Canning-Kishver v Sandwell & West Birmingham Hospitals NHS Trust [2008] EWHC 2384 (QB)

[2008] EWHC 2384 (QB)

Case No TLQ/08/0620

IN THE HIGH COURT OF JUSTICE

QUEEN'S BENCH DIVISION

Venue Royal Courts of Justice, Strand, London, WC2A 2LL

Date 13 th October 2008

Before

SIR CHRISTOPHER HOLLAND

Between

AYESHA CANNING-KISHVERClaimant

SANDWELL & WEST BIRMINGHAM HOSPITALS NHS TRUSTDefendants

Simeon Maskrey QC and Adam Korn (instructed by Irwin Mitchell) for Claimant

Neil Block QC (instructed by Bevan Brittan LLP) for Defendants

Hearing Hearing dates: 25 th to 31 st July 2008

Judgment

Sir Christopher Holland :

[1]A claim for damages is brought on behalf of Ayesha Shamin Canning-Kishver (“Ayesha”). She was born prematurely on the 15th July 1997 and she sues the Defendants as the body responsible for the City Hospital, Birmingham, alleging that the treatment of her as a premature baby was negligent so as to cause her to suffer a brain injury, in its turn causative of a significant level of permanent disability. Liability and quantum are respectively in issue. By way of Case Management, liability is sensibly before the Court as a separate, preliminary issue – quantum abides the outcome. As to liability, two essential issues are raised: was there any breach of an admitted duty of care? and, if so, was such legally causative of the brain injury? Having heard the evidence, it is my task to resolve these issues and I do so as follows.

NEONATAL UNIT

[2]Ayesha was delivered by way of Caesarean section after a gestation of just 25 weeks and 3 days. She was immediately admitted to the Neonatal Unit at the City Hospital. A description of this Unit and its staffing is a necessary preliminary to a recital of the history, focussing upon the material period, that is the night 22nd/23rd July 1997. Thus, the Unit featured three rooms: Intensive Care (with 6 cots); High Dependency (with 6 cots); and Low Dependency (with 10 cots). Inevitably Ayesha went straight into a cot in the Intensive Care Room and she remained in such at all times material to her action. Her cot featured a servo-controlled incubator that by way of response to her skin temperature provided an environment of appropriate warmth. At all times she was attached to monitors that provided visual readings, in particular as to heart rate and respiratory rate. Her care was the subject of regular monitoring, such resulting in hourly entries of a comprehensive kind made in a High Dependency Chart. Other charts were maintained for specific separate purposes, as in the Blood Gases and Ventilator Settings Instruction Chart. The required level of Intensive Care necessarily demanded concentrated, skilled, specialist nursing, subject to similarly skilled and specialised clinical direction. In the event for the night of the 22nd/23rd the nurse tasked with her care was Staff Nurse Wright (now, Sister Henry). This nurse started her shift at 9.15 pm and was on duty to 7.45 am. In the course of this shift she had two neonates to care for: Ayesha and another similar baby. I interpose: I was told that ideally any such nurse should be tasked to care for just one baby but that the exigencies of the NHS regime made caring for two babies pragmatically inevitable. Staff Nurse Wright had been caring for neonates since 1988. She gave evidence before me: she presented as caring, dedicated and knowledgeable.

[3]Sister McCarthy was the other nurse involved in the Intensive Care Room that night. She too was tasked to care for two babies – there appear to have been concurrently four babies then in Intensive Care. Her shift hours were similarly 9.15 pm to 7.45 am. She was exceptionally experienced having been on the Neonatal Unit since 1979. She too gave evidence before me, giving a similar presentation. As was to be expected, she covered for Nurse Wright when circumstances required the latter to leave her patients, whether for a break or for other duties – and vice versa.

[4]For the night of the 22nd/23rd July immediate medical cover for the Unit was to be provided by the Duty S.H.O, Dr Ulrika Schmidt (now Ulrika Prume). However, that doctor’s cover had to be shared by the Unit with other wards, particularly the Labour Ward. As at that date Dr Schmidt had had six months’ neonatal training; yet further, on various earlier occasions, she had been concerned in the care of Ayesha, as is apparent from entries made by her in the clinical notes. She gave evidence, again to good effect. Seemingly, she retained some memory of that night’s duty.

