Introduction
[1] This is a clinical negligence action in which the District Judge directed that there should be split trials, with the first trial being confined to the issues of liability and causation. This is my judgment on those issues.
[2] The claim arises out of the birth of SL ('S') in the Royal Victoria Infirmary ('the RVI') on 16 March 1989. At the time of S's delivery, his mother LL ('Mrs L') suffered from significant blood loss and it was discovered that she had suffered a placental abruption shortly before the birth.
Placental abruption is "the process by which the placental attachment to the uterus is disrupted by haemorrhage."[1] S suffers from quadriplegic cerebral palsy and it is the joint opinion of the paediatric neurologists who have been instructed that, on the balance of probabilities, S's condition was caused by birth hypoxia, secondary to the placental abruption.
[3] The case primarily advanced on behalf of S has to do with the administration to Mrs L during labour, through a drip, of a drug known as syntocinon (intravenous oxytocin infusion). The purpose of syntocinon is to induce or enhance labour so as to establish a pattern of contractions similar to that of normal labour. This aspect of the case raises questions of both liability and causation. As to liability, it is said that there were during the labour warning signs which should have led those responsible for the management of the birth to discontinue, or to reduce the dosage, of syntocinon: in fact, the dosage was inappropriately increased. As to causation, it is said that the placental abruption was, on the balance of probabilities, the result of the administration of an excessive quantity of syntocinon and that, if the syntocinon had been turned off or reduced, the placental abruption would not have occurred. All these propositions are disputed by the defence.
[4] There is a secondary claim relating to the delivery of S. S was born by Caeserean section, which was carried out as an emergency following an unsuccessful attempt at delivery by the use of Kiellands forceps. This attempt was made at a time when, if it had succeeded, S would have been born without mishap. It is said on behalf of S, and again disputed by the defence, that the failure to achieve a forceps delivery was negligent.
History
[5] Mrs L was born on 25 April 1969. Her first child is L, who was born on 14 October 1995. Mrs L had no previous medical history of significance. She suffered few ill effects during her pregnancy with L, who was carried to full term and was delivered by forceps. L weighed 4.0 kg (9 lbs) at birth. He is now a normal, healthy boy aged 10, and is proceeding through school without difficulty.
[6] Mrs L became pregnant again in 1997. The original expected delivery date was 23 February 1998 but, after a scan in October 1997, this was amended to 6 March 1998. Once again, the pregnancy proceeded uneventfully. Mrs L describes herself as having "bloomed in pregnancy", so much so that her general practitioner twice asked her to attend her surgery so that medical students could observe a "text book pregnancy." She attended all her antenatal classes and went to the RVI for scans. On 13 March 1998, when the baby was 7 days overdue, she again attended the hospital and was booked to come in for an induction of labour three days later, on 16 March.
[7] The sequence of events on 16 March 1998 is clear, both from the oral evidence and from the hospital records. There are one or two queries over the precise timing of events, but that is all. The manually compiled records consist of the labour progress sheet kept by midwives and doctors, written notes of vaginal examinations (made by completing boxes on the left hand side of the labour progress sheet), and a monitoring sheet or partogram (which is the reverse side of the labour progress sheet). The partogram contains, among other details, timed records of
(1) the fetal heart rate;
(2) contractions;
(3) the rate of administration of syntocinon;
(4) the dilatation of the cervix; and
(5) the descent of the baby's head.
[8] The fetal heart rate is recorded in beats per minute ('bpm').
[9] The number of contractions and their strength were obtained by palpating Mrs L's abdomen. The number of contractions was expressed as so many per 10 minutes. The strength is indicated by the relative "blackness" of the lines drawn to record the number, the blacker the line the greater the strength.
[10] The rate at which syntocinon was being administered was shown in millilitres per hour.
[11] The dilitation of the cervix was shown in centimetres.
[12] The descent of the baby's head was obtained by palpating the abdomen and expressed in the conventional manner on a scale running in fifths of the head which can be felt above the pelvic brim. 5/5ths is the highest point, where the whole of the head is wholly above the pelvic brim and is still in the mother's abdomen. The lowest point, 0/5ths, is where the whole of the head has passed beyond the pelvic brim and is on the pelvic floor. On a vaginal examination, the descent of the head is expressed differently, in centimetres from 0 where the head has come down to the level of the ischial spines to —5 where it is 5 cm above that level. A head with the leading edge at the level of the ischial spines and therefore 0 on vaginal examination is between 2/5ths and 3/5ths palpable.
[13] Besides these manually compiled records, there is the trace from a cardiotocograph ('CTG') to which Mrs L was connected. This produces a continuous timed record of two matters, the fetal heart rate and the uterine contractions. The monitoring equipment is attached to belts which are strapped around the mother's abdomen, and it is generally accepted that the quality of the recording is inferior to the intra-uterine devices which were more commonly used in the past but are now regarded as unduly invasive.
[14] As regards the fetal heart rate, the CTG shows, at its most basic, the bpm. The baseline fetal heart rate is the rate between contractions. In 1998, the acceptable limits of the baseline rate were 150 or 160 and 110 bpm. A baseline rate above 150 or 160 bpm is known as tachycardia, a rate below 110 bpm as bradycardia: either is indicative of possible fetal distress. Increases and decreases in the rate, known as accelerations and decelerations, can be related to the mother's contractions. The rate normally remains steady, or accelerates, during contractions. Decelerations may be early or late. An early deceleration starts at or around the onset of the uterine contraction which provokes it and is not usually a cause for concern. A late deceleration follows the relevant contraction, with a time lag between the two, and, if recovery from the deceleration is delayed, will give cause for concern. Finally, there is beat to beat variability ('btbv'). The baseline rate should vary by at least 5 beats over every period of 1 minute. Loss of btbv is another indicator of possible fetal distress.
[15] As regards contractions, the CTG shows the frequency and duration (but not the strength) of contractions. The level to which the graph on the printout from the CTG returns between contractions is the baseline and, if there is no return to the baseline, this is indicative of increased uterine pressure.
[16] The relevant history on 16 March 1998 runs from about 0900, when Mrs L was admitted to the RVI, and 2103, when S was delivered. Two midwives and three doctors were the persons principally involved in caring for Mrs L. Alexandra Waterston (then Alexandra Angel) was the midwife on duty until 2000, when her shift ended and her place was taken by Sarah Fellows. Umo Esen was the obstetric specialist registrar who was on duty until 2000, when another specialist registrar, Robert Wood, came on duty. Finally, Philip Bullen was the "senior" specialist registrar who was on call from 1700 onwards. Dr Esen, Dr Wood and Dr Bullen are all now consultants at other hospitals.
