sufficient for it to be a more than immaterial contribution to the damage (assuming it to have been caused by a period of hypo-perfusion at this time).”

However, on a closer reading of the judgment as a whole, the judge plainly in that earlier part of the judgment was dealing with the primary case of the claimant then being advanced: namely, that it was the (undetected) PNT and cardiac arrest which was the cause of all the relevant damage. The judge was simply saying that if all the damage had been caused thereby within 9 to 10 minutes then the negligence (as found) lasting some 3 minutes would have made a material contribution. In the event, on his ultimate findings, that never was established as the situation and he rejected that claim. It is also, in any case, rather unclear as to what was the basis for the judge’s allusion to a “potential 9 - 10 minutes of damaging hypo-perfusion”: a point to which I will revert.

Dr Powers realistically accepted that he could not at this stage challenge the judge’s findings that there was not enough time for all the hypoxic ischaemic injury to have been incurred as a result of the PNT and subsequent cardiac arrest (the primary case as pleaded and advanced): and there is thus no appeal against the finding that brain damage was caused during the bypass. Nevertheless, Dr Powers queried how the judge could attribute all the damage to the bypass procedure (even allowing for Grace’s already sick state) and none to the 9-10 minutes of potentially damaging hypo-perfusion (as referred to by the judge) within which the watershed injury could have occurred. However Dr Powers conceded that he could not say simply by reference to this period of time that a proportion of the injury must without more be taken as attributable to the latter period mentioned by the judge rather than all being attributable to the bypass period. Indeed, in common with Mr Block, he frankly accepted that it was not altogether clear from where the judge had derived his reference to 9-10 minutes of damaging hypo-perfusion within which the watershed injury could have occurred. But Dr Powers’ central point was that on the actual evidence at least some material contribution to the overall damage was made in the 2-3 minutes prior to cardiac arrest and thereafter.

At some stages, all the same, Dr Powers did seem to me to be arguing that it was really a matter of logic that additional damage must have been caused both in the 2 to 3 minutes prior to the cardiac arrest (when, as found, the signs should have been detected) and in the period after cardiac arrest before circulation was restored. But this is not a matter of logic, it is a matter of evidence. And in my view the judge was fully entitled to conclude that the evidence did not support the appellant’s case on this.

First, the judge accepted the evidence of Dr Rennie (and Dr Rosenbloom and Dr James) in this regard. This evidence was against the appellant’s “double-hit” theory. We were carefully taken through extensive passages of the transcripts of their evidence by Dr Powers and Mr Block. There is no doubt at all that, taken overall, they support the judge’s conclusion.

Second, and reflecting the first point, the conclusion is consistent with the important paper of Barkovich, based on extensive research. In that paper, there is a full discussion of auto-regulation. It is also stated at page 169 of the report:

“The duration of the hypo-perfusion is a critical factor in determining whether brain damage results from an episode of hypo-perfusion…we have found no damage in neonates who suffered hypo-perfusion for less than 10 minutes…if the hypo-perfusion is profound, with severely reduced blood flow to the brain, we have found that nearly all gray matter is injured…in contrast less severe hypo-perfusion results in damage to the intervascular boundary zones…”

Barkovich goes on to identify three primary factors for the patterns of brain injury as a result of hypoxic-ischaemic episodes: severity of hypotension; maturity of the brain at time of injury; and duration of event. On severity of hypotension, Barkovich among other things reports this:

“When blood flow to the brain is mildly or moderately reduced (mild to moderate cerebral hypotension with impaired auto-regulation) blood flow is shunted from the anterior to posterior circulation…As a result damage is limited to the intervascular boundary zones of the cerebral hemispheres. However when reduction of cerebral blood flow is severe (profound cerebral hypotension)…shunting of blood is no longer adequate to save the deep structures from damage…”

Barkovich then deals with the second factor (maturity of the brain). As to the third factor (duration of the injury) Barkovich says this at page 171:

“Duration of the event is another important factor in interpreting an imaging study of an asphyxiated child. It is not possible to know the precise duration of an arrest, particularly in a neonate who may have arrested before delivery. Our experience, however, is that no brain damage is found in infants who have arrested for less than about 10 minutes. Patients who have arrested for 10 to 15 minutes typically suffer damage that is limited to the ventrolateral thalami, globus palladus, posterior putamen, perirolandic cortext, and sometimes hippocampi. As the duration of the arrest becomes longer, the amount of injured brain increases to include the superior vermis, optic radiations, and calcarine cortex. Ultimately, when the arrest extends into the 25-30 minute range, nearly all of the gray matter is injured and the child is left with diffuse multicystic encephalomalacia and shrunken basal ganglia…

The duration of cerebral ischemia necessary to cause injury to the watershed zones and periventricular white matter is probably similar to that needed to cause damage from circulatory arrest. However, because the region suffering hypo-perfusion is limited, the region that is damaged does not extend as the duration of the hypotension progresses unless the hypotension becomes more severe. Therefore, in our experience, patients who suffer mild to moderate ischemia for many hours, or even days, have watershed patterns of injury similar to those who suffer injuries of shorter duration.”

This accords with the respondent’s case. Further, the judge was entitled to attach, as he did, great weight to Mr Yates’ typed-up note which among other things records: “At no time was there any significant period of circulatory arrest,” and which also records that on the tension PNT being relieved the heart regained normal rhythm and “a good circulatory status”. Moreover, the note records external cardiac massage being administered. The experts were agreed that external cardiac massage would not necessarily have been effective: but equally there was evidence to indicate that it was not to be taken as entirely ineffective either.

Dr Powers maintained – as he had to the judge - that the situation was not to be assessed simply by reference to the duration of the event: regard had to be had to the profundity of the hypo-perfusion. That is no doubt so and accords with Barkovich. But it simply does not justify putting to one side, as it were, the duration of the event. The evidence of the respondent’s experts, to which we were taken, was clear on that: as is Barkovich. Thus Dr Rosenbloom (for example) made clear his opinion that sustained impaired perfusion was needed for extra damage to be caused. Dr Rennie said that no further damage would arise if on the second occasion of the alleged “double hit” the same “threshold” was reached as on the first occasion (the bypass): there would only be extra damage to the border zones if the degree and depth lasted on the second occasion even longer and even more severely than on the first occasion. Indeed, the point was inevitably made on behalf of the respondent that if the (postulated) injury lasted around 10 minutes then the level of profundity required to add to the damage would be expected also to give rise to injury to the grey matter. Yet no such injury occurred in this case. The judge, in my view, was justified in rejecting this argument, on the evidence, as he did.

Reflecting all this, the difficulty, as it seems to me, in the way of Dr Powers’ argument is this. The theory advanced – following the sprinkler example considered, within limits, useful both by the experts and by the judge –would, if right, require, among other things, that the level of hypo-perfusion occurring after the negligence of Dr Hasbury arose was more profound than that pertaining at the time when damage was caused (as found by the judge and as not challenged on appeal) at the time of the bypass – see Barkovich at p.171 (op.cit) and as confirmed by Dr Rennie and other expert evidence. But there was no evidence of that in fact being so in this case: and in my view, contrary to Dr Powers’ submission, it is not a matter which can be inferred as having happened.

Looking at it overall, there was, to maintain the appellant’s case, neither sufficient evidence before the judge of the overall period of allegedly damaging hypotension; nor sufficient evidence as to its alleged profundity preceding or following the cardiac arrest. In such circumstances, it is unsurprising that the judge concluded that the appellant had not made out her case on causation.

With all respect to Dr Powers, it also is not right to say, as he did, that the judge’s approach was simply to ask which was the more likely period during which the brain damage occurred (bypass or PNT); rule out PNT as the cause because there was insufficient time for all the damage to have occurred; and thus conclude that all the damage must have been caused by the bypass. On the contrary, the judge plainly addressed the alternative scenario – viz as to whether the undetected PNT at least materially contributed to the brain damage – and rejected it as not in accordance with the evidence. At the very least, and as Mr Block submitted, the judge’s conclusion to the effect that there was no second period which added to the damage already sustained was a finding within the range of findings he was entitled to make.

It was really a necessary part of Dr Powers’ argument that the damaging injury allegedly occasioned as a result of the “second hit” arose not only in the 2-3 minutes before the arrest but also in the period – a short period, as found by the judge – of the cardiac arrest until circulation was restored. Dr Powers in reality was invoking this further period to bolster his case on duration and profundity. Dr Powers was entitled in this regard to point to the finding that the cardiac arrest was the consequence of the developing PNT. He was also entitled to make the point that, until circulation was restored, there would have been no perfusion.