[5]Yet further medical cover could be obtained from that night’s Duty Registrar, Dr Douglas Simkiss. His evidence was to the effect that he retained no memory specific to that occasion. However, he was able to cite his invariable working practice as a Duty Registrar and the resultant surmise was supported in part by the evidence of Dr Schmidt. Thus, he told me that it was his invariable practice to do a full round of all the wards under his potential care, starting at about 10.00 pm. and accompanied by the Duty S.H.O. before retiring to bed. This round was done for ‘my own peace of mind’ and was aimed at identifying and tackling ‘issues of concern’, in part by discussion with the nursing staff. He too presented as caring and knowledgeable. He had been practising in paediatrics since 1989 and he attained Consultant status in 1998.

[6]Other doctors provided comparable daytime cover for the Unit and the forthcoming history will introduce Dr Nik Rashid as another S.H.O. With respect to Consultant cover, nominally this was the responsibility of Dr Jeffrey Bissenden but in the event Ayesha also received Consultant attention from Dr Pal. The history will further introduce the Grand Round; it was the practice of the available Consultants to conduct a round of all the wards at 8.30 am each day, accompanied by the other medical staff then on duty and available.

HISTORY

[7]By way of preface, I draw attention to the impact of delay upon individual recollections of the material events, that is, those of the night 22nd/23rd July 1997. The first intimation of a claim was not made until 2005 and these proceedings commenced as late as early 2007. Inevitably there is little that can be offered by way of direct memory and there has to be much reliance upon contemporaneous records and such inferences as can fairly be drawn from them. I have had the potential for injustice, particularly to those defending belated allegations of negligence, much to mind as will be apparent when I make my judgments hereafter.

[8]Period 15th – 22nd July. Ayesha was delivered by way of Caesarean section after just 25 weeks of gestation – the estimated date of delivery had been the 25th October. Following delivery she was immediately admitted to the Intensive Care Room described above and there she remained at all material times. Her progress during the first week of life as is apparent from the records has been carefully recited and reviewed by the experts, principally by Dr Sian Harding. For present purposes I need only identify certain features which, whether or not ultimately significant, meant that her clinical presentation in terms of totality was unusual.

[9]Thus,(a) From birth her albumin level was low.

(b) She had an enlarged heart.

(d) She had become jaundiced and was accordingly exposed to a blue phototherapy light.

(e) There had been a pericardial effusion calling for an aspiration of some 7 mls.

(f) There was a recurring build-up of lactic acid in the tissues for some unestablished reason, resulting in metabolic acidosis. The fact of this condition was to be established by analysis of a capillary blood sample taken from the baby’s heel. Ideally this should reveal a Ph level of the order of 7.35 or 7.45 and a base excess of + or – 2 or 3. A Ph figure at significantly less than that range together with a higher base excess evidence an ongoing acidosis. The response to the latter could be a cure (such necessitating investigation), or treatment with a view to alleviation by way of administration of sodium bicarbonate. In the event the question of a cure had not been addressed and as and when the blood sample readings had demanded such, she had been treated with sodium bicarbonate.

(g) Finally, there had been a pneumothorax requiring aspiration by a chest drain.

[10]A crucial feature of this early history was an extubation on the 21st July. Thereafter she breathed air assisted by a Continuous Positive Airways Pressure device. It was deemed appropriate to support her in the newly extubated state with a course of steroids, that is,dexamethasone. It is common ground that following such extubation the ensuing 36 hours present a struggle for the neonate.

