AW AGAINST GREATER GLASGOW HEALTH BOARD

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OUTER HOUSE, COURT OF SESSION

[2015] CSOH 99

 

A10/07

OPINION OF LORD BRAILSFORD

In the cause

AW

Pursuer;

against

GREATER GLASGOW HEALTH BOARD

Defenders:

Pursuer:  Clancy QC, Lake;  Drummond Miller LLP

Defender:  MacLean QC, Dawson;  Norma Shippin

24 July 2015

[1]        In view of the length of this opinion and the number of distinct issues which require to be addressed, it may be helpful if at the outset I give an overview of the case and thereafter set out a list of contents and issues.

 

Overview
[2]        The pursuer, “AW”, is the mother of a male child, “LW”, who was born on 8 October 1996. The first day of AW’s last menstrual period was 25 February 1996.  She saw her GP regarding pregnancy on 4 April 1996.  The GP informed the Queen Mother’s Hospital (“QMH”), Glasgow where AW’s pregnancy was ‘booked’ on 21 May 1996 following her attendance at a clinic.  Care for her during her pregnancy was to be shared by her GP and QMH. On 21 May 1996 she had an ultrasound scan at QMH. At this visit gestation was estimated at  “12 + 2”, that is twelve weeks and 2 days, foetal heart was noted as “heard seen” and no problems were noted.[1]  She was given a number of antenatal appointments, all of which she attended.  In August 1996 she enquired as to the possibility of a home delivery.  She discussed this option with a doctor from QMH, Dr McLelland on 20 August, was advised against it but was told by the doctor of the possibility of being admitted to the “Domino scheme” which was run by community midwives for low risk patients.  Within the scheme antenatal care was provided at home by community midwives but delivery took place in hospital.  AW qualified for admission to the scheme, wished to participate and was admitted.  Isobel Giles.[2] was appointed as her lead midwife.  As part of her care under this scheme AW had an antenatal home visit on the morning of 5 October.  Mrs Giles attended at that visit accompanied by another midwife, Mrs Evelyn Mohammed (“Mrs Mohammed”). The circumstances of this visit and what occurred during the visit are the subject of dispute between the parties and will be dealt with in detail at a later stage in the opinion.  At the end of this visit an appointment was made by the midwives for a further routine antenatal visit two weeks following.  On 8 October at 10am AW attended at QMH for a routine antenatal class of 2 hours duration. Following this class AW was given an unscheduled ultrasound scan by Dr Lena Macara[3], then a senior registrar in the hospital, following which immediate admission to hospital was arranged. The circumstances by which AW came to be scanned and the circumstances thereof are disputed by the parties and will be dealt with at a later stage.  Following admission AW was monitored by cardiotocograph (“CTG”), examined by a midwife, a senior registrar in obstetrics and a consultant obstetrician.  Thereafter LW was delivered by caesarean section, undertaken in an emergency situation.  LW was born some 8 weeks premature.  LW has cerebral palsy and associated with that condition significant learning and motor disabilities.  In the present action AW alleges that LW’s said condition was caused by fault and negligence on the part of midwifery staff employed by the defenders who spoke to and attended on AW on 1, 2, 3 and 5 October 1996, that is in the period immediately prior to the birth.  AW seeks damages in respect of loss and damage occasioned by the alleged fault and negligence.

 

Procedural history
[3]        The summons in the present action was signetted on 21 November 2006 and after sundry procedure was set down for a proof scheduled for 8 weeks to commence on 24 September 2013.  Shortly before the proof was due to commence the pursuer enrolled a motion seeking to split the proof, with an initial proof on liability and causation and a subsequent proof, if required, on quantum of damages.  The stated grounds for the motion were that the allocated diet of 8 weeks was unlikely to be sufficient to deal with issues of both liability and quantum.  This motion was opposed. I heard argument on the first day allocated for the proof and continued the matter to allow the proof to commence and enable me to determine progress in the first week of proof.  At the end of that period it was apparent that the pursuer’s concerns in relation to timing were justified and I accordingly granted the motion. In the event proof on the issue of liability and causation occupied 51 days of court time between September 2013 and July 2014.

[4]        The proof involved hearing the evidence of 30 witnesses. Witnesses to issues of fact spoke to the pursuer’s medical condition in the final week of her pregnancy, the midwifery care provided to AW in that period and the circumstances surrounding her admission to hospital on the day of LW’s delivery. Expert evidence was heard in relation to the following specialities; midwifery, obstetrics, neonatology, neuroradiology and paediatric neurology.

Contents and issues

1. The factual position
2. Neonatal care of LW and the diagnosis of Cerebral Palsy
3. Obstetric issues
   • Prof. Timothy Draycott –consultant in Obstetrics and Gynaecology, Southmead Hospital Bristol
   • Prof. Michael de Swiet – Emeritus Professor of Obstetric Medicine, Imperial College School of Medicine, London formerly consultant physician at Queen Charlotte’s Hospital, University College Hospital and Whittington Hospital, London
   • Prof. James Walker – Professor of Obstetrics & Gynaecology, St James University Hospital, Leeds
   • Prof. Deirdre Murphy –Professor of Obstetrics, Trinity College, Dublin, consultant Obstetrician Coombe Women & Infants University Hospital, Dublin

      

4. Neuroradiological issues
   • Dr Brian Kendall – retired Consultant Neuroradiologist
   • Dr Daniel Connolly - Consultant Paediatric Neuroradiologist, Sheffield Childrens Hospital, Consultant Neuroradiologist, Sheffield Teaching Hospitals Trust, Royal Hallamshire Hospital, Sheffield
5. Neurology issues
   • Dr Colin Ferrie – Consultant Paediatric Neurologist, Leeds General Infirmary
   • Dr Martin Kirkpatrick – Consultant Paediatric Neurologist & Honorary Senior Lecturer, Tayside Children’s Hospital, Ninewells Hospital & Medical School, Dundee
6. Neonatal issues
   • Prof. Richard Pearse – neonatal expert for pursuer
   • Prof. Malcolm Chiswick – neonatal expert for the defenders

      

7. Midwifery issues
   • Sandra Tranter – midwifery expert for the pursuer
   • Dr Jean McConville – midwifery expert for the pursuer
   • Dr Julia Sanders – midwifery expert for the defenders
8. Relevant law
9. Reliability and credibility of witnesses of fact.
10. The grounds of negligence.
11. Causation:the effect of referral to hospital earlier than 8 October.

    (i)   Admission on Saturday 5 October

    (ii)  Admission on Monday 7 October

12. LW’s cerebral palsy - causation

The factual position
[5]        In 1996 AW became pregnant for the first time. She was 30 years old and healthy, did not smoke, took exercise and drank alcohol moderately before her pregnancy.  After becoming pregnant she abstained from drinking alcohol and was careful about her diet. She had a healthy lifestyle.  She saw her GP and the pregnancy was “booked” at 7 weeks gestation.  She was informed that her care during pregnancy would be shared between her GP and QMH.  She had an ultrasound scan at 12 weeks gestation and at that time was provided with a “Pregnancy Care Plan” (“PCP”) booklet [4].  Amongst other matters the PCP booklet contained a table where antenatal appointments were recorded and the details of examination at such appointments noted by the examining medical professional.  AW did not want a medicalised pregnancy and was accordingly interested in having a home delivery and an appointment was arranged with Dr Dina McLelland, then a senior registrar in obstetrics at QMH, on 20 August 1996 to discuss this possibility.  Dr McLelland advised against a home delivery but at the same meeting informed AW about the possibility of her entering the “Domino” scheme as an alternative. “Domino” is an acronym of ‘domiciliary in and out’ and was a scheme operated by community midwives where the majority of antenatal care was provided at home but delivery was carried out in hospital.  A woman on the scheme would have an identified community midwife as the first point of contact for antenatal care.  The purpose and intention of the scheme was to allow women who met certain criteria to commence labour at home, go into hospital at a late stage in labour for delivery and then return home within a short period, ideally 4 or 5 hours, of giving birth.  The scheme was only available to healthy women who had experienced no difficulties during pregnancy.  Women experiencing their first pregnancy were discouraged from the scheme.  AW fell into the latter category but otherwise met the criteria for admission to the scheme.  She was keen to participate.  She had a further meeting on 28 August 1996 with a community midwife at QMH, Mrs Giles.  GW[5] also attended this meeting.  Because she was healthy and, at least as a matter of inference, had experienced no problems during the pregnancy she was admitted to the scheme.  She was told that Mrs Giles would be her main midwife.  The PCP booklet contained a list of the community midwives based in QMH.  Mrs Giles circled her name on that list and put a sticker on the PCP booklet with a telephone number for contacting the community care midwives.  AW was also told about her antenatal appointments.  Her recollection was the usual day for appointments would be Tuesday.  She was also advised that her primary contact should be with the community midwives but that in the event of an emergency she should go directly to QMH.

[6]        Following admission to the domino scheme AW’s next antenatal appointment was on 19 September, a Thursday. This appointment was fixed by telephone call to AW. The midwife who attended on that occasion was Muriel Patterson, who did not give evidence. AW recalled feeling well at the time of this appointment.  There are no adverse health recordings noted in the PCP booklet for this meeting.  At the rear of the PCP booklet is a box entitled “Return Appointments”.  This has been completed by Muriel Patterson with the entry “W/B 30^th September 1996”, broadly two weeks ahead.  AW’s expectation, unchallenged in evidence, was that contact would be made by a community midwife prior to 30 September to arrange an appointment in the week beginning on that date.

[7]        Over the weekend of 28-29 September AW stated that she started to feel unwell.  She said she experienced flu like symptoms and started to have headaches.  She spoke of having blurred vision, a swollen face and of feeling tired.  She also said that she began to have concerns about the size of her, using the term she employed, “bump” and of what she felt was a reduction in both the number and strength of foetal movements.  She recalled a chance meeting with the mother of a friend at a swimming pool on 29 September where that lady “….said I was looking small, and that triggered, you know, I was already concerned that I thought I was looking small. Ehm, so that registered with me.”[6]  AW continued to feel unwell, experiencing the symptoms already noted in the following week.  On the Friday of that week (4/10/96) she attended the funeral of the brother of a friend who had died at a young age.  She said she was upset at this and had to leave the funeral following the burial without attending a reception because of this.  She did not dispute that this might have contributed to her feelings about her health.  The account of how she felt in this period and of the symptoms she was experiencing was supported in evidence by her husband.  He described a period he put as being “maybe” 10 days prior to the visit on 5 October during which AW had been developing cold or flu like symptoms.  He said that she had complained of headaches, of blurred vision, of the baby not kicking so much and of her being generally worried and not feeling well.

[8]        AW was expecting an appointment for a routine antenatal check in the week beginning 30 September.  Her expectation was that an antenatal appointment would normally be on a Tuesday.  She stated that she did receive an appointment, arranged by telephone call, for Tuesday 1 October.  She did not recall anything about the telephone call but said that she did have reason to recall that the appointment was fixed for that day because she also had an antenatal class on the morning of that day.  She did not raise any concerns about feeling unwell at the antenatal class because she was going to see her midwife that afternoon.  She further said that she did not in any event have serious concerns about her health.  There was no visit by a midwife on the afternoon of 1 October.  AW stated that because there was no appearance by a midwife that afternoon she telephoned the number she had been given, spoke to Mrs Giles, told her that she was feeling unwell and wanted to see a midwife.  She said she was given another appointment 2 days later on Thursday 3 October.  This account was not contradicted by Mrs Giles.  The appointment on 3 October was not kept by the midwives, albeit AW stated she was telephoned about lunchtime that day, informed of a delay, but assured that she would be seen later that afternoon or the following day.  Again this account was not contradicted by Mrs Giles.  There was no visit on the Thursday or the following day, Friday 4 October.  On that later date AW attended the funeral already mentioned, but left feeling unwell.  She did not however consider there was anything that constituted an emergency in her situation, a position supported by her husband who stated that had he considered it such he would have taken her to hospital.

[9]        It is common ground between the parties that AW was visited by midwives on the morning of Saturday 5 October.  AW’s position was that she was not expecting a visit that day, no visit had been arranged in advance.  At about 10am Mrs Giles, accompanied by Mrs Mohammed, arrived at her house.  They explained that they had come straight from a home confinement where they had been engaged since the early morning. The confinement had been successful and they had delivered a healthy baby.  AW’s husband admitted the midwives and took them to the living room.  AW had not met Mrs Mohammed previously and therefore Mrs Giles made introductions.  AW recalled Mrs Giles referring to her as the “boring case”, albeit accepting that this was probably said in a good natured way and was designed to put her at ease.  AW’s recollection was that both midwives were in a “giggly” or jokey mood.  She talked of light hearted banter between them and went so far as describing their mood as “erratic and delirious”[7].

[10]      The evidence of AW and her husband was that the consultation that morning fell into two distinct parts, the first in the living room and the second in AW’s bedroom.  This evidence was not contradicted by either midwife.

[11]      The initial consultation, with both AW and her husband present, was in the living room.  During this part AW stated that she reported that she was concerned and had been feeling unwell for about one week.  She reported headaches, something that was unusual for her, vision blurred round the edge of the eyes, feeling hot and puffy in the face, of being tearful, again something that was unusual for her, feeling tired and having experienced both reduced foetal movement and foetal movements of a different nature, very light and like flutters, than those she had been experiencing prior to the onset of symptoms. She mentioned having attended a friend’s funeral the previous day and of having left because she felt unwell, accepting that she said she was unsure if this was because of flu or grief.  AW recalled that in relation to her complaint of blurred vision Mrs Giles informed her that this could happen in pregnancy, that eyesight could change, but that it would revert to normal on conclusion of pregnancy.

[12]      AW said that she also mentioned concerns about the size of her unborn child, said that she felt her stomach had not grown in size since she had last seen a midwife and reported remarks about her size made to her by her friend’s mother at the swimming pool.  In response to this AW recalled Mrs Giles saying “Oh dear do you think something is wrong”, a comment which she did not find re-assuring and which caused her to become tearful.  AW’s husband recalled Mrs Giles saying at this point “nothing’s wrong you know”, a comment which he found re-assuring.  At this juncture AW recalled the previously light hearted approach of the midwives changed and they becoming more serious.  One of the midwives suggested that they move to the bedroom in order to facilitate a physical examination.

[13]      The second phase of the consultation took place in the bedroom.  Again AW and her husband and both midwives were present.  AW said that she lay on the bed throughout the examination.  One of the midwives, she was not sure which, listened to the foetal heartbeat for a period she estimated as being between 15–30 seconds.  She was told the heartbeat could be heard and was “fine”.  Both midwives checked her abdomen.  She remembered being asked by Mrs Giles whether she was experiencing 12 foetal movements in 24 hours which she answered in the affirmative.  She reported her perception of a change in both number and character of the movements and was told that these could change during the course of pregnancy, varied from woman to woman and, further, that the most important thing was that she was getting movements.  AW’s husband gave no evidence about the discussion on foetal movement.  Mrs Giles had no recollection, but said that in the sort of discussion described by AW she would not have asked about 12 movements in a 24 hour period, but would have asked if the woman was experiencing 10 movements in that period and that she might have said that “babies act differently at different parts in the pregnancy.”[8]

[14]      After the initial examination AW said that Mrs Mohammed asked her to put her left arm out to the side of the bed and the midwife then took a blood sample.

[15]      The next matter arising from the consultation that day is the issue of a urine sample.  AW stated that, because the midwife visit was unarranged and unexpected, she did not have a urine sample prepared.  She said that throughout the period in the bedroom she was neither given a container nor asked to provide a urine sample.  She did not leave the room and go to the lavatory to provide a sample.  AW’s husband corroborated all these matters.  He was in the room throughout, confirmed that his wife did not leave the room and, further, thinks that he would have remembered if he had been left alone in the room with the two midwives.  Mrs Giles again had no recollection of these events but said “well, I’ve recorded the urine analysis as being clear/clear, so I would not record anything like that if I had not tested the urine.”[9]  The PCP entry for 5 October 1996 under the column heading “urine” records “CC” indicating a urine reading clear for both sugar and protein.  Mrs Mohammed had no recollection of this aspect of matters.

[16]      AW’s recollection was, further, that her blood pressure was not taken on 5 October. She said that at that date she was familiar with the procedure for taking blood pressure and knew the type of equipment used in this procedure. She was clear in her recollection that no blood pressure equipment was used and that neither midwife used a stethoscope which would have been required during the procedure. Her husband corroborated this position. He too was familiar with the equipment used having had his own blood pressure tested in the past.  He did not see such equipment that date.  He had a clear view of the examination on the bed and did not see AW’s blood pressure being taken.  AW’s PCP has no blood pressure recording for the consultation on 5 October.  Both Mrs Giles and Mrs Mohammed accepted that there was no blood pressure recorded in the PCP, that this was a departure from normal practice, and that no explanation could be offered for this.  Both recognised the importance not only of taking a patient’s blood pressure at every consultation but also of recording blood pressure in order that a complete clinical picture was available to all clinicians subsequently examining the patient.  Notwithstanding her general position in relation to recollection of these events on this matter Mrs Giles’s position was emphatic: “I absolutely know that we would have taken her blood pressure. It may not have been at that point but my normal practice would definitely have been to take her blood pressure, especially on a lady of 31 plus weeks and also someone who had mentioned that they were having headaches. We would not, erm, not take the blood pressure.”[10]

[17]      The meeting of 5 October ended with the midwives saying they would see AW in 2 weeks time.  No date was fixed.  Mrs Giles completed the PCP in the bedroom and returned it to AW.  AW remained lying on the bed while her husband took the midwives to the front door.

