Case No: 8NE90052
Neutral Citation Number: [2013] EWHC 4023 (QB) 
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION

Royal Courts of Justice
Strand, London, WC2A 2LL

Date: 20/12/2013

Before :

HHJ MCKENNA
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Between :

	MS DAWN CHAPPELL (as personal representative of Callum Lee Chappell)	Claimant	
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	NEWCASTLE UPON TYNE HOSPITALS NHS FOUNDATION TRUST 	Defendant	

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Julian Matthews (instructed by Simpson Millar Solicitors) for the Claimant
Steven Miller QC (instructed by Ward Hadaway Solicitors) for the Defendant

Hearing dates: 25, 26, 27, 28, 29 November and 4 December 2013
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Judgment
HHJ McKenna : 
Introduction
1.	In this action, Callum Lee Chappell (“Callum”), or more accurately his estate, seeks damages for injury and loss said to have been caused by the negligence of the Defendant’s medical and midwifery staff, in the management of Dawn Chappell, the Claimant’s mother’s, labour at the Royal Victoria Hospital, Newcastle upon Tyne (“the RVI”) on 4th /5th March 2000
2.	Callum was delivered at 05.38 on 5th March 2000 by caesarean section carried out under general anaesthetic following a failure to progress in labour. Callum was in a reasonable condition at birth but his condition soon deteriorated and it very quickly became clear that he had extensive brain damage.  In particular, he suffered from cerebral palsy with severe learning difficulties and visual impairment, he was tube fed, had little meaningful motor control and  required 24 hour care, which was provided predominantly by his family up until the date of his death on 29th December 2012.
3.	This claim, which was originally brought within Callum’s lifetime, is continued on behalf of his Estate by his mother, and this court is concerned with the determination of the issues of breach of duty and causation. In particular, two key issues in the case concern (i) the obstetric care provided to Callum’s mother during labour, and (ii) the cause of Callum’s brain injury. These issues are inter-related.
4.	The Claimant’s case is that the management of Callum’s mother’s labour was inadequate and that as a result Callum suffered intra-partum hypoxia during the course of his mother’s labour, which resulted in hypoxic brain damage, which would have been avoided with appropriate obstetric care. In essence, it is said that a Syntocinon infusion caused the mother’s uterus to contract too frequently thus preventing adequate recovery time between contractions and this coupled with allowing labour to go on too long caused Callum to sustain a prolonged period of chronic partial hypoxia which in turn led to acidosis and interference with the peripheral circulation in the brain.
5.	The use of Syntocinon is governed by hospital protocols concerning its use and the rate of administration. The aim is to induce labour whilst avoiding hyperstimulation of the maternal uterus, which, it is agreed by the expert Midwives in their Joint Statement, is an expression used to describe “a pattern of excessive contractions in response to stimulation by Syntocinon or Prostaglandin. In 2000 a reasonable definition of hyperstimulation was more than 5 contractions in a 10 minute period for two or more consecutive periods” [Bundle B pages 231-2], and by the Obstetricians in their Joint Statement to be “tachysystole (that is “a contraction frequency of more than 5 in 10 minutes for a period of over 20 minutes”) with abnormal fetal heart rate patterns”. [Bundle B pages 159-160]
6.	The  Royal College of Obstetricians and Gynaecologists (“RCOG”) Guideline on Induction of Labour 2001 states that in induced labour the aim should be to maintain a contraction rate of 3-4 contractions every 10 minutes, and that “in case of uterine hypercontractility with a suspicious or pathological CTG the oxytocin infusion should be decreased or discontinued.” [Bundle C page 44] Hypercontractility is agreed between the Obstetric experts to occur when “there are more than 5 contractions every 10 minutes” [Bundle B page 152]. However the RCOG Guideline also states that “the frequency of contractions with oxytocin use should not exceed three to four contractions in every ten minute interval.” See section 4.4, page 20 at Bundle C2 page 56. It is common ground that those are guidelines, deviation from which does not of itself constitute evidence of breach of duty.
7.	The Obstetric experts also agree “that it is important when using Syntocinon to allow the uterus to relax between contractions sufficiently to ensure that the placental bed fills with oxygenated blood, to avoid reduction in the oxygen supply to the fetus.” [Bundle B page 152]
8.	The expert Midwives agree that “when administering Syntocinon the aim is to stimulate contractions until a rate of 3-4 every 10 minutes is achieved; that the maximum desirable would be 5:10 and that any increase above 5:10 can cause fetal hypoxia as the placenta may not be able to reoxygenate between contractions” [Bundle B page 224] and that it “is essential to monitor the number of contractions at any given time during the course of labour assisted by Syntocinon in order to be able to titrate the rate of infusion to avoid uterine hyperstimulation”. [Bundle B page 225]
9.	The Defendant’s case is that there was nothing untoward about the obstetric care, and that in any event Callum’s injury was the consequence of infection, passed from his mother during labour which led to neonatal meningitis and is thus unrelated to any obstetric care.
10.	Each party contends that the opposing party’s analysis of events and its thesis as to the cause of Callum’s injury, whilst possible, is implausible. It is fair to say that the case turns primarily upon the expert evidence, and that the issues are complex. Only one set of experts can be right, and there would appear to be no middle ground.
11.	The Claimant also relies on the fact that the paediatric staff at the Hospital responsible for Callum’s care following his delivery, whilst initially considering the possibility of infection, decided after 4 days, on the basis of his presentation over that period, that the cause was not an infection but was intra-partum hypoxia with sufficient certainty to feel confident about discontinuing the intravenous antibiotics that had been started shortly after delivery. Despite that early discontinuance, there was no relapse, which the Claimant’s experts regard as an important indicator in favour of a hypoxic rather than an infective cause of Callum’s brain damage.
The Evidence
12.	The factual evidence consists of statements from Callum’s mother and    grandmother [Bundle A pages 34-41, 42-54] and statements from the clinical staff on duty at the material time consisting of Midwife Deborah Raymond, Rekha Shroff, a Senior House Officer, Gillian Black, a Registrar and Fiona Cullinane, a Senior Registrar, all in the RVI’s Obstetrics and Gynaecology Department.[ Bundle A pages 55-101] It is fair to say that given the passage of time each of the Defendant’s factual witnesses are reliant on the Labour and Delivery Notes [Bundle E page 1] and following and other notes when giving their evidence. 
13.	So far as the factual evidence adduced on behalf of the Claimant is concerned, the short point is that it is accepted that nothing turned on it and to the extent that it conflicts with the Defendant’s contemporaneous records in my judgment the latter are to be preferred and I do not therefore propose to refer to their evidence further in this judgment.
14.	Turning now to the Defendant’s factual witnesses, it is plain from the way in which the case has been argued that the allegations made against Midwife Raymond, such as they were, are not pursued, nor could they be in the light of the agreed midwifery evidence and in those circumstances, little would be gained by lengthy recitation of the evidence of midwife Raymond or indeed that of the midwifery experts, the Claimant’s criticisms being aimed at the actions of Dr Black. 
15.	In these circumstances I propose to limit my reference to the Defendant’s factual evidence to matters relevant to the decisions the subject of criticism and to include such references in the next section of the judgment under the heading “Factual Background”.
16.	That said, I should make the point at this early stage that I found each of the Defendant’s factual witnesses to be impressive each doing their best to assist the court.
17.	The expert reports and joint statements are in Bundle B and are in the disciplines of midwifery and obstetrics in relation to the issue of breach of duty and paediatric neurology, neonatology and neuroradiology as far as causation is concerned as follows:
Claimant	Defendant	
Fact (Bundle A)
Jacqueline Chappell (34 – 41)               Dawn Louise Chappell (42 - 54)
	Fact (Bundle A)
Deborah Raymond (55 – 61)                  Dr Gillian Black (65 - 71)                        Dr Rekha Shroff (72 – 74) and (75 – 90)                                                     Dr Fiona Cullinane (99 – 101)                                  
	
Expert (Bundle B)
Katrina Erskine (obstetrician) (102 - 112) and (113 - 114)

Debra Kroll (midwife) (168  - 198)

Dr Mordekar  (consultant paediatric neurologist) (242 – 258)

Dr Smith (neonatologist) (296 – 315)  and 316

Dr Kendall (neuroradiologist) (397 – 403)
	Expert (Bundle B)
Derek Tufnell (obstetrician) (115 – 138) and (139 – 144)

Susan Brydon (midwife) (199 - 219)

Dr Ferrie  (consultant paediatric neurologist) (259 – 295)
  
Dr Newell (neonatologist) (328 – 367) 

Dr Forbes (neuroradiologist) (404 – 413)
	