[17] After Mrs L had arrived at the RVI, she was seen by Ms Waterston. Ms Waterston wanted to carry out an artificial rupture of the membranes (amniotomy), but was unable to do so, and called for assistance from Dr Esen. Dr Esen saw Mrs L at 1000, performed the amniotomy, and formed a plan for management of the labour. This was that syntocinon infusion should be started within 2 hours if Mrs L was not by then contracting satisfactorily.
[18] It will, I think, make for easier understanding of what occurred over the next few hours if I reproduce in tabular form some of the material which is to be found in the records to which I referred a few moments ago.
| Time |
Palpated contractions |
Dilatation of cervix |
Descent of head |
Syntocinon |
| 1000 |
|
4 cm |
—2 |
|
| 1145 |
|
|
|
1.2 |
| 1200 |
|
|
|
↑2.4 |
| 1230 |
3:10 varying in strength |
|
|
↑3.6 |
| 1300 |
4:10 weak |
|
|
|
| 1345 |
4:10 thereafter getting stronger |
|
|
|
| 1422 |
4:10 varying in
length and strength |
|
|
↑7.2 |
| 1530 |
4:10 |
8 cm |
3/5ths; —1[2] |
|
| 1630 |
4:10 |
6-7 cm |
—1 |
|
The final two entries relating to dilatation of the cervix, which come from records of vaginal examinations performed by Ms Waterston, cannot both be correct, because the cervix does not contract during labour.
[19] Thus far, the labour had been unremarkable. At 1422, however, Ms Waterston had noted occasional early decelerations on the CTG trace, with the fetal heart rate baseline going down from 135 to 120 bpm. At 1430 she informed a junior doctor, but the doctor was busy and did not attend. There was decreased variability on the trace at 1450. At 1510 Mrs L was given diamorphine and stemetil at her own request. Ms Waterston spoke to Dr Esen, who instructed her to wait until 1530 before carrying out the vaginal examination due at that time. Vaginal examinations were carried out by Ms Waterston at 1530 and 1630, as noted in the table above. She informed the medical staff of her findings: she believes that she did so because of the difference between her assessments of the cervix on the two examinations.
[20] At 1650 Mrs L was seen by Dr Esen. His note reads:
"Reviewed.
CTG = early decelerations.
Rather slow progress.
Plan
For [vaginal examination] + [fetal blood sample]
[Discuss with senior registrar]."
A fetal blood sample is taken by a doctor from the baby's scalp: the object is to discover whether the fetus has become acidotic as the pH of its blood is lowered. Around 1700 Dr Esen discussed this plan with Professor Davison, who was the consultant on duty, and Dr Bullen, but it seems from the evidence as a whole that these two doctors did not themselves see Mrs L.
[21] There is uncertainty about some of the timings which follow, but the likely sequence of events is this. Preparations will have been made for the taking of the fetal blood sample. These will have included getting Mrs L on to her left side, with her left leg drawn up to her chest as far as possible and her right foot in a stirrup; the doctor washing and scrubbing; and the covering of the patient with sterile drapes. Dr Esen's evidence was that there are usually about 4 minutes between the completion of the procedure and the analysis of the sample. As the analysis here was timed at 1733, it seems that the sample was taken just before 1730. Dr Esen then carried out, according to his plan, a vaginal examination. He timed this at 1733, and he says that he will have performed the examination between the taking of the sample and the result coming back.
[22] The pH reading of the blood sample was 7.35, which was within normal, healthy limits.
Dr Esen's note of the vaginal examination records the dilatation of the cervix as 8 cm and the level of the baby's head as —2. He decided to increase the rate at which Mrs L was receiving syntocinon to 9.6, and noted that the case should be discussed with Professor Davison in 2 hours. His note includes the phrase "CTG much better now." I will leave until later discussion of the readings which could be seen on the trace around this time.
[23] One matter arising out of Dr Esen's vaginal examination at this time assumed an unexpected significance in the course of the trial. His note records the position of the fetus as occipito-anterior, i.e. the back of the baby's head facing to the front of the mother (which is a favourable position for delivery). It is agreed by the two expert witnesses that this finding must have been wrong. The reason is that, as will be seen, the fetus was eventually in the right occipital transverse position, which is a position that can be reached from occipito-posterior but cannot be reached from occipito-anterior.
[24] The next block of time which I wish to consider runs from 1735 to 1925. Throughout
this period, palpated contractions were being recorded at 4:10 and strong, and Mrs L was continuing to receive syntocinon at 9.6. Ms Waterston made full notes, and I think that the progress of labour can best be seen from a straightforward reproduction of those notes.
| Time |
Ms Waterston's notes |
| 1735 |
Syntocinon ↑9.6 mls/hr. LL lying on left side, contractions very painful -
does not want to have an epidural - may have diamorphine at 1800 -
wishes to wait for it. |
| 1745 |
Discussion re epidural/analgesia. LL not coping well at present, contractions too painful & close together. |
| 1750 |
Decided to have epidural. Anaesthetist informed. |
| 1810 |
Epidural sited - main dose. |
| 1825 |
Prolonged bradycardia. [Heart rate] ↓ 80 bpm. Turned on to [left] lateral.
BP 120/60. IVT full on. Medics informed. Slow recovery to baseline = 125 bpm.
Dr Esen busy. |
| 1830 |
CTG improving. |
| 1845 |
CTG [seen by] Dr Esen (reg). LL more comfortable now - aware of contractions
but not too painful. Maternal observations stable. |
| 1910 |
Further early deceleration. Dr Esen informed for next [vaginal examination]
15 mins. |
| 1925 |
New syntocinon syringe commenced (on 9.6). |
There is, it appears to be agreed, one probable error in these notes. The increase in syntocinon was almost certainly at 1748, not 1735. There is uncertainty, which I shall have to resolve, whether the entry for 1735 (apart from the reference to increase in syntocinon) and that for 1745 are correctly timed: it is at least possible that they are not and that they refer to events shortly after the increase in syntocinon. Once again, I shall leave until later any matters which emerge from the CTG trace.
[25] At 1930 a further vaginal examination was carried out by Dr Esen. His note on the labour progress sheet reads:
"Fully dilated. RoT [right occipital transverse].
Allow descent/rotation + 1 hr, then to push."