[11]Period 22nd – 23rd July. I trace the essential history as follows:- 22nd July 8.00 pm A comprehensive clinical note is made by Dr Rashid reviewing her condition and establishing a plan for future treatment. 9.15 pm The night nursing shift of Sister McCarthy and Staff Nurse Wright took over with Ayesha the latter’s patient. 10.00 pm onwards. Dr Simkiss conducted his round, probably accompanied by Dr Schmidt. Whether or not he gave Ayesha any examination there is no doubt but that he looked at her nursing charts so as to note that there had been no Ph check since about 8.00 am. He requested that such be done. 23rd July 12.10 am A note is made by Dr Schmidt. She had taken a blood sample and the analysis gave Ph 7.177 and base excess -14.5. She spoke to Dr Simkiss about this result, such plainly indicative of ongoing metabolic acidosis, and it was agreed that sodium bicarbonate should be administered at a half rate. Unfortunately there was at this point a breakdown in communication. Nurse Wright was engaged elsewhere and Sister McCarthy misunderstood or failed to act upon the S.H.O’s requirements. No sodium bicarbonate was then administered. 3.50 am Dr Schmidt sought to check the effect of the administration of sodium bicarbonate only to discover that there had been none such. She took a further capillary blood sample and had this analysed. Happily there had been no significant deterioration since 12.10 am: the Ph was 7.22 and the base excess was -14.9. The administration of sodium bicarbonate now started. I interpose: it is common ground that given the lack of significant deterioration, the delay in administering sodium bicarbonate was not in the event significant. 7.45 am There was a change of nursing shift. 8.00 am Dr Schmidt went to check on Ayesha’s progress, initially by taking another blood sample for analysis. She found it difficult to induce bleeding and, upon switching off the phototherapy light, she saw that Ayesha was pale and ‘oddly perfused’. It was at about this time that an alarm sounded, indicating that the heart rate had dropped to 90 beats per minute. As soon as the results of the blood analysis were to hand the startling figures were Ph 6.43 and base excess -13.29. It was obvious that Ayesha’s condition was all but terminal. Happily, participants in the Grand Round were assembling in the vicinity and Ayesha received extensive life saving measures, principally re-intubation and aggressive fluid resuscitation, from the doctors then in attendance.

THE CLAIM

[12]Initially, there were three essential allegations of breach of duty. Two such proved to be, in my judgment, unarguable. First, it was contended that Dr Simkiss and/or Dr Schmidt were in breach of duty inasmuch as they sought only to alleviate the metabolic acidosis and not to cure it. Had they exercised an appropriate standard of care, they would have conducted investigations such as would have established what is contended to be the case, namely that the acidosis was caused by infection, and would have administered the appropriate ‘second line’ antibiotics. As to this, I regarded it as unrealistic to hold that the admitted failure of those two doctors to do more in the course of the night than treat the acidosis could conceivably amount to a breach of the duty of care. If the problem was infection and if the duty of care demanded a cure rather than treatment then the spotlight falls, if at all, on the Consultants giving daytime care specific to Ayesha.

[13]This then leads into the second allegation of breach of duty that proved to be quite unarguable. Still proceeding on the premise that the metabolic acidosis was caused by infection calling for ‘second line’ antibiotics, complaint is made that this approach to Ayesha’s problems was not in the event adopted by those who participated in the Grand Round as led by Dr Bissenden. The consensus then adopted by the constituent doctors did include an investigation by way of lumbar puncture into a possibility of meningitis (in the event ruled out), but essentially focussed upon the potential for a cardiac explanation for the near catastrophe. The fact that this was the contemporaneous approach adopted by those seised with Ayesha’s immediate care tends, in my view, to undermine rather than support this part of the Claimant’s case. The obvious inference is that the proffered focus on infection has to be treated with caution and in any event it was not the practice accepted as proper by the Grand Round – that is, it was not “accepted as proper by a responsible body of medical men skilled in that particular art”, see Bolam v Friern Hospital Management Committee

(1957) 2 All ER 118

, 121.

[14]The remaining allegation is plainly arguable; does it serve to establish liability, subject to causation? The claimant’s case has to be that the condition of Ayesha so deteriorated between 5.00 am and 7.00 am as to give rise to signs that could and should have impacted upon the nursing staff so as to occasion the summoning of a doctor long before drastic resuscitation with its capacity to damage became necessary. As to this, it is common ground that the condition of Ayesha at 8.00 am did call into question the prior conduct of the nursing staff and indeed forthwith there was an enquiry, albeit limited to the circumstances in which Ayesha failed to receive sodium bicarbonate before 3.50 am. That said, the Defendants contend that on a proper and fair interpretation of the available evidence, nothing further can be laid at the door of the nursing staff in terms of breach of duty of care. It is to the available evidence that I now turn, starting with the charts.