18.	There had been meetings between all of the relevant liability and causation experts and the extent of agreement/disagreement was set out in the minutes signed by each expert in Bundle B as follows
•	Obstetric:   13th  October 2013 - Bundle B/5 pages 145 - 158  and Bundle B/6 pages 159 - 167  
•	Midwifery: 31st  October 2013 - Bundle B/9 pages 220 - 227  and Bundle B/10 pages 228 – 241
•	Paediatric neurology: 16th October 2013 - Bundle B/15 pages 368 – 373, B/16 pages 228 – 241 and Bundle B/17 pages 386 – 396
•	Neonatology: 16th October 2013 - Bundle B/15 pages 368 – 373, Bundle B/16 pages 228 – 241 and Bundle B/17 pages 386 – 396 In fact, the paediatric neurologists and the neonatologists all met together and considered three separate agendas.
•	Neuroradiology:  15/10/2013 – Bundle B/20 pages 414 – 418
In addition, during the course of the trial, some further documents were produced by the experts. These consisted of two letters each of which was dated 19 November 2013 from Dr Smith, copies of which appear at Bundle B page 316 and Bundle B page 317 and following, together with responses to those letters from Dr Ferrie by letter dated 25 November 2013, copies of which are at Bundle B page 295A and following and from Dr Newell by way of a Supplementary Note date 25 November 2013 a copy of which is at Bundle B page 367A and following. 
Factual Background
19.	Dawn Chappell was initially referred to the RVI by her General Practitioner on 26th July 1999 at which point she was 16 years old having been born on 9th February 1983. She was given an estimated date of delivery of 18th February 2000, which was subsequently adjusted to 20th February 2000 following ultrasound scanning. She had no significant problems in the antenatal period. There were a number of false alarms in the run up to the admission with attendances at the RVI and which are described by Callum’s mother and grandmother in their witness statements but nothing turns on them.
20.	On 4th March 2000, by which time she was just 17 years old, Ms Chappell was admitted to the RVI for induction of labour at 41+ 6 weeks. She was not at that point in labour. She was booked in at 18.30. The admission note reads:
“Admitted from home for ARM & Syntocinon infusion. See VEopposite. Dawn feels she would like an epidural before commencing Syntocinon. CTG in progress. Obs[ervations] stable as charted. Abdominal palpation: Fundus at term, Lie long[itudinal] Pres[entation] = cephalic, position ROA. 3/5ths palpable(Bundle E page 1)”
21.	The vaginal examination had led to a decision to rupture the membranes and this was done at 18.30. The fluid that was released (liquor) was described as “pinky”.
22.	The health of the fetus was monitored by a cardiotocograph machine (CTG). This has a sensor attached to the maternal abdomen or the fetal scalp which gives a fetal heart rate (FHR) reading, and an abdominal belt (the tocograph) which records maternal contractions. These readings are recorded on a continuous paper trace. The RVI guidelines at the time [Bundle C1 page 48 at page 26m] provided that a normal FHR was in the range 110 to 150 beats per minute (bpm), and that reduced variability of the FHR was between 6-10 bpm; silent being below 5. Reactivity (i.e. accelerations of the FHR) and variability of the FHR are indicators of good fetal health. Reduced reactivity and variability can occur at times of fetal sleep, but if ongoing can indicate poor fetal health.
23.	The RVI’s Guidelines at the time included the following definitions:
“Acceleration Transient rise in heart rate of 15 bpm or more lasting 15 secs or more
Decelerations Transient decrease in heart rate of more than 15 bpm and lasting 15 seconds or more
Early deceleration Onset with contraction and recovery within contraction. Usually benign
Late Deceleration Onset nadir and recovery out of phase compared with contraction. Usually pathological
Variable decels Commonest. Onset with contraction but delayed recovery and vary in shape and timing. May or may not indicate hypoxia and are often associated with cord compression”
24.	The Guidelines also provided the following summary of FHR patterns and their significance:-
Pathological	Tachycardia with reduced variability Prolonged bradycardia >10 min (lethal and needs immediate action)                          Late deceleration pattern                              Severe variables	
Suspicious	Tachycardia +/- reduced variability             bradycardia +/- reduced variability              moderate variable pattern  	
Reassuring	Normal baseline                                            normal variability                                         acceleration pattern	