The doctor's note of the level of the head is "0." What one gets from this is, quite simply, that the cervix is now fully dilated (i.e. to 10 cm), that the head has come down to the level of the spines, but that the baby is in the right occipital transverse position. A baby cannot be delivered directly from this position: the head must first rotate naturally, or be rotated. Dr Esen's plan, as appearing from the note, was to allow over an hour for a natural rotation, and further descent, after which Mrs L would be asked to push.
[26] At 1940, according to Ms Waterston's note, Mrs L complained of pain in her left side and requested a top-up of epidural. This was carried out by an anaesthetist at 1950.
Ms Waterston's note at 1950 states:
"Good effect. Maternal & fetal observations static.
CTG more reactive and variable."
[27] At 2000 there was a changeover of staff. Dr Esen was replaced by Dr Wood. Ms Waterston was replaced by Ms Fellows.
[28] Ms Fellows' first note is timed at 2015. Mrs L was complaining of left-sided discomfort in her abdomen. Ms Fellows called on the anaesthetist for a further top-up of epidural, which was administered at 2020. Five minutes later, at 2025, the CTG showed that the fetal heart rate had gone down to 90 bpm and was not recovering. Ms Fellows at once realised that there was now a medical emergency. She moved Mrs L on to her left side, administered facial oxygen, and summoned the doctors.
[29] There is, once again at this point, a little uncertainty about precise timings. Dr Bullen and Dr Wood arrived in the delivery room at times between 2030 and 2036.[3] It was apparent that the level of concern as to the condition was such that the medical team should proceed to active delivery of the baby. Mrs L's first child had been a forceps delivery after failure of a ventouse to effect delivery. Dr Bullen was aware of this and it very probably prompted the decision, which was made at 2040, to go straight to a forceps delivery.
[30] Delivery by the use of Kiellands forceps was attempted by Dr Wood at 2045.
The relevant parts of his operating note read as follows:
"[Per abdomen 0/5]…
[Cervix] fully dilated.
RoT at spines…
Easy application of blades (ant[erior]) wandering/post[erior] direct.
No rotation of head although blades rotated x 2."
Put shortly, two attempts at a forceps delivery failed, because the blades slipped from the baby's head. After the second attempt the fetal heart rate had dropped to 80 bpm.
[31] At 2050 Mrs L was taken to theatre. The fetal heart rate was by now down to 50 bpm. At 2103 S was delivered by emergency Caesarean section. He was in poor condition. It was apparent that placental abruption had occurred. Irrespective of any questions of fault or causation, the outcome was, whether in terms of obstetrics or in ordinary language, a calamity.
Summary of issues
[32] The issues which arise for decision have been framed in rather different ways at different stages of the litigation. At the conclusion of oral submissions, there remained for decision four main questions:
(1) Was it negligent to increase the dose of syntocinon from 7.2 to 9.6 at 1748?
(2) Was it negligent not to turn off or reduce the syntocinon at 1825 or subsequently?
(3) If negligence in either respect is established, did the syntocinon cause uterine hyperstimulation which in turn led to the placental abruption?
(4) Was the failure to achieve delivery by Kiellands forceps negligent?
(4) is a question discrete from (1) to (3). It is agreed that the placental abruption occurred at or before 2020 and that, if delivery had taken place by 2049, S would have been born undamaged. Accordingly, no question of causation arises on (4). So, in order to succeed, there has to be established on behalf of S either negligence with regard to syntocinon together with causation or negligence with regard to the failed forceps delivery.
Witnesses
[34] Mrs L gave evidence on behalf of S. She was plainly an honest and reliable witness, who did her best to recall the events of what turned out to be a traumatic day and evening. No one who heard her testimony could fail to have the utmost sympathy for her.
[35] There were five witnesses of fact for the defence. They were Dr Esen, Dr Wood, Dr Bullen, Ms Waterston and Ms Fellows. I had no reservations about the evidence of the last four mentioned, all of whom were plainly assisting the court to the best of their ability. Dr Esen gave evidence in a rather more defensive fashion than the others and at times his answers were given with more than a hint of dogmatism. I think, however, that to criticise him on this basis would be superficial and that his faults, if faults they were, were ones of manner rather than substance. He is the practitioner who has been most prominently in the firing-line and it is understandable he should feel the pressure of the litigation more acutely than the other witnesses. Having considered the matter carefully, I have concluded that he was not in any way "covering up" and that he recounted to the best of his ability what he observed and did on the relevant day.
[36] The expert witnesses were Mr Anthony Johnson, who was before his retirement the senior consultant surgeon in obstetrics and gynaecology at the Jessop Hospital for Women in Sheffield, and Professor James Thornton of the University of Nottingham and the Nottingham City Hospital NHS Trust. Mr Johnson gave evidence on behalf of S and Professor Thornton on behalf of the defendant. Both are distinguished obstetricians and there was nothing in the nature of a "battle of qualifications." Nor was either more obviously a more impressive witness than the other. There were, however, two planks in S's case, which appeared late in the day and had been foreshadowed neither in the pleadings nor in any of Mr Johnson's reports. These were the significance (if any) of Dr Esen's error as to the position of the fetus at 1733 (which goes to issue (1)) and the allegation as to negligence in the use of the forceps at 2045 (which covers the whole of issue (4)). The lateness of these developments of S's case raised difficulties both for the defence and for the court; and, putting matters as gently as one can, it does not engender confidence in the soundness of either aspect of the claim. I shall return to these matters later.
Issue (1): increase of syntocinon from 7.2 to 9.6 at 1748
[37] There is, to start with, a question of fact to be resolved, although it is not one on which either side has pressed strongly for one rather than the other of the two possible findings. The question is whether Ms Waterston's notes of 1735 and 1745 are mistimed and in fact record events which occurred shortly after the syntocinon was increased at 1748. In my judgment, the strong probability is that the notes are mistimed. On their face, they record a sequence of events or observations which begin, and do not end, with the raising of the dosage. Further, the pain from contractions of which Mrs L complained twice would be more likely to follow stimulation from an increased dose of syntocinon than to have occurred when she had been receiving a static dose for some 3.5 hours.
[38] Mr Johnson regards the decision to increase the syntocinon (and, indeed, the failure to reduce it) as treatment which was "sub-standard" to a degree which was negligent. I think that one can put the considerations which support or undermine this opinion into three categories, contra-indications, indications and what might broadly be called surrounding circumstances. I must, however, in order to avoid being unduly analytical, look at the treatment in the round. In doing so, I bear in mind that I am asking, not whether the increase in syntocinon was "right" or "wrong", but whether it was something which no responsible practitioner, acting with reasonable care, would have authorised.
[39] The possible contra-indications come from the CTG, both with regard to the fetal heart rate and to the mother's contractions.