[18]      In relation to recollection of these events Mrs Giles initially stated in evidence that she had no memory of the meeting with AW on the morning of 5 October.  In relation to AW’s evidence that she complained of blurred vision Mrs Giles maintained that a complaint of this nature would have led to a clinical assessment by her consisting of taking blood pressure and asking questions about blurred vision and headaches.  Mrs Giles did however respond to cross examination about her alleged remarks about eyesight changing during pregnancy by saying “that can happen”.[11]  Having initially taken the position that she had no recollection of the meeting on 5 October Mrs Giles position changed during the course of her evidence.  On her second day in the witness box she stated that she did not accept the accuracy of AW’s account of the meeting.  This position was subsequently modified and her position ultimately came to be that it was possible that AW had reported her symptoms to her, but if that was the case she would have carried out a clinical assessment.[12]  Mrs Mohammed had no recollection of the meeting of 5 October at all.  She accepted that a meeting had taken place that day, because it was recorded in her work diary.  She was unable to explain how she knew that she accompanied Mrs Giles, as that was not something disclosed in her work diary.  Her only meeting with AW was on that date.  She had no source of knowledge about the events on that date other than her work diary.

[19]      Following the departure of the midwives on the morning of 5 October AW stated that she continued to experience the symptoms she complained of throughout 6 and 7 October.  As a result of what had been said by the midwives neither AW nor her husband felt any need to consult any doctor or midwife in the period before a planned antenatal class on the morning of Tuesday 8 October.  AW continued to monitor her foetal movements in this period.  She said that she continued to think that they were not as strong as they had been previously.  On the evening of 7 October AW retired to her bed earlier than her husband.  He went to bed about midnight and found her in considerable discomfort, “doubled over” and complaining of very sharp pains in her abdomen. The pain subsided after a short period.  The couple discussed it and both attributed the pain to indigestion caused by a curry they had eaten for dinner.

[20]      On 8 October AW’s husband had a business meeting in the Scottish borders and left early, before AW got up, to drive to the meeting.  AW had an antenatal class at QMH commencing at 10am and scheduled to last for 2 hours.  The class was split into two halves, the first taken by a midwife, the second by a physiotherapist, Dot Sorley[13].  AW continued to experience the same symptoms  she had described to the midwives on 5 October on the morning of 8 October.  She walked from her house to QMH.  Despite remaining concerned about the health of her unborn child she made no mention of any symptoms to the midwife who took the first half of the class.  She explained that she did not like to make a fuss and was concerned that she might be embarrassed in front of the class if she raised these matters.  She had however previously met Dot Sorley, appears to have been impressed by that lady and thought she might listen sympathetically to her concerns.  Accordingly she waited till the end of Dot Sorley’s class at 12 noon and then spoke to her.  AW said that she told Dot Sorley that she was feeling anxious, had headaches which were not usual events for her, felt hot and puffy in her face, was tearful, had reduced foetal movements, had experienced no movements in the course of that morning, thought she was small for her dates and had experienced sharp pains in her abdomen the night before. AW’s position was that on receipt of that information Dot Sorley indicated that she was going to arrange for a scan in order to put AW’s mind at rest.

[21]      The chronology of events and the medical staff involved in the care of AW during the afternoon of 8 October can be set out before considering the events in more detail. AW was seen initially by Dr Macara who performed an ultrasound scan. The records for that procedure show that it took place between 1300 and 1311.[14] She was then admitted to the west wing. The exact time of admission is not recorded in the nursing note but at 1327 she was examined by a midwife, Mrs Ovens.[15] A CTG trace was commenced in the west wing. She was then seen by a senior registrar in obstetrics, Dr McLelland, there is no time in the records for this examination. Dr McLelland decided to transfer AW to the labour suite where she was admitted at 1445.[16] The CTG trace had been discontinued during the transfer to the labour suite but was recommenced on arrival. At 1510 AW was seen by a consultant obstetrician, Dr Hanretty, who commenced the hypertensive protocol and determined that delivery by caesarean section was to be performed when AW’s blood pressure stabilised.[17] At 1605 the decision was taken to transfer to theatre.[18] The transfer took place at 1630.  At 1639 a spinal anaesthetic was administered by Dr Thorburn, a consultant anaesthetist. LW was delivered by caesarean section performed by Dr MacLean assisted by Dr Hanretty at 1652.[19]

[22]      I move from the outline chronology to examine these events in more detail.  In the absence of evidence from Dot Sorley there was no information to explain how that lady arranged a scan.  There was evidence from Dr Macara, the clinician who performed the scan, that it was not normal practice for physiotherapists to arrange scans. What is however clear is that Dr Macara performed an ultrasound scan on AW during her lunch break on 8 October.  Dr Macara was at that date a senior registrar in QMH.  She was very experienced in conducting and interpreting the results of ultrasound scans on pregnant patients.  At the time of proof she was a consultant obstetrician in Aberdeen Maternity Hospital.  Because of the circumstances she remembered the events of 8 October 1996.  She had agreed to perform an unscheduled scan anticipating it would take 10 minutes and would re-assure a patient.  In fact it turned out to be “anything but that,” had occupied about half an hour and that had caused her to keep patients waiting all afternoon.[20] She had a recollection of AW being in the scan department waiting room with another person, could not specifically remember if that person was Dot Sorley, but accepted that Dot Sorley was involved. She had no note of the reason for performing the scan but said that “my vague memory was that it was something to do with pain, or not feeling the baby move. ………It was certainly something that I felt at least merited an emergency, unscheduled appointment.”[21]

[23]      So far as the scan itself was concerned AW recalled that it had been carried out by Dr Macara in the presence of a midwife. Dr Macara did not examine her before performing the scan.  She tried to raise her concerns about her health with Dr Macara but was asked by the doctor to be quiet as she was concentrating.  Dr Macara did not ask her about any symptoms she was experiencing.  Dr Macara had no memory of these matters but accepted they were plausible and could have happened.  She also explained that as she was not assessing AW’s health she would neither have questioned her about that matter or examined her.  Dr Macara did recall that on seeing AW’s abdomen when she applied gel before the scan her “…memory was that it seemed quite a small bump.”[22]  On examination of the scan she determined an estimated foetal weight of 8-900 grammes, an abnormal Doppler, reduced liquor and that there was a possible retroplacental clot.  She recorded a biophysical profile score of 0/8.  As a consequence of these findings she was extremely concerned about the health of the foetus. Her note in the comments box of her clinical note was “needs admission stat: CTG steroids and Kleihauer and lupus”.[23]  She informed AW that the baby was small, that she was going to be admitted to hospital immediately, have steroids and that a CTG trace would be started.  She further indicated that she thought the baby would be delivered within 48 hours.  Thereafter she arranged for AW’s immediate admission, the performance of CTG and for the administration of steroids. 

[24]      Following the scan AW recalled being taken to a separate room where she was transferred from the care of the community midwives to hospital care.  She said that she met Mrs Giles at that time in the room.  She recalled that Mrs Giles took her PCP from her and also offered to telephone her husband and leave a message from her.  In relation to telephone messages the evidence from AW’s husband was that on return from work that afternoon he discovered a number of messages on the answering machine.  These messages came from Mrs Giles.  The last message, which he followed, requested that he attend at QMH urgently.  AW said that the PCP was never returned to her after Mrs Giles removed it in the circumstances described.  Moreover, she was never asked whether she had any complaints about the care she had received from the midwives.  Despite this her PCP bears the entry “No complaints” in the box for comments.  AW did not know who made that entry.  At this point it is also of note to observe that Mrs Giles made an entry in AW’s clinical notes for 8 October.  The note is in the following terms:  “EMSCS for IUGR and reduced liquor baby ventilated in paediatric department”[24] .  The entry would have been made after LW’s birth.  The entry is, to some extent, erroneous in that the reason for the Caesarean section was not IUGR but pre-eclampsia.   Mrs Giles had no recollection of a meeting with AW in QMH on 8 October.  She maintained she had no recollection of telephoning AW’s husband.  She maintained she had no recollection of making an entry for 8/10/96 in AW’s clinical notes, nor had she any explanation for the erroneous material in that entry.

[25]      AW was taken from the room where she was admitted into hospital care to the west wing of QMH.  She was received there by Mrs Ovens, a midwife.  She was put on a CTG and administered steroids.  Mrs Ovens took her blood pressure which was recorded as 174/118.[25]  As a result of these findings, Mrs Ovens asked for the urgent attendance of the duty registrar.  The duty registrar, Dr McLelland duly attended and decided to transfer AW to the labour suite for a caesarean section.  Mrs Ovens gave evidence.  She had no recollection of AW but was able to speak to the medical notes that she had compiled.  She noted from those records the blood pressure recording she had taken and commented that it was high and that she would have been concerned about it.  She said that she would have been concerned that the patient may have had pre-eclampsia.  She noted that in the relevant records she had written after her recording of blood pressure the word “asymptomatic”. In this context she explained that she would have asked AW if she had a headache, or had had a headache, if she had had abdominal pain, if she had blurred vision because these are the symptoms of pre‑eclampsia and the fact that she had written “asymptomatic” would be because AW had said that she did not have any of those symptoms.  Mrs Ovens’ clinical notes do not bear an entry as to the time when her examination took place. 

[26]      The next clinician involved with AW that afternoon was Dr McLelland, at that time a senior registrar in QMH.  At the time of proof she was a consultant obstetrician at Wishaw General Hospital. Dr McLelland made a clinical note of her examination of AW.[26] The note is untimed.  The note records that AW was admitted for foetal monitoring having been “referred by community midwife this am”.  She noted the results of the ultrasound scan as: “IUGR + oligohydramnios - BPP 0/8 - ?RPC”, an accurate précis of Dr Macara’s clinical note which was presumably before her. She further recorded that AW was complaining of “..2 episodes of diarrhoea + irregular u/a today – no pv bleeding”. She then records that on examination AW was “Well anxious”. The note goes on to record Dr McLelland’s findings on clinical examination and her interpretation of the CTG trace to that point. Her impression as a result of her examination was of intra-uterine growth retardation and the possibility of abruptio placenta. She had concerns arising from the CTG trace, from which she noted “low to absent variability” and the possibility of decelerations. She regarded the CTG trace as “worrying”. Her clinical decision based on these considerations was to transfer the patient to the labour suite.

[27]      Dr McLelland said that she did have a vague recollection of AW’s case because it was unusual and because she had “...followed through later in the day to see what happened.”[27].  AW’s recollection of the examination by Dr McLelland was that she told her of the abdominal pain she had experienced at about midnight the previous night (7 October).  She said Dr McLelland characterised this as irregular uterine activity, this was not a term used by AW.  AW also said that she told Dr McLelland about reduced foetal movements.  Dr McLelland could not recall this but accepted that it may have been said.  She did not in any event think this of any significance as she had information on foetal movements from the ultrasound scan which superseded any subjective information conveyed by AW.  AW said that Dr McLelland did not ask her about how she was feeling, whether she had any headaches or otherwise take any detailed medical history from her.  She was asked in cross-examination why she herself did not volunteer information about her symptoms to Dr McLelland.  Her explanation was that by this stage she was being told that the situation was an emergency, that she was going to have a caesarean section in a very short period of time, that she was anxious and therefore confined herself to answering questions put to her. 

[28]      Dr McLelland’s clinical assessment following her examination and consideration of the test results was that AW was “..an acute obstetric emergency that had to be managed.”[28] She appeared to consider this to be a case of severe pre-eclampsia, or at least proceeded on that basis[29]. The plan formulated by Dr Macara to deliver within 48 hours was changed to delivery as soon as safe, that was when the high blood pressure had been stabilised.  Dr McLelland informed AW of the change of the plan.  She commenced AW on the severe pre-eclampsia regime.  AW was moved, in a bed, to the labour suite.  The CTG was discontinued during the course of the move but commenced again on arrival in the labour suite.  Dr McLelland could not remember introducing the case to the consultant on call, Dr Hanretty, but confirmed that the case was sufficiently serious to have merited that and, given the consultant’s involvement shortly thereafter, did not demur from the proposition that she must have called him.

[29]      Dr Hanretty was, in 1996 and remained at the time of the proof, a consultant obstetrician.  He was the consultant on call on the afternoon of 8 October.  On the basis of the medical records he first saw AW in the labour suite at 1510 on 8 October[30].  He would have had sight of the clinical notes made by Mrs Ovens and Dr McLelland and of the CTG trace.  He would have had regard to these. His clinical note records: “IUGR and pre‑eclampsia. Foetal assessment concerning.”  On examination Dr Hanretty found AW to have exaggerated reflexes.  He noted “small foetus”. He noted his clinical conclusion and instruction as follows: “I think delivery is indicated in both the foetal and maternal interest. … Plan delivery when BP stable – put on protocol”.  Given AW’s gestational period he considered there was significant risk of stroke.  AW’s recollection of these events was broadly similar to the account given by Dr Hanretty.  She recalls him using the term pre‑eclampsia.  She recalls him tapping her knees and commenting to a colleague on her exaggerated reflexes.  He did not carry out any further examination but told her they were going to administer a drug to lower her blood pressure and that when that was done there would be an urgent delivery.  AW did recall Dr Hanretty reading her hospital notes and asking her when she had last been seen.  She told him that she had been seen by midwives on the previous Saturday.  She recalled that he commented to a colleague, on reading her notes, “Can you believe it, this woman was seen three days ago and her blood pressure wasn’t taken”[31]. 

[30]      AW’s recollection was that Dr Hanretty remained in the labour suite with her after his involvement at 1510.  Dr Hanretty’s evidence was slightly different in that he thought he would have been in and out of the room as he attended to giving instructions and preparing for a caesarean section.  What is clear if that by 1547, a time determined from AW’s medical notes, her blood pressure was stabilising.  By this time, on the basis of the CTG trace the predicament of the foetus was deteriorating.  At this time Dr Hanretty decided it was safe to proceed with a caesarean section.  AW was prepared for that procedure.  The CTG trace was discontinued between 1605 and 1630 because AW was being transferred to the operating theatre.  Dr MacLean, assisted by Dr Hanretty, carried out a caesarean section operation without complications and the child LW was delivered at 1652. 

[31]      Immediately after the birth AW was told that her child was small.  She did not see the child immediately following the birth.  AW was ill and was administered morphine.  Her husband had not been present throughout the events prior to LW’s birth.  He had been absent from Glasgow on business that day and efforts to contact him had been unsuccessful.  As noted in paragraph [27] messages had been left on the answerphone in his house.  He returned home between 5.30 and 6.00pm and listened to the messages.  He recalled there being three messages.  The first was quite relaxed and informed him that AW was in hospital for some tests.  The second message advised him that LW was going to be delivered and that he needed to get to the hospital.  The third, which he described as “more panicked”, was from Mrs Giles and advised him of the urgency of the situation.  On receipt of these messages he drove to the hospital as fast as he could arriving between 6.00 and 6.30pm.  On arrival at hospital he was informed by nursing staff that AW was dangerously ill.  He was also advised that he should take a photo of LW in case the child died.  He saw AW and confirmed that she was unwell.  He indicated that initially she did not appear to be completely understanding the seriousness of the situation.  Later that evening he took AW in a wheelchair to see LW but she vomited on arrival at intensive care where the child was and had to return to her own ward.  AW also said that she was vomiting that evening, had blurred vision with black spots and felt unwell.  She said that the following morning (9 October) she fainted and collapsed while having a shower.  She continued to receive medication for high blood pressure.  She was discharged on 16 October.

[32]      Turning to the position regarding LW, following delivery the child was, in accordance with normal medical practice, taken into the care of Dr Gallacher, then a senior house officer specialising in neonatology.  In October 1996 Dr Gallacher had held that post for two months.  At the time of the proof Dr Gallacher was a consultant paediatrician of eight years standing specialising in acute paediatrics and childhood diabetes.  She had a recollection of LW in the neonatal unit but had no recollection of the delivery or resuscitation which had followed delivery.  Her evidence on these matters was taken from the medical records.  These records indicated that LW had an endotracheal tube inserted and was ventilated following birth.  Dr Gallacher started cardiac compression which she continued until the child’s heart rate came up to 100bpm, which occurred at six minutes after birth.  During this period LW required the administration of two doses of adrenaline.  On LW’s heart rate reaching 100bpm Dr Gallacher was comfortable that circulation had been secured.  He remained on ventilation.  Dr Gallacher considered LW to be very comprised.  He was at this stage transferred to the neonatal unit.  Subsequently he required ventilation by spontaneous intermittent mandatory ventilation. 

[33]      LW remained in hospital for 99 days following birth.  During this period he was under the care of Drs Coutts and Turner.  LW was initially incubated, catheterised and administered a range of drugs, blood transfusions and antibiotics.  He had a bradycardia and required ventilation on an oscillating ventilator.  He suffered from respiratory difficulties including respiratory distress syndrome and required ventilation, administration of surfactants, sedation and transfusions.  He had hypoglycaemia, desaturations and agitation.  During his first week of life he received phototherapy for jaundice.  He had suspected early necrotising enterocolytis treated with antibiotics as a precaution.  He suffered from a patent ductus arteriosus and likely ductal ligation which was treated conservatively and which closed spontaneously.  He also had an inguinal hernia which required surgery.  Neither Dr Coutts or Dr Turner considered that there was an encephalopathy.  By the time of his discharge, LW was no longer oxygen dependent.  There was however radiological evidence of chronic lung disease.