25.	An anaesthetist attended to insert an epidural at 18.55, but he was called away to deal with an emergency in theatre at 19.00. The midwife noted (Bundle C page 1) at 19.00 that the FHR baseline on the CTG was 115 – 120 (which was thus within the normal range), the variability appeared reduced, but there were some accelerative periods noted. Half an hour later, the midwife noted that the variability had improved. At 20.05 care was taken over by Midwife Raymond.
26.	Midwife Raymond’s notes are full and in the course of her evidence she explained how she would ascertain the contraction rate by palpating the abdomen to ascertain both the strength and the rate rather than simple relying on the CTG which, as she explained, and as I accept, would tend to pick up extraneous features such as maternal movements and breathing and sometimes, as indeed was the case here on occasions, the CTG would not pick up anything at all. The recorded rates in the Notes and the Partogram were very largely obtained in this manner and in my judgment are more likely to be accurate than the CTG trace. 
27.	At 20.30, the epidural was in fact set up and shortly afterwards, Ms Chappell was seen by Dr Black and Dr Cullinane on their evening ward round. Dr Cullinane authorised the  Syntocinon infusion and this was started by Midwife Raymond at 21.00 at 1.2 mls per hour in accordance with the RVI’s Guidelines. Ms Chappell was said to be contracting 3:10 (three contractions in every 10 minutes), they were lasting for 45 seconds and were of moderate strength. [Bundle E page 2]
28.	At 21.30, the Syntocinon rate of infusion was increased to 2.4 mls per hour, again in accordance with the RVI’s guidelines which provided that the rate of infusion could be increased by 1.2ml increments at stated intervals until a satisfactory rate and strength of contraction had been achieved. The baseline FHR increased from 130 to 140bpm (see Joint Statement of Obstetric experts at Bundle B page 221) Ms Chappell was not comfortable and the epidural was topped up at 21.35. At 22.00 it was noted that the FHR was less reactive with reduced variability. At 22.05 the rate of infusion was increased to 3.6 mls per hour again in accordance with RVI Guidelines. The contraction rate was noted  by the midwife to be 4:10 and of moderate strength. (see the Joint Statement of the Obstetric experts at Bundle B page 221 although the tocograph indicated a contraction rate of between 6 and 8 in 10 minutes according to the Claimant’s expert Dr Erskine.) 
29.	At  22 30 a vaginal examination was performed which was  recorded as showing the mother’s cervix to be 9cm dilated ( 10cm being full dilatation) with the fetal head at -1 above the ischial spines of the pelvis and  thought (inaccurately as it turned out) to be in a left occipito transverse position. The FHR was 140-145 bpm and the mother was contracting at 5:10. The Partogram [Bundle E2 page 7] noted contractions between 4 and 5 in 10 minutes with the midwife’s note recording 5:10. [Bundle E page 2]
30.	The Claimant’s Obstetric expert Dr Erskine’s review of the CTG showed, she said, at least 7 contractions in this period whilst the Defendant’s midwife expert Susan Brydon concluded that the peaks in the tocograph could be unreliable and might or might not represent contractions. 
31.	At 22.55, the obstetric senior house officer (SHO) Dr Shroff reviewed the CTG trace at the request of midwife Raymond because she said the mother was contracting at 6:10 and there appeared to be reduced variability. She noted:
“- baseline ↑[increased] from 120 to 130 to 140 bpm
  - Baseline now 135 bpm
  - bt – bt variability 5 – 10 bpm
	   º accelerations”[Bundle E page 2]
The infusion rate of the syntocinon was reduced to 2.4mls per hour.
32.	Dr Shroff said that she would review the trace again in 20 minutes and she in fact saw Ms Chappell again at 23.20 by which stage the trace had improved. In her oral evidence to the court she explained that she could not recall whether she discussed increasing Syntocinon with the midwife but concluded that there was nothing to suggest that she didn’t recommend an increase. She was certainly not concerned enough to have suggested that it not be increased. 
33.	At 23.10, contractions were noted to be 4-5 in 10 and the Syntocinon was increased to 3.6 mls per hour. Dr Erskine’s view was that there had been reduced baseline variability from 22.40 so becoming suspicious (after 40 minutes) whilst Mr Tuffnell considered that the CTG showed a normal baseline, normal baseline variability and the presence of accelerations and so was entirely normal.  
34.	At 23.35 Syntocinon was increased to 4.8 mls per hour, because Midwife Raymond did not believe that the mother was contracting effectively. 
35.	At 23.20 the CTG was noted to be satisfactory by Dr Shroff. 
36.	At 23.28 there was a deceleration of the FHR to 80-85 bpm with a quick recovery (Bundle B pages 147 and 222)
37.	Between 23.00 and midnight the baseline FHR was around 150 bpm and says Dr Erskine there was reduced baseline variability. It rose from 150 to 160 bpm in the period 00.00 to 01.00. There were no accelerations and the baseline variability was more than 5 bpm. The FHR was therefore normal. Contractions were around 6 in 10 though the tocograph is difficult to interpret. Dr Erskine again points to what she perceives to be reduced baseline variability. 
38.	At 00.30 a further vaginal examination was performed to assess cervical dilatation. Midwife Raymond considered that the cervix was fully dilated. The baseline heart rate was noted at 140 – 145 bpm (normal). The contraction rate was 5:10 and the contractions were still of moderate strength . The midwife decided that they should allow an hour for the head to descend before the mother started pushing.
39.	At 01.00 Midwife Raymond asked Midwife Robinson to review and she in turn asked for a doctor to review the CTG trace because of a perceived reduction in variability between 23.40 and 01.00 and an increase in the baseline. Dr Black noted that the fetal heart baseline rate had risen and that the variability had reduced. She also noted that the mother’s temperature had risen to 38º and that the mother was tachycardic; that is to say that her heart rate had risen abnormally and the assumption would be that the fetus also had an infection. Dr Black advised that a fetal blood sample (FBS) should be taken in order she said in her oral evidence to find out what was the cause of the rise in baseline FHR i.e. whether it was the result of fetal compromise or infection. A FBS is obtained by making a small cut in the baby’s head using an instrument inserted in the vagina. The acid (pH level) is measured, since when the body is deprived of oxygenated blood it switches to anaerobic metabolism and the blood becomes more acid. The purpose of the test is to see whether the fetus is becoming starved of oxygen and therefore  becoming acidotic. Dr Black also suggested  that Ms Chappell should be provided with intravenous antibiotics which again she suggested in the course of her evidence were not just for the benefit of the mother but also the fetus. She also advised that if the blood samples were satisfactory the mother should be allowed to push, but that if the samples were abnormal or if the CTG deteriorated there should be an instrumental delivery (forceps or ventouse). 
40.	Dr Black was challenged as to why she did not assess the position of the fetus’s head at the time of the 01.50 vaginal examination. Her response, quite candidly, was that in an ideal world she should have assessed its head position at that time in order to consider further the cause of the lack of progress in labour since 22.30 but she couldn’t now recall what else was happening on the ward but she would have had to prioritise. 
41.	Between 01.30 and 01.40 Dr Schroff the SHO made attempts to obtain a fetal blood sample. This took some time because she had to get the mother into the right position. In fact the blood samples which she obtained, it is common ground, were not accurate. This was recognised at the time and Dr Black repeated the exercise at 01.55. She took three separate blood samples, which on analysis, produced the following results: 7.296, 7.340 and 7.309. [Bundle E/3 pages 13-15]. Again it is common ground that these were normal results and were indicative of a healthy fetus. She also performed a vaginal examination and concluded that the cervix was not in fact fully dilated and that a rim of cervix remained.
42.	At about 02.00 the Syntocinon rate was increased by midwife Raymond to 7.2mls per hour, a decision which the midwifery experts agree was a reasonable decision. The FHR baseline was 150-160 bpm rising to 170 bpm. Again the obstetric experts disagree as to the interpretation of the CTG with Mr Tuffnell identifying an acceleration confirming fetal wellbeing and Dr Erskine identifying reduced baseline variability and what she described as “possible atypical acceleration such that fetal wellbeing cannot be assured”. They also disagree as to beat to beat variability of the FHR between 02.00 and 03.00 with Mr Tuffnell being of the view that it was more than 5 bpm whilst Dr Erskine suggested that it was less than 5 bpm and as to whether a further FBS should have been taken. At 02.45 the CTG was noted to be reactive (i.e. there were accelerations) but there was evidence that the baseline FHR was high. It is the Defendant’s case (which is broadly accepted by the Claimant) that if the mother has a fever the baby’s heart rate would be likely to go up. The contraction rate was 5–6:10.
43.	At 03.00 a vaginal examination undertaken by Dr Black showed that the cervix was now fully dilated and that the baby was in an OP (occipio-posterior) position that is to say with the back of its head facing towards the mother’s spine which was confirmed by an ultrasound scan. If this position persists, it may lead to a prolonged labour and ultimately the need for some sort of intervention. The mother’s temperature was 38.8 with caput++  and moulding++. 
44.	Dr Black concluded that the mother should commence pushing, her reasoning being that there had been a good FBS at 01.00 hours and the CTG was reassuring. There were accelerations and variability had improved. She was challenged as to why a further FBS was not taken given that this was no longer a straightforward case in the light of the delay since 22.30 to which she replied that it was common for babies presenting in the way that Callum did to take a long time. In her judgment there was no need either to call for more senior help because she felt she had the necessary level of expertise nor to undertake a further FBS in the light of the information she had and the need to balance the risk of infection if the FBS were to be repeated.  
45.	It is the Claimant’s case that as at 03.28 the CTG showed late deceleration of the FHR and reduced baseline variability such that the CTG was pathological, there having been reduced baseline variability for more than 90 minutes. [Bundle B page 155] Again the Defendant’s obstetric expert disagrees. In his view the baseline variability was normal and there had been no significant period of abnormal baseline variability [Bundle B page 155]. Moreover some decelerations were to be expected with pushing.
46.	At 03.10 the contraction rate was 5-6:10 and the fetal heart rate baseline was 165 bpm.
47.	At 03.22 the mother commenced pushing. There followed on the CTG what appeared to be a series of decelerations which the midwifery experts and Mr Tuffnell agreed was the likely explanation. Dr Erskine, on the other hand suggested that they could be indicative of hypoxia. The CTG shows that at around 03.30 for a short period the mother’s uterus was contracting at around 6:10 (six contractions in every 10 minutes). This, it is common ground, should have led to a reduction in the Syntocinon infusion but again it is common ground this made no difference to the outcome although the Claimant relies on it as indicative of the need for more senior input. It was also noted that the mother’s contractions were 5:10 moderate.
48.	At 03.45 the mother was being encouraged to push more effectively. At 03.50 there was a deceleration of the FHR to 90 – 100bpm with contractions and a quick recovery. Advice was sought from Dr Black (obstetric registrar) who sanctioned an increase in the rate of Syntocinon infusion to 9.6mls per hour, because it was felt that the mother’s contractions were not very effective. In her evidence to the court she accepted that this was probably not a correct decision, but there is no evidence to suggest that it made the slightest difference to the outcome.
49.	At 04.05 the  contractions were noted at 5-6:10. The state of the labour was again reviewed by Dr Black.  She carried out another vaginal examination. The position was confirmed as OP and deflexed meaning that the chances were that the delivery would be prolonged and that there was caput ++ and moulding. +++ The CTG, however, was reassuring, apart from the tachycardia (fast heart rate) which Dr Black considered was explicable by the mother’s fever. She concluded, however, that spontaneous delivery was unlikely, because of the position of the head and the ineffectual pushing to date and asked for the Senior Registrar, Dr Cullinane to review the position.
50.	Dr Cullinane did so at about 04.40. Her detailed note was as follows:-
“Asked to review
I[nduction] O[f] L[abour] (42/40) ARM 18.30 on 4.3.00 
Fully dilated x 90mins
CTG – baseline 165 b/min, good variability, no decelerations, accelerations present
Clear liquor
Abdo 1/5th palpable
VE see over