[40] As regards the fetal heart rate, there were decelerations at 1348, 1600 and 1720. Mr Johnson said of the first two in his oral evidence that "no one takes much notice of short, isolated decelerations like these. You just note it and keep an eye on it." Mr Johnson attached more significance to the deceleration at 1720, when there was a deep late deceleration to 80 bpm. I cannot, for my part, go along with him on this, for the reason advanced by Professor Thornton (which is confirmed by an examination of the trace) that, immediately after this isolated deceleration, the heart rate returned to the baseline and remained steady until the increase in syntocinon at 1748.
[41] As regards the rate of contractions, they appear from the trace to have been running at 4:10, 4-5:10 or 5:10 from 1420 on. The rate goes more to the progress of labour, or, more accurately, what is said to be the slow progress which was an indication for increasing the syntocinon. What was of greater concern to Mr Johnson as a contra-indication is the raised baseline on the tocograph, which appears very clearly on the trace between about 1700 and 1750. The question is whether this should have been regarded by the defendant's staff as indicative of increased uterine pressure. Was this, as Mr Redfern QC put it to Professor Thornton in cross-examination, "good evidence of hyperstimulation"? Professor Thornton thought that it was not, on the ground that there must at this stage have been a good deal of movement on the part of Mrs L, who was being made ready for the taking of the fetal blood sample. It is recognised that, where CTG monitoring is taking place via an external transducer attached to a belt round the mother's abdomen, accuracy may be lost over a period when the mother is being moved around. This is readily understandable. In my judgment, it would over the period under consideration simply not have been possible to say one way or the other what was causing the increase in baseline. It should, however, have been something to which those attending Mrs L were alert. Indeed, as Mr Hart QC correctly pointed out in his closing submissions, Mr Johnson's view changed over the course of his evidence: his opinion had been that there was positive evidence of uterine hyperstimulation between 1700 and 1750, but it shifted to regarding hyperstimulation over this period as something that could not be excluded.
[42] The debate on whether an increase in syntocinon was indicated has been focused on the question whether Mrs L's progress in labour up to 1748 should be regarded as slow.
Progress can be assessed with regard to dilatation of the cervix and descent of the head.
As regards dilatation of the cervix, obstetricians use 1 cm per hour as a rule of thumb, but allow for marked variations from one woman to another. Dilitation was 4 cm at 1000. Given that no unassisted progress in labour had been made by 1200, it was probably still 4 cm by then. One should ignore Ms Waterston's finding at 1530, as it cannot stand with the result of her examination at 1630. At 1733 dilitation was 8 cm. So, if one goes from 1000 to 1733, there is only 4 cm progress over 7.5 hours; if one goes, as seems to me to be more probably correct, from around the introduction of syntocinon at midday, one gets 4 cm over 5.5 hours. As regards descent of the head, Dr Esen has recorded —2 at both 1000 and 1733.
There are intervening findings from Ms Waterston of —1, but one is dealing in small units and in an area in which precision must be almost impossible, so there is no significant difference. In sum, the head has failed to descend over a period of 7.5 or 5.5 hours (depending on what is taken as the starting time). Dr Esen's view, which was supported by Professor Thornton, was that this amounted to slow progress. Eventually, as the evidence proceeded, Mr Johnson's opinion was not very different. According to my note, he said:
"[Dr Esen's] view that there was 'rather slow progress in labour' is a subjective view which I don't criticise. It is on the slowish side. The doctor's mind should turn to - 'why is it on the slowish side? - do I need to do anything about it?' This position does not cross any action line."
[43] I will come to Mr Johnson's question "why?" in a moment. But before I do, I must clear out of the way a matter on which a considerable amount was written in the early stages of this case. This has to do with the rate of contractions. Prior to the increase in syntocinion, the contractions had been running at 4:10 and at times touching 5:10. In a nutshell, Mr Johnson's view is that contractions which are 4:10 and strong are sufficient and all that is to be desired. 5:10 is a rate which "he could live with" but not, as I understood his evidence, a rate which should be increased by means of additional syntocinon. The RCOG/NICE clinical guidelines published in June 2001 state that the minimum dose possible should be used and that it "should be titrated against the uterine contractions aiming for a maximum" of 3-4:10. It is submitted on behalf of S that this publication is sufficiently proximate in time to 1998 to indicate what acceptable practice was in that year. Professor Thornton, on the other hand, says that 5:10 was the desired rate in 1998.
[44] The fetal blood sample produced a normal pH reading. This is said by the defence to indicate that the baby was healthy and that further artificial stimulation of labour could be safely attempted. Mr Johnson throws doubt on the value of a fetal blood sample while syntocinon is being administered, and refers to the following passage from a standard work on fetal monitoring:[4]
"There is little merit in performing a fetal blood scalp pH measurement in a patient receiving oxytocin since the FHR [fetal heart rate] changes are iatrogenic. If the test is done soon after a prolonged bradycardia or after ominous decelerations, it may show acidosis prompting the performance of an emergency caesarean section; on the other hand, if a fetal blood sample is not taken and time is allowed, the FHR recovers and within 30-40 minutes the scalp blood pH is likely to be normal."
Professor Thornton says that there is, in general, no lack of value in a fetal blood sample taken while syntocinon is being administered. The first sentence of the passage quoted must, he says, be read in context: so read, it is simply a warning against the hasty drawing of an adverse inference from a poor pH reading.
[45] I come now to Mr Johnson's question "why?" In his view, the key to the case lies in the positional disproportion of the fetus. He said in his oral evidence that anything other than the occipito-anterior position is to be regarded as positional disproportion. If you have positional disproportion, "you absolutely do not crank up the contractions." You have an irresistible force (which I took to be the contractions) and an irresistible object (as Mr Johnson described the uterus) and to increase the contractions is to risk rupturing the uterus.
"There is no virtue in forcing a baby out too quickly." This evidence was then linked to Dr Esen's error as to the position of the fetus, which Mr Johnson regarded as negligent. Mr Johnson had read "OA" in Dr Esen's 1733 note as "OP." Dr Esen had persisted in his own error as to position when giving evidence in court, but Mr Johnson (who was present) had not noticed the mistake and so Dr Esen had not been given the opportunity to deal in his own evidence with this aspect of Mr Johnson's criticisms. This was unfortunate, given that the matter was "now critical to my [Mr Johnson's] analysis of the case." In other words, if I have understood this evidence correctly, Mr Johnson's view was that it would not be acceptable practice to increase syntocinon if the position of the fetus had been correctly ascertained as occipoto-posterior. Professor Thornton was of the opinion that the error as to the position of the fetus was not negligent. It could, in his opinion, stem from mistaking one fontanelle for the other, which "is a mistake easy to make, unless one is making a forceful examination. Getting it right is crucial when one is going to do a forceps delivery, but not at this stage."