Nevertheless, and as reflects the first ground, this too has very great difficulty. The judge’s justified finding, based on Mr Yates’ note, was that there was no significant period of circulatory arrest: and good circulatory status was regained almost immediately. He in terms (in paragraph 70 of his judgment) had found that there was “no significant time after the cardiac arrest within which under-perfusion of the brain could be supposed to have continued”.

As the judge noted when refusing permission to appeal it would have been speculative to conclude that the cardiac arrest contributed to the brain damage; and there was insufficient evidence before him so to conclude. When asked, Dr Powers was not himself able to point to such evidence establishing this. On the contrary, and as noted above, both Dr Rennie and Dr Rosenbloom, whose evidence the judge accepted, had stated that if watershed damage greater than that which occurred during the bypass had been occasioned, that would have required a sufficiently long period (“prolonged” or “sustained” were epithets variously used) of a deeper level of hypo-perfusion than occurred during the bypass. As Dr Rennie put it: “If, however, the degree and depth lasted on the second occasion even longer and even more severely than the first occasion then the border zone, as in the lawn sprinkler, would potentially enlarge but the cells that had already died could not die any further”. When questioned about her contention putting all the damage in the bypass period as opposed to the later period, she was asked whether the issue was one of time rather than profundity. Her answer, however, was: “It’s both, because the blood pressure has to be low enough for long enough”.

Dr Powers maintained, nevertheless, that hypo-perfusion following the cardiac arrest would have been worse. He latched on to one particular answer of Dr Rosenbloom given in evidence. Dr Rosenbloom agreed that there was a period of hypo-perfusion before the cardiac arrest. The cardiac arrest would “not have improved” the hypo-perfusion. The question then put was: “In fact, quite the reverse?” To which Dr Rosenbloom answered “Probably.” But that isolated answer cannot displace the overall evidence of Dr Rosenbloom, to the effect – consistently with Dr Rennie - that a worsening of the level of perfusion over a significant period of time would have been called for for extra damage to be caused. Dr Rennie’s evidence in chief, on which she was not shaken in cross-examination (and she ultimately being a witness whose evidence generally the judge preferred) was that Grace did not sustain any damage as a direct result of the cardiac arrest. The judge’s findings in paragraph 70 of the judgment were justified.

Overall the evidence of Dr Rennie and Dr Rosenbloom was to the effect that there was not evidenced a sufficiently prolonged degree of perfusion over a significantly sustained period to give rise to extra damage or to contribute materially to the overall brain damage. The judge was entitled to accept that evidence.

This ground can be subsumed into my discussion on the cross-appeal relating to the finding of breach of duty. As there appears, in my view this ground has no validity.

This ground also is not made out. It presupposes that the judge made a positive finding that there were about 10 minutes of significant and detectable damaging hypo-perfusion. The judge made no such finding. On the contrary his finding was that the negligence, as found, was in the 2-3 minutes before the cardiac arrest; and that after the cardiac arrest, as the note records, circulation was “speedily” restored. It is true that the judge, in paragraphs 72 and 73 of the judgment, refers to a “potential” 9 to 10 minutes of “damaging” hypo-perfusion. But, as I have previously said, it is not altogether clear where this derives from. In any case he makes no actual finding to the effect that is what in fact occurred here; and his other findings elsewhere in the judgment are to different effect.

In advancing the cross appeal Mr Block reemphasised the difficulties occasioned by the lapse of time and stressed that Dr Hasbury had not been alive to defend himself. He emphasised the difficulties in reconstructing events precisely. He further emphasised that the appellant’s case connoted that a skilled and experienced consultant anaesthetist – and perhaps too the supporting team present at the operation – had failed to make important and basic observations: something, he submitted, which was inherently unlikely (although of course claims in negligence cannot be rebutted solely on such a basis, as the judge pointed out).