Plan    * Transfer to theatre
*  Anaesthetist informed 
* Prof Davison informed 
* Blood cultures, ºHVS” [Bundle E page 5]
51.	At 04.45, the Syntocinon was discontinued and at 04.55, Ms Chappell was transferred to the operating theatre. There, at 05.00, Dr Cullinane decided that delivery should be by caesarean section. The CTG showed FHR of 160 bpm with good variability, accelerations and no deceleration. Initially it was thought that  delivery could be carried out under spinal anaesthesia, but when this proved difficult, the operation was carried out under general anaesthetic. 
52.	The baby was born at 05.38. It is common ground that the delay of 58 minutes between the decision to perform the caesarean section and actual delivery is acceptable in all the circumstances of this case. Callum was given Apgar scores ( a measure of fetal well being out of 10) of 3 at 1 minute and 6 at 5 minutes. His first gasp was at two minutes and he had regular respiration at eleven minutes of age.  His cord blood samples (taken at birth from umbilical vessels) yielded pH values of 7.29 (arterial) and 7.297 (venous). It is likely that both samples were, in fact, venous, but in any event, the results were normal and indicative that Callum was not acidotic at that point.
53.	The Claimant’s mother  had a persistent fever after her son was born and Chlamydia was subsequently grown from a high vaginal swab.
54.	Callum’s condition declined after birth. He suffered from frequent episodes of apnoea associated with a blank stare and twitching of both legs, which were thought to be fits. These commenced within 4 ½ hours of his birth. He was treated with Penicillin and Gentamycin. Full details of the neonatal care are set out in the report of Dr Smith at [Bundle B page 301] onwards, and Dr Ferrie at [Bundle B page 268] onwards.
55.	As I have already indicated, it is the Defendant’s case that this decline was caused by an infection which he acquired from his mother which led to meningitis. It was not a fulminant infection, because it was partially treated by the antibiotic treatment which the mother had received during and after her labour.
56.	CSF was taken by lumbar puncture at about 10 hours of age. Cranial ultrasound scans on the 5th and 6th March 2000 were reported as normal. A further scan on 7th March 2000 was reported as being markedly abnormal with diffuse echogenicity and focal hyperlucency in the left subcortical region and abnormally small ventricles.
57.	Callum continued to suffer from fits and an EEG was markedly abnormal. He was commenced on Phenytoin therapy. A metabolic screen was normal.
58.	On 20th March 2000 a further cranial ultrasound showed diffusely increased echogenicity throughout the cerebral hemospheres. The ultrasonographer reported subdural fluid on the left side.
59.	By July 2000 the head circumference (38cm) indicated a failure of normal head growth with acquired microcephaly. There was a developmental delay, spastic quadriparesis and usual impairment. 
60.	A cranial MRI scan was performed on 22nd March 2001 and showed a normal brain stem and cerebellum but very severe changes of a generalised cerebral multi-cystic encephalomalacia gliosis and atrophy involving the frontal and parietal regions in particular.
The Law
61.	There is no issue between the parties as to the relevant legal principles to be applied in this case. In order to establish vicarious liability in negligence on the part of the Defendant, the Claimant must prove that the Defendant’s obstetric medical and/or midwifery staff did some act (or failed to act) in a way in which no reasonably competent obstetrician or midwife would have acted or failed to act.
62.	The Claimant must then show that any negligence proved, caused or made a material contribution to Callum’s injury and damage; in the context of this case the Claimant has to prove that but for the negligence of the midwives and/or obstetricians (if proved), Callum would have been born unharmed.
63.	The standard by which the individual doctor or midwife is to be judged is the standard of a reasonably competent doctor or midwife carrying out the functions expected of him/her in the delivery suite of a hospital providing maternity services. (See: Bolitho v City & Hackney Health Authority [1998] AC 232).  
Breach of duty
64.	It’s the Claimant’s case that from 01.00 there was a clearly documented maternal infection with maternal tachycardia and pyrexia which, it is common ground, can have a potential effect on the fetus as it reduces the capacity of the fetus to withstand hypoxic stresses and increases its susceptibility to injury from peripheral profusion failure in the brain as it increases the metabolic rate and lowers the threshold for ischaemic damage. [Bundle B page 418]. That pyrexia was still present at 03.00.
65.	In addition there had been poor progress in labour since 22.30 when the Claimant’s mother was 9cm dilated and there was still a possible small rim of cervix remaining as at 03.00 some 4 1/2hours later by which time the position of the fetus was noted to be OP, that position being confirmed on a scan, and which is the least favourable position for a vaginal delivery. There had been no descent of the head and there was caput++ and moulding++.
66.	Moreover by 03.00 during the use and increase in the infusion rate of Syntocinon, it is said, in reliance on the expert evidence of Dr Erskine,  that the baseline of the FHR had increased from 110-120 bpm to 160-165 bpm with prolonged periods exceeding 160 bpm, in conjunction with reduced baseline variability of the FHR and no clear accelerations and there had been evidence of hypercontractility during the early part of the induced labour which meant that the CTG was suspicious as defined by the guidelines to which I have already referred. There were also occasional decelerations in the FHR particularly after pushing commenced at 03.20 which was a non-reassuring factor which in combination with the above normal baseline heart rate rendered the CTG pathological and which were not negated by the presence of accelerations the existence or significance of which were, in any event disputed.  
67.	In the circumstances what is said on behalf of the Claimant is that senior input should have been sought immediately since although Dr Black had some experience as a registrar over two years in locum training posts, she was only six months into her first substantive registrar post and her level of experience and knowledge was accordingly limited. In this regard the Claimant also points to the admissions made by the Defendant that it was negligent both not to reduce the level of Syntocinon at 03.30 and actually to increase it at 03.55 as well as the failure to assess the station of the fetal head. 
68.	By 03.00, the continued and progressive use of Syntocinon was significantly outside the guidelines for its use and therefore to continue with it required very careful consideration of the various complex risk factors which it is said Dr Black failed to do. 
69.	Labour could only reasonably have been permitted to continue if reassurance could be obtained that the fetus was in good condition by a repeat FBS. In the absence of a reassuring FBS then the only appropriate course was to stop the Syntocinon immediately and to proceed to delivery by caesarean section in which case, relying on the evidence of Dr Erskine, the Claimant says that delivery would be likely to be by 03.40. In particular it was not appropriate and likely to be damaging to the fetus to continue and or to increase the infusion rate of Syntocinon in these circumstances and that accordingly Callum’s mother and Callum were not provided with an appropriate standard of obstetric and midwifery care applying the principles established in Bolam and in Bolitho to which I have referred above. 
70.	In support of the argument that the appropriate standard of obstetric and midwifery care was not provided, the Claimant relies heavily on the opinion of Dr Erskine whose first report dated 14 October 2010 is at Bundle B pages 102 and following and includes the following material passages: 
“4.3 at 01.00, the doctor was asked to review because of anxieties about the CTG; furthermore, Ms Chappell had developed pyrexia. It was appropriate to perform a FBS and administer antibiotics. At this time, the doctor noted that the cervix was still not fully dilated – she had therefore been approximately 9cm dilated from 22.30 until this time – 01.50…
4.4 when the junior registrar reviewed her at 03.00, the cervix was still not definitely fully dilated – after 4 ½ hours at 9cm – and the doctor scanned Ms Chappell and realised that the baby was OP – a much more difficult position to push the baby out. Ms Chappell had a persistent significant pyrexia. At this time the junior registrar, who clearly was not able to take an independent decision to perform a caesarean section, should have immediately summoned a senior registrar. Either a further FBS should have been carried out, or, more likely, a decision to perform an immediate caesarean. If the senior registrar had arrived within 10 minutes, i.e. by 03.10, a decision could have been taken to either proceed to caesarean at 03.20 (allowing 10 minutes for the senior registrar to assess the situation), and the Syntocinon would then have been stopped. This would have allowed delivery of the baby by 03.50. If the decision had been made to do an FBS, and it had been reassuring, the senior registrar may have allowed labour to continue a short while longer, but should have reduced the Syntocinon.”
71.	 She continued:-
“5.3 it was substandard not to either decide to deliver, or repeat the FBS at 03.00, one hour after the first attempt, in the light of continuing anxiety about the fetal heart and the possible abnormal results earlier.
5.4 It was substandard for the registrar to recommend increasing the Syntocinon without personally reviewing the patient when there had been anxieties about the fetal heart.”
72.	Under the heading “Conclusions” she continued:-
“6.1 The care given to Ms Chappell antenatally was standard. The care given to Ms Chappell during her induction process until 01.00 was satisfactory. However at 01.00 there were clear anxieties about this labour. There was a delay in obtaining FBS results and there are two results which are clearly abnormal which are not commented on satisfactorily. Even if these were erroneous, in view of the continued fetal heart rate abnormalities, a further FBS should have been carried out by 03.00 if there had not been a decision to deliver Ms Chappell.
6.2 The senior registrar should have been summoned by 03.10. At that time, there was clear evidence of pyrexia, fetal heart rate abnormalities, and very slow progress despite very frequent contractions. At that time, the senior registrar should have either opted for immediate caesarean, and stopped the Syntocinon, or very carefully supervised the labour for a short time more with a reduction in the Syntocinon.” 
73.	In her Supplementary Report dated 21 June 2012 [Bundle B pages 113 – 114] Dr Erskine addressed the issue of excessive contraction frequency which did not feature in her first report as follows:-