Contrary to Mr Johnson, Professor Thornton said that the use (and, presumably, increased use) of syntocinon would be acceptable with a fetus in the occipoto-posterior position, and the head would (or, perhaps, should) rotate naturally prior to birth.
[46] As to surrounding circumstances, Mr Redfern pointed to evidence that the day in question was a busy one at the obstetrics department of the RVI, to the number of occasions on which midwives called for medical assistance, and to the fact that (as undoubtedly appears from the notes) a doctor was not available to answer every such call. All this showed that the circumstances were ones which were conducive to care being given below the proper level and to the making of mistakes which amounted to negligence.
[47] For the reasons which I shall now set out, I have come to the conclusion that, in relation to the increase in syntocinon at 1748, negligence has not been established.
[48] The starting-point is that the plan to increase the syntocinon was not formed by Dr Esen "on the hoof" or without consultation with his seniors. His decision in principle was discussed with, and approved by, Professor Davison and Mr Bullen at 1700; and, before he implemented the plan, Dr Esen had obtained the result of a fetal blood sample and had carried out a vaginal examination. This seems to me to put on the periphery, at any rate of this aspect of the case (matters may be different in relation to issue (2)), the assistance which Mr Redfern attempted to derive from surrounding circumstances.
[49] In my judgment, the progress of labour by the time of the vaginal examination can fairly be regarded as slow. Mr Johnson conceded as much. One had therefore a state of affairs in which further progress could reasonably be induced by increasing the syntocinon unless there were contra-indications. The possible contra-indications were the fetal heart rate and what is said to be evidence of hyperstimulation from the tocograph. As to the heart rate, the recovery from the deceleration at 1720 was a rapid one (it looks to be about 1 minute on the trace), and I accept Professor Thornton's evidence that it was not such as should give cause for concern. As to the raised baseline on the tocograph, it is at this stage impossible to say definitely whether it showed hyperstimulation or was the result of movement on the part of Mrs L during the various procedures which were carried out over the 40 minutes or so following 1700. But, for a reason which I hope is not simplistic, the latter appears to me to be the more probable explanation, because after 1750 the baseline goes down notwithstanding the fact that the dose of syntocinon (which would itself have a stimulating effect) had been increased.
[50] The next question is whether the rate of contractions was such that no increase in syntocinon should have been authorised. It seems to me, having heard both experts, that it is impossible to find that there was in 1998 an optimum rate of contractions on which all obstetricians would have agreed. Professor Thornton says that 5:10 was the desired rate in 1998, while Mr Johnson "could live with" that rate. Mrs L's contractions were not running consistently at 5:10, although they had at times hit that rate. She was accordingly, as it seems to me, just below what might be called the cusp of what at least some obstetricians would have regarded as the desirable rate. If this is right, it cannot have been negligent to take steps to increase the rate, so long as other indicators were favourable.
[51] Other indicators were favourable. As I have already stated, the rate of progress in labour could reasonably be regarded as slow, and the fetal blood sample showed that the fetus was healthy. In my judgment, the passage from the work on fetal monitoring which was quoted earlier in this judgment does not support Mr Johnson where the finding from the sample is a favourable one.
[52] This leaves the evidence as to Dr Esen's error about the position of the fetus.
This is forensically troubling for reasons to which I have already adverted, at perhaps too great length. The matter appears as an unforeseen addendum to the claimant's case, it is not something dealt with by Dr Esen in the witness-box nor by the experts in their reports or their joint statement, yet – after the conclusion of all the evidence of fact – it is advanced by Mr Johnson as being crucial to his analysis. The questions which arise are whether Dr Esen's error amounted to negligence; and, if it did, whether the correct assessment of the position of the fetus would (or at least should) have led to a decision not to increase the syntocinon. On both questions, I have little more to go on than assertion from Mr Johnson and counter-assertion from Professor Thornton, with no reference to literature in support of any of the views put forward. As to the nature of Dr Esen's mistake, I found Professor Thornton's opinion the more convincing. It does not appear to me that precision as to the position of the fetus was critical at the time of the relevant vaginal examination. If that be so, Dr Esen would have been justified in carrying out as minimally invasive an examination as he could and, as he did not have the opportunity to deal with the matter, I am bound to assume in his favour that this is what he did. Then, on the basis advanced by Professor Thornton, that one fontanelle can easily be mistaken for the other, there will have been a simple error but no negligence. If I were wrong about this, then I would say without hesitation that Mr Johnson's assertion as to the inappropriateness of administering syntocinon where the fetus is in the occipto-anterior position, unsupported by citation and controverted by Professor Thornton, would be far too weak a peg on which the court could hang a finding adverse to the defendant.
Issue (2): failure to turn off or reduce syntocinon at 1825 or subsequently
[53] By 1800 Mrs L had been placed on her left side in anticipation of the administration of the epidural. At this stage the trace from the CTG shows the fetal heart rate running at around 155 bpm. Mrs L was contracting at 4-5:10. Ms Waterston's notes state "epidural sited main dose" at 1810, and it seems as though the dose was actually given around 1820. The trace contains a note "Epidural" at 1810; and a longer note, running across the time-points on the paper from 1820 to 1828, in these terms:
"Sat upright.
(L) lateral.
BP 120/60.
IVT full."
Ms Waterston in her oral evidence supported a timing of 1820 for the main dose of epidural, and said that it would have been preceded by a small, test dose in order to see whether there was any adverse reaction on the part of the patient. I am sure that neither she nor anyone else involved would say that all the notes which were made accurate to within a minute or so but, doing the best one can, the timings are: 1810, test dose; 1820, main dose.
[54] At 1825, as appears both from Ms Waterston's notes and from the trace, there was a prolonged bradycardia. It seems from the trace (which is quite difficult to read) as though, prior to the bradycardia, the baseline fetal heart rate had been around 140-150 bpm. It then fell and for about 3 minutes the heart rate was at or below 80 bpm. Recovery, which took about 4.5 minutes from the start of the bradycardia, was to a baseline of 130 bpm. Ms Waterston noted "CTG improving." Thereafter the baseline increased to 150 bpm.
[55] Ms Waterston said in evidence that, when the bradycardia occurred, Mrs L was placed on her left side: this is supported by the note on the trace to which I have referred. At around 1830 Ms Waterston made this further note on the trace:
"Medical staff informed.