Those are valid points. But it is quite clear that the judge had regard to them. Further, the judge had accepted that many of the signs of a developing tension PNT, as indicated by Professor Hatch (expert paediatric anaesthetist called by the claimant) as potentially present, would have been difficult to detect and that it was not negligent to fail to spot such signs. In making the finding of breach of duty, the judge’s principal emphasis was on the existence of monitors of both arterial and central venous pressure. The judge found, reviewing the expert evidence and medical literature (including papers by Paige and Barton) that the developing tension PNT would give rise in combination to lowered arterial pressure and raised central venous pressure. The judge found that “at some stage” before cardiac arrest, Grace’s arterial pressure would have gradually risen before falling abruptly and that her central venous pressure would have risen. He accepted, preferring Dr James’ evidence on this, that these would have been late signs before the cardiac arrest occurred.

Some of the judge’s remarks leading up to the central paragraph 65 of his judgment (set out above) relating to breach perhaps indicate a receptiveness to the notion that it was likely that one or more of the team would have been alert, prior to transfer from the operating table, to signs of compromise of the circulation, if there really had been such signs for any appreciable length of time prior to arrest. The judge at all events accepted that it was possible that, if readings required action for between 90 seconds and 2 minutes, attention was understandably distracted elsewhere prior to preparations for removal to the incubator. Further, of course, as the evidence showed, there would have been a time when the monitors would have had to be disconnected just prior to Grace’s transfer to the incubator.

That said, on the whole I do not think the judge was disentitled from finding that there was a slightly longer period within which the monitors displayed readings indicating a need for urgent investigation. It may be that the team was distracted in preparing for removal at that time: but, as Mr Jones crisply submitted in argument, all the more reason for the anaesthetist himself (having prime charge of these aspects) at that stage to keep a close eye on the monitors before disconnection. As to the length of time involved, as the judge himself said there could be no “point precision”. He acknowledged the point made by Dr James – and repeated by Mr Block in argument – that there may have been a time when there was an equilibrium of pressures. All the same a conclusion, reconstructing as best as possible, that the likely range for detectable worrying pressures was 2-3 minutes was a conclusion which on the evidence, in my view, the judge was entitled to reach. The judge was thus entitled to go on to conclude that there was a breach of duty in that, those signs being there in that period, they should thereafter have been detected within seconds.

Mr Block complained that the judge had in effect plucked a figure out of the air in giving a range of 2 to 3 minutes and must have misunderstood Dr James’ evidence in this regard. I do not think that a well-founded criticism: indeed the very fact that Dr James advanced in the course of his oral evidence the suggestion that members of the team could for a period of 90 seconds to 2 minutes have been distracted in preparing Grace for removal (a point alternative to Dr James’ other point that it was very unlikely that the team would have ignored significant changes in the monitored pressures) is capable of being supportive of the judge’s approach. In fact, during the course of his cross-examination Dr James himself at one stage had said, with regard to the observable signs available from the arterial and central venous pressures, “it is my suspicion that either they were noticed or just not noticed or something happened around the time of (sic) about to be moved to the incubator…which has pushed everything out of equilibrium and caused hypotension there.” Moreover to put, as the judge did, the time range of such pressure signs as 2-3 minutes is at least consistent with Professor Hatch’s overall evidence, as well as Professor Hatch’s acceptance that they would have been “late” signs: even if Professor Hatch also had said the rise in central venous pressure would have been a relatively early sign. The judge, at all events, was not bound to accept the evidence of Dr James to the effect that the blood pressure changes were part of the process of what was called the cardiac arrest nor that the pressures could have been in equilibrium until just before Grace was transferred and the cardiac arrest.

For corresponding reasons, the argument advanced as Ground 3 on behalf of the appellant must itself also fail. For the reasons given above, it is not to be taken that the judge did in fact make a finding that there had been a 9-10 minute period of damaging hypoperfusion. In paragraph 65, indeed, the judge had in terms said that “I cannot think that the readings would have invited action for as long as 5 minutes”. To find that the detectable signs were there for 2-3 minutes was, as I have indicated, a finding open to the judge on the evidence. Mr Jones carefully took us through the relevant parts of the papers of Barton and Paige and of the expert evidence, particularly of Professor Hatch and Dr James. Suffice it to say, in my view those did not in any way require a conclusion (contrary to the one which the judge reached) that the signs were detectable for a period of significantly longer than 2 to 3 minutes.

For my part, I would dismiss the appeal and I would dismiss the cross-appeal.

I agree

I also agree.