“1…By 22.20 on 4.3.2000, Ms Chappell was clearly contracting 8 times in 10 minutes – i.e. there was hypercontractility. This pattern continues, although the tocographic pick up of the uterine activity was occasionally poor. The fetal blood sample (FBS) indicates that the baby was not hypoxic at approximately 01.50. After the FBS, there was continuing hypercontractility with reduced baseline variability (less than 5) and a fetal tachycardia – i.e. hyperstimulation was occurring. From 02.40 the tocographic pick up was poor until 03.30 when there was clearly hypercontractility, again with an abnormal fetal heart rate pattern. At 03.30 there were recurrent decelerations with reduced baseline variability and a wandering baseline. At 04.00 there are approximately 8 contractions every 10 minutes with a persistent abnormal fetal heart rate. At approximately 04.45 the Syntocinon was stopped prior to transfer to theatre; the recording restarted in theatre at 04.59, when the contractions appeared to be considerably reduced prior to the caesarean. There is clear evidence of hyperstimulation from 01.50, which continues until the Syntocinon is stopped prior to transfer to theatre. In theatre the CTG is reassuring with a baseline of approximately 160 with fetal heart accelerations.
2 In my opinion there is clear evidence of hyperstimulation – hypercontractility associated with fetal heart abnormalities – from 01.50 until the Syntocinon is stopped. When the Syntocinon stops, the fetal heart rate improves. 
3 It is well recognised in the presence of maternal pyrexia, babies are less able to cope with hypoxic insults.
4 It is well recognised that if a baby is receiving a hypoxic insult due to hyperstimulation, stopping/reducing Syntocinon, or giving a tocolytic may alleviate the hypoxic insult (RCOG Guidelines on the Induction of Labour 2001.) Thus stopping the Syntocinon prior to transfer to theatre may well have resulted in the hypoxic insult being reduced/abolished in this case, allowing a degree of recovery. The CTG tracing in theatre shows an improvement, with heart rate accelerations.”
74.	In her oral evidence to the court, Dr Erskine maintained her views and indicated that in her view for a lot of the relevant period baseline variability was low; that’s to say less than 5 bpm. She summarised the position in this way. By 01.50, the Defendant was faced with a very high risk scenario. There were a number of risk factors; the mother was seventeen; she was 42 weeks pregnant; she was being induced; had a pyrexia; she had dilated to 9cm two hours previously with no further progress suggestive of a potentially obstructive labour. Moreover it was plain that there was fetal tachycardia with reduced baseline variability and in those circumstances the risk of hypoxia couldn’t be ignored. Such accelerations as there were were non-reassuring or atypical. These were expressions which she had used in the Joint meeting with Mr Tuffnell. In the circumstances therefore at 03.00 the mother should have been re-examined and an FBS undertaken because of what she regarded as non-reassuring CTG particularly in the light of the mother’s sepsis. The decision not to undertake a second FBS on the evidence available was, she said, a decision which no competent doctor would have made. Furthermore a more senior doctor should have been involved.
75.	The Defendant for its part suggests that there was never any fetal heart abnormality demonstrated on the CTG suggestive of hypoxia. There were periods of reduced variability but these were noted before Syntocinon was started and the normal results of the FBS taken made it clear that the fetus was not at that time (01.55) hypoxic. The rising fetal heart baseline rate (tachycardia) was explicable by the fact that the mother was noted to have a fever and neither the reduced variability or the rising fetal heart baseline rate were or should have been considered to be suggestive of hypoxia particularly as recurrent decelerations, a characteristic feature of hypoxia were absent from the CTG. In the circumstances there was no clinical reason for taking another FBS or deciding to intervene to deliver the baby at any earlier time.
76.	The Defendant relies on the opinion of Mr Tuffnell who sets out his views in his first report dated July 2011 Bundle B page 115 and following as follows at Bundle B page 127.
“35. At the examination at 03.00 hours the reason for the delay was diagnosed. This was because the baby was occipito-posterior and this was actually confirmed on an ultrasound on the labour ward. The head was also deflexed which makes the presenting part of the baby seem much larger to the pelvis. A decision was made to see if the head would rotate with pushing and if not consider caesarean section. I believe this was a reasonable decision. This was a young woman and in general one tries to achieve a vaginal delivery given the importance of caesarean section in future reproductive performance. Under these circumstances I believe that most doctors would have attempted to achieve a vaginal delivery. It is also important to realise that the mother showed signs of infection and that caesarean delivery has an increased risk in women with signs of infection in labour. The CTG showed a baseline heart rate above the normal range but this was accounted for by the maternal tachycardia and pyrexia. The actual baseline variability was normal and accelerations were present. There was therefore no reason to consider that there would be immediate concern about fetal wellbeing. It was entirely reasonable to try and encourage delivery of the baby.
36. The one slight area of concern is the contraction frequency at the time. The midwives are recording the contractions were 5 to 6 in each 10 minutes and the Syntocinon was increased. This does not represent good practice. There must have been concern that this could have caused hyperstimulation which could have caused problems from the fetal point of view. I believe it would have been more appropriate for the Syntocinon to have been left at the same level. However, as I will detail below I do not believe that the baby did develop hypoxic problems in labour relating to an increased dose of Syntocinon so I think it is extremely unlikely that this action is related to the outcome for the baby. 
37. At around 04.00 hours it was clear the head was not descending and the case was reviewed by the registrar and senior registrar and a decision was made to take the mother to theatre. There were some delays in performing the caesarean section, predominantly because the anaesthetist had difficulty with inserting the spinal. However, at that point there was no immediate concern about fetal wellbeing and it is far more important to perform a safe caesarean section that to rush a caesarean section and cause problems for the mother as well as the baby. I therefore do not think that the time delays are unreasonable in this case. The CTG was continued and although it continued to show a baseline tachycardia the variability was normal and accelerations which are taken to be the hallmark of fetal health, were present. I do not believe that there was any unreasonable delay in the delivery taking into account all the factors that were present.
38. Once the baby was born the baby was initially a little slow to respond to resuscitation but the clear gases were entirely normal. It has to be acknowledged that the only principle by which fetal monitoring in labour can work is by consideration of the development of acidosis. The reason to perform electronic fetal monitoring is to determine abnormalities which might be indicative of acidosis in the baby. In this case there were no changes in the CTG that made that seem likely. There was a rising baseline heart rate but this was explained by the maternal temperature. A fetal blood sample in labour was normal. The fact that the fetal blood samples and the cord samples were also normal is entirely in keeping with the fact that the baby was not acidotic in labour. It is therefore from an obstetric point of view extremely difficult to suggest that the outcome of this pregnancy, in terms of the developmental problems from which the baby has suffered, are related to hypoxia in labour.”
77.	As for Dr Erskine’s suggestion in her Supplemental Report that there was hypercontractility, Mr Tuffnell in his Supplemental Report dated 4 November 2012 (Bundle B page 139) points out both that the assertion was lacking in Dr Erskine’s main report and that he fundamentally disagrees with her interpretation of the CTG. In his oral evidence, Mr Tuffnell made the point that he had been unable to find any reference in the medical literature to the expression “atypical acceleration” used by Dr Erskine. The phrase was not one with which he was familiar.
78.	In his view the most relevant period was 03.00 onwards and throughout that period there were clearly accelerations present right up until the birth of Callum from which the Defendant’s clinical team were entitled to take reassurance since in his view the likelihood of a baby having a problem if there were accelerations was extraordinarily low. In cases of chronic partial hypoxia, in his experience, there would often but not always be tachycardia and reduced baseline variability and in the vast majority of cases there would be significant and worsening decelerations although occasionally such decelerations might be very shallow but it was completely outside his knowledge to have ongoing hypoxia caused by hyperstimulation as suggested by Dr Erskine without a significant pattern of decelerations in the fetal heart rate which would have shown up on the CTG and which were entirely lacking in this case.
79.	So far as the CTG was concerned, in his view it showed that baseline variability was maintained at more than 10 bpm and there was evidence of a number of accelerations and an isolated (and therefore unconcerning) deceleration with no non-reassuring features other than what he regarded as borderline tachycardia. In the circumstances his view was that he personally would not have considered it necessary or even appropriate to undertake a further FBS at 03.00. Moreover it would be very unusual not to give the mother an opportunity to push the baby out in these circumstances and he also disagreed with the assertion that Dr Black should have sought the opinion of a more senior doctor at that time.
80.	He went on to emphasise that the FBS taken at 01.50 was reassuring. It would be remarkable for the fetus to have been severely acidotic so as to cause the severe brain injury actually sustained and yet to have recovered by the time of delivery and all the more so in a case where the mother had pyrexia. 
Discussion
81.	What then am I to make of the competing expert evidence on obstetrics? At the heart of the Defendant’s case is the assertion that accelerations of the fetal heart rate could be found on the CTG throughout labour and right up until delivery and that this negatived the presence of fetal hypoxia. This is what the midwives and doctors thought at the time, as is clear from their notes, which refer throughout to the presence of accelerations. This was not contradicted by Dr Erskine in either of her two reports but for the first time in the Joint meeting with Mr Tuffnell she introduced the concept of “non-reassuring” and/or “atypical” accelerations. When challenged at the meeting to disclose the origins of these terms she was unable or unwilling so to do. That remained the position at trial although she did make reference to the National Clinical Infant Human Development Forum in America as having dictated the guideline and to the RCOG of Australia and New Zealand but did not produce any literature. 