Doctors busy."
She agreed under cross-examination that at 1825 the index of suspicion
"was well and truly raised, and a doctor's intervention was necessary. From this time on, the situation became more and more suspicious."
[56] At 1828 there is a doubtful tocograph reading. Mr Johnson found it difficult to say whether this was a sign of uterine irritability or "just that the belt on the tocograph had not been properly adjusted." Professor Thornton's view is that it was the latter.
[57] Dr Esen, who had been dealing with another patient, arrived at 1845. He reviewed the trace and found it satisfactory.
[58] Between 1840 and 1850 the trace shows that Mrs L was contracting at the rate of 5-6:10. There is a controversy as to the interpretation of the trace with regard to the fetal heart rate over this period. Mr Johnson says that the heart rate went up to 155 bpm, while Professor Thornton regards recordings of 155 bpm as no more than intermittent. At this point, I find the trace relatively easy to read. The baseline appears to me to be 150 bpm, with the rate varying (as one would expect) above and below this, at times touching 155 bpm.
[59] At 1909 the trace of the fetal heart rate shows a deceleration from a baseline of about 160 bpm, taking about 2.5 minutes to recover to a baseline of about 150 bpm. It is difficult to tell from the trace what the deepest point of the deceleration was, but at one point the rate went to 90 bpm.
[60] I do not think that subsequent readings throw any light on the issue of negligence, and I shall therefore proceed to deal with that issue at once.
[61] The principal question which arises here has to do with the proper response to the prolonged bradycardia which began at 1825. Mr Johnson's view is that this should have been treated as evidence of fetal distress and have led to the immediate turning off or reduction of the syntocinon. Professor Thornton is of the opinion that the proper response (which was adopted by Ms Waterston) was to summon a doctor. That having been done, Professor Thornton regards the decision not to take any steps in relation to the syntocinon was one which is defensible for reasons at which I shall look in a moment.
[62] The presentation of this aspect of the case on behalf of S has not been consistent over the course of the litigation. The particulars of claim contained, amongst other allegations of negligence, failure to observe or react to the fetal distress at 1828 and failure to turn down or switch off the syntocinon at the same time. The former allegation was withdrawn in a subsequent pleading. In Mr Johnson's original report (20 February 2001) there was no criticism of the management of Mrs L's labour around 1828, but in his revised report (30 September 2003) one gets a single sentence, stating that "[i]t was substandard care that the syntocinon was not switched off at that time." Then, in a letter of 1 March 2005, he stated that
"They did react appropriately to the episode of fetal distress at 1828. I have not made any criticism about this in my report."
Not surprisingly, the issue was not addressed by Professor Thornton in his report of 22 September 2005, but the allegation of a negligent failure to turn off the syntocinon was revived by Mr Johnson at the experts' meeting on 12 December 2005. At the hearing, it played a prominent part in his criticism of the defendant.
[63] The following passage from a textbook on high risk pregnancy was put to Professor Thornton:[5]
"According to the data sheet currently supplied with syntocinon, the manufacturers recommend that it should never be administered if there is any evidence of fetal distress, and in practical terms this means if there is any abnormality of the [fetal heart rate]. If such an abnormality occurs during syntocinon infusion, the infusion should be stopped immediately."
Professor Thornton's evidence was to the effect that he did not regard the last sentence as universally prescriptive. "You take every case on its own." It was put to Dr Thornton that at any rate by 1840, when the rate of contractions began to increase and Dr Esen had not yet arrived, the syntocinon should have been stopped. He disagreed, for reasons which were helpfully summarised in Mr Hart's written submissions at the end of the hearing:
"(i) the doctors knew the baby was in excellent condition [from the fetal blood sample at 1733];
(ii) bradycardia following epidural is common;
(iii) so long as the bradycardia returns to normal it was reasonable to continue the syntocinon;
(iv) the bradycardia did return to normal."
[64] The question which arises under issue (2) is a short one, but I have not found it to be an easy one, and it has given me greater difficulty than has issue (1). I have, after some hesitation, concluded that negligence has not been made out.
[65] The situation which was disclosed by the trace from 1825 to 1828 was such as to give rise for real concern and it was certainly unfortunate that medical staff were not in a position to respond more rapidly to the call from Ms Waterston. It may well have been that, at this stage, pressure of work elsewhere in the department caused a delay in attending to Mrs L. That is, however, something of a diversion from the real path of enquiry, because a failure to turn off the syntocinon at 1840 or 1845 must, in my judgment, have been no more and no less culpable (if culpable at all) than a corresponding failure to do so at 1825 or 1828.
[66] I have to say that I find Professor Thornton's approach convincing. I accept it, but not without scrutiny at each of its stages. As to (i), I simply underline the fact that the fetal blood sample was a recent one, taken within the hour which preceded the bradycardia. I shall have to dwell somewhat longer on (ii). It is accepted by Mr Johnson that fetal bradycardia does frequently follow upon epidural, but he points out that the bradycardia could reasonably be attributed to the epidural only if it were combined with a fall in the mother's blood pressure. Mrs L's blood pressure was recorded between 1820 and 1830, but there is nothing to suggest that the reading (120/60) was other than normal. It is, I think, common ground that the proper response to bradycardia following epidural is to place the mother on her left side and await a recovery. This is what occurred here, the fetal heart rate did recover and so Professor Thornton's points (iii) and (iv) are made good. That cannot, however, be an end of the matter: because, even if each stage of his reasoning process thus far is unimpeachable, there may have been other signposts pointing to the need to discontinue the syntocinon.
[67] I do not think that there were any such signposts. Given the movement of Mrs L which was involved in the administration of the epidural, the likelihood is that the state of the tocograph around 1828 was attributable to such movement. Anything that happened thereafter was, as I understood Mr Johnson's evidence, confirmatory of an error already made rather than the provision of a warning belatedly to correct that error.
Issue (3): causation
[68] Mr Johnson said in his report:[6]
"I would say that in my opinion it is more likely than not that had they turned the syntocinon down at 1700 that the dysfunctional uterine activity would have settled down and that Mrs L would have gone on to achieve full dilatation. It may have taken a little longer but in the absence of dysfunctional uterine activity I think it is improbable that there would have been any significant fetal distress…
The defence deny that the syntocinon caused the abruption. I think that they are wrong. They are clearly wrong if they are suggesting that an abruption is always a rapid and and precipitous event. Placental abruptions can and do evolve over a finite period which can be a matter of hours. I would agree with the defence that an abruption cannot be foreseen by gradual changes on a CGT. In this case I would not and indeed I have not suggested that the abruption was particularly foreseeable."