THE CHARTS

[15]Each hour throughout the night entries were made by one or other nurse on Ayesha’s High Dependency Chart. For present purposes, I need only cite certain of the entries as recorded from midnight onwards. As to the selection, some entries cannot bear upon Ayesha’s deterioration and others do not need detailed recital being, for all intents and purposes, consistent.

[16]I start with the latter.(a) Throughout this period the percentage oxygen saturation was consistent in the acceptable range, 90-99%.

(b) Similarly, as to colour, Ayesha was consistently noted to be ‘pink’.

[17]I turn to those entries that do bear upon the circumstances in which the deterioration came about and I produce them as follows:- Time 24 01 02 03 04 05 06 07 08 Respiratory Rate 77 75 83 57 61 57 52 39 30 Heart Rate 156 169 171 172 164 161 111 110 115 Incubator Temp 36.6 36.7 36.2 35.1 34.9 35.5 37.1 38.5 38.6

THE NURSES

[18]Both Staff Nurse Wright (as she then was) and Sister McCarthy presented as caring, skilled and concerned, necessarily hampered by fading memory. They told me that which was accepted by all the experts, namely that, with experience, deterioration in a neonate can be discerned. They laid emphasis on the appearance, the ‘feel’ and the demeanour of the child as well as such on inferences as flow from the chart readings. Indeed they tended to down-play the latter: as ‘snapshots’ recorded on the hour, they may not evidence a significant trend. As to Ayesha, Nurse Wright pointed out that at about 3.00 am (as noted on the chart) she underwent ‘cares’, that is, as a matter of routine she had her temperature taken, her nappy changed and her mouth and anus cleaned, along with other checks. Had Ayesha then been deteriorating she, the nurse, would undoubtedly have noticed this through the necessary handling, not least because for these activities the phototherapy light had to have been pushed to one side so as temporarily to remove a distortion of the baby’s colour. In the event, she noticed nothing then nor, save in certain respects, during the rest of the shift. It was in such circumstances that her end of shift report read “Stable on CPAP ….. maintaining saturation above 90%. No bradycardias or apnoeas”.

[19]As to what she did notice, between 5.00 am and 6.00 am, she saw old blood in the aspirate obtained from mouth suction and accordingly she checked the nappy and found blood in the meconium. She had to react to these signs and did so. As she was empowered to do, she omitted the next feed at 6.00 am. As to what she further did is not wholly clear. On the chart there is a 7.00 am entry, “Food stopped”. For that order she would have to contact a doctor, presumably the S.H.O. In evidence before me she said that between 6.00 and 6.30 am she had ‘contacted’ a doctor communicating the fact of blood findings. Inferentially, this was by ‘phone because she said that she retained the syringe and nappy for subsequent inspection. As to information then put before the doctor, she included, as she now thinks, the fact of a recent fall in the heart rate from 161 to 111.

[20]So much for evidence before me; in her witness statement she put matters differently: “Normally the doctors are back on the Unit by around 5.30 to 6.00. It is standard practice for the junior doctors to come to the Unit at that time in order that they can carry out the bloods and various tests that will be required for the ward round later that morning. I think it is very likely that I would have mentioned to the doctor my findings in respect of old blood in the aspirate and meconium when she arrived on the unit. I would also have mentioned that I had felt it appropriate to omit her 6.00 am feed”.

[21]It remains to add that the S.H.O., Dr Schmidt, had no recollection of attending the Intensive Care Room between 5.30 and 6.00 am, nor indeed of being spoken to by Nurse Wright if such was the case. Nurse Wright cannot now remember which doctor she spoke to. Dr Schmidt’s belief is that she was there of her own volition at 8.00 am, similarly to pave the way for the Grand Round.

[22]One further matter: at no time during the night shift was Ayesha’s blood pressure checked. Nurse Wright’s evidence as to this was “In hindsight it looks bad”.