[34]      Following discharge from the neonatal unit LW continued to attend at the child development clinic at QMH.  AW and her husband were told by the discharging nurse that LW should be treated like a normal baby.  They were advised at this stage that there was no indication that there would be any long-term health problem.  Problems did however develop over time.  LW experienced feeding problems and generally failed to thrive.  He suffered from developmental delay and did not meet milestones for sitting up and crawling.  Comparison with growth charts showed his weight to be tailing off.  AW spoke to realising that he had disabilities.  These disabilities manifested themselves more obviously as time passed.  LW was at the date of proof a teenager.  He attended a special needs school and experienced learning difficulties. 

[35]      There have been a number of attempts to determine the cause of LW’s disabilities.  Initial genetic testing designed to determine whether there was a congenital feature to the disability were conducted by Dr Joss in 2001.  These tests were negative.  Further testing was carried out by Dr Joss in conduction with Dr Zuberi who determined that an MRI scan was required to check whether LW had a developmental brain abnormality.  An MRI was performed in 2002.  This scan showed that all major brain structures were present and that there was no evidence that LW’s brain had developed abnormally.  The scan did however show an acute ischaemic hypoxic event affecting the basal ganglia and possibly the hippocampi.  On review by a consultant radiologist areas of damage were found in the periventricular white matter of LW’s brain. 

 

3.   Obstetric issues
[36]      Evidence was heard from seven obstetricians.  Four of these persons, Drs Crichton, McLelland, Hanretty and MacLean were involved in the treatment of AW on 8 October 1996 and fall therefore to be regarded primarily as witnesses of fact.  Drs Crichton, McLelland and MacLean were at the time obstetric specialists below consultant rank.  All three of these doctors have since 1996 attained consultant rank.  Dr Hanretty was a consultant in 1996.  Questions seeking to elicit his expert opinion on various obstetric matters were asked by counsel for the defenders.  Initially these were objected to by counsel for the pursuer, this objection was however subsequently withdrawn.  Accordingly the court had the benefit of some expert testimony from Dr Hanretty.  In addition evidence was heard from four experts.  Professors Draycott and De Swiet gave evidence on behalf of the pursuer.  Professors Walker and Murphy gave evidence on behalf of the defenders.  The evidence of the treating clinicians has already been dealt with and I do not propose to repeat it in this part of the opinion.

[37]      The pursuer adduced evidence from Professor Timothy Draycott.  Professor Draycott currently holds the post of consultant in charge of the labour ward at Southmead Hospital Bristol, a major teaching hospital in the south-west of England.  He has a research interest in the management of obstetric emergencies and shoulder dystocia in particular.  He prepared a report in relation to the present case dated 23 May 2013[32] and spoke to this report at proof.  For the purposes of preparing his report Professor Draycott had considered AW’s GP records and hospital records, had seen medical legal reports from Dr Brian Kendall and Professor Michael de Swiet, had seen a witness statement from AW and had seen question and answer sheets prepared by Drs MacLean, Hanretty, Macara and McLelland.  In addition he had seen the draft summons.  He noted at the outset of his opinion that, for cost reasons, he had not dictated a formal chronology.  He proceeded thereafter on the basis of a short narrative which he termed “Facts of the case” based on the above mentioned documentation which he had considered.  He then considered the CTG traces taken on 8 October 1996.  His conclusion was that the CTG was “abnormal from admission”.  He made comments on the standard of care received by AW.  He considered that AW’s antenatal care was within normal standards expected up to 1 October 1996.  In relation to the midwife’s visit to AW on 5 October 1996 he noted that “[AW] is adamant that neither her BP nor urine were checked.”  He also noted that “The BP was not recorded”.  In relation to the urine analysis section he observed that the letters “CC” therein used were “…not an abbreviation commonly used in my practice or experience.”  He further observed that on the basis of the information he had obtained AW had described almost all the relevant symptoms of pre-eclampsia to the midwives and that therefore this possibility should not have been excluded.  He referred to Professor de Swiet’s analysis, which I will deal with subsequently, and agreed that on the balance of probabilities there would have been both hypertension and proteinuria detectable had the appropriate test been carried out on 5 October.  He then expressed the view that had both hypertension and proteinuria been detected on 5 October AW would have been referred to hospital that day for further investigations. 

[38]      Professor Draycott thereafter reviewed the treatment received by AW at QMH on 8 October 1996.  He had no criticisms of any aspect of the treatment AW received that day. 

[39]      His conclusion on the basis of the foregoing was that AW would have been referred to hospital for assessment on Saturday 5 October 1996.  He thereafter considered the implications this would have and hypothesised on a likely clinical management regime if this had occurred.  He noted that the first blood pressure assessment on 8 October was “very high at 172/118” and postulated that “therefore it is likely that [AW]’s BP would have been high enough to merit admission on the 5^th October.”  He further expressed the opinion that the threshold for admission to hospital would have been reduced by consideration of AW’s reported symptoms, particularly blurred vision, headaches and reduced foetal movements.  On the basis of his views as to the likely blood pressure level and symptoms he considered it “extremely likely” that on admission AW would have been subjected to four hourly observations, blood tests, foetal monitoring and possible management of her hypertension.  He thought that given that AW’s blood tests were normal up to the time of delivery it is likely that they would also have been normal on 5 October.  In relation to hypertension he agreed with the analysis of Professor de Swiet.  In relation to proteinuria Professor Draycott observed that since AW had only 1+ proteinuria on 8 October he considered it “less clear” that there would have been significant proteinuria on 5 October.  He did however consider it likely that she would have been started on a 24 hour urine collection to accurately quantify her proteinuria if she had been admitted on 5 October.  He did not think it likely that AW would have undergone ultrasound scanning on 5 October if admitted, because it was unlikely that formal scanning facilities would have been available over a weekend.  He did however consider that ultrasound would have been performed on Monday 7 October and that it was “extremely likely” that “the same findings as on the 8^th”, foetal growth retardation, reduced liquor volume and abnormal Dopplers, would have been demonstrated.  In relation to CTG Professor Draycott considered that this would “definitely” have been performed on admission of 5 October.  He did think that it was “difficult” to know exactly what this would have shown but expressed the view that “it is unlikely to have been completely normal”.  Lastly he considered that AW would have been administered antenatal steroids on admission to hospital and would have derived benefit from this. 

[40]      Professor Draycott considered the incident on the evening of 7 October when AW suffered acute abdominal pain.  On the hypothesis he was considering of admission to hospital on 5 October he considered that by the evening of 7 October “the following are likely to have been the case: 48 hours post-steroids, established IUGR, reduced liquor volume and abnormal Dopplers, probably, or at least likely, to be an abnormal CTG, BP controlled by oral anti-hypertensives, normal serology”.  On the basis of such findings he considered it would be “a difficult decision” that would require input at senior consultant level but that “most consultants would have advised delivery on the evening/night of the 7^th October”.  He did however concede that it might have been reasonable to have waited until the morning of 8 October to take a decision.  On the basis of all the foregoing Professor Draycott concluded that AW been admitted to hospital on 5 October it was most likely that LW would have been delivered by caesarean section during the evening of 7 October or at least overnight that night.  He considered that the latest that LW would have been born would have been by 10am on 8 October. 

[41]      Professor de Swiet is emeritus professor of obstetric medicine at Imperial College Faculty of Medicine, London.  He is a specialist obstetric physician, that is a physician specialising in pregnancy complicated by medical problems such as high blood pressure or heart disease.  He was first appointed a consultant physician in obstetric medicine at Queen Charlotte’s Hospital, London in 1973.  He thereafter held further appointments as a consultant physician at the Hammersmith Hospital Trust, University College Hospital Trust and the Whittington Hospital Trust, all London.  Between 1995 and 2011 he was a central assessor in obstetric medicine for the UK Confidential Enquiries in Maternal Mortality.  He has been made an honorary Fellow of the College of Obstetricians and Gynaecologists of South Africa and an honorary Fellow of the College of Physicians of Ceylon in recognition of his services to the development of obstetric medicine.  He has been the author or co-author of over 130 refereed papers, 110 chapters in books and more than 200 abstracts, reviews and other publications in relation to obstetric medicine.  He edited a definitive textbook on obstetric medicine “Medical Disorders in Obstetric Practice” from 1984 until it was replaced by “de Swiet’s Medical Disorders in Obstetric Practice”. 

[42]      Professor de Swiet prepared a report in the present case dated 5 May 2013[33].  His brief for the preparation of this report was a single question: “What is the likelihood that [AW] would have had proteinuria and hypertension had these signs been looked for when the midwives came on 5/10/96”?  In relation to the factual background against which Professor de Swiet considered the foregoing question he primarily relied upon details given to him in his letter of instruction.  Professor de Swiet expressed the view that “It is generally believed that significant proteinuria develops in women with pre‑eclampsia about three weeks before delivery is necessary.  Therefore it is highly likely that [AW] had proteinuria and hypertension on 5/10/96 only three days before she was delivered.”  Professor de Swiet stated that the general proposition contained in the foregoing expression of opinion was a general belief held by senior obstetricians.  He also referred to a passage in a paper by Chua and Redman as support for this proposition[34].  Professor de Swiet further expressed the view that “…on balance of probability [AW] would have had proteinuria for 15 days before she required delivery on 8/10/96 i.e. proteinuria would have developed on 23/9/96… well before 5/10/96 when it is alleged that the visiting midwives did not check [AW]’s urine or measure her blood pressure.”  This proposition was based upon a study of 122 cases of symptomless proteinuric pre-eclampsia presenting in Oxford before 32 weeks gestation in a period spanning the years 1980/85[35].  The professor then went on to consider the possibility that because AW, on the instruction given to him, displayed symptoms of pre-eclampsia her case fell to be regarded as more severe than the cases in the Oxford study where the patients were symptomless before presentation at hospital.  The professor therefore posited the view that her symptoms of elevated blood pressure and proteinuria could have developed more rapidly than was the case in relation to the persons reported on in the Oxford study.  In relation to this proposition, Professor de Swiet again relied upon the paper by Chua and Redman where the study had been of 42 women with more severe disease.  On the basis of  the findings of this paper the median time for delivery after the onset of signs, proteinuria and in most cases severe hypertension, was between four and seven days.  Having regard to this, Professor de Swiet expressed the view that “…on balance of probability even allowing for [AW]’s severe pre-eclampsia, proteinuria would have been present for more than four days before she needed delivery on 8/10/96 i.e. on balance of probability proteinuria would have been present by at least 4/10/96.”  On the basis of the foregoing, Professor de Swiet’s conclusion in his report, which he supported and reiterated in evidence, was that it “…is highly likely that significant proteinuria would have been present in [AW]’s urine, had it been tested on 5/10/96.”  Further from this, the professor considered that since high blood pressure usually appeared before proteinuria and pre-eclampsia it was also highly likely that AW would have had hypertension on 5/10/96. 

[43]      Professor Walker gave evidence on behalf of the defenders.  Professor Walker holds the chair of obstetrics and gynaecology at the University of Leeds and is an honorary consultant in obstetrics and gynaecology in the United Leeds Teaching Hospital Trust.  He has practised in obstetrics and gynaecology since 1977.  He is a senior vice president of the Royal College of Gynaecologists and chair of the Global Health Board of the Royal College of Gynaecologists.  He is a former clinical advisor (obstetrics) to the National Patient Safety Agency, former Chairman of the Centre for Maternal and Child Health Enquiry, the medical director of Action on Pre-eclampsia, an international board member of the International Society for the Study of Hypertension and Pregnancy and the medical advisor to the Miscarriage Association.  He has over 200 peer reviewed publications, review articles and chapters in textbooks covering the aetiology and management of hypertension in pregnancy. 

[44]      Professor Walker was instructed by the defenders to review the pregnancy and delivery of AW and how actions or inactions may have contributed towards the damage sustained by LW prior to his delivery.  To assist him he had the medical records relative to the case, statements from the treating doctors at QMH and the midwives involved in the care of AW.  He had also seen an expert medical report from Professor Chiswick and had sight of various pleadings in the case.  In his report he dealt with the antenatal care received by AW and noted her position that she stated she had symptoms of headache, felt unwell and blurred vision which were reported to midwives.  He then dealt with her admission to QMH on 8 October 1996, her progress in the delivery room and the delivery itself.  In relation to the child LW he noted the difficulties experienced immediately post birth and the subsequent developmental problems.  In relation to this he expressed the opinion that the child “…has developed a mixed pattern of abnormalities suggestive of underlying abnormality and long-term intrauterine growth deficiency and not an immediate pre‑delivery acute hypoxic insult.”[36]  He considered the pathology of the placenta and on the basis of this expressed the view that “[T]he retro placental clot must have antedated the admission since there was no evidence on the CTG of an acute event and no evidence of ongoing bleeding at delivery.”  He considered the CTGs and foetal monitoring performed at QMH on 8 October 1996.  His view was that “It would appear to be a trace of a sick baby that has been in trouble for some time and the CTG abnormality is the result of this problem not a sign of an ongoing cause.  There is no evidence of an acute event on that day that could have been prevented.”  He found support for this view in the biophysical profile score which had been recorded by Dr Crichton.  He also considered that the fact the baby was only 920g, the weight of an average baby around 27 weeks, indicated an intrauterine insult which had been ongoing for some time.  He also pointed to a number of other factors, problems of head growth suggestive of symmetrical growth restriction compatible with first or second trimester insult, the fact that the baby had only one umbilical artery, 13 ribs and hypospadias as further support for a longstanding cause possibly due to abnormality.  He could find no evidence of acute hypoxia at or immediately prior to the time of delivery.  He did not consider that earlier delivery on 8 October or even some days earlier would have made any substantial difference to the outcome. 

[45]      Professor Walker was of the view that AW “did not have pre-eclampsia by any definition.”[37]  He considered that she had an acute elevation of blood pressure which was easily controlled by a relatively low dose of appropriate medication.  Her elevated blood pressure did not require any treatment after delivery, albeit that it remained mildly elevated for a number of days thereafter.  It was his opinion that “Women with established pre‑eclampsia normally have ongoing problems after delivery, often with worsening signs and parameters.”  He also expressed the view that the length of problem after delivery is a reflection of the degree and duration of problems prior to delivery.  The absence of any problems after delivery for AW was to him suggestive that there was no longstanding problem prior to delivery.  He also noted that AW’s blood results, particularly platelets and liver enzymes remained completely within the normal range.  He also founded upon the lack of documented symptoms at delivery.  He accepted that a retro placental clot was found but could find no evidence of the abruption having occurred at a given time.  There were no indicative symptoms apart from the sharp pain on the evening of 7 October and there was no evidence of massive blood loss at delivery.  He considered that this was not a significant abruption.  He thought the fact the child was delivered live implied that the area affected by the infarct was small, had happened some time previously and was not a factor in the child’s long term outcome.

[46]      Professor Walker considered the issue of whether AW should have been diagnosed with any condition which merited referral to hospital on 5 October.  His view was, as already noted, that AW did not have pre-eclampsia on admission  to hospital on 8 October and she would not therefore have had that condition on 5 October.  He therefore considered that her blood pressure would have been as a matter of probability normal at that time.  He also observed that after catheterisation on admission to hospital she only had “plus” of proteinuria and therefore, in his opinion, would have had no more than that on 5 October.  That level of proteinuria would not prompt a referral to hospital.  His position was that even if the symptoms of headache or blurred vision were present then in the absence of other clinical features of pre-eclampsia no action would have been taken on 5 October.

[47]      The professor’s conclusion was that LW suffered from a longstanding intrauterine insult arising as a result of either congenital abnormality, infection or gross placental insufficiency or a combination of those.  The problems were in his opinion longstanding, of at least six weeks and probably longer than that.  There was no acute event in utero that contributed to or caused the problems.  AW did not suffer from pre-eclampsia and would not have displayed symptoms of that condition on 5 October.  He did not consider that delivery on 5 October or anytime between that time and the time of actual delivery would have made any substantial difference to the outcome. 

[48]      The defenders supplemented the opinion of Professor Walker with evidence from Professor Murphy.  Professor Murphy holds the chair of obstetrics and is head of department at Trinity College, Dublin.  She is a consultant obstetrician with lead responsibility for the labour ward at the Coombe Women and Infants University Hospital, Dublin.  This unit handles almost 9,000 deliveries per year.  She was Chairman of the Guidelines and Audit Committee of the Royal College of Obstetricians and Gynaecologists and a member of both the Standards Board and Scientific Advisory Committee of the Royal College of Gynaecologists between 2004 and 2007.  Her primary research interests are in perinatal epidemiology with a particular interest in the aetiology of cerebral palsy. 

[49]      Professor Murphy was instructed by the defenders to provide a report on the obstetric aspects of the case and any issues of causality that lay within her expertise.  For the purposes of preparing this report she had access to AW’s medical records from QMH, LW’s medical records from QMH and Yorkhill Hospital, Glasgow and the pleadings in the case. 