82.	The concepts of “non-reassuring” and/or “atypical” accelerations were questioned by Mr Tuffnell who was in fact one of the authors of the 2007 NICE Guidelines and of a further undated version which is to be published in 2014. As leading counsel for the Defendant submitted, it would be surprising, if such guidelines or a different definition of an acceleration existed elsewhere in the world that Mr Tuffnell was unaware of it. To my mind Dr Erskine’s evidence on this aspect of the case is to be treated with considerable caution and that caution should, in my judgment, be extended to her evidence more generally insofar as it conflicts with that of Mr Tuffnell for a number of reasons. First, she expressed the view that she would not necessarily expect to see fetal heart decelerations on the CTG trace if the fetus was being subjected to an episode of prolonged partial hypoxia as opposed to an acute near total event. This was surprising given that all of the obstetricians as well as Mrs Brydon and Dr Newell disagreed with her and it is notable that Dr Smith, who like Dr Newell would as a neonatologist be used to seeing and evaluating CTG traces after birth in the event of a problem, did not suggest that he would not have expected decelerations if the fetus was suffering from sustained periods of hypoxia. Second, Dr Erskine was the only witness not prepared to attribute the short period of decelerations that plainly does appear on the trace between 03.20 and 03.40 to maternal pushing. Overall therefore I find myself forced to conclude that Dr Erskine was an unimpressive and unreliable witness who seemed more determined to argue the Claimant’s case than to give objective assistance to the court and when important features of the records of labour on which the other experts had relied were pointed out to her she sought to explain away their significance rather than accept their significance. 
83.	Mr Tuffnell, by contrast, on any view, was an impressive witness on whose opinion I felt the court could place considerable weight. First of all he was uniquely placed to assist the court on the interpretation of the CTG having been a member of the committee which put together the 2007 version of the NICE Guidelines and which is in the process of producing a further update to which I have already referred. His explanation that practitioners had complained that the 2001 Guidelines had not placed sufficient emphasis on the fact that accelerations were a positive feature and that as a consequence, the 2007 Guidelines had stressed that even where there was reduced variability, the presence of accelerations should be taken as a reassuring feature was, as it seems to me telling.
84.	In addition, he seemed genuinely perturbed at the suggestion that what he considered to be accelerations were not in fact accelerations properly so called. He seemed equally perplexed at the suggestion that if the fetus was being subjected to a period of prolonged partial hypoxia, you would not expect to have decelerations of the fetal heart developing on the CTG trace. They represent the same fetal response to the need to resort to anaerobic metabolism that would occur, albeit more abruptly, in the face of an acute event. 
85.	Overall, Mr Tuffnell’s views were to my mind authoritative and I have no hesitation in preferring his evidence to that of Dr Erskine and accepting as I do the thrust of that evidence I conclude as follows:
i)	The period of heart rate monitoring between 23.40 and 01.00 shows reduced variability but still within the normal range of between 5 and 10bpm. Apart from that period the variability was normal.
ii)	Callum’s mother developed a high temperature (pyrexia) during labour (such that by 22.15 on 4 March it was recorded at 37 degrees and by 01.00 on 5 March it had risen to 38 degrees).
iii)	At the same time the fetal heart rate baseline rose from its starting point of 120bpm so that by 01.00 on 5 March it was 160bpm [Bundle E page 7]
iv)	The appropriate responses to these three features were for the midwife to ask for a review by a doctor and the doctor, in turn, to take a FBS to see whether there was any evidence that the fetus was becoming hypoxic. The normal results from the three fetal blood samples taken by Dr Black at 01.55 would, and in my judgment, should have reassured the doctors that the maternal pyrexia and fetal tachycardia were probably linked and that, whatever the CTG showed, the baby was not becoming hypoxic.
v)	The Defendant’s clinical team would and in my judgment should have been reassured by the continued appearance of accelerations. The 2001 NICE Guidelines make it clear that a moderate tachycardia i.e. 161-180bpm is not associated with hypoxia in the presence of accelerations with normal baseline variability [Bundle C/1 page 24] and that was the position here. Dr Erskine’s thesis that the increases in FHR shown at this time were not typical of the type which are reassuring, even if accurate, which I do not accept in the light of Mr Tuffnell’s evidence, does not assist since Dr Erskine was forced to concede that Dr Black could not have been expected to recognise the difference by the standards applicable in 2000 in any event. 
vi)	After 01.55 although the tocograph may have appeared to show contraction rates higher than 5-6:10 this is, on the balance of probabilities, incorrect having regard to midwife Raymond’s evidence and indeed that of Mrs Brydon. As leading counsel for the Defendant submitted, this proposition could be tested by looking at the trace in two places: the first at the 10 minute period between 03.28 and 03.38 where Dr Erskine said that if these decelerations were each with contractions, the rate was 8:10 where it was only 5:10. Secondly at the 20 minute period between 03.58 and 04.18 when the mother was pushing the true contraction rate looks like 5 or a maximum of 6:10. It was Mr Tuffnell’s evidence, which I accept, that you would not be concerned at a 5-6:10 contraction rate at that stage of labour even if it was slightly higher than you would be aiming for since the midwife would quite properly be striving to get effective strong contractions.
vii)	The management after the FBS had been obtained was standard. It was correct to increase the Syntocinon infusion rate. Pushing could not start because Dr Black had determined on vaginal examination that the cervix was not quite fully dilated. There would have been no reason or justification for taking another FBS at 03.00. The only non-reassuring feature was the fetal tachycardia and this had not increased and was legitimately considered to be due to maternal pyrexia. The Guidelines state that moderate tachycardia is not associated with hypoxia in the presence of accelerations, normal baseline variability and no deceleration, which was the position in this case. In the circumstances therefore caesarean section of a 17 year old having her first baby was not appropriate at that stage.
86.	In all the circumstances in the light of the results of the ultrasound, Dr Black had a credible explanation for the delay in dilatation and descent of the head and this coupled with the fact that there was no indication from the CTG that the fetus was in danger and the continued appearance of accelerations leads me to conclude that the management of the labour and delivery, supported as it is by Mr Tuffnell and indeed Mrs Brydon throughout, were of an appropriate standard applying the principles established in the cases of Bolam and Bolitho. It follows that I reject the criticism levelled at Dr Black who on the totality of the evidence available to her was in my judgment entitled to proceed in the way she did without recourse to advice from a more senior doctor.
87.	In the light of my findings on breach of duty, there is strictly speaking no need for me to proceed to deal with the competing theories put forward on behalf of the Claimant and Defendant as to causation but since both parties led significant amounts of expert evidence on the causation issues which were fully argued I turn now to deal with those issues albeit relatively shortly. 
Causation
88.	The Claimant’s case on causation is that Callum’s brain injury was caused by hypoxic ischaemia resulting indirectly from hyperstimulation of the uterus by the infusion of Syntocinon because it is said that the frequency of the rate of contractions was such as to prevent the foetus from recovering between contractions.
89.	In support of this theory the Claimant relies on the fact that it is common ground among the neuroradiologists that Callum’s brain injury showed multi-cystic leuko-encephalomalacia (MCLE) caused close to the time of birth [Bundle B page 417] and that the MRI scan taken on 27th March 2011 showed diffuse generalised involvement similar to that seen following prolonged asphyxia from whatever cause and that the distribution of the damage was suggestive of peripheral perfusion failure [Bundle B page 417] and that the scan did not show changes consistent with an uncomplicated infective neo-natal meningitis.
90.	The Claimant also points to the fact that no infective agent was ever cultured and that intravenous antibiotics were stopped after four days post the birth as the treating clinicians had come to the conclusion that the cause of  Callum’s injuries was hypoxia and not infection and yet there was no relapse, both of which factors, the Claimant’s causation experts believe, make the possibility of meningitis as the cause much less likely [Bundle B page 394].   
91.	In further support of the Claimant’s theory what is said is that there was an improvement in the fetal heart rate pattern after the Syntocinon was turned off at 04.45 since the CTG became more reassuring.  Here the Claimant relies on the evidence to that effect of Dr Erskine (contradicted by Mr Tuffnell whose evidence I have already indicated I prefer) and argues in the light of that evidence that it is therefore perfectly possible that Callum could have been exposed to a chronic hypoxic insult due to excessive stimulation of labour by the infusion of Syntocinon in the presence of maternal pyrexia which would increase the fetus’s susceptibility to hypoxia and which would have rendered him acidotic but that his gas readings recovered to more normal levels when the Syntocinon was discontinued in the light of the neurological and neo-natal experts agreeing that “it is possible for the acidosis that is likely to have been present at the end of any hypoxic ischaemic insult to have resolved in the fifty three minutes after the Syntocinon was discontinued”  [Bundle B page 377].  What is said is that the cessation of Syntocinon would have removed the continuing cause of the fetal distress and hypoxia and led to recovery just as it is said actually occurred following actual cessation at 04.45.  Given the normal blood gasses result at 01.55 and that permanent injury would not occur until about an hour after the onset of hypoxia, cessation of infusion of Syntocinon at 03.00 is likely to have avoided all injury.
92.	The Defendant by contrast asserts, and, this is not disputed, that the normal FBS at 01.55 precludes the possibility of any hypoxic ischaemic damage up to that point and relying on the evidence of Mr Tuffnell and his interpretation of the CTG, the Defendant asserts that there is no evidence from the CTG after 01.55 that Callum was becoming hypoxic in the absence of persistent decelerations of the fetal heart and moreover the normal blood gasses at birth preclude any damaging hypoxic ischaemia in the period leading up to delivery.
93.	As for the Claimant’s argument as to intra uterine recovery after the turning off of Syntocinon at 04.45, what is said by the Defendant is that it is inconceivable that the evidence of hypoxia severe enough to cause MCLE (as a consequence of which Callum would have been profoundly acidotic) would have completely disappeared to allow the pH to be normal in such a short period of time.
