Cowley v Cheshire & Merseyside Strategic Health Authority

Introduction. The Claimant, Jamie Andrew Cowley (hereafter “Jamie”) was born prematurely at the Defendant’s Countess of Chester Hospital (“the hospital”) on 16^th April 1991 at 23:38. At delivery, Jamie was 27 weeks 6-plus days’ gestation by dates. Sadly, Jamie has significant brain damage that can be broadly described as cerebral palsy.

It is the essential thrust of Jamie’s case in these proceedings that betamethasone (a cortico-steroid) should have been administered to his mother (“Mrs Cowley”) following her admission to hospital in the late afternoon of 15^th April 1991, rather than at the time it was actually administered (i.e. approximately 24 hours later at 6pm on the 16^th April), and that if that had been done the brain damage suffered by Jamie would have been notably reduced. The Defendant disputes both breach of duty and causation if breach of duty is established. This trial is concerned only with the determination of those liability issues.

The Facts. I now turn to give an account of the relevant facts as I find them to be, following consideration of all the evidence that I have heard and read in the course of this trial. In doing so, I have taken fully into account the detailed and helpful oral and written submissions made by Mr Robert Francis QC on behalf of Jamie and Mr Michael de Navarro QC on behalf of the Defendant.

Prior to the pregnancy that led to the birth of Jamie, Mrs Cowley had given birth to two other preterm children: in 1987 to a boy, Gary, at 35 weeks gestation and in 1990 to another boy, Ben, at 33 weeks gestation. These pregnancies appear to have been complicated respectively by (in Gary’s case) a urinary tract infection and (in Ben’s case) by a significant ante-partum haemorrhage, most likely a placental abruption. Mrs Cowley has also had a subsequent pregnancy in 1994, leading to the birth of another boy, Jack, at 35 weeks gestation. Gary, Ben and Jack were all healthy babies, albeit having been born prematurely. In each case, Mrs Cowley was treated and the baby was born at the hospital.

In Gary’s case, the pregnancy went smoothly until 35weeks, when Mrs Cowley went into premature labour. She had been experiencing regular abdominal “tightenings” at home and so she went to the maternity unit at the hospital and told the attending staff that she thought she was going into labour. Although attempts were made to reassure her that this was not the case, Mrs Cowley nevertheless was kept in hospital that night for observation.

During the night, Mrs Cowley continued to have regular abdominal tightenings. Initially the tightenings were not accompanied by pain. However, there came a stage when she began to experience regular tightening and pain at the same time and, by the following morning, the pain had become quite severe. On a couple of occasions during the night, Mrs Cowley’s condition was checked by staff, but each time she was told that she was definitely not in labour and she was given a modest amount of analgesics to ease the pain. Eventually, a passing midwife agreed to give Mrs Cowley an internal examination. As a result, Mrs Cowley was taken to the delivery room within minutes where Gary was delivered very shortly afterwards. Mrs Cowley was then told that it was accepted that she had, in fact, been in labour all night.

In Ben’s case, at 33 weeks Ms Cowley experienced pain and abdominal tightenings that appeared to her to be exactly like those she had experienced in Gary’s case. In light of her experience with Gary, Mrs Cowley was taken into hospital by her husband. Her waters broke almost as she was going through the doors of the hospital and Ben was delivered within about an hour after that.

Mrs Cowley became pregnant with Jamie in November 1990. On 27^th December 1990, her GP referred Mrs Cowley to the hospital for shared care. In his referral letter, Mrs Cowley’s GP stated: “… She had two normal deliveries in 1987 and earlier this year, both very early, one at 35 weeks and the second at 33 weeks. Her LMP [last menstrual period] was 3^rd October.”

On 14^th January 1991, Mrs Cowley attended her first antenatal clinic in relation to her pregnancy with Jamie. The expected date of delivery was estimated to be 10^th July 1991 and her two earlier premature deliveries were noted as a “special consideration”. Her next antenatal clinic was arranged for the 28^th week of her pregnancy. Mrs Cowley also underwent an ultrasound scan on 11^th February 1991. Neither then nor at any of her GP attendances were any abnormalities noted.

On the morning of 15^th April 1991 Mrs Cowley attended the hospital for her 28-week clinic. She was seen by a registrar who told her that it was almost certain that she would again have a premature birth and that, at the first sign of anything hinting at her going into labour, she should come into the hospital immediately. The gestation period was calculated to be “27 +” weeks (it appears to have been 27 weeks 5 days) and no abnormalities were noted.

After the antenatal clinic, Mrs Cowley returned home. During the afternoon of the same day (i.e. 15^th April) she began to experience regular “slight”, pain-free abdominal tightenings and, when she went to the toilet at about 3.30 pm she had a “show”, i.e. a discharge of bloodstained mucous. Mrs Cowley described what she saw as a “brown, mucous, jelly-like show”. Mr Stephen Andrew Walkinshaw (“Mr Walkinshaw”), who gave expert obstetric evidence on behalf of the Defendant, readily acknowledged that, with the benefit of hindsight, there was no reasonable doubt that what Mrs Cowley described was indeed a “show”. Mrs Cowley had not experienced this before. She was alarmed and became concerned that she was going into labour. So it was that Mrs Cowley went to the hospital, arriving there at about 4.15 pm on 15^th April. She was then admitted to the labour suite at about or shortly before 5 pm, by which time she was experiencing “some measure of pain” at the same time as the abdominal tightenings. In the event, although the regular tightenings continued, the associated pain ceased during the afternoon/evening of the 15^th April and did not start again until the afternoon of the 16^th April.