[50]      After narrating her understanding of AW’s clinical history during the pregnancy up until 8 October 1996 Professor Murphy then considered in detail the ultrasound scan conducted by Dr Macara on that date.  She expressed her own view on the ultrasound scan report as follows: “The scan findings are best summarised as severe symmetrical IUGR, oligohydramnios, and abnormal biophysical profile as a result of placental insufficiency, with possible placental abruption and reduced perfusion to the foetal bowel.”[38]  She then considered the treatment and tests conducted on AW during the afternoon of 8 October 1996.  In relation to this she observed that “…all of the blood tests were entirely normal and are not in keeping with either severe early onset pre-eclampsia or an acute onset placental abruption”[39].  She considered the post-delivery health of AW and the placental pathology.  She also noted that AW subsequently had two further pregnancies both of which went to full-term without any antenatal complications.  She considered the CTG traces from 8 October 1996.  Her view of the first, shorter CTG was that it “should be classified as pathological and requires an urgent medical review.”  In relation to the second CTG she stated:

“This CTG has a normal baseline foetal heart rate with markedly reduced variability and unprovoked decelerations.  There are two abnormal features and the CTG is classified as pathological.  Each of the two CTGs are pathological from the outset suggesting foetal compromise that predates the start of the first CTG.” 

 

Professor Murphy then noted the neonatal history of LW and recorded her knowledge of his current problems. 

[51]      On the basis of the information that was available to Professor Murphy she concluded that there was no strong evidence of an underlying genetic, metabolic or structural aetiology for developmental delay.  She therefore concluded that “The possible origins of his cerebral damage lie in the antenatal and neonatal period.”  She considered that these were not mutually exclusive and thought that “the most likely origin of developmental delay in this case relates the combination of adverse factors in the antenatal and neonatal periods.”[40] 

[52]      In relation to antenatal causes she expressed the view that pre-eclampsia, intrauterine growth restriction and placental abruption are conditions that constitute a syndrome of “ischaemic placental disease” (IPD).  Whilst these conditions have different clinical manifestations she considered they shared a common underlying pathophysiology.  The professor considered that AW’s pregnancy was complicated by all these elements “underpinned by long-standing placental maladaptation and insufficiency over many weeks prior to delivery.”[41] 

[53]      Professor Murphy developed her hypothesis of IPD by noting that the ultrasound assessment conducted on 8 October 1996 revealed severe symmetrical intrauterine growth restriction with foetal measurements consistent with 25-27 weeks gestation.  She thought that this degree of compromise was likely to have evolved over a number of weeks, probably from as early as 22-24 weeks gestation.  The ultrasound scan’s finding of oligohydramnios and increased resistance in the umbilical artery Doppler supported a diagnosis of placental insufficiency.  The presence of dilated loops of bowel, and later concern about necrotising enterocolitis she thought was suggestive of longstanding reduced profusion to non-priority foetal organs.  The very poor biophysical score indicated to her that the foetus was conserving energy due to diminished availability of energy sources through the placenta.  She thought that the area on the scan identified as retroplacental clot indicated a poorly functioning placenta which was beginning to separate from the uterine wall.  She regarded this as being consistent with chronic maladaptation and end stage deterioration in an ischaemic placenta.  She noted that at delivery there was an area of approximately 25% of the placental surface that revealed retroplacental haemorrhage, which was in keeping with the ultrasound scan, and that the placenta was thin and friable.  She observed that these findings were confirmed at pathological examination both macroscopically and histologically.  She noted in addition that placental histology revealed widespread excess syncytial knots and many villi showing stromal fibrosis.  She thought that these placental findings were indicative of premature maturation/deterioration of the placenta and expressed the view that they were commonly found in pregnancies complicated by severe pre-eclampsia and/or intrauterine growth restriction[42].  In relation to placental abruption she considered that in this case it was likely that placental abruption developed as part of a chronic vascular process.  In relation to pre-eclampsia she considered that the diagnosis was correct albeit that the maternal affects apart from hypertension were mild[43].  She noted that in a UK based control study of antenatal and intrapartum risk factors for cerebral palsy amongst very pre-term singleton babies pre-eclampsia was associated with a reduced risk of cerebral palsy.  The same consideration applied to delivery without labour.  There was no increased risk of cerebral palsy with intrauterine growth restriction. 

[54]      In relation to a possible neonatal origin of LW’s cerebral palsy Professor Murphy noted a number of factors associated with an increased risk of cerebral palsy among very pre-term babies which applied to LW.  These were patent ductus arteriosus, hypotension, blood transfusion and prolonged ventilation. 

[55]      In conclusion Professor Murphy expressed the opinion that all the information available to her “supports an aetiology for developmental delay/cerebral palsy of antenatal and neonatal origin with an onset many weeks prior to delivery due to ischaemic placental disease, aggravated by subsequent pre-eclampsia and placental abruption, and further compromised by significant neonatal complications including recurrent episodes of respiratory desaturation, hypotension, bradycardia and hypoglycaemia.”[44]

[56]      Professor Murphy considered the antenatal care received by AW and made no criticisms. 

[57]      In relation to the question of whether admission to hospital at a date earlier than 8 October 1996 was merited or required, Professor Murphy noted that whilst AW had marked hypertension and +1 proteinuria on admission to QMH on 8 October clinical findings on that day were “not at all in keeping with severe maternal pre-eclampsia”, that blood tests were normal and that urine output was good and that hypertension resolved rapidly with minimal anti-hypertensive medication.  Having regard to these considerations her view was that “…it is highly speculative to suggest that the blood pressure and urine would have been abnormal on Saturday 5^th October…”  She went further and stated “if pushed to speculate” she would “not be at all surprised if both were normal”.  She then noted that the clinical course of early onset – that is before 34 weeks gestation – pre‑eclampsia is highly unpredictable and variable in presentation, severity and rate of deterioration.  Having regard to these factors, she considered that even if AW had been admitted to hospital on 5 October 1996 it would be entirely speculative whether blood pressure and urine would have been abnormal at that time.  She considered, apparently in common with Professor Draycott, that in any event it is likely that an ultrasound scan would have been delayed until Monday 7 October.  She therefore considered that in the event that AW had been admitted to hospital on 5 October the only important difference was that she would have received antenatal corticosteroids which would have reduced the risk of respiratory distress syndrome and therefore the duration of ventilation which would have been required.  She does not consider that the outcome would have been different. 

 

4.   Neuroradiological issues

[58]      The pursuers adduced evidence from two neuroradiologists.  Dr Brian Kendall is a retired neuroradiologist.  He was a consultant radiologist at various hospitals been 1962 and 1974.  Between 1974 and 2000 he was a consultant neuroradiologist.  Between 1975 and 1994 he was a consultant neuroradiologist at the Hospital for Sick Children, Great Ormond Street, London.  Between 1979 and 1981 he was visiting professor at the University of California, San Francisco.  Between 1994 and 2000 he was a consultant neuroradiologist at the Royal Free Hospital, London.  Between 1994 and 2011 he was an honorary consultant neuroradiologist at the Hospital for Sick Children, London.  Between 1994 and 2011 he was an honorary consultant neuroradiologist at the National Hospital for Neurology and Neurosurgery.  Between 2001 and 2012 he was a consultant neuroradiologist at Wellington Hospital, London and during the same period held the same post at the London Imaging Centre.  In 1977 he was awarded the Barclay Prize by the British Institute of Radiology for contributions to neuroradiology.  In 1988 he was awarded the Barclay Medal for original contributions in neuroradiology.

[59]      Dr Kendall’s brief was to “analyse the neuroimaging in order to diagnose the pathology underlying [LW]’s neurological disabilities and by correlation with the history to comment on the causation and timing of brain damage.”  In order to do this Dr Kendall had sight of the medical records of LW and the obstetric records of AW.  He saw a statement from AW, reports from two midwifery experts and medical reports from Professor Draycott, Dr Pearse, Dr Ferrie and Professor de Swiet.  He also saw neuroimaging relative to LW. 

[60]      Dr Kendall’s report was dated February 2013.[45]  He initially narrated a brief outline of his understanding of AW’s pregnancy, the delivery of LW and the child’s medical difficulties following birth.  I need only make mention of two aspects of this narrative.  Dr Kendall reported that “foetal bradycardia was noted prior to delivery.”[46]  He further recorded that LW “now suffers from dystonic quadriparesis.”[47]  So far as interpretation of radiological data was concerned he considered ultrasound studies relative to LW made on 9, 14 and 23 October 1996 and 8 November 1996 and expressed the view that these suggested “slight increase in echogenicity in the region of the lentiform nuclei.”  Of more direct relevance was his consideration of a cranial MRI of LW performed on 10 September 2002.  Dr Kendall expressed the view that on review of this material he could detect the following abnormalities:

“1. There is high signal in the putamina of the lentiform nuclei, which are atrophic.

2.  There is increased signal from the white matter in the regions of the pre- and post‑central gyri.”

 

Dr Kendall’s opinion was that these abnormalities were “indicative of brain damage and signal change associated with a gliotic response… in regions of high metabolism in the maturing foetus.”  He expressed the view that such regions were vulnerable to profound circulatory insufficiency.  In support of this view he made reference to mammalian experiments and clinical experience which suggested that damage in those regions in previously normal foetuses begins after about 10 minutes of profound circulatory insufficiency.  He further expressed the view that a continuation of circulatory insufficiency for longer than 25 minutes would result in death or extensive and severe brain damage.  Dr Kendall further noted from the MRI scan “increased signal on the FLAIR sequence in the deep cerebral white matter and that the lateral ventricles were slightly dilated.”  He considered that these features were also consistent with a period of profound circulatory insufficiency which he thought would be of relatively long duration, “probably close to 25 minutes”.  Dr Kendall could find no other abnormality on the MRI scan and saw no evidence of any additional brain damage.  He considered there was no evidence of any malformation in the brain.  He considered that the brain damage which he did see was the “pathology underlying the dystonic cerebral palsy suffered by LW.”  He considered that it was not possible to determine from the MRI in isolation the timing of the brain damaging period.  His view was that this required “detailed correlation” with the other clinical history. He explained that in clinical practice this was a familiar process where neuroradiologists would discuss their findings with other clinicians involved in the delivery and subsequent care of a child who developed cerebral palsy, obstetricians and paediatricians, in order to determine from the history the probable causation of the condition in a given sufferer. 

[61]      Neuroradiological evidence was also adduced by the pursuers from Dr Connolly, a consultant paediatric neuroradiologist.  Dr Connelly’s expertise and experience included the reporting of CT and MRI scans of children as part of his everyday practice.  For the purposes of preparing his report he considered the same four cranial ultrasounds and the same MRI scan of LW that had been considered by Dr Kendall.  As he had been instructed shortly before the proof commenced he did not have time to consider either AW or LW’s medical records.  He relied for a clinical history from information in Dr Kendall’s report.  From his own consideration of the imaging he first identified a number of areas where there were no problems, thereby discounting possible alternative explanations for LW’s disability.  In relation to adverse findings he considered:

“There was focal high T2 signal with volume loss affecting the posterior putamen bilaterally.  There was minor high T2 signal without volume loss demonstrated on the coronal T2 sequences in the right anterolateral thalamus.  There was mild generalised dilatation of the lateral ventricles without any irregularity of the lateral borders.  There was minor, high T2 signal within the deep white matter of both cerebral hemispheres without there being a focal periventricular distribution.”

 

He explained these findings as demonstrating damage to the posterior putamen bilaterally and the right anterolateral thalamus.  In his opinion these features were entirely in keeping with an acute profound asphyxia.  He also considered the features were entirely consistent with the dystonic quadriparesis suffered by LW.  He also considered there was evidence of brain volume loss “with prominent lateral ventricles and some white matter high T2 signal.”  He considered that this pattern of injury was likely to be associated with a severe acute profound asphyxia. 

[62]      Dr Connolly also gave evidence, which was unchallenged, that his clinical work involving the investigation into the causes of cerebral palsy in children was collaborative and involved working with clinicians from other specialities such as neonatologists, paediatric neuro-oncologists, paediatric neurologists and neurosurgeons[48]. 

[63]      The defenders did not call a neuroradiologist to give evidence.

 

5.   Neurology issues
[64]      The pursuers adduced neurology evidence from Dr Colin Ferrie, consultant paediatric neurologist, Leeds General Infirmary who produced a report dated 3 March 2013[49].  For the purposes of preparing his report Dr Ferrie had sight of the medical records of AW and LW, had seen a statement from AW, statements from Mrs Giles and Mrs Mohammed, Dr Macara, Dr MacLelland, Dr MacLean and Dr Hanretty.  He had also seen expert reports from both midwives and doctors involved in the case.  In addition to this material he had also examined LW and undertaken a medical evaluation of him on 27 March 2012.

[65]      In his opinion Dr Ferrie first outlined his understanding of the facts which were relevant for the purposes of formulating his opinion as based on his understanding of the aforesaid material and of his examination of LW.  On the basis of this material he expressed the opinion that LW had cerebral palsy, learning difficulties and behavioural problems.  He defined cerebral palsy as a term “used to denote a group of conditions characterised by abnormalities of movement and posture caused by non-progressive disorders of the developing brain.”[50]  He observed that a number of professionals had characterised LW’s cerebral palsy in different ways.  His opinion was that LW’s “cerebral palsy is quadriplegic in distribution but his lower limbs are more severely affected than his upper limbs.  The predominant feature is dystonia, indicating that his cerebral palsy is predominately dyskinetic in type. … His tendon reflexes are excessively brisk, indicating a degree of spasticity.”[51]  He classified LW’s cerebral palsy as “mild”.  He further noted that LW displayed evidence of significant bulbar muscle involvement in his cerebral palsy which affected processes such as chewing, swallowing and the articulation of speech.  He observed that cerebral palsy commonly coexisted with learning difficulties.  Estimation of the degree of learning difficulties was a matter he considered appropriate for psychological assessment.  In the absence of psychological assessment his impression was that LW had severe learning difficulties.  He also noted that LW had significantly challenging behaviour, which he again thought very common in children with cerebral palsy and learning difficulties.  He noted that LW did not suffer from epilepsy.

[66]      In relation to the causation of LW’s cerebral palsy he was aware that the contention of the pursuer was that LW’s problems had arisen as a consequence of a hypoxic ischaemic insult immediately prior to his delivery.  He noted that a number of criteria are regarded as “useful in determining the likelihood of an individual’s neurodevelopmental problems as having arisen as a consequence of intrapartum hypoxia.”[52]  These criteria were:

(1)  evidence from foetal monitoring in the intrapartum period suggestive of hypoxia;. 

(2)  the condition of the baby immediately following delivery should be that expected following intrapartum hypoxia;

(3)  the baby should develop features of a hypoxic ischaemic encephalopathy and also evidence of multi-system hypoxic damage; 

(4)  the subsequent condition of the baby should be compatible with that known to arise following intrapartum hypoxia;

(5)  other potential causes for the subject’s condition should, as far as possible, have been excluded.

Dr Ferrie recognised that LW having been delivered by caesarean section could not technically fall into the category of those who had suffered intrapartum hypoxia, labour being a necessary pre-condition.  He did however express the view that the criteria could usefully be applied “…to consider whether [LW]’s neurodevelopmental problems are likely to have risen, wholly or in part, as a consequence of hypoxic ischaemia immediately prior to his delivery.”[53] 

[67]      In applying these criteria he firstly considered, having regard to the evidence as known to him, that foetal monitoring in the hours prior to LW’s delivery showed features suggestive of significant foetal hypoxia.  He further considered that LW’s condition in the immediate newborn period was that expected in cases of damaging hypoxic ischaemia immediately prior to delivery.  He considered LW’s clinical picture in the days following his delivery and on the basis of that material considered that there was equivocal evidence that LW developed both a hypoxic ischaemic encephalopathy and multi-system hypoxic damage.  On the basis of these considerations Dr Ferrie concluded that it was “clear that [LW]’s current condition is consistent with that expected following hypoxic ischaemic insults immediately prior to delivery.”[54]  Dr Ferrie’s report concluded by him considering other possible causes for LW’s presentation and excluding the same. 

[68]      The defenders’ neurological expert was Dr Martin Kirkpatrick.  He produced a report dated 16 October 2011[55].  For the purposes of preparing his report Dr Kirkpatrick had sight of the pleadings, precognitions from the treating midwives and doctors, the medical records of AW and LW, access to a CD containing pictures of LW’s MRI scan performed in 2002 and various expert reports.  Dr Kirkpatrick also had the opportunity to examine LW in the context of a visit to that person’s home in 2011.  At that stage he met both LW’s parents and his two siblings.  On the basis of all the foregoing material Dr Kirkpatrick set forth his understanding of LW’s delivery and neonatal course, his subsequent progress and his understanding of LW’s prognosis. 