94.	The damage is much more likely to have been caused by infection which led to meningitis.  In this regard there is no doubt that the mother had an infection and it is well recognised that infections can pass from mother to fetus during labour and indeed afterward. The fact that no infecting organism was identified after delivery is accounted for by the fact that the mother was treated with antibiotics during labour and this would have treated the infection and masked its presence.  
95.	The Defendant also relies upon the results of the cranial ultrasound scan undertaken on day thirteen which showed extra axial collections which it is said points towards infection rather than hypoxia as the cause of the brain damage.  
96.	Dr Smith, a consultant paediatrician instructed on behalf of the Claimant, in his oral evidence expressed the view that whilst he accepted that there was no biochemistry which supported a diagnosis of hypoxia, in his view the neo-natal illness and complicated outcome were consistent with hypoxic ischaemic damage. Moreover in his view the threshold for injury would have been lower in Callum’s case because of the maternal pyrexia and this might well explain the normal pH result at birth.
97.	He was unpersuaded by arguments in favour of meningitis being the cause in the light of the raised CSF white cell count since the interpretation of the count was complicated by the large number of red cells and he also took the view that the normal CSF glucose finding would be very unusual in a case of severe meningitis.  Moreover there were no organisms of significance in the CSF and he would have expected a positive culture from the CSF given the severity of the illness.  Alternatively, if the organisms in question were so sensitive as to have been eradicated by the antibiotics, then he would have expected a better outcome in terms of the injury suffered by Callum.  Finally, he also noted that the blood culture was negative and he would have expected a positive blood culture [see Bundle B pages 317-318].
98.	Having concluded that the cause of the damage to Callum was unlikely to have been infective he was driven to the conclusion that it was caused pre-natally and the fact that early observations appeared satisfactory, led him to conclude that the only cause which fitted the facts was hyperstimulation in the hours before delivery causing prolonged partial asphyxia and given the involvement of pyrexia the degree of acidosis necessary to have caused the injury might not have been profound.  Moreover given that, having stopped the Syntocinon, there was evidence according to Dr Erskine of fetal recovery, the absence of fetal acidosis at birth was not so surprising.  
99.	Overall Dr Smith’s conclusion as to the probable cause of the injury to Callum was hypoxic ischaemic injury to the brain.  The findings on CSF, whilst of interest, were the only evidence supportive of meningitis but in his view the pattern of illness and the glucose level did not fit with the cause of Callum’s injury being neo-natal meningitis.
100.	Dr Santosh Mordekar, a paediatric neurologist instructed by the Claimant, in effect agreed with Dr Smith expressing the view that this did not look like a case of meningitis. He made no independent contribution to the joint statements and in cross examination conceded that his conclusions relied heavily on the evidence of Dr Erskine.  
101.	Dr Colin Ferrie, a consultant paediatric neurologist instructed by the Defendant sets out his conclusions as to the probable cause of Callum’s injury in his first report dated December 2012 [Bundle B page 284] as follows:
“3.46	Only a few of the criteria I previously outlined as useful in helping decide whether an individual’s cerebral palsy has arisen as a consequence of intrapartum hypoxia have, in Callum’s case, been met.  These include the fact that he developed features consistent with an hyopoxic ischaemic encephalopathy and equivocal features of multisystem hypoxic damage in the newborn period and that his current condition is compatible with having arisen by this mechanism.  However, his condition in the immediate newborn period, although compatible with this mechanism, cannot be said to have been typical and, in particular, the lack of evidence of a severe metabolic acidosis on blood gas analysis, coupled with a lack of clear evidence from fetal monitoring in labour suggestive of damaging intrapartum hypoxia makes it extremely unlikely that Callum’s condition has arisen by this mechanism 
3.47	However, the fact that his head circumference at delivery was normal and subsequently showed the rapid development of microcephaly and that initial ultrasound scans were normal followed by the development of very severe brain damage makes it clear that his condition has occurred as a consequence of an insult at or around the time of birth.  There are multiple pieces of evidence suggesting that Callum’s brain damage arose as a result of a severe infection around the time of delivery.  This can be summarised as follows:
(i) His mother developed a fever towards the end of labour
(ii) The membranes were described as smelly
(iii) There was pus on the placenta
(iv) Callum had a significantly raised white blood cell count in his CSF – a cardinal feature of meningitis.
3.48	In my opinion, on a strong balance of probabilities Callum’s condition has arisen as a consequence of brain damage caused by infection around the time of his birth.  Neonatal infection, particularly meningitis, is often a devastating condition, which can rapidly cause death.  Multicystic encephalomalacia is a well recognised pattern of brain damage in survivors.  It is probable that the antibiotics given to Callum’s mother in labour and to him in the hours and days following delivery effectively treated the responsible bacterium responsible for the infection, but not before permanent brain damage had occurred.  Although neonatal meningitis is usually treated with longer courses of antibiotics than were given to Callum, it is well-recognised that relatively short courses of antibiotics are often sufficient.
3.49	The Particulars and Amended Particulars of Claim assert that Callum’s condition is a result of prolonged partial hypoxic ischemia in labour.  This is unlikely both because the usual criteria used to assess the likelihood of an individual’s cerebral palsy as having arisen as a consequence of intrapartum hypoxia are mostly not met, and because there is strong evidence of an alternative explanation, namely infection.  The Claimant alleges that both cord blood samples were likely to be venous, rather than one being venous and the other arterial.  The implication is that if an arterial sample had been taken this would have shown a severe metabolic acidosis as expected in intrapartum hypoxia.  However, the Claimant also alleges that the hypoxic insult in labour was of the chronic partial type.  Had this been the case both the venous and the arterial cord blood samples would have been expected to show a severe metabolic acidosis.  It is with sudden severe hypoxic insults in labour that one can have a normal venous cord blood result.”
102.	In his oral evidence he maintained his view that the raised white blood count was a very significant factor which, taken with other facts such as the evidence of maternal infection and the lack of any good evidence of intra-partum hypoxia and the lack of evidence of significant intercranial bleeding on early ultrasound scans and the development of extra-axial fluid collections led him to conclude that infection was the probable cause of injury in this case.
103.	He disagreed with Dr Smith’s approach to the raised white blood count since in his view it was not merely slightly above expected values but was ten times higher than that expected even after correction for the contamination as a result of the so-called traumatic or bloody tap.
104.	Equally he did not agree with Dr Smith about the significance of the CSF glucose level since whilst meningitis was commonly associated with a low CSF: blood glucose ratio, a normal CSF glucose does not provide strong evidence against meningitis because the absolute CSF glucose level is often normal when the ratio is abnormally low and it is accepted that in many cases of bacterial meningitis the absolute glucose level is normal (see Dr Ferrie’s letter dated 25th November 2013 at Bundle B page 295 A and 295 C).
105.	Dr Simon Newell, a consultant and honorary senior clinical lecturer in neo-natal medicine and paediatrics instructed by the Defendant, in his oral evidence maintained his view that, although possible, it was extraordinarily unlikely that the severe damage caused to Callum had occurred without severe metabolic acidosis which could have cleared in the relatively short period after the discontinuance of the infusion of Syntocinon and delivery, particularly where labour was still going on and contractions were still taking place.
106.	In his view Callum’s injuries were most likely to be the result of neo-natal infection and meningitis because there was evidence of maternal infection and very importantly the results of the lumbar puncture where the white blood cell count at 230 was both abnormal and elevated and of the ultrasound on day 13 which showed evidence of extra-axial fluid both of which he regarded as characteristic of meningitis.  By contrast, he would not have expected subdural fluid on day 13 which had been absent on days one, two and three, following asphyxia.
107.	So far as the raised white blood count was concerned he agreed with Dr Ferrie and explained that in his view the Garges paper [Bundle C/14 page 188] which looked at different white cell counts and their predictive power for meningitis was strongly supportive of the theory that the cause of Callum’s injury was infective.  He also referred to the latest edition of Rennie and Robertson’s Textbook of Neonatology (2012) which confirmed that the maximum white cell count in the CSF should be about 20 and dealt with the need for any corrections as a result of the so-called bloody tap to be made with great care and the importance when looking at the level of glucose of having a simultaneous specimen of blood for analysis in order to avoid the effects of stress (which is lacking in this case).
108.	So far as the neuroradiologists are concerned, Dr Brian Kendall, instructed by the Claimant, and Dr Forbes, instructed by the Defendant, in their joint statement dated 10th October 2013 (Bundle B page 414 and following) agreed the following propositions:
“It is agreed by both neuroradiologists that the ultrasound scans of 5th and 6th March were reported as normal.  Both neuroradiologists agree that the reported absence of cerebral oedema does not exclude perinatal hypoxia ischaemia as a cause for the Claimant’s damage.
Both neuroradiologists agree that the diffuse abnormalities demonstrated on the scan of 7th March do not exclude an insult occurring in the early neonatal period.  It is agreed that the diffuse abnormalities are equally consistent with but not more consistent with an insult occurring in the early neonatal period.
Both neuroradiologists agree that MCLE is a histological appearance which occurs with several pathologies and is therefore not causally specific.  Dr Kendall considers that the distribution of the abnormality is strongly supportive of perfusion favour.  Dr Forbes considers that the appearances are consistent with perfusion failure or infection.
Both neuroradiologists agree that the brain damage shown on the imaging in particular the cranial ultrasound scan was caused close to the time of birth.
Both neurologists agree that the imaging shows diffuse generalised involvement similar to that seen following prolonged asphyxia from whatever cause.