In a supplementary letter Mr Johnson said:
"The defence are on strong ground when they say there is nothing in the literature to indicate that syntocinon causes placental abruption. I have made that clear in my own report, however though, in this case, there is a clear association."
[69] Professor Thornton in his report said:[7]
"I have been asked to consider whether use of oxytocin in general, either in normal or raised dosage, is associated with placental abruption.
Response. In my opinion it is not. I can find no reference to the association in the oxytocin data sheets or in the relevant chapters of large textbooks of obstetrics which deal with the aetiology of abruption."
[70] At least one of the data sheets for syntocinon, which neither expert had seen when writing his report, does in fact mention placental abruption. The ABPI Compendium of Data Sheets and Summaries of Product Characteristics (the copy in evidence is undated) contains the following passages relating to syntocinon produced by Novartis:
"Overdosage. The fatal dose of syntocinon has not been established…
The symptoms and consequences of overdosage are those mentioned under 'Side-effects.' In addition, as a result of uterine overstimulation, placental abruption and/or amniotic fluid embolism have been reported…
Side-effects…
When oxytocin is used by iv infusion for the induction or enhancement of labour, its administration at too high doses results in uterine overstimulation which may cause fetal distress, asphyxia and death…."
The edition of the same publication for 1999-2000 contains similar passages.
[71] Two of the leading textbooks were referred to. According to Turnbull's Obstetrics[8]
the aetiology of placental abruption, which in the 1970 British Births Study was found to have occurred in about 1 per cent of pregnancies, "remains an enigma." Apart from cases of direct trauma to the uterus, e.g. in a road accident, which are uncommon, "the cause is obscure." The editors go on to consider three particular cases (abdominal trauma, uterine decompression, and prolonged rupture of the membranes). Similarly, Creasy and Resnik in their Maternal-Fetal Medicine: Principles and Practice[9] say:
"Numerous factors have been suggested to pay a causal role in abruption placentae, but a unifying etiologic concept is still lacking. Underlying disease of the deciduas and uterine blood vessels seems best to explain the diversity of associated factors that have been described… [A]bruptio placentae may be viewed as the final, dramatic expression of long-standing pregnancy disorder…
Some factors that have been suggested to play an etiologic role in the development of abruptio placentae are as follows…."
The authors go on to consider trauma, short umbilical cord or uterine anomaly, inferior venal caval compression, maternal hypertension, folic acid deficiency, cigarette smoking, maternal age, and cocaine abuse.
[72] It appears to be agreed on all sides that, whilst placental abruption is an uncommon phenomenon, for it to take place during labour is an extremely rare occurrence.
[73] Each of the expert witnesses adhered in his oral evidence to the view expressed in his report. Mr Johnson said that, from the time when the syntocinon was increased at 1748, there was an excessive amount of syntocinon which "caused uterine hyperstimulation which is compatible with the cause of the abruption." The cause of the placental abruption must either be the syntocinon-induced hyperstimulation or something unknown. The warning on the drug sheets and the temporal connection between the increase in the syntocinon and the abruption pointed to the former. My note of Professor Thornton's evidence includes these two passages:
"I have never before come across the suggestion that hyperstimulation causes abruption. Abruption is the separation of the placenta. I don't see a mechanism. If you squeeze the uterus, you just push around the baby. Syntocinon was used in 20 to 30 per cent of labours at this time. Abruption in labour is very rare, but not unheard of…
The data sheets simply say that these cases have occurred. You can't infer causation from that. The textbooks don't mention it. This is the first time I have heard the suggestion."
[74] If causation had been relevant to the decision of this case, I would have been unable to find that it had been established.
[75] The first point on which Mr Johnson and Professor Thornton disagree is whether there is, as a matter of fact, sufficient evidence of hyperstimulation following the increase in syntocinon at 1748. They agree that hyperstimulation is accurately defined as "excess pressure and/or excessively long and/or excessively frequent contractions."[10] Mr Johnson in a tabular chronology identified raised baseline pressure on the CTG at 1800, definite hyperstimulation at 1840, and what he called instances of uterine irritability at 1910 and 1945. I have to say that, in accordance with Professor Thornton's view, I am unable to discern any significant changes on the trace at any of these times other than 1840, particularly in view of the accepted limitations of monitoring by an external transducer. 1840 marks the beginning of the period of 10 minutes during which Mrs L was contracting at 5-6:10. That is, on any view, hyperstimulation, but it seems to me to stand alone in the chronology. It was transient: thereafter the contractions returned to an acceptable rate. This isolated instance would not, in my judgment, be sufficient to ground a finding that this was a hypersimulation case.
[76] Further, Mr Johnson and Professor Thornton disagree as to hyperstimulation being a cause of placental abruption, whether generally or in this case. It is clear that recognised authorities in the field of obstetrics have considered the possible causes of placental abruption and none has suggested uterine stimulation as one among such possible causes.
All that the data sheets do is to say that placental abruption has been reported following hyperstimulation, but there is no indication of when and where this occurred and nothing in the nature of an analysis of the case or cases concerned. The statement is, perhaps, typical of the bald ex abundanti cautela warnings which are familiar on drug sheets. This, in my judgment, is insufficient as a basis on which I could find either that hyperstimulation may lead to placental abruption or that it in fact did so in this case. Mr Johnson does, as I have indicated, rely on the temporal relationship between the increase in syntocinon and the abruption. I hope that I will not be regarded as making a point cheaply, and it is certainly not my intention to do so, when I say that, in the particular circumstances of this case, he is coming close to the post hoc, propter hoc fallacy.
[77] Lastly, under this heading, I should deal with certain material which was placed before me by Mr Redfern.
[78] Between the conclusion of the evidence and closing submissions, Mr Johnson received a letter from Michelle Clarke of Alliance Pharmaceuticals Limited, who publish the data sheets, stating that she had heard from Novartis that an overdose of syntocinon
"may lead to placental abruption as a result of the uterine overstimulation.
The link between the cause and the effect is in the mechanism of action itself."
Even if one were to treat this as admissible evidence, it would not, in my judgment, add anything to what is in the data sheets.