THE EXPERTS

[23]As to breach of duty, I had the benefit of oral evidence from three independent experts of high calibre: Dr Sian Harding of University College, London Hospital; Professor Malcolm Levene of the University of Leeds; and Professor David Field of the University of Leicester. Circumstances supplemented the foregoing with evidence that inevitably mixed fact and expertise from Dr Bissenden. I was indebted to all such and I was particularly impressed by the thought and research dedicated to the issues and no one will begrudge a specific acknowledgement of the contribution tirelessly made by Dr Harding. Again, I am indebted to the respectively well researched and well presented final submissions of Mr Block Q.C. on behalf of the Defendants and Mr Maskrey Q.C. (aided by Mr Korn) on behalf of the Claimant. All this leads to my own pragmatic decision not at this stage to burden this inevitably long judgment with successive recitals of the expert opinions and the resultant submissions. I propose to proceed immediately to my ‘breach of duty’ judgment in the course of which my indebtedness and consequent findings will be hopefully fully apparent. I intend no discourtesy and certainly no lack of appreciation.

JUDGMENT AS TO BREACH OF DUTY

[24]My first concern is to make a finding as to when Ayesha’s condition so deteriorated as to require urgent medical attention. As to this, first, it is common ground that shortly after 8.00 am she was in a parlous state. Dr Bissenden categorised her as the most acidotic baby he had ever seen, with a Ph 6.4 as the lowest level he had ever encountered. There was thus far no dissent. Could Ayesha’s collapse have occurred shortly beforehand, that is, after 8.00 am when Dr Schmidt took over from the nursing staff? Professor Field suggested this as a possibility for my consideration. This suggestion came from him belatedly and by way of response to a degree of personal incredulity at the possibility that the nurses he had seen give evidence could conceivably have been so in error as to be in breach of duty. He postulated a baby that was due to collapse, quite possibly because of a cardiac condition, quite possibly because of unresolved metabolic acidosis. He further postulated the sodium bicarbonate given at 3.50 am acting as a ‘buffer’ staving off the collapse until its beneficial effects wholly expired whereupon there would, in his opinion, be a sudden catastrophic collapse within minutes. He suggested that this analysis was consistent with the nurses’ failure to discern any seriously untoward sign up to and including the 8.00 am readings. Further, such was consistent with the unaffected saturation level and the continuous recording of the colour as pink.

[25]That said, Professor Field had to concede, first, that at the joint meeting of neonatologists he had agreed “that there were signs of decompensation by 5.00/6.00 am and a blood gas at that time would have shown a severe metabolic acidosis and this would have mandated intervention…”. True, he had then expressed a reservation that at that time the changes might reasonably have been missed by the nursing staff but before me he was constrained to agree that at 6.00 am the 50 beat change from 161 to 111, which change was maintained at 7.00 am, could not be ignored. At the least, in his opinion, it required the staff to review the baby’s condition, to make a decision about calling a doctor and, importantly, to note any assessment that had been made.

[26]My initial approach to my task echoed that of Professor Field. Having heard the evidence of the two nurses and taking into account their respective skills and dedication, I too found it difficult to envisage a sound basis for a finding of breach of duty against either or both. However, having appreciated the force of the expert evidence of Dr Harding and Professor Levene, having appreciated the near concession made by Dr Bissenden and having realised that Professor Field was almost constrained to acknowledge some lack of good practice, I am driven to make the following findings.

[27]I find that the acidosis was only temporarily alleviated by what Professor Levene categorised as a relatively low administration of sodium bicarbonate. Thus, by about 5.00 am the acidosis was impacting. Her circulatory insufficiency consequent upon the acidosis was increasing. That insufficiency demanded increased cardiac output. Ayesha’s heart beat was then at 161: there was no scope for an increase and in any event the circulatory insufficiency was by then impacting upon cardiac efficacy. Circulatory insufficiency started to dominate and the progress to a shutdown got underway. At 6.00 am there was recorded the drastic 50 beat drop to a heart rate of 111; that this was no ‘blip’ was confirmed at 7.00 am with a recorded rate of 110. At 6.00 am the respiratory rate was falling at 52; at 7.00 am it was in freefall at 39. Further, as Professor Levene pointed out, the skin temperature was only being maintained by increases in the incubator temperature. Decompensation that started, as theneonatologistsagree, at about 5.00 am was by 7.00 am serious and manifest.