[69]      In relation to the issue of causation Dr Kirkpatrick noted that LW had a “complex clinical picture”.  He considered that the “significant components” of that picture were his learning and behavioural difficulties, diplegic cerebral palsy, and some soft dysmorphic features.  All the foregoing had to be considered in the context of LW’s intrauterine growth retardation and prematurity.  Dr Kirkpatrick then considered whether these difficulties could have arisen from early on in pregnancy.  In relation to that issue he noted that at birth LW was noted to be markedly small for the size expected for his gestational age.  Given that all LW’s three growth parameters at birth were very low he considered that his growth retardation was symmetric, that is affecting both his body and head to an equal extent.  He further observed that it is “commonly accepted that symmetrical growth retardation reflects a cause or event that occurs in the first trimester (or third) of pregnancy.”[56]

[70]      In relation to the issue of the contribution of hypoxia and/or ischaemia in the immediate prenatal period of LW’s disabilities Dr Kirkpatrick, in agreement with Dr Ferrie, recognised that there were established criteria to fulfil a diagnosis of hypoxic ischaemic encephalopathy.  He set forth the criteria as follows:

• A sentinel hypoxic event;
• Foetal acidosis demonstrated from a foetal blood sample or umbilical cord sample taken at the time of birth;
• A depressed Apgar at 5 minutes of age;
• A neonatal encephalopathy (a disturbance of conscious level with or without neonatal seizures);
• Evidence of transient ischaemic damage to other organ systems;
• A pattern of neurological damage consistent with an intra-partum hypoxic-ischaemic episode to the baby; and
• Brain imaging studies, if available, that are also consistent with such a brain damaging perinatal hypoxic-ischaemic event.[57]

In Dr Kirkpatrick’s opinion of these criteria the most important in the present case was the presence or otherwise of a neonatal encephalopathy.  He thought that without evidence of such an encephalopathy the chain of linked evidence needed to demonstrate causation would be broken[58].  On the basis of the information available to him there was no suggestion of a neonatal encephalopathy.  Dr Kirkpatrick indicated that there was a major caveat in the use of the criteria he had referred to.  This caveat was, as had been pointed out by Dr Ferrie, that the criteria referred to babies born after labour at term and LW having been delivered by caesarean section eight weeks prematurely did not fall into this category.

[71]      Dr Kirkpatrick concluded by considering the MRI brain scan findings.  He considered that these findings required to be “interpreted in the context of the sequence of clinical events and subsequent outcomes.”[59]  He acknowledged that there was evidence in these scans of basal ganglia damage and perhaps hippocampal damage.  He agreed that these findings might represent damage resulting from acute circulatory collapse at the time of labour.  He did however consider that the result of this type of insult “…is typically that of a child with a severe form cerebral palsy known as choreo-athetoid or dyskinetic quadriplegia, often accompanied by major speech and swallowing difficulties but with intact cognitive skills.  This is not the overall neurological picture of [LW].”[60]  He further considered that even if the MRI findings reflected an acute ischaemic perinatal event then this “has a relatively minor material contribution to his existing neurological difficulties.”[61] 

 

6.   Neonatal issues
[72]      The pursuer adduced neonatal evidence from Dr R J Pearse, retired senior consultant neonatal paediatrician at the North Trent Neonatal Intensive Care Unit at the Jessop Wing in Sheffield Teaching Hospitals NHS Foundation Trust.  For the purposes of preparing his report Dr Pearse had sight on the summons in this action, statements and correspondence from the pursuer, photographs of LW, both general practitioner and hospital records relative to the pursuer and LW and, in addition, had seen reports from Dr Ferrie, Professor Draycott, Mrs Tranter and Professor Hutton (not a witness).

[73]      Dr Pearse reviewed the clinical history of LW from birth until his discharge from hospital three months later.  In addition he had regard to the continuing medical history of LW after discharge from hospital essentially to date.  In essence Dr Pearse was attempting to determine whether or not he could find a causal connection between LW’s perinatal history and the development of cerebral palsy.  His views were expressed in a report.[62]  Before expressing his opinion on causation Dr Pearse initially noted that

“Most studies suggest that overall a relatively small proportion (no more than about 10 - 20%) of cases of cerebral palsy in term babies, is caused by perinatal events.  The figure is significantly higher in the pre‑term.”[63]

 

Dr Pearse then noted that no genetic disorder had been identified as a cause of LW’s cerebral palsy.  He then considered AW’s pregnancy.  In this regard he noted that the pregnancy was not normal and that AW had severe pre‑eclamptic toxaemia and that LW was very growth retarded at delivery.  He further noted that LW’s head circumference at birth was below the mean.  Dr Pearse considered that these features suggested that LW had severe asymmetric growth retardation and that AW’s placenta had not been functioning well for some time prior to birth.

[74]      In relation to the issue of birth asphyxia Dr Pearse deferred to the opinion of Professor Draycott in relation to obstetric interpretation of the birth and to Dr Kendall in relation to interpretation of the MR scan.  That said he proceeded by accepting Professor Draycott’s opinion that the pursuer should have been admitted to hospital earlier than she was and that as a consequence LW would have been delivered at an earlier time than was in fact the case.  He also accepted Dr Kendall’s opinion that the damage seen on MR scan occurred from a period of acute profound asphyxia lasting in the region of 25 minutes immediately before and after delivery of LW.  On the basis of this it was Dr Pearse’s opinion that:

“On the balance of probabilities this continuous period of hypoxic‑ischaemic insult, occurring immediately before and immediately after [LW’s] delivery caused the cerebral damage which, at the very least, made a material contribution to the problems from which [LW] now suffers.”[64]

 

[75]      Dr Pearse thereafter considered the perinatal evidence to seek support for his view that the injury was caused or materially contributed to by hypoxic‑ischaemic insult immediately before and after birth.  In this regard he firstly expressed the view that LW was “clearly asphyxiated at delivery”.  He then considered whether LW demonstrated signs of hypoxic‑ischaemic encephalopathy in the neonatal period.  He acknowledged the difficulty in determining retrospectively whether this condition had developed.  He concluded that“[LW] did not really show any incontrovertible signs of hypoxic‑ischaemic encephalopathy …” but qualified this by stating that “…one does not necessarily expect these in babies at 32 weeks gestation.”[65]  He considered whether there was a rise in the nucleated red cell count after LW’s birth but did not think this issue was of assistance in LW’s case because his growth retardation and date of birth made this factor impossible to interpret.  He considered whether there was evidence of organ failure in the immediate post‑natal period.  Although he could find no evidence of patent organ failure he did note that LW had some oliguria in the day following delivery followed by a period of polyuria which he said was suggestive that the infant had acute tubular necrosis.  He also observed that LW developed suspected necrotizing enterocolitis.  He considered the list of LW’s disabilities and considered that “… the most important, if not all, of [LW’s] current problems” were on the balance of probabilities the result of the period of acute profound asphyxia which he considered that LW suffered in utero.

[76]      The defenders’ neonatal expert was Professor Malcolm Chiswick.  Until 2006 Professor Chiswick was Medical Director of Central Manchester and Manchester Childrens’ University Hospitals NHS Trust.  He has since that date held the post of Honorary Professor of Neonatal Paediatrics at the University of Manchester and Honorary Consultant Neonatal Paediatrician with Central Manchester and Manchester University Hospitals NHS Foundation Trust.  For the purposes of this proof he produced a report dated 26 August 2013[66].

[77]      Professor Chiswick’s report followed the same basic structure of that as Dr Pearse in that he considered the birth of LW and subsequent neonatal history during his period of three months in hospital and subsequently.  He observed LW’s current medical position and noted the same constellation of difficulties observed by Dr Pearse, namely cerebral palsy, learning difficulties and behavioural problems.  He acknowledged that:

“Causation in this case is complex because there are risk factors operating in the antepartum period, immediately after birth, and in the weeks after his birth.”[67]

 

Professor Chiswick further acknowledged:

“Any discussion on causation must rely in part on the appearance of brain imaging.”[68]

It is to be noted that in this regard the opinion of Professor Chiswick is to be differentiated from that of Dr Pearse.  As already noted Dr Pearse had the benefit of sight of a report from Dr Kendall, which report was subsequently spoken to at proof, and was the subject of cross‑examination.  By contrast Professor Chiswick had seen a number of cranial ultrasound scans (also seen by Dr Kendall and Dr Connolly) and beyond that had a MR brain scan interpreted and reported upon by Dr McPhillips, a Consultant Paediatric Radiologist at the Royal Hospital for Sick Children Edinburgh.  This report was not produced and Dr McPhillips was not a witness.  Notwithstanding these issues Professor Chiswick considered on the basis of the imaging he had seen and on the report of the MR scan that LW did suffer an acute profound hypoxic incident.  He considered the principle issue was to determine insofar as possible the timing of that incident.  His view on this matter was that the damage to the basal ganglia and thalami in LW’s brain probably started at delivery and that the appearances of damage to these structures were consistent with a six minute period of damage.[69]  His view was that it was likely that LW was compromised as a result of failure to thrive in utero, probably as a result of placental insufficiency, and that this resulted in him being unable to sustain the six minute period of hypoxia.  He accordingly attributed the causation of LW’s deficits to placental insufficiency rather than an acute hypoxic incident at birth.

 

Midwifery issues
[78]      The pursuer led evidence on midwifery from Mrs Sandra Tranter and Dr Jean McConville.  Mrs Tranter practiced as a midwife between 1966 and her retirement in November 2002.  At the time of her retirement she was Joint Head of Women’s Services at Brighton Sussex University Hospitals NHS Trust based at the Princess Royal Hospital, Haywards Heath, West Sussex.  She had represented her profession at a statutory level by membership of the Specialist Register, Midwifery of the English National Board for Nursing Midwifery and Health Visiting between 1994 and 1997 and had between 1994 and 2002 been a member of the Association of Supervisors of Midwives.  She was a member of the Royal College of Midwives.  For the purposes of preparing her report she had seen the written pleadings in the case.  She had also seen reports from Dr Jean McConville, midwife, Professor Draycott, Professor de Swiet, Dr Pearse, and Dr Kendall.  She had seen the relevant medical records in the case and a number of statements taken from clinicians and midwives involved in the care of AW during her pregnancy in 1996. 

[79]      Mrs Tranter’s report was dated 3 May 2013[70].  The format of Mrs Tranter’s report was to set out and consider the management and care of AW from the date of the booking of her pregnancy on 21 May 1996 until the delivery of LW on 8 October 1996.  Having considered that material she expressed the view that she had no criticism of the standard of midwifery care “apart from the antenatal assessment at home on 5/10/1996.”[71].  In relation to that assessment Mrs Tranter’s criticisms focused on four matters.  First, she considered the information she had to the effect that midwife Giles listened to the foetal heart rate by pinnard for a period of about 15 seconds.  She considered that this was not a reasonable time “to make sure that the foetal heart rate was within normal limits.”[72].  She considered that it was usual to listen for at least a minute.  She regarded listening for 15 seconds as amounting to insufficient time to be reassured about foetal heart rate.  Second, proceeding on the hypothesis that AW had reported her symptoms of feeling unwell and her concern that her baby was small for dates to the midwives, Mrs Tranter considered that no mention of these factors had been made in the “Comments” section of the PCP booklet.  She regarded this as a departure from normal practice.  Third, she noted that in the column of the PCP relative to the examination of urine an entry contained the notation “C/C”.  She had not come across the use of this term before and therefore queried its meaning.  Fourth, she noted that there was no recording of blood pressure in the PCP.  Failure to record blood pressure, if the same was taken, would, in her view, amount to a departure from ordinary practice by a midwife.  Mrs Tranter did however go further and express the view that the failure to record blood pressure was indicative that that procedure had not been undertaken.  Having regard to these features she was of the view that the conduct of the assessment by the two midwives involved on 5 October 1996 had departed from ordinary standards to be expected of a midwife.  She considered that the information which she understood AW to have conveyed to the midwives regarding how she was feeling and her concern for her baby’s size should have prompted the midwives to consider the possibility of the development of pre‑eclampsia.  This in turn should have led to “…them taking particular care to check her blood pressure.”  She further expressed the view that “Had her blood pressure been raised, then it should have been rechecked and if it remained raised, the attending community midwives should have referred [AW] into hospital for a medical review.”[73]. 

[80]      The pursuer also led evidence from Dr Jean McConville.  She had practised as a midwife between 1984 and 2011.  At the date of giving evidence she remained a member of the Nursing and Midwifery Council.  In all its essentials the evidence of Dr McConville supported that given by Mrs Tranter. 

[81]      The defenders led the evidence of Dr Julia Sanders, a registered midwife with over 25 years’ experience.  Dr Sanders was at the time of the proof employed as a consultant midwife by Cardiff and Vale University Health Board as lead clinician for a midwifery LED unit providing intrapartum care to around 2,000 women annually.  In addition she was employed by Cardiff University as a senior clinical research fellow. 

[82]      Dr Sanders’ report was dated 19 August 2013[74].  The format of Dr Sanders’ report was essentially the same as that adopted by Mrs Tranter.  In relation to the midwifery examination and assessment on 5 October 1996 which was the subject of criticism by Mrs Tranter, Dr Sanders opinion on the matters raised by Mrs Tranter was as follows.  Firstly in relation to the midwives listening to the foetal heart with a pinnard, Dr Sanders considered that there was no departure from ordinary practice by the midwives.  She considered that the period for which the midwife was estimated to have listened to the heart rate was sufficient to form an opinion as to the foetal heart rate and, moreover, was in accordance with midwifery practice.  It was her view that “…observation and practice would suggest many midwives listen for as little as five seconds.”[75].  In relation to urine testing she had no difficulty with the use of the notation “C/C” which she understood, and accepted, was a notation used to denote nothing abnormal detected in clinical practice in the West of Scotland in 1996.  In relation to Mrs Tranter’s criticism that the midwives failed to record AW’s alleged complaints about her general health and the size of her baby Dr Sanders expressed the view that:

“Midwives do not necessarily record all pregnancy related complaints or discomforts discussed during antenatal check-ups.  Women commonly vocalise general pregnancy related symptoms during check-ups and although these are discussed, such discussions are frequently only recorded if symptoms are severe.  It is not possible to determine from the records of October 5 which, if any, pregnancy related symptoms were reported by [AW], or what discussion took place.”[76]

 

In relation to the issue of whether or not AW’s blood pressure was taken on that date, Dr Sanders acknowledged that no blood pressure finding was recorded in the PCP.  She observed that “This implies that either it was not taken or taken and not recorded.  Either is possible and which is correct cannot be determined from the notes.”[77].  She then went on to observe that the taking of blood pressure was a part of routine practice and that the recording of the patient’s blood pressure was an “essential component” of a midwifery antenatal examination.  She observed that both midwives involved in the examination on the relevant date were experienced community midwives and would have understood and been aware of that requirement.  She observed that having regard to those considerations she thought there were two scenarios:

“…either the midwives omitted to check [AW]’s blood pressure, which suggests symptoms were absent or sufficiently mild not to prompt two experienced midwives to remember to check it, or it was taken and found to be completely normal, giving no grounds to prompt the midwives to record the finding or plan additional surveillance.”

 

[83]      Having regard to all these factors Dr Sanders conclusion was that “Apart from the failure to record [AW]’s blood pressure, the antenatal check performed on October 5^th, 1996 appears to be otherwise completely standard and suggest the midwives provided an acceptable level of care.”

 

8.         Relevant law
[84]      There was no material dispute between the parties as to the relevant law applicable to the determination of this case.  It was accepted that the court required to determine whether there had been professional negligence on the part of those blamed by the pursuer for the delictual act complained of, in this case midwives.  Beyond that there was the issue of delictual causation, whether any departure from ordinary professional standards by those complained against had caused the damage sustained by the harmed party. 

[85]      In relation to negligence the claim is based upon alleged professional negligence on the part of the two midwives Mrs Giles and Mrs Mohammed.  It is said that they acted as no ordinarily competent midwives would have acted in 1996 if they had exercised reasonable or ordinary skill and care in the exercise of their professional duties owed to AW.  The law remains as stated by Lord President Clyde in Hunter v Hanley 1955 SC 200 at page 205 as follows:

“In the realm of diagnosis and treatment there is ample scope for genuine difference of opinion and one man clearly is not negligent merely because his conclusion differs from that of other professional men…  The true test for establishing negligence in diagnosis or treatment on the part of a doctor is whether he has been proved to be guilty of such failure as no doctor of ordinary skill would be guilty of if acting with ordinary care…”

 

It was common ground between the parties that the test adumbrated by Lord President Cooper is to be applied on the basis of scientific and technical standards at the time of the alleged negligence.  It was further agreed that the test can only be met by a pursuer leading expert evidence that supports their position from a suitably qualified expert.  It was also accepted that if the defender’s lead expert evidence which supports the actions taken by the treating clinician demonstrated that there was a body of suitably qualified experts who take a view different from that expressed by the pursuer’s experts and consider that the treating clinician has not acted negligently then that view will prevail as showing that Lord President Cooper’s test has not been met unless the defender’s experts are found to have been unreasonable.  It is not the function of the court to adjudicate between experts (Honisz v Lothian Health Board [2006] CSOH 24, Dineley v Lothian Health Board [2007] CSOH 154). 