[79] Mr Redfern cited a passage from Clerk and Lindsell on Torts[11] in support of the proposition that, in an exceptional case and for reasons of policy and fairness to a claimant, the court may relax the requirement that he should prove his case on the balance of probabilities and treat conduct which increases the risk of damage to him as proof of the causal link between them. The accuracy and scope of this proposition was not investigated in submissions. I cannot, however, see that it could possibly carry the day in a case like the present. If textbook writers had adverted to the question of causation in a sense which was favourable to the claimant's case and there were stronger evidence of hyperstimulation specific to this case, matters might be different. But, given the twin obstacles which stand in the path of success, to disregard the normal rule as to the claimant's obligation to prove each element of the tort alleged would be to decide the issue of causation on a purely speculative footing.
Issue (4): failure to deliver by forceps
[80] On 7 December 2005 the solicitors acting for S notified the defence of a proposed amendment to the particulars of claim, adding as an allegation of negligence that the defendant had "failed to deliver the claimant by Kiellands forceps by 2049." The matter is only briefly addressed in the record of the experts' meeting of 12 December 2005, the doctors simply stating that there was no clear explanation or evidence for the failure.
[81] There had so far been no detailed evidence as to the attempted delivery, which was not surprising, given the absence of any relevant criticism. On 9 January 2006 Dr Wood provided a further witness statement, in which he said:
"I can say that all forceps deliveries have a failure rate. In this case I put the forceps blades on the baby's head and although the forceps rotated it was apparent that the head had not. I then took the blades off and re-applied them but the same thing occurred, namely that the blades had rotated but the head had not… The attempt at forceps delivery took only a couple of minutes…
I had thought it would be feasible to deliver the baby vaginally. The head was low enough and the pelvis was adequate…
I chose to use Kiellands forceps due to the position of the head which required rotation."
A pair of Kiellands forceps was produced in court. It was explained by one of the experts, without dissent from the other, that the blades are placed on the narrowest part of the baby's skull, around the lower part of the cheek and on the side of the chin. When they are properly applied, the handles of the forceps are parallel with each other. The instrument must be used with caution, so as not to exert undue pressure on the head. Mr Johnson described Kiellands forceps as the most dangerous tool in obstetrics, which could cause immense damage, but which were nonetheless valuable.
[82] At the beginning of the trial, permission to make the amendment was given without opposition from the RVI. But, until Dr Wood came to be cross-examined, the precise nature of the allegation against him remained unclear. The forceps issue had not been addressed in Mr Redfern's opening, written submission. In his evidence in chief Dr Wood described in detail the technique which he employed in applying the forceps. He said that, after he applied the forceps, he had introduced a finger as to as check exactly where the forceps were in relation to the head. He would then push up the baby's head about 0.25 cm towards the mother's head and rotate the blades. This was the exercise through which he had gone twice in this case. He had twice attempted to rotate S's head through 90° but on each occasion the blades had slipped round the head and rotation was not achieved. Dr Wood said that he had carried out around 130 to 150 deliveries by Kiellands forceps and had experienced slipping on three occasions: on one of these he had been successful on a second attempt.
[83] Early in his examination in chief Dr Wood had said that, in this case, he had "felt the head low enough down in the pelvis." In cross-examination it was put to him, and he denied, that the delivery had failed "because the head was higher than you thought." When Mr Johnson came to give evidence, he said that the most likely explanation for the failure was that, when the attempted delivery was made, the head was above the ischial spines and Dr Wood made an error as to its position. Mr Redfern in his closing submissions asked me to make a finding of fact that the head was above the spines.
[84] One has at once to face the fact that there is an inconsistency as to the position of the head within Dr Wood's operating note. This records a position on palpation of 0/5ths and, on vaginal examination, of "RoT at spines." 0/5ths on palpation is the equivalent of 3 cm below the spines on vaginal examination.[12] It follows that a mistake was made. But, it seems to me, the nature of the mistake, that the head was below the spines when it was at the spines or vice versa, is not such as to lend credence to the possibility that the head was higher than suggested by either part of the note.
[85] Mr Hart enumerated what are, in my judgment, powerful reasons for rejecting the "head too high" explanation. First, accepting the explanation would involve a finding that Dr Esen also was wrong when on his vaginal examination at 1930 he recorded the level of the head as "0", i.e. at the spines. It was, I should observe, never put to Dr Esen in cross-examination that he was mistaken in this respect. Second, I see no reason to reject Dr Wood's evidence when he said that the handles of the forceps were parallel when he attempted rotation. Mr Johnson accepted in cross-examination that, if this evidence were accepted, his theory could not be right. Third, the manner in which the criticism of Dr Wood has crystallised into the "head too high" form is not such as to lend credence to it. Mr Johnson is an acknowledged expert in, and teacher of, the use of Kiellands forceps: yet, as he acknowledged in evidence, he only thought of "head too high" 2 or 3 days before he started to give evidence, and that is in a case in which he has been considering the papers at intervals over a period of close on 5 years.
[86] There are, as Professor Thornton stated, other possible explanations for what happened. It may be that S, who was somewhat bigger than L had been, was "a tight fit in the mother's pelvis and more resistant to rotation." Or it may be that Dr Wood was unfortunate in the forceps with which he was provided: forceps vary, and these could have had a larger than normal separation of the tips. Professor Thornton thought that either explanation was more probable than the making of an error as to the position of the head. He thought the latter explanation highly unlikely, because it involved finding that three mistakes had been made in assessing the position of the head (one by Dr Esen and two by Dr Wood) and also because it seemed inconsistent with Dr Wood's evidence that he had pushed the head up about 0.25 cm.
[87] For reasons which will now be apparent, I prefer Professor Thornton's approach. It is not possible to say why the forceps delivery failed; but, whatever the reason, it is, in my judgment, improbable in a high degree that the failure is attributable to the position of the head being above the spines.
[88] Mr Johnson also had what Mr Hart called his fallback position. There is some uncertainty as to his evidence on this but, taking it at its highest from the claimant's point of view (from the note of Mr Redfern or his instructing solicitor), Mr Johnson would also criticise an attempted forceps delivery being made when the head was at the spines save in a real medical emergency. That criticism, which might or might not have merit in other circumstances, does not, in my judgment, do anything to advance the claimant's case. Whatever happened or did not happen at 2045 on the evening in question, I have no doubt as to the existence of a real emergency.
Conclusion
[89] It follows that the claim fails. This is not a result which can give satisfaction to S's parents. I am sure that their lawyers have done what was, in the circumstances, the very best that could be done in attempting to make good S's claim. I must, however, say, without intending any criticism either of the lawyers or of Mr Johnson, that the various shifts in the nature of the claimant's case have fortified me in my conclusion that it is not one which can succeed. The longer I have studied the material which is before me, the more clearly it appears that what occurred was not the fault of any of the doctors or midwives at the RVI who were involved in the care of Mrs L.