[28]In the overall result, I am entirely satisfied upon the evidence of Dr Harding and Professor Levene that by 7.00 am, if not earlier, exercise of reasonable care and skill by the nurses demanded the urgent calling of a doctor by way of response to the drastic falls in the heart and respiratory rates of an acidotic neonate. I am further satisfied that had there been timely medical intervention the decline in Ayesha’s condition could have been stayed and reversed (such again being the opinion of those experts) without the trauma necessarily attendant upon intervention after 8.00 am. It follows that by failing so to react to the available signs as to secure medical intervention, the nursing staff were in breach of duty and thus negligent. All such findings are on the balance of probabilities. I add in the failure to record a blood pressure.

[29]I return to Professor Field’s concerns. How did it come about that there was this unexpected negligence? I am satisfied, again on balance of probabilities, that various factors contributed:(a) At all material times Ayesha’s saturation level was within normal limits. There is no obvious explanation for a sign that in isolation was reassuring. In the event, it may have served to militate against anxiety, albeit that it should not have gainsayed the overwhelming significance of the falls in heart and respiratory rates.

(b) For the purpose of the chart, Ayesha was consistently noted as ‘pink’, that is, as apparently perfused. It may well be that the persistent use of the phototherapy light to counter Ayesha’s jaundice served to mask the loss of colour that had to have been a feature from, say, 6.00 am onwards. It is to be remembered that when Dr Schmidt intervened she only noticed the change of colour when she switched the light off.

(c) There are indications that this was a demanding shift so as to render concentration upon an individual patient difficult. When Dr Schmidt had her initial dealings with Ayesha’s acidosis Nurse Wright was busy elsewhere. The Doctor’s instructions to Sister McCarthy were not acted upon. At 6.00 am it was Sister McCarthy that made the chart entries. Further, it may well not be a coincidence that the failures to react came towards the end of a shift, that is, at a very busy time as preparations are made for handover. I add in Dr Harding’s evidence as to the ideal patient/staff ratio.

(d) Finally, I draw particular attention to the extract cited above from Nurse Wright’s witness statement. If she believed that the S.H.O. would be in attendance at about 6.00 am in any event then a failure specifically to call for such attendance becomes less difficult to understand. Indeed, giving weight to that passage in the statement, I am satisfied on balance of probabilities that she never called for a doctor’s attendance, even to inspect the syringe and the nappy, believing that there would be attendance in any event and that there was no particular urgency. It is for that reason that the conscientious Dr Schmidt did not attend until after 8.00 am – and then only on her own initiative. Had Ayesha’s crisis occurred earlier in the shift when routine attendance by the S.H.O. was not anticipated then, as I like to think, similar signs in terms of heart and respiratory rates would have led to specific summoning of a doctor as a matter of urgency.

CAUSATION

[30]Under this head there are further difficult issues for me to resolve. It is convenient to start by reciting that which is common ground for present purposes:(a) Ayesha has continuing disabilities, principally dysarthria, ataxia, intention tremor and manual clumsiness. All such would correlate with atrophy of the cerebellum. They found the claim for quantum purposes.

(b) MRI scans of Ayesha’s head taken in, respectively, 2001 and 2007 reveal atrophy and some deformation of the cerebellum, that is, per Dr Harding’s glossary, part of the vertebrate hindbrain concerned primarily with somatic motor function, the control of muscle tone and the maintenance of balance. Additionally the scans reveal that a feature immediately adjacent to the cerebellum, the 4th ventricle, is enlarged.

(c) Whatever caused the features to be seen on the scans occurred very early on, that is, before or relatively shortly after delivery.

(d) Research into the potential cause or causes of cerebellar atrophy occurring in a neonate is in its early days and is ongoing – the current issues were at the ‘cutting edge’!