[86]      The position where there are divergent or conflicting views between the parties’ medical experts was considered by Lord Hodge in Honisz (supra).  His statement on the applicable law in that situation has since its pronouncement been regarded as authoritative.  In that case in relation to the issue Lord Hodge stated:

“[39]   First, as a general rule, where there are two opposing schools of thought among the relevant group of responsible medical practitioners as to the appropriateness of a particular practice, it is not the function of the court to prefer one school over the other (Maynard v West Midlands Regional Health Authority, Lord Scarman at p.639F-G). Secondly, however, the court does not defer to the opinion of the relevant professionals to the extent that, if a defender lead evidence that other responsible professionals among the relevant group of medical practitioners would have done what the impugned medical practitioner did, the judge must in all cases conclude that there has been no negligence. This is because, thirdly, in exceptional cases the court may conclude that a practice which responsible medical practitioners have perpetuated does not stand up to rational analysis (Bolitho v City and Hackney Health Authority, Lord Browne-Wilkinson at pp.241G-242F, 243A-E). Where the judge is satisfied that the body of professional opinion, on which a defender relies, is not reasonable or responsible he may find the medical practitioner guilty of negligence, despite that body of opinion sanctioning his conduct. This will rarely occur as the assessment and balancing of risks and benefits are matters of clinical judgment. Thus it will normally require compelling expert evidence to demonstrate that an opinion by another medical expert is one which that other expert could not have held if he had taken care to analyse the basis of the practice. Where experts have applied their minds to the comparative risks and benefits of a course of action and have reached a defensible conclusion, the court will have no basis for rejecting their view and concluding that the pursuer has proved negligence in terms of the Hunter v Hanley …  As Lord Browne-Wilkinson said in Bolitho (at p.243D-E), ‘it is only where the judge can be satisfied that the body of expert opinion cannot logically be supported at all that such opinion will not provide the benchmark by which the defendant's conduct falls to be assessed.’

 

[40]   An example of such a rare case is that of Hucks v Cole [1993] 4 Med L R 393, which Lord Browne-Wilkinson discussed in Bolitho. In that case a general practitioner failed to give penicillin to a lady in a maternity ward who had a septic spot and as a result she developed fulminating septicaemia. The defendant knowingly took a risk that the lady could develop puerperal fever because the risk was small and he was supported in his decision by distinguished expert witnesses. Nevertheless the judge concluded that he was negligent and the Court of Appeal upheld his decision, Sachs LJ holding that there was a lacuna in professional practice and that the defendant knowingly took an easily avoidable risk which elementary teaching had instructed him to avoid. As, in the court's judgment, there was no proper basis for the practice of not giving penicillin it was not reasonable for the medical practitioner to expose his patient to that risk.”

 

[87]      In relation to causation there appeared to be agreement between the parties that if the pursuer established that the midwives had acted negligently she then had to further establish the existence of a complex chain of causation from those failures the end result of which was an outcome, so far as LW was concerned, which was different from that which in fact pertained.  There was no dispute that those matters had to be proved on the balance of probabilities.  It was also accepted that there was an esto case stated on behalf of the pursuer that if there was proven negligence on the part of the midwives then the outcome for LW would have been materially better than that which in fact pertained. 

 

9.         Reliability and credibility
[88]      There are four separate allegations of negligence pled against the defenders’ midwifery staff.  The first allegation of negligence is in relation to the midwifery staff’s response to AW’s telephone calls to them on 1 and 3 October 1996.  It is pled that in response to AW’s complaints by telephone of feeling unwell it was the midwife’s duty “to attend….to advise her to count foetal movements, or to attend the hospital for investigations”.  This case is against only Mrs Giles.  The second allegation is of a failure to take or record AW’s blood pressure on 5 October.  The third allegation is of a failure to obtain a urine sample on the same date.  The fourth allegation is of a failure to refer AW to hospital on the same date in relation to her reported symptoms.  The last three cases of negligence are made against both Mrs Giles and Mrs Mohammed.  The second and third grounds of fault, failure to take or record blood pressure and failure to take a urine sample, turn entirely on the factual issues of whether these failures occurred, a construction of the case which was accepted by the pursuer.  The reliability and credibility of AW and her husband are central to the determination of the factual issues which underlie each of these cases of fault.  The credibility and reliability of AW and, in a less focused manner, her husband as witnesses was the subject of challenge and submission by the defenders.  The evidence of Mrs Giles and Mrs Mohammed is also important in the determination of these issues and the reliability and credibility of these witnesses therefore also requires to be considered. 

[89]      I deal firstly with the reliability and credibility of AW and her husband.  In relation to AW the challenge upon her in this regard relates both to her account of the events before and on 5 October and to the account she gave of the events on 8 October.  In relation to AW’s husband his evidence was primarily of relevance to the events of 5 October.

[90]      The position of counsel for the pursuer in relation to AW was that she gave all her evidence in a straightforward manner.  She narrated her account of what she had told midwives, and latterly doctors, about her symptoms without exaggeration and as accurately as she could recall having regard to the significant passage of time since the events.  It was submitted that she did not exaggerate and was not guilty, either consciously or unconsciously, of confabulation.  In relation to AW’s husband it was noted that he had stated in evidence that he had a very clear recollection of the events of 5 and 8 October 1996.  The events of those days were, he said, “stuck in our memories”.  It was submitted that there was no reason to doubt his evidence that he remembered these days clearly. 

[91]      By contrast the position of the defenders was to submit that the “…pursuer’s evidence disclosed very significant issues with regard to her credibility and reliability, such that the court cannot safely rely on her evidence on any of the critical issues in this case.”  This was developed by a submission that AW was an intelligent woman, from a high achieving family and who, in addition, was “creatively talented”.  It was said that the “stakes” in the litigation were very high, a reference to the sum sued for.  AW was said to be aware that her role in the whole case was “pivotal” and that she was consequently under a “great deal of pressure to remember”.  As a result of all this it was said that AW had a “huge incentive to ‘remember’ things she does not actually recall” and used her creative mind “…to confabulate so as to enable the claim in negligence to be put together.”  An example of what was submitted to be her “extreme commitment” to the case was the fact that she attended throughout every day of the proof.  Beyond this it was submitted that the pursuer had in evidence accepted the existence of the concept of confabulation, which was said to be  a recovered memory, sometimes strongly held, which turns out to be false.  This was submitted to be a “significant feature” of the case.   The defenders’ further submitted that AW’s memory was extremely patchy.  The defenders’ position was that she could recall things which supported her case but could not recall matters which were, or might be, regarded as adverse to her interests.  In this regard it was noted that her precise recollection of some facts, for example the events of and surrounding the antenatal class of 8 October, were precise whereas in other respects her evidence was far less clear.  It was also submitted that examination of correspondence, reports obtained and the pleadings showed that the pursuer’s case had developed over time and that this reflected an adaptation by her of the facts to suit the case she required to present.  In this regard it was said that AW had made extensive and detailed study of her medical records and the other medical reports and papers prepared for the case and again tailored her evidence to suit these reports.  In conclusion the defenders’ submission was that the accounts of critical events given by AW was not really a recollection “…but a construct, a creed that she has come to believe in because it matters so much to her and her family and to [LW] that it should be accepted, however unlikely it may be, because that is the way she thinks [LW] will get the money she feels he deserves.”  On this basis the defenders’ submission was that AW should be found incredible and/or unreliable in every critical respect of her evidence.

[92]      In relation to AW’s husband the defenders’ submitted that it was apparent on the evidence that he had taken “a far less prominent role than his wife in almost every material area of the pregnancy and birth”.  As a result of this it was submitted that his recollection of events were “pretty vague”.  It was said that he did not support his wife in a number of the key details of the evidence of the events of 5 October.  He of course was not involved in any of the key events of 8 October. 

[93]      AW gave evidence over five court days.  At the time of her giving evidence, most of the matters about which she was asked had occurred 16 years in the past.  This long passage of time is, in my view, likely to have some effect on a person’s ability to recall events accurately and reliably.  That factor must however, again in my view, be balanced against consideration of the significance or importance of the events to the person recounting them.  In that regard it is obvious, and was spoken to by both AW and her husband, that the events being recalled by them were the most significant events in their lives.  This was AW’s first pregnancy.  The pregnancy was planned and was desired by both her and her husband.  The pregnancy had been routine and uneventful until the events with which this case is concerned.  In the week preceding the critical midwives visit of 5 October, AW had experienced, on her evidence, symptoms which caused her to have a degree of concern about her health and the unborn baby’s wellbeing.  The meeting of 5 October was on the evidence of both AW and her husband, and, at least to some extent, the two midwives involved, somewhat out of the normal routine of an antenatal midwifery visit.  On any view the events of 8 October were for AW both out of the ordinary and, for most unfortunate reasons, highly memorable.  It is, in my view, against that background narrative of circumstances, that the evidence of AW requires to be considered. 

[94]      In my view AW gave her evidence in a calm, thoughtful and for the most part unemotional manner.  There were a number of instances when she became tearful and required to compose herself.   Having regard to the nature of the subject matter about which she was giving evidence, I consider these displays of emotion were appropriate and understandable.  I saw nothing in the conduct or demeanour of AW over her very lengthy period of giving evidence that would cause me to have reservations as to whether she was doing other than attempting to tell the truth.  I accept the defenders’ submission that AW was an intelligent woman.  There was also evidence which would support the defenders’ contention that she was a member of a “high achieving family”.  I fail to see how the academic and professional achievements of AW’s family can have any bearing on the issues of her reliability and credibility in this proof.  I also accept that AW would fall to be regarded as “creatively talented” in the sense that there was evidence that she had been a student of architecture and had studied photography.  Again however I fail to see how creativity in an artistic sense can, in the absence of precise and objective evidence, be used as a basis for the suggestion that someone may have invented factual evidence.  Viewed objectively and reasonably, against the background I have already outlined,  I did not find the precision in some aspects of AW’s evidence particularly surprising having regard to the importance of the events to her.  I accept that confabulation can occur and is a recognised psychological trait.  There were however no submissions to me as to when confabulation can occur and how it can, in an objectively veritable way, be recognised by a judge.  The dictionary definition of the term is “to fabricate imaginary experiences as compensation for loss of memory”[78].  The defenders’ submission amounted, in my view, to no more than an assertion, unsupported by any evidence, that AW confabulated.  I do not consider that this assertion can be accepted.   I do accept that the defenders are correct, at least as a matter of fact, to submit that AW expended very considerable effort, time and application to the pursuit of this case.  I do not however consider that it can be asserted that simply because she has devoted so much energy to this case then it must follow that she is guilty, whether consciously or unconsciously, of confabulation.  I reach this conclusion first, because in my view her account of the events of 5 October were substantially supported by the evidence given by her husband.  Moreover, many aspects of what she said about the meeting on that day were accepted as being plausible by the two midwives involved.  Second, so far as the events of 8 October were concerned her version of events was at least in a broad sense supported by the medical records.  It is true, as was pointed out by the defenders, that her evidence did not accord in all respects with matters noted in the medical records.  AW did not hide from these discrepancies in her oral evidence, but simply narrated in a straightforward manner what she recalled of that day.  Having regard to all these considerations I am of the view that AW at all times was attempting to give evidence which was truthful.  I find her in general a witness who was reliable and credible, albeit there are a number of matters in her evidence which I am not prepared to accept. 

[95]      I can be much more brief about AW’s husband.  He gave his evidence in a straightforward and unemotional manner.  He did not appear to me to be exaggerating at any stage.  He accepted there were gaps in his memory and did not attempt to cover or fill in these gaps with invention.  Quite simply when he did not remember anything he said so.  I accept his evidence as reliable and credible. 

[96]      I turn now to consider the reliability and credibility of the midwives.  The position of both midwives was that they had no recollection of the events of 5 October.  In relation to the critical aspects of their examination of AW on that date they both stated that it was absolutely routine and standard midwifery practice to test a patient’s urine during a routine antenatal examination.  They both adopted exactly the same stance in relation to the taking of a patient’s blood pressure.  Their position in relation to the routine and structured nature of these tests was supported by all the midwifery experts.  It was the position of both midwives that having regard to the routine nature of these practices they would both have been undertaken.  In relation to the urine sample Mrs Giles position was that the notation “C/C” was a normal one used at that time in the West of Scotland.  Mrs Mohammed stated that she herself normally used the notation “NAD” when there was no adverse finding in a urine test, but the entry could be explained by the possibility that, with two midwives present, she did not write the entry in the PCP.  In relation to the absence of any record of blood pressure both acknowledged that was a mistake, but both maintained that the mistake must, on the basis of their practice, have been limited to a failure to note the result of a test not a failure to perform the test.

[97]      So far as Mrs Mohammed is concerned her only contact with AW was on 5 October.  She had no further involvement with the case, and could not recall the case ever having been brought to her attention again until she was questioned after the intimation of a claim.  Having regard to the fact that her involvement was so limited I do not find it difficult to accept Mrs Mohammed’s evidence that she had no recollection whatsoever of any aspect of the examination of 5 October. 

[98]      The position in relation to Mrs Giles is somewhat different.  She had had involvement with AW, albeit somewhat limited, before 5 October.  She was the allocated midwife for AW.  Moreover, on the basis of AW’s evidence, she had some, albeit limited, engagement with AW on 8 October in hospital.  There is also the consideration that Mrs Giles made an entry in AW’s medical records relative to the birth of LW on 8 October and, further, on AW’s husband’s evidence left telephone messages for him that day.  Having regard to all these factors I find it surprising that Mrs Giles claimed to have no memory whatsoever of the events of 5 October.  She was an experienced midwife.  On any view of the evidence she was aware on or about 8 October that AW had been admitted to hospital suffering from pre-eclampsia and had subsequently been delivered of a premature baby.  These occurrences are, fortunately, relatively unusual even for an experienced midwife.  In these circumstances I find her alleged complete lack of memory of events to be surprising.  Further, Mrs Giles demeanour whilst giving evidence was, in my view, less than wholly satisfactory.  During the course of her evidence, whilst maintaining a general lack of memory of the events, she did at times appear to indicate that she had some knowledge of these events from her memory.  Having regard to all these factors I am not prepared to accept the evidence of Mrs Giles as entirely credible and reliable.  When her evidence conflicts with that given by AW and her husband I prefer the evidence of the latter. 

 

10.       The grounds of negligence
[99]      AW was expecting a home visit from a midwife on 1 October 1996.  That appointment was not kept.  AW telephoned the midwives and spoke to Mrs Giles.  She told Mrs Giles that she was feeling unwell, that she had concerns and that she wanted to see a midwife.  This account was not contradicted by Mrs Giles.  She did say that she “would have” advised AW to phone her GP or contact the hospital if she was particularly worried.  AW was given another appointment two days later which, again, was not kept by the midwives.  AW telephoned the midwives at around lunchtime that day and was told that she would definitely be seen later that day or the following day.  There was no visit by the midwives that day or the following day.  On the face of this appears to amount to poor service however neither of the pursuers expert midwives expressed any criticism of this aspect of care. 

[100]    I turn to the examination on Saturday 5 October.  The critical issues are whether or not a sample of urine was taken and tested and whether or not AW’s blood pressure was taken.  In relation to both these issues AW is clear that they were not performed.  In relation to the urine sample she stated that as the visit was not arranged and was unexpected she had not prepared a urine sample.  This was confirmed in evidence by her husband.  Moreover AW said she would have remembered being asked to go to the lavatory and prepare a sample and was sure this had not happened.  Likewise her husband did not recall her at any stage leaving the room to go to the lavatory.  Whilst the midwives have no recollection of the examination they both point to the entry “C/C” in the appropriate column of the PCP as evidence that the test was undertaken.  There was some evidence that the notation “C/C” is not a standard one in midwifery, or for that matter medical, clinical practice.  Whilst I accept the veracity of that evidence I equally accept that there might have existed in 1996 areas of the country where other notations were in use.  In that regard there was evidence from a number of clinicians practicing in the Glasgow area in 1996 that the form of notation employed in the PCP was used by doctors and midwives in that area at that time.  There was also evidence from Mrs Mohammed that she did not use the notation “C/C” but employed the more usual “NAD”.  From this evidence I take it that the entry in the PCP was likely to have been made by Mrs Giles.  The issue is therefore whether I accept that the entry was made at the time following a urine sample test or, for some reason unexplained in the evidence, it was completed at another time.  In relation to the issue of when the entry “C/C” was made in the PCP the pursuer’s submission was that the onus was not on her to establish or explain when the entry was made.  I accept that is correct.  There was evidence, effectively unchallenged, that AW had handed the PCP to Mrs Giles in QMH following her admission to hospital at lunchtime on 8 October.  A patient is meant to keep possession of her PCP at all times and a request to hand over the booklet made by Mrs Giles and acceded to by AW is difficult to understand.  There are however no inferences I feel I can properly draw from that part of the evidence.  I am however prepared to accept the evidence of AW and her husband in relation to the events of 5 October and accordingly hold that no urine test was performed on that date.  In relation to blood pressure testing the issue is more straightforward.  There is no recording of blood pressure in the PCP.  That was accepted by both Mrs Giles and Mrs Mohammed as a failure or mistake.  They did however maintain that as a matter of practice they would have taken the blood pressure.  Again there is contradictory evidence from both AW and her husband.  Again I accept the evidence of AW and her husband and hold that no blood pressure recording was made. 

[101]    The last issue in relation to the examination on 5 October is whether or not AW reported symptoms suggestive of pre-eclampsia to the midwives on that date.  Having regard to the clear evidence of AW and her husband I hold that such symptoms were reported and that the midwives failed to record them in the appropriate part of the PCP.  More importantly the issue arises as to whether the symptoms which I accept AW reported to the midwives necessitated a referral to hospital on 5 October.  Mrs Tranter’s evidence was that the symptoms reported, headaches, visual disturbance and blurred vision merited referral to hospital regardless of the presence of other signs of pre‑eclampsia such as hypertension and proteinuria.  She was supported in this opinion by Dr McConville.  I am satisfied that the evidence represented the procedure of ordinarily competent midwives in 1996 and accordingly hold their failure to “make a referral” to be established as negligence.

[102]    It follows from the foregoing that I consider that all three of the grounds of negligence pled against the midwives have been established.  The implications of that finding are that AW should have been referred to hospital on 5 October 1996.  This gives rise to the issue of causation to which I now turn.