Both neurologists agree the distribution of the damage suggests that it was cause by perfusion  failure.
Both neurologists agree that the brain damage shown on the imaging is the underlying basis of Callum’s neurological deficits but defer to expert paediatric opinion.
Both neurologists agree ischaemia can be a cause of multi-cystic leuko-encephalomalacia (MCLE).”
109.	They disagree however about the significance of the presence of extra axial sub arachnoid collections and a sub-dural collection on the left on the cranial ultrasound scan dated 17th March (day thirteen) with Dr Kendall considering that they do not help in excluding or confirming brain injury caused by a partial asphyxial insult whilst Dr Forbes considers that their presence is more likely to indicate infection.   They also disagree as to the issue of whether the scan results are more consistent with perinatal chronic asphyxia or infection as the cause of the neurological problems in the neonatal period with Dr Kendall considering that the timing of the seizures at four and a half hours post birth are more consistent with an insult occurring before birth than after birth and consistent with peripheral perfusion failure whilst Dr Forbes considers that it is not possible on the basis of the available imaging to time the insult causing the brain damage which could be either infection or peripheral perfusion failure.
Discussion
110.	What then am I to make of the competing theories?  What is plain is that this is not a clear cut case either way.  There are plainly a number of factors present which tend to support either one or the other theory whilst there are yet other factors which are consistent with either theory. What is also plain is that all of the causation experts have sought to assist the court with what is clearly an unusual set of circumstances. 
111.	Counsel for the Claimant urges me to focus on the nature of the damage as it appears on the MRI and ask myself what is the most likely cause.  He prays in aid the evidence of Dr Kendall and Dr Smith and indeed the Defendant’s own radiologists, copies of whose reports appear at Bundle E pages 101 and 102, coupled with the expert radiologists’ agreement that the cause could not be simple meningitis in support of the Claimant’s assertion that the more likely mechanism for the brain injury is pyroxic ischaemia.
112.	Whilst the Defendant’s alternative thesis is possible it is not it is submitted probable, particularly in circumstances where there are no suggestions that Callum sustained any asphyxial injury between the time or birth and the onset of seizures and no documented evidence of hypotension after birth, a necessary ingredient to cause the damage albeit that Callum did need CPR, IPPV ventilation and suffered from apnoeic attacks in the last few hours of his life.  In fact, submits counsel for the Claimant, the evidence of Callum’s condition in the period between birth and the onset of fits four and a half hours of age strongly suggests that there was no such period of hypertension which he says leads to the conclusion, on the balance of probabilities, that the cause of the brain damage must have been a prolonged partial asphyxia.
113.	The evidence relied upon in support of the submission that Callum’s condition in the period between birth and the onset of seizures was inconsistent with a period of hypotension included the following:
(1)	With resuscitation following delivery he recovered to have regular respirations at 11 minutes of age and his tone came back to normal over the following 15 minutes.  [Bundle E page 28]
(2)	A first paediatric check at 06:20 found Callum to be alert, active and pink. [Bundle E page 270]
(3)	Callum was given to his mother and her family in the recovery room where he was described as “looking all right” by his grandmother and had taken a feed of approximately 20 mls and was noted to be sucking very well.  [Bundle E page 35]
(4)	The first note of any concern was when a paediatrician, Dr Woods, attended to assess Callum at about 09:30 but he did not think there was any respiratory distress and found Callum to be “pink, well perfused, alert, handles well”.  [Bundle E page 28]
114.	Moreover the assessment of the CSF results for the lumbar puncture taken at ten hours of age is complicated by contamination (the so-called bloody tap) and whilst the white cell count was higher than normal, given the contamination, the result, whilst an indicator of infection, was not as clear cut as the Defendant and its experts would have me think. In making that submission counsel relied on the evidence of Dr Smith that the increase was not as dramatic as he would have expected in a severe meningitis.
115.	Again relying on the evidence of Dr Smith it is said that if infection was the cause of the injury the CSF glucose would be expected to be very low yet it was normal at 3.6 mmol/L.  There is then also the fact that no infective agent was ever cultured and that, despite the fact that intravenous antibiotics were stopped after four days, there was no relapse.  
116.	On the other hand, the major difficulty with the Claimant’s theory as to the mechanism of injury is the need for hypoxia which can be identified from the presence of acid in the blood measured by the PH level or from abnormalities in the CTG.  However, as I have already concluded, there was no evidence of either in this case.  On the two occasions on which the acid was measured by reference to the PH and base deficit (BD) levels in the blood at around 01:55 in the FBS and on delivery in the cord blood samples, the results were normal which is suggestive that there was no acidosis at the respective times that those samples were taken.  To my mind if Callum was profoundly acidotic because of the Syntocinon driven contractions, the acidosis would have continued and would have deepened up to the point at which the Syntocinon was discontinued at 04:45.  There was therefore only a 53 minute period before the delivery took place, at which point there was no evidence at all of acidosis.  As I have already recorded, neither Mr Tuffnell nor Dr Newell can accept that the acidosis would have cleared in such a short period of time, particularly as Callum was still being subjected to the hypoxic stresses of labour up until the point of actual delivery.  
117.	Furthermore, as it seems to me, the absence of an infective agent having been cultured and the absence of any relapse does not assist in the circumstances of this case.  The mother had been treated with antibiotics during labour and the baby had been started on penicillin and Dr Newell’s opinion, the force of which I accept, was that he would have expected a negative CSF culture 8 hours after antibiotic treatment had started which is borne out by what is said in Clinical Practice Guidelines where the following appears:
“Prior antibiotics usually prevent the culture of bacteria from the CSF.” [Bundle B 15C page 216]
118.	In addition, a 14 day course of Erythromycin was continued and it has to be said that the conclusion eventually reached as to the cause of damage by the treating clinicians was somewhat lukewarm so that, for example, Dr Milligan, writing to Callum’s GP five months after birth, remained unconvinced.  He said as follows:
“One of the difficult things is that we still do not have a clear idea of the underlying pathology here.  There are no good grounds to suppose that this was a perinatal hypoxic ischemic insult and all the various metabolic investigations have so far been negative …. It is important that we try and make a definitive diagnosis if possible as it may have implications for future children”. [Bundle E page 161]
119.	There are, of course, two important pieces of evidence which point towards infection as the cause and which are relied on heavily by Dr Ferrie and Dr Newell.  These are the raised white blood cells and the ultrasound scan at 13 days to which I have already referred.
120.	To my mind, the existence of the raised white blood cell count is significant.  It is plainly a marker of infection in the central nervous system and, given the very high level, is in my judgment strongly suggestive of infection, accepting as I do the evidence on this aspect of Dr Ferrie and Dr Newell in preference to that of Dr Smith who seemed to me to be at odds with the most recent literature including Renny and Roberton and, of course, the Garges paper [Bundle C page 192]. Dr Newell particularly was an impressive witness who, in my judgment very plainly has weighed all the evidence very carefully, making concessions when he felt it appropriate, before coming to his conclusions.
121.	In my judgment, the evidence of the significantly raised white cell count, coupled with the results of the ultrasound scan at 13 days showing the presence of bilateral echogenic subarachnoid collections with an additional subdural collection on the left which, according to the evidence of Dr Newell and Dr Forbes which I accept,  are much more commonly seen after meningitis rather than hypoxic ischemic injury are strongly suggestive of infection as the cause of Callum’s injury, particularly where there is no reasonable alternative explanation for the subdural collection.  During the course of cross-examination Dr Kendall expressed a theory that perhaps the arachnoid had in some way been damaged and let fluid leak in the subdural space, but there is no evidence to support this theory.
122.	Some criticism was levelled at Dr Forbes for expressing his views in this case without ever having seen a print of the scan which, it is said, undermined the quality of Dr Forbes’ evidence.  However, the fact that Dr Forbes had not seen a print of the scan does not detract from what the radiologist has reported he has seen, still less Dr Forbes’ expertise in commenting on its likely significance.  
Conclusions 
123.	In my judgment there was plainly a material pyrexia and a credible explanation for the absence of any infecting organism having been grown from the blood or CSF samples. There was also some important evidence in the form of the raised white cell count and the results of the ultrasound scan which plainly, on the evidence of Dr Ferrie and Dr Newell which I have accepted,  points to meningitis as the likely cause. On the other hand there was positive evidence of the absence of hypoxia as 01.55 when the FBS was taken and at birth with the cord blood samples and, on the basis of Mr Tuffnell’s interpretation of the CTG, no evidence of hypoxia in the intervening period coupled with what I regard, again on the basis of the evidence of Dr Ferrie and Dr Newell, as the inherent unlikelihood, given the appallingly severe injury to Callum, that there could have been damaging hypoxia and therefore a profound acidosis after 01.55 and running up until 04.45 when Syntocinon was discontinued, the evidence for which would have completely disappeared by the time of delivery some 53 minutes later, simply as a result of discontinuing the infusion of Syntocinon.  Taken together, all these factors lead me to conclude, on the balance of probabilities, and,   notwithstanding the absence of any documented evidence of hypotension after birth, that the cause of the injury sustained by Callum was infection and not hypoxia. 
124.	It follows, in my judgment that this claim fails. 
125.	I hope that the parties will be able to agree a form of order that reflects the terms of this judgment.
126.	Finally I would like to take this opportunity to thank counsel for the helpful and constructive way in which they approached this difficult case and for their very helpful focussed closing arguments.