[31]What then are the issues? The case for Ayesha is that on balance of probability the cardiac collapse of the 23rd July and the measures taken in reaction served to cause or make a material contribution to the cerebral atrophy and the disabilities consequent upon such. This case is based upon the expert evidence of Professor Levene, of Dr Harding and of Dr Brian Kendall, a vastly experienced Consultant Neuroradiologist. The Defendants contend that the atrophy and its consequences amount to risks inevitably attendant upon the neonate and that there is no sufficient evidence to establish the causal connection relied upon. In this they rely on the evidence of Professor Olof Flodmark of Karolinska Hospital, Stockholm, a Consultant Neuroradiologist. Uncomfortably aware of the difficulties attendant upon resolution of this issue, I propose successively to review the opinions of the respective experts as follows.

[32]Professor Levene(a) By way of background, he contends that a baby born at 25 weeks’ gestation has a 50% chance of disability of some sort, assuming survival. Focussing on the disability so risked, 50% of those with disability will have major functional impairment such as such arising from cerebral palsy. The balance will have lesser, more subtle disorders.

(b) Ayesha falls in this latter group.

(c) Her ataxia is an unusual disability as suffered through simple immaturity and is more likely to have occurred through brain pathology.

(d) Having regard to the MRI scans, this pathology is likely to be the atrophy and deformation of the cerebellum as identified by the neuroradiologists.

(e) There are three possible causes of an atrophied cerebellum in a baby: a congenital malformation, a metabolic disorder or an insult to the cerebellum during fetal or neonatal life so as to damage a previously normal organ. He cannot rule out a congenital cerebellar haemorrhage as a possibility; he can rule out a metabolic disorder as highly improbable; but he thinks that a cerebellar haemorrhageoccurring as a result of an insult is most likely as a cause.

(f) As at her collapse, Ayesha’s CO² level would have been high representing conversion of the administered sodium bicarbonate. CO² can have a profound effect on the brain causing its blood vessels to be maximally dilated. As and when there were the resuscitative measures there would have been a rapid rise in blood pressure so as to cause rupture of these dilated vessels, particularly the fragile capillaries, and hence a cerebellar haemorrhage.

(g) Whereas the science on this topic is at an early stage, such limited material as is afforded by the academic papers is not hostile to these views and he draws particular attention to Roberton’s Textbook of Neonatology 4th Edition at p. 1153 where the factors potentially contributing to an intra-ventricular haemorrhage are specified by way of a flow chart. Those factors were, to a significant degree, present as at the time of the collapse: hypercarbia, acidosis and very low blood pressure.

(h) It is accepted that Ayesha was from time to time subjected to ultrasound scanning; that one such scan was performed on the 23rd July at the behest of Dr Bissenden; and that none such served to depict a brain haemorrhage. That said, given ultrasound scanning technique and its limited scope, it would not have served to reveal a haemorrhage in the cerebellum area, that is, in the lower posterior area.

(i) Some help for fixing the timing of the damage to the brain is afforded by a lumbar puncture of the 25th July which showed a large number of fresh red blood cells consistent with intercranial haemorrhage that was pre-existing. The haemorrhage is likely to have occurred between the 22nd and 25th July.

[33]Dr Harding(a) It is not possible to be certain that the atrophied cerebellum did not arise from Ayesha’s premature state.

(b) That said, the appearance of Ayesha’s cerebellum by way of the MRI scan is entirely consistent with a pattern of cerebellum injury first described by Messerschmidt et al in a paper ‘Disruption of cerebellar development; potential complication of extreme prematurity’, AJNC 26, 1659. Thus, there is a markedly reduced cerebellum alongside an enlarged 4th ventricle. In the paper the authors postulate an ‘insult’ to the cerebellum at 24-32 weeks’ gestation such as disrupts the fundamental steps in cerebellum development.

(c) Yet further, it is not possible to be certain as to the exact mechanism of injury that could and did lead to Ayesha’s pattern of cerebellar damage.