 

Causation:  the effect of referral to hospital earlier than 8 October
[103]    The causative effect of the midwife’s negligence requires to be considered.  In order to do this it is necessary that the case on causation be set forth clearly.  The pursuer’s case on causation is to be found in article 8 of condescendence in the closed record.  The following passages are, in my view, critical:

“Had the pursuer been referred to hospital (as she should have been) by the midwives on 5 October 1996 she would have gone there that day without delay.  On her attendance at hospital the pursuer would have been reviewed by an Obstetric Registrar.  The pursuer’s blood pressure would have been elevated and given her symptoms which include blurred vision, headaches and reduced foetal movements she would have been admitted to hospital that day.  She would have undergone four hourly observations, blood tests, foetal monitoring and management of her hypotension.  She would have been given oral ante-hypotensives.  She would have been given ante-natal steroids at her gestation after her admission.  By the morning of 7 October at the latest the pursuer would have undergone an ultrasound scan which would have shown foetal growth retardation, reduced liquor volume and abnormal dopplers.  Had the pursuer been admitted on 5 October, a CTG would have been performed on admission, particularly with the pursuer’s history of reduced foetal movements.  Monitoring would have continued into 7 October.  The CTG would have been abnormal by 7 October at the latest showing intermittent decelerations consistent with cord compression secondary to the reduced liquor volume.  If the pursuer had been in hospital (as she should have been) on the night of 7 October when she suffered the sharp abdominal pain hereinbefore condescended upon she would have been assessed by the Obstetricians on duty who would have noted: the IUGR, reduced liquor volume and abnormal dopplers;  the abnormal CTG;  48 hours post-steroids;  blood pressure controlled by oral ante-hypotensives;  normal serology.  They would have concluded that there was a very low threshold for immediate delivery by Caesarean Section.  By the morning of 8 October the CTG would have continued to be abnormal.  LW would have been delivered by section.  Had the pursuer been admitted to hospital on 5 October her management would have been optimised such that LW would have been born by Caesarean Section on the evening of 7 October or at least overnight that night.  The latest LW would have been born would have been by 10am on 8 October.  Likewise if the ultrascan had been performed on 5 October.  In any event the CTG traces were continuously abnormal from the point that monitoring actually commenced at about 1400 on 8 October 1996.  There was a significant decline in the trace at about 15.30 with reduced baseline and variability, absence of accelerations and multiple decelerations.  But for the midwife’s breaches of duty a Caesarean Section could and would have been performed immediately with LW being delivered unharmed by about 1600 at the latest.  At the latest LW would have been born between 1559 and 1604…..In the circumstances which actually occurred on 8 October 1996 the Caesarean Section was delayed because the pursuer was still being treated for hypotension and the obstetricians were still waiting for the results of essential tests which were being carried out on a sample of the pursuer’s blood and for steroid treatment to take effect.  If the midwives had performed the duties incumbent on them and the pursuer had been seen at the hospital by 7 October 1996 these delays would not have occurred.  The pursuer’s hypotension would have been treated, the steroid treatment would have been effective and the blood test results would have been available before 1530 on 8 October.  The pursuer’s blood pressure would have stabilised, permitting delivery as soon as the CTG became abnormal”.

 

Having regard to these averments examination of the issue of causation requires consideration of the evidence of what would have occurred had AW been referred to hospital following the midwives’ visit on 5 October.

[104]    The first issue to dispose of is whether or not AW would have attended at hospital on 5 October.  In my view this question is very easily answered.  All the evidence in the case supports the proposition that AW was a careful and thoughtful expectant mother who followed advice given to her by doctors and midwives.  There was no reason to doubt that she would have followed either advice or an instruction given to her by midwives to attend hospital on 5 October.

 

(i)         Admission on Saturday 5 October
[105]    The pursuer’s position is that had AW been referred to hospital on 5 October it is highly likely that pre‑eclampsia would have been diagnosed.  This is because she would have been reviewed by an obstetric registrar, have reported her symptoms and had her blood pressure taken and urine tested for the presence of protein.  The blood pressure would have been elevated and the urine test would have disclosed the presence of protein and she would therefore have been admitted to hospital.  These propositions in relation to elevated blood pressure and the presence of protein in the urine, as I understood it, depended critically upon the evidence of Professor de Swiet.  The key issue had been identified by the professor in his report in the following way:

“What is the likelihood that [AW] would have had proteinuria and hypertension had these signs been looked for … on the 5 October 1996?”[79]

 

As already noted Professor de Swiet answers the foregoing questions he posed in the affirmative in the sense that he considered that both proteinuria and hypertension would have been detected.  This argument is then developed by the pursuer with a submission that referral to hospital on 5 October, which was a Saturday, would have resulted in foetal monitoring by CTG and an ultrasound.  Even if the ultrasound department had as a matter of fact been closed over the weekend a consultant could, if that person wished, have undertaken such an examination.  In any event the very latest when an ultrasound scan would have been performed would have been on the following Monday morning (7 October).  On the evidence of Professor Draycott the pursuer submitted that an ultrasound scan carried out at any time between 5 and 7 October would have shown the same negative signs as when that procedure was performed by Dr Macara on 8 October and that because all of the features noted on that date, reduced liquor, intrauterine growth restriction and abnormal dopplers take days to develop they therefore on the balance of probabilities would have been present at any time on and following 5 October.  Professor Draycott’s position was, further, that a bio‑physical profile taken on 7 October would have been abnormal.  Moreover a CTG carried out on that date was likely to have been abnormal because the foetus would not have been moving or breathing normally as a result of low nutrition.

[106]    On the basis of the foregoing the pursuer’s submission was that a caesarean section would have been performed by at the latest Monday 7 October.  Support for this proposition was said to be obtained from the evidence of Dr Hanretty the treating consultant on the afternoon of 8 October.  His evidence was that had the clinical picture been the same on Saturday 5 October as it was on 8 October he would have delivered the child on the former date.  He also expressed the view that he would have delivered the child earlier than 8 October because of the intrauterine growth restriction alone even in the absence of signs of pre‑eclampsia.[80]  Dr Hanretty’s position appears to have been that an ultrasound carried out on Monday 7 October would have shown:

“Isolated growth restriction in the sense of absence of hypertension and this was a seriously concerning, severely compromised foetus and he would have been delivered … on the Monday”.[81]

 

Dr Hanretty would not have delayed delivery for a course of steroid treatment.  He also thought that if an ultrasound scan had been carried out on 7 October the foetus’ condition would have been the same as that on the Tuesday because of long‑standing placental abnormality.

[107]    It followed, on the pursuer’s submission that admission of AW to hospital on Saturday 5 October would, on the balance of probabilities have resulted in the delivery of her child by caesarean section during the course of 7 October.  It follows that the child would have been delivered before she experienced the sharp abdominal pains on the night of 7/8 October which may have been the abruption signs of which were found on examination of the placenta after the birth.   It follows that the child would have been delivered before he suffered brain damage from an acute hypoxic insult which on the pursuer’s submissions occurred in the few minutes either side of his delivery at about 16.52 on the afternoon of 8 October.

[108]    The defenders’ primary position was, of course, on the basis that there was no negligent failure to refer on 5 October by the midwives.  Counsel for the defenders did however make full submissions in relation to what he submitted to be the position if, as has transpired to be the case, the defenders’ primary position was rejected by the court.  His position was that on the evidence a referral to hospital on Saturday 5 October would have resulted in AW being initially assessed not by an obstetric registrar but by midwives.  This was spoken to by both Dr Macara and Dr McLelland.  The admitting midwife would have tested blood pressure, urine for protein and sugar, temperature and pulse.  An examination of the foetus and measurement of fundal height would have been undertaken.  In the event blood pressure was found to be abnormally elevated, protein detected in the urine or that fundal height was found to be inappropriate for the stage in gestation the patient would have been admitted and would have remained in hospital until an ultrasound scan could have been performed, which would have occurred on the following Monday.  Whether or not a CTG would have been undertaken was dependent upon whether or not the patient was admitted.  The threshold for admission on the evidence of Drs Macara and McLelland was the existence of abnormal blood pressure, abnormal urine tests or fundal height not commensurate with the period in gestation or any of those symptoms.

[109]    There was no evidence in the case that on 5 October the fundal height was inappropriate for the stage in gestation.  On the contrary, the evidence of both midwives who attended the pursuer on 8 October is that fundal height was measured on that date and no abnormality recorded.  The pursuer confirmed that her “bump” was measured.  It is therefore relatively easy to conclude that that criteria for admission to hospital on that date would not have been met.  There remains the critical issues of blood pressure and the presence or absence of protein in AW’s urine on that date.  As already observed the pursuer’s position on these two critical issues is dependent upon acceptance of the evidence of Professor de Swiet.  The defenders challenged Professor de Swiet’s evidence and submitted that it should not be accepted.  They noted that in his instructions the professor was not asked to address the general causation question of what caused LW’s disabilities.  Consequently he did not require to rely on the evidence of the other clinical experts when preparing his report.  This was submitted to be contrary to normal clinical practice in which teams of experts from various medical disciplines formulate diagnosis of cerebral palsy.  As I understood it this was a complaint on the defenders’ part that Professor de Swiet failed to have regard to the entire clinical picture that is necessary to determination of questions of the causation of cerebral palsy.  Further it was noted that Professor de Swiet was a physician and not an obstetrician and that the majority of his clinical experience involved advising women in an out‑patient setting who were experiencing problems in pregnancy or women who were not pregnant and were concerned about potential problems in future pregnancies or who had experienced problems in previous pregnancies and wanted to discuss how best to approach future pregnancies.  The principle criticism of Professor de Swiet’s position was however, again as I understood it, that his work was theoretical and based entirely on the interpretation that could be placed upon a number of academic papers.  The conclusions he drew were essentially inferences in relation to the development of pre‑eclampsia made upon the basis of findings in academic studies.  The studies he relied upon did not actually prove the propositions advanced by the professor.  His views were inferences which he said could and should be drawn from the data in the papers he relied upon.  The inferences which the professor made from the papers were not, it was said, supported by the views of the clinicians who had dealt with AW during the course of her stay in QMH on 8 October.

[110]    In relation to the views expressed by the clinicians who gave evidence there was, firstly, a degree of reservation as to the degree of proteinuria detected on 8 October.  Whilst both Dr McLelland and Dr Hanretty considered that the diagnosis was of pre‑eclampsia they both considered that there was only a very slight elevation in the level of protein found in the urine.  Whilst both considered that the findings, taken by the relatively crude dipstick test method, could not be ignored there was the possibility that the slight degree of elevation in proteinuria recorded was a false positive.  The presence of a small amount of protein in the urine could be accounted for by the presence of traces of blood caused by the taking of the sample.  In both these clinicians’ views it could not be said that the degree of protein detected on 8 October established that any testing of urine on 5 October would have resulted in a positive finding.  Similar scepticism was expressed in relation to Professor de Swiet’s opinion that the presence of high blood pressure on 8 October would of necessity have produced the same result if testing had taken place on 5 October.  None of the treating clinicians considered that there was any means of knowing what a person’s blood pressure would have been three days before it was actually tested.  Dr Hanretty stated that pre‑eclampsia was unpredictable and that hypertension could resolve quickly particularly in circumstances where the onset of that condition had been rapid.  He said that as an experienced obstetrician he was familiar with this phenomenon.[82]  The defenders’ obstetrics expert Professor Walker went somewhat further.  He was not satisfied that AW in fact was suffering from pre‑eclampsia on 8 October.  He considered there were a variety of reasons for AW’s hypertension on that afternoon, most probably the underlying placental pathology.  He also noted that AW’s hypertension responded well to the administration of appropriate drug therapy after her admission in the afternoon of 8 October and did not persist at an abnormally high level for a particularly long period after the delivery of the child.  Having regard to these considerations his view coincided with Dr Hanretty that there was no way of determining the blood pressure on 5 October by consideration of blood pressure results on the afternoon of 8 October.

[111]    Having regard to all these considerations the submission of the defenders was that AW had failed to establish that she would have been admitted to hospital on the afternoon of 5 October even if she had been referred thereto by the midwives.

[112]    In my opinion the defenders are correct in their submission that the pursuer requires to prove on the balance of probabilities that she would have been admitted to hospital on 5 October.  In answering the question of whether or not she would have been admitted I have to have regard to the evidence before me in relation to the criteria which would require to be satisfied before she would have been admitted on that date.  In that regard there appears to be no dispute that notwithstanding anything which might have been said by the referring community midwives a further examination and assessment would have been made on arrival at hospital.  The evidence available to me from Drs Macara and McLelland establish that such an initial assessment would have been performed by midwives.  There is no dispute that measurement of fundal height would have revealed no abnormality.  This criteria is not therefore fulfilled.  The questions of whether urine testing and blood pressure recordings would have revealed abnormalities depend, in my view, critically, on the view taken of Professor de Swiet’s evidence.  It is plain from his CV that the professor has enjoyed a distinguished professional career, has practiced extensively in the area of obstetric medicine and has specialist knowledge of the diseases which pregnant woman encounter.  Whilst his hands on experience of obstetrics is, as he readily and properly acknowledged, less than that of the obstetricians who gave evidence I do not consider that factor to be of particular significance.  The problem in relation to Professor de Swiet’s approach is, as I interpret it, that no matter how elegant his reasoning it is entirely theoretical.  There is in fact, as he quite properly and readily acknowledged, no means of actually proving the inferences he makes from the academic papers he relied upon.  This is quite simply because when a patient is admitted with pre‑eclampsia the disease is established.  Plainly recordings of features of the disease, such as proteinuria and high blood pressure, were not made before the patient was examined in connection with her complaints.  This absence of proof and dependence on inferential conjecture might not be problematic but for the powerful clinical and expert evidence that the pre‑eclamptic process is highly unpredictable.  In my view the opinion of Professor de Swiet cannot meet the challenges and observations made by Professors Walker and Murphy based upon their extensive clinical experience and, moreover, similar observations made by the treating clinicians in this case.  These other views appear to me to express a body of professional opinion in relation to the development of pre‑eclampsia which contradict Professor de Swiet’s opinion.

[113]    Having regard to my view on the opinion of Professor de Swiet I reach the conclusion that the pursuer cannot prove that had she been admitted to QMH on 5 October it would have been established that she had high blood pressure or an abnormal urine test.  That being the case the evidence before me was that AW would have been sent home on 5 October.  This gives rise to the next question which I require to answer, would she have been told to return to hospital on 7 October and, if so, what would have been the outcome?

 

(ii)        Admission on Monday 7 October
[114]    It is fair to state that the question of admission on Monday 7 October was not directly addressed in the submissions of either the pursuer or the defenders.  This is not a criticism of these submissions.  Both parties analysed the evidence and framed their submissions in a slightly different way to that which I have adopted in this opinion.  As will have been seen the pursuer’s primary position is that referral to hospital should have occurred on 5 October, that examination following such referral would have detected hypertension and proteinuria which findings would have resulted in management of AW’s case in such a way that an ultrasound would have been performed by at latest 7 October and CTG monitoring would also have been undertaken by that date.  As a consequence of this management the pursuer submits that delivery of the child would have occurred by at latest 7 October.  By contrast the defenders’ primary position is that there was no basis for referral to hospital on 5 October, but even if they are incorrect (as I have determined) in that submission referral to hospital on that date would not have resulted in AW being admitted.  Whilst there is some discussion in the defenders’ submission as to what results might have been detected on appropriate clinical examination on 7 October there is no discussion as to whether midwife assessment on 5 October not followed by admission on that date would have resulted in an instruction to AW to return to hospital for a further assessment on Monday 7 October.

[115]    It is equally fair to say that amongst the many hypothetical questions posed to witnesses the issue of what would have occurred if AW had been referred to hospital sometime on 5 October but not then been admitted was not addressed.  Beyond these considerations I also have to consider that, at least inferentially, a decision not to admit following midwife assessment on 5 October would only have arisen because those carrying out the assessment were not satisfied that the threshold criteria for admission, which have already been discussed, had been met.  The implication of this inference is, of course, that there was at this stage nothing of sufficient severity to cause concerns and merit admission.  Any midwife who carried out the assessment would also have been aware that AW had a routine ante-natal appointment at the hospital three days later on the morning of 8 October.  In these circumstances, and in the absence of any direct evidence to the contrary, it seems reasonable to conclude that it is unlikely that AW would have been instructed to return for further assessment on 7 October.  That conclusion depends of course upon drawing a number of inferences.  Another way of approaching the same issue is that in my view it cannot be said that the pursuer has proved on the balance of probabilities that had she been referred to hospital by the midwives on 5 October but not, following assessment in hospital on that date, been admitted she would have been instructed to return for further assessment on 7 October.  It follows from that conclusion that the second part of the question I have posed, namely the outcome of assessment on 7 October is not a question I require to answer.

[116]    The conclusion from my foregoing analysis of the situation from 5 October is that on the evidence AW has not proved that she would have been admitted to hospital prior to her actual attendance there on 8 October and admission in the early afternoon of that date in the circumstances I have already described. 

[117]    There are a number of implications arising from this finding.  First, AW not being in hospital on 7 October means that the abdominal pains she experienced during the night of 7/8 October, whatever may have been the cause of those pains, have no direct relevance to the issue of liability.  Second, AW would not have experienced any of the clinical interventions desiderated in the pleadings as likely to have occurred had she been in hospital on 7 October.  The result is that the course of what occurred on 8 October requires to be considered from the causation standpoint as that which in fact occurred.  There is, of course, no criticism of the management of the pursuer and the treatment she received following her first contact with a member of the medical clinical staff, Dr Macara, at the hospital on that latter date.  The result is, in my view, that the pursuer cannot prove a causative link between the midwives’ negligence and the injuries sustained by LW.

[118]    The result of these findings is that, strictly, there is no requirement to consider the issue of the causation of LW’s cerebral palsy.  Having regard to the length of this proof and to the importance of these issues I do not however consider that it would be appropriate not to undertake that exercise.  Accordingly I now turn to consider the issue of the causation of LW’s cerebral palsy.

 

LW’s cerebral palsy – causation
[119]    There is no dispute that LW suffers from cerebral palsy.  The exact nature of LW’s cerebral palsy and the extent of his disabilities as a result thereof are the subject of dispute but that issue was not to any material extent the focus of evidence in a proof limited to issues of causation.  There was, further, no dispute that LW had sustained an insult to his brain which was causative of his deficits and which had first been clinically determined by MRI scan performed by Dr Zuberi in September 2002.  The issue was not whether the insult to the brain was causative of LW’s deficits but whether the cause of the brain insult was an event or events for which the defenders were responsible as a result of negligence on the part of their employees, the midwives.

[120]    There was further agreement between the parties that there are numerous possible causes for cerebral palsy including genetic or constitutional problems caused by ante-natal or perinatal insults including chronic, partial and acute hypoxic insults and neo-natal events such as infections, respiratory problems, jaundice or hypoglaecemia.  In addition there are known risk factors pre-disposing towards development of the condition of which the most pertinent appear to be prematurity and abnormally small birth size, both factors relevant in the case of LW.  Having regard to these considerations, it was common ground amongst all the expert clinicians who gave evidence that in clinical practice diagnosis of cerebral palsy is a process of teamwork amongst a range of clinicians expert in a number of fields including obstetrics, neo-natology, genetics, paediatric neurology and paediatric neuroradiology.  Evidence from experts in all these disciplines, with the exception of genetics, was adduced at proof in this case.

[121]    Against that background the pursuer’s position in relation to the issue of causation was that LW’s brain insult had been caused by an hypoxic ischaemic insult which occurred in the period immediately before and after his delivery.  A hypoxic ischaemic insult is caused by lack of oxygen and/or blood capable of damaging the organs of an unborn baby or a new-born.  An acute hypoxic event lasts approximately 30 minutes or less during which there is complete or near complete deprivation of blood or oxygen or both.  This type of event is distinguished from partial reductions in the supply of blood and/or oxygen, described as peripheral perfusion failure or, if existing for a longer period of time, chronic partial asphyxia.  It was submitted that in the present case evidence of an acute hypoxic ischaemic insult was obtained from expert examination of neuro-radiological imaging which showed damage to the deep cerebral white matter of LW’s brain and consideration of these findings by radiologists in conjunction with paediatrician and paediatric neurologists.  The pattern of damage in the present case, where radiological evidence showed damage to an area of the brain known as the putamina, was consistent with and only explicable by an acute hypoxic incident at the said time.

[122]    Whilst it was accepted that diagnosis of cerebral palsy required input, as already discussed, from a number of medical disciplines the pursuer’s submission, adopting a phase used in evidence by Dr Turner, was that neuro-radiological evidence was the “gold standard” when assessing and weighing clinical evidence regarding the causation of cerebral palsy.  As I understood senior counsel for the pursuer’s submission by this he meant that whilst consideration of the views of specialists in other medical fields was relevant to the determination of a diagnosis of cerebral palsy, the input of views from other disciplines was subject to a degree of subjective analysis and interpretation whereas neuro‑radiological evidence in the form of an MRI scan was more objectively based and therefore took precedence over other fields in assessing the likely causes of this condition.  Dr Turner, a witness called by the defenders, who used the phrase “gold standard” to describe MRI scans, indicated that the scans in this case were indicative of an “episode of acute profound brain damage.”  The importance of neuro-radiological imaging evidence, and the interpretation of that evidence by experts in the field was of particular importance in this case in the submission of senior counsel for the pursuer because the defenders did not produce any such evidence or call an expert in neuro-radiology.  This feature in the defenders’ case was described by senior counsel for the pursuer as a “huge flaw” and had the result that “…their other experts take no proper account, in some instances no account at all, of the true significance of the MRI”. 

[123]    The pursuer’s analysis was that LW’s cerebral palsy was caused by an acute hypoxic ischaemic insult which occurred over a period of minutes ending with his resuscitation which occurred approximately 6 minutes after his delivery at about 1652 hours on 8 October 1996.  Senior counsel for the pursuer accepted that the precise length and exact timing of this incident could not easily be established from the evidence.  The CTG was stopped in theatre at 16.39, albeit the clock on the machine appears to have been inaccurate, on the evidence probably running some three or so minutes fast.  The theatre midwife present noted that the last foetal heart rate recording was taken at 16.39.  If those timings are accepted then there was a period of thirteen minutes between the last recording of foetal heart rate and delivery at 16.52.  There was no bradycardia at the time of the last reading of foetal heart rate.  The pursuer’s submission, based primarily on the evidence of Dr Kendall and Dr Connolly, was that at some time in the period between the last recorded foetal heart rate and delivery a bradycardia occurred giving rise to sudden reduction in oxygenation of the foetal brain.  The period of reduction in oxygenation has a known terminus at six minutes post-delivery.  Dr Kendall estimated the period of profound circulatory insufficiency as lasting about 10 minutes and, further considered that it was preceded by a short period of peripheral perfusion failure, with the whole brain damaging event lasting less than thirty minutes.  Dr Connolly was of slightly different view considering that the damaging event lasted about seven to eight minutes but that it was proceeded by a few minutes of resilience, a time when no brain damage occurred because of the baby’s utilisation of reserves of oxygen and nutrients.  There was one further strand to the pursuer’s submissions in relation to the length of the period of profound circulatory insufficiency.  On the basis of analysis of readings taken by Dr Thorburn, the anaesthetist at the delivery it was submitted that the period was at least nine minutes.

[124]    The result of this period of profound circulatory insufficiency was said to be damage to the putamina, the right anterolateral thalamus, the deep cerebral white matter and the white matter in the regions of the pre and post central gyni.  These findings arise from the evidence of the pursuer’s expert paediatric neuro-radiologists Drs Kendall and Connelly whose evidence on these matters was characterised by senior counsel for the pursuer as “essentially unchallenged”.  Both these experts expressed the view that the putamina are areas of high metabolism which are vulnerable to profound circulatory insufficiency from about 30 weeks gestation.  Similarly both doctors reported damage to the white matter in the regions of the pre and post-central gyri.  Dr Kendall explained that the pre and post-central gyri are areas of high metabolism in the brain.  They are amongst the earliest regions of an unborn baby’s brain to be myelinated, that is coated with myelin.  Once the brain is fully mature all of the white matter is myelinated.  The process of myelination requires a lot of energy which is derived from oxygen and glucose.  The brain does not store energy.  This means that the developing brain requires a high blood supply carrying oxygen and glucose to the pre and post-central gyri as they are developing.  The implication of these findings are that the damage seen on the MRI to these regions cannot have occurred before that time.  On the pursuer’s argument this means that the damage could not have occurred earlier than that time.

[125]    The evidence of Dr Kendall and Dr Connolly was that the type of brain damage they described as seeing in the MRI of LW’s brain, that is damage to the putamen, the anterolateral thalamus and the paracental white matter are three components of a triad which form textbook examples of damage caused by an acute hypoxic ischaemic insult.

[126]    Beyond these findings the pursuer further relied upon analysis by Dr Connelly of four ultrasound scans of LW’s brain taken in the first month of his life.  These scans show no evidence of periventricular cysts or intraventricular haemorrhage, both of which are features of a condition known as periventricular leucomalacia.  Periventricular leucomalacia is associated with chronic partial asphyxia and the absence of that condition is supportive of LW’s brain damage being caused by a single acute hypoxic incident.  Moreover the evidence of a single causative event to explain the damage to LW’s brain was submitted to be consistent with the evidence of Drs Ferrie and Pearse who regarded LW’s antenatal history as consistent with such an explanation.

[127]    In response to these submissions the defenders’ position was that it was inappropriate to rely entirely upon interpretation of an MRI scan as an explanation for all LW’s disabilities and, further, that on the basis of all the medical evidence it was implausible that such disabilities could best be explained by a single acute hypoxic ischaemic insult.  The pursuer’s analysis was said to rely too heavily on the analysis of neuro-radiological evidence presented by Doctors Kendall and Connelly.  A number of specific criticisms were levelled against the pursuer’s approach.  These are as follows:

• The pursuer’s approach was said to ignore limits to the use of neuro-radiological evidence as explained by Professors Chiswick and Walker;
• Dr Kendall’s evidence depended critically upon the identification of the acute hypoxic ischaemic incident and its timing.Both these matters depended upon information which could only come from others and, further where the timings relied upon were the subject of challenge;
• Dr Connelly relied upon Dr Kendall’s timings with the result that they were subject to the same criticism, as made immediately above;
• There was some dispute as to the interpretation of the MRI images between Dr Kendall, Dr Connelly and Dr MacLennan, the consultant radiologist in the hospital at the time of LW’s birth;
• There was over-reliance on academic studies which depended upon controlled laboratory studies conducted on non-human primates which were criticised insofar as their ability to give any clear guidance as to how any process of asphyxiation on the brain of a primate foetus would affect the same process on a pre-term growth restricted human foetus;
• The differences of opinion between Drs Kendall and Connelly as to the length of insult that was involved or as to whether it was acute or partial and acute;
• Lack of time available during the period from the end of the CTG trace to the time of return of heart rate to about 100bpm to accommodate the supposed period of birth asphyxia; and
• Possibility, based upon the evidence of Drs Henratty, Pearce and Professor Walker that the period of birth asphyxia was even shorter than that contended for on the basis that in 1996 there was a common practice of checking for heart rate just before caesarean section was performed.

[128]    When these criticisms were considered the defenders submitted that it could not be said that the pursuer had proved on the balance of probabilities that an acute hypoxic ischaemic insult was the cause of LW’s brain damage.  The defenders further maintained that even if there was a single acute hypoxic insult then given that on their argument the pursuer had failed to establish that but for the negligence LW would have been delivered earlier it follows that he would have suffered the consequences of the single insult in any event.  This consideration would also result in the failure of the pursuer’s claim.

[129]    Beyond attacking the pursuer’s reliance on the single insult theory the defenders’ submission, based on the evidence, was that the entirety of LW’s disabilities were likely to have been caused by the failure of his brain to develop properly in-utero as a result of longstanding intra-uterine growth restriction and a consequent longstanding chronic insult to his brain resulting from placental insufficiency.  The pursuer’s submission was that this combination of problems was “likely to include an element of a genetic condition”. 

[130]    The defenders also submitted that beyond intra-uterine growth restriction and placental insufficiency LW’s disabilities were also attributable to his prematurity and what was described as his “stormy neo-natal course” which it was submitted he would have suffered anyway regardless of any negligence.

[131]    Beyond those arguments the defenders yet further submitted that if any aspect of LW’s disability required to be explained by an acute insult to his brain, that acute insult is likely only to have resulted in the damage to his basal ganglia which contributed only “a minute” part of his movement disorder to his overall disability.  It was submitted that any such basal ganglia damage is likely to have occurred anyway.  It is likely to have been caused by the placental abruption or cord compression pre-dating the pursuer’s admission to hospital on 8 October, which would have happened anyway.

[132]    For all these reasons it was submitted that the pursuer had failed to establish the single insult theory of causation upon which her case critically depended.

 

Conclusions
[133]    As I have already made clear I am satisfied that the midwives employed by the defenders and blamed by the pursuer in this action were negligent, in the respects pled by the pursuer, in the management of her labour on 5 October 1996.  In relation to this negligence the most important aspect appears to me to be the failure to refer the pursuer to hospital following assessment by the midwives on the morning of that date.  In relation to what follows that failure I am satisfied as a matter of fact that had the pursuer attended at hospital on 5 October 1996 she would not have met the admission criteria then in operation.  It follows from this that in my view she would have been sent home that day.  I do not consider that the pursuer has proven that she would have been asked or instructed to have attended at the hospital two days later on Monday 7 October.  I am, further, satisfied that she would only have attended hospital when in fact she did on the morning of Tuesday 8 October 1996.  As a consequence of that finding I am of opinion that there is no negligent act for which the defenders are responsible which caused any delay in the delivery of LW.

[134]    On the basis of that finding there is, strictly, no requirement for determination of the issue of causation of LW’s admitted cerebral palsy.  I have however considered that the issue would therefore state the following.  The pursuer’s case is critically dependent on the cause of LW’s disability being a single event, that being an acute ischaemic hypoxic insult commencing at some time immediately prior to delivery and ending on his resuscitation 6 minutes after delivery.  The occurrence of such an event is not in doubt, albeit its timing is.  It appears to me that criticisms of the timing made by the defenders have some force.  I do not consider that it is established on the basis of the evidence exactly how long the event occurred.  So far as the MRI scan and an interpretation thereof is concerned with the exception of the timing of the acute hypoxic event, I am satisfied that I can rely on the evidence of Drs Kendall and Connelly.  Both were highly and relevantly experienced.  Both gave their evidence clearly and precisely.  In my view neither overstated the implications of their evidence, nor importantly did either suggest that their evidence on its own was conclusive of a diagnosis of cerebral palsy caused by any particular factor.  Both Dr Kendall and Dr Connelly were clear that the causation of cerebral palsy depended upon teamwork from a number of medical disciplines.  When that consideration is taken into account I find it difficult to accept the pursuer’s proposition that the single insult theory must be accepted in this case.

[135]    In my view there is a very considerable body of expert opinion, most notably that of Professors Walker and Murphy, that cogently and persuasively suggests the admitted features of severe intra-uterine growth restriction and placental insufficiency cannot be ignored for their potential causative effect so far as LW’s condition is concerned.  It is significant in my view that the treating clinicians in this case all recognised and accepted that these features were likely to have played a part in the development of LW’s deficits.  Whilst I recognise that there are other features in LW’s case, his prematurity and his difficult neo-natal history that cannot be ignored it appears to me that the majority of the medical opinion I heard was to the effect that intra-uterine growth restriction and placental insufficiency were the most significant features in LW’s clinical history.

[136]    Having regard to that consideration the present case appears to me to raise issues similar to that faced by the court in Honisz (supra).  There is a body of clinical opinion presented by the pursuer which supports a single insult theory as establishing causation for LW’s disabilities.  Against that there is another body of expert opinion which does not accept that theory and presents an alternative hypothesis to the effect that as a result of intra-uterine growth restriction and placental insufficiency LW’s deficits were in existence before 8 October 1996 and would have caused his condition regardless of the date of his delivery.  I have no objective reason to reject that second body of evidence.  In these circumstances I cannot be satisfied that the pursuer has established her case.

 

Incidental matters
[137]    I require to deal with a number of incidental issues which arose during the course of proof.  In their submissions the defenders made quite detailed criticisms of all of the pursuer’s experts.  The purpose was, of course, to seek to persuade the court that the pursuer’s experts were less reliable in their evidence than the defenders’ experts and, in the event of conflict of evidence, the views of the latter should be preferred.  In the event the issue of conflict of view between experts has not figured prominently in the formulation of my views expressed in this opinion.  Insofar as determination of the outcome of the litigation is concerned the issue of difference of opinion of expert witnesses is only relevant in respect of midwifery issues, and then only to a minor extent, and in the obstetric evidence of Professor de Swiet, which evidence was rebutted by that of Professors Walker and Murphy.

[138]    So far as the midwifery issue was concerned the finding of negligence turned on matters of fact in respect of which the experts could only offer views in relation to their experience of routine practice.  These considerations were of no material weight in the formulation of my opinion in relation to the grounds of negligence which I have held to be established.  Accordingly I need say nothing further in respect of the midwifery experts.

[139]    In relation to the obstetric issue I have preferred and found in favour of the views expressed by Professors Walker and Murphy.  My reasons are stated in the body of my opinion and again I need say nothing further on that matter.

[140]    It follows that I do not require to address the detailed criticisms made of expert witnesses by the defenders.  I should however state that whilst I accept that some errors could be identified in the evidence of some of the experts I regarded these as understandable having regard to the volume of material the experts required to consider and the complexity of the subject matter.  In my opinion all of the experts who prepared reports and gave evidence did so conscientiously and to the best of their ability.  I found no reason to criticise any expert witness in this case.

[141]    The other incidental matter to be addressed is the question of outstanding objections.  Although a substantial number of objections to lines of evidence were made by both parties during the course of proof these had, following the conclusion of evidence, narrowed to a relatively small number.  I arranged a hearing to deal with these objections by which time only three objections by the pursuer and a similar number by the defenders remained extant.  As it happens none of the areas to which objections to evidence were made featured in my reasons for reaching the opinion that I have.  In these circumstances I do not consider that there is any need, nor would I regard it as productive, to make rulings on any of the outstanding objections.

[142]    In the result I will uphold the defenders’ second and third pleas‑in‑law and pronounce decree of absolvitor.