(d) That said, first, a convincing mechanism of injury can be postulated. The brain features the germinal matrix: a cellular area where primitive brain cells form which has a rich blood supply and thin wall of blood vessels which readily bleed. As at the 23rd July Ayesha, then in a virtually moribund state, was the subject of aggressive fluid resuscitation. Granted that this was essential to save her life as it served to re-perfuse her, certain fragile blood vessels in vulnerable areas could be thereby made to bleed so as to institute haemorrhaging. Such blood vessels include the germinal matrix. Bleeding from this highly vascular area could have directly entered the cerebellum so as to cause a haemorrhagic infarct, alternatively it could have entered the 4th ventricle there coagulating so as to become a haematoma and to give rise to the enlargement there is to be seen on the scan, such impacting on an adjacent area of the cerebellum that is particularly concerned with balance of control of gait. Whatever the course taken by the bleed from the matrix, the result would be poor, atrophied growth of the cerebellum.

(e) Second, the absence of cardio-vascular instability prior to the 23rd July taken in conjunction with the evidence of intercranial haemorrhaging provided by the lumbar puncture of the 25th July point away from Ayesha’s premature state as a cause of her atrophied cerebellum.

(f) “It is my professional opinion that she sustained cerebellar damage from haemorrhage that occurred as a complication of the episode of severe acidosis/hypotension on 23.07.97”.

[34]Dr Kendall(a) There is marked cerebellar atrophy; there is marked enlargement of the 4th ventricle.

(b) These features are similar to those described by Messerschmidt et al. op.cit.

(c) As to causes, bleeding around the cerebellum is postulated, not bleeding into the cerebellum. A blood clot around the latter when immature interferes with its development,

(d) Bleeding from germinal matrices is postulated. There are two such which are material. Both had a high vascular content and were fragile. This bleeding formed a blood clot such as distended and enlarged the 4th ventricle before clearing. Careful examination of the scans reveal other structures which have been distorted by something that is not now there to be seen: an ultimately clearing blood clot is postulated.

[35]Professor Flodmark(a) The explanation postulated by Dr Kendall is possible but improbable.

(b) I accept that shortly before or shortly after delivery there was an insult to the cerebellum. One cannot say what the cause was. The finding of atrophy of the cerebellum is non-specific and the list of possible causes is long.

(c) As to the 4th ventricle, it is as possible that it is enlarged because the atrophy of the cerebellum gave it space to expand.

(d) Given the explanation as postulated, I am surprised that there was no hydrocephalus, that nothing was to be discerned by way of the ultrasound scans and that there was no damage elsewhere, say, to the supratentorial region.

JUDGMENT

[36]In the course of his final submission Mr Maskrey Q.C. helpfully referred me to a very recent decision of the Court of Appeal, Bailey v Ministry of Defence

[2008] EWCA Civ 883

. A medical negligence case, it suffices to record that a causation issue arose. Having reviewed the authorities, Waller L.J., in giving the judgment of the Court, concluded at paragraph 46:

“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….. 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.”

[37]The evidence does not establish on balance of probabilities that Ayesha’s brain injury arose simply from her immaturity. That cannot be excluded as a possibility but there is nothing that suggests that that non tortious cause was probable. As to this, Professor Flodmark’s essentially open mind was contemplating a range of possibilities rather than any one probability and Professor Levene identified the incidence of ataxia as militating against immaturity as an explanation. All that said, the fact of residual possibilities militates against success for Ayesha by reference to a ‘but for’ test. However, I am entitled to find – and I do find – that on balance of probabilities the contribution of the collapse occasioned by the breach of duty constituted a contribution to the atrophy of the cerebellum than was more than negligible so that the claim succeeds. As to this, the Claimant’s experts have satisfied me that, notwithstanding the necessary speculation as to cause and effect in this ‘cutting edge’ sphere, the probabilities are that it was the impact of events leading up to and following the collapse that resulted in the atrophy of the cerebellum. Of course, as between Professor Levene, Dr Harding and Dr Kendall there are differences but the overall thrust is uniform, obviating the need for me to make specific findings as between their respective views. That said, I ought to record a strong impression of weight behind the evidence of Dr Kendall, not least when he talked me through the scans.

[38]In the overall result there must be judgment for the Claimant for damages to be assessed. If an Order can be agreed the judgment can be handed down without further attendance. I reiterate my indebtedness to Counsel.