On admission to the labour suite, Mrs Cowley was initially assessed by a midwife who recorded a history of “lower abdominal pain and a show today at 15.30”. The midwife went on to note that Mrs Cowley was well, that the fundal height was appropriate for gestation and that the presenting part was cephalic. The midwife did not make any record or note of tightenings or contractions. A CTG was performed and was said to be reactive. The trace was timed at 1702 and continued until 1725. According to Mr Walkinshaw, the CTG trace records some uterine activity and there are indications of 2 possible uterine contractions during a period of just over 20 minutes and separated by an interval of about 10 minutes. The variability on the trace was normal and it is likely that the baseline rate of the foetal heartbeat was 155 bpm.

Shortly after Mrs Cowley had been seen and assessed by the midwife, she was examined by Dr Kathryn Fishwick (“Dr Fishwick”), a Senior Senior House Officer. It is to be noted that Dr Fishwick is now a Consultant Obstetrician and Gynaecologist. However, for convenience, I will continue to refer to her as Dr Fishwick rather than as Miss Fishwick. Although, understandably after such an interval of time, Dr Fishwick has no present recollection of her examination of Mrs Cowley, I am satisfied that the written notes that she made at the time were both adequate and accurate as to detail and that she was therefore able to and did give a fair and balanced account of the examination and her findings based on those notes.

Dr Fishwick’s attendance on and examination of Mrs Cowley lasted for some 10 to 15 minutes and took place shortly after 5 pm and before 5.40 pm. Dr Fishwick noted that Mrs Cowley was at 28 weeks’ gestation and that she had experienced two previous preterm labours. Based on information that she obtained from Mrs Cowley (but not necessarily using her words), Dr Fishwick recorded that Mrs Cowley had attended the hospital with “? Braxton Hicks [contractions] but associated with supra-pubic pain & [urinary] frequency.” Braxton Hicks contractions are quite commonly experienced during pregnancy and differ from the painful contractions to which a patient is subject during the onset and course of labour. Braxton Hicks contractions are characteristically pain free (although this can depend on the patient’s subjective perception of what constitutes pain) and do not result in any cervical dilatation and vaginal delivery.

However, during her attendance and examination, Dr Fishwick did not herself observe or detect any contractions, nor did Mrs Cowley appear to be distressed by any pain. I am satisfied that Dr Fishwick would have made an appropriate note of any such condition had it happened during her examination. Equally, if Dr Fishwick had been given a history of regular and/or significant contractions, she would have recorded that in her notes. As Mrs Cowley herself accepted, her abdominal tightenings were occurring at intervals of about 10 minutes and the pain associated with the tightenings had ceased at some stage during the afternoon/evening of the 15^th April, although she was unable to say precisely when. In my view, it is very probable that the pain associated with the tightenings had actually ceased at some stage shortly before Dr Fishwick’s attendance and examination, hence the content and terms of Dr Fishwick’s notes. As a matter of routine, Dr Fishwick considered the possibility of a urinary tract infection and so she noted a requirement for a mid-stream sample of urine to be taken for the purposes of analysis.

On examination Dr Fishwick found Mrs Cowley’s abdomen to be soft, with no evidence of tenderness. The uterus was consistent with 28 weeks’ gestation. Dr Fishwick was able to feel the foetal parts easily. She determined that the presentation was cephalic and that the head was free in the abdomen. Dr Fishwick drew a diagram in the notes and noted the findings of her abdominal examination both in and beside the diagram.

Having carried out an abdominal examination of Mrs Cowley, Dr Fishwick then performed a vaginal examination and found Mrs Cowley’s cervix to be posterior, soft but not dilated. I accept her evidence that her clinical findings revealed no evidence of cervical change that would support a diagnosis of pre-term labour nor were there any factors suggesting that pre-term labour was likely – in particular, there was no evidence of any significant uterine contractions: see paragraph 4 of Dr Fishwick’s supplemental witness statement. She therefore correctly concluded that Mrs Cowley was not in actual pre-term labour. However, in view of Mrs Cowley’s previous history, Dr Fishwick decided that it was appropriate to keep her in for observation and later reassessment. Dr Fishwick recorded her findings and conclusions in the notes and Mrs Cowley was transferred to Ward 34, apparently arriving there at 1740. I accept that, had Mrs Cowley not had a previous history of premature deliveries, Dr Fishwick would not have considered admitting Mrs Cowley to hospital on the basis of her presenting symptoms: see paragraph 4 of Dr Fishwick’s supplemental witness statement.

The Consultant Obstetrician and Gynaecologist under whose care Mrs Cowley was admitted to the hospital was Mr John Davies-Humphreys. I accept his evidence concerning the hospital’s policy in 1991 in relation to the administration of cortico-steroids in cases of premature labour (“the hospital’s premature labour policy”), as set out in paragraph 5 of his witness statement, as follows:

“5.

Our Policy in Chester in 1991 (which was agreed by all the Consultants in post at that time) was to administer Betamethasone only to those women in whom premature labour had been diagnosed as opposed to being possible or likely. The diagnosis of labour is made by the concurrence of regular painful uterine contractions and cervical dilatation. If the relevant criteria for the diagnosis of labour were present, then Betamethasone was administered and a Ritodrine drip commenced to try and delay delivery for sufficiently long to allow the Betamethasone to exert its beneficial effect. One would be hoping to delay delivery by 24 hours, but this is not always possible.”

Mr Davies-Humphreys stated that the hospital’s premature labour policy had existed since about 1987 and, although it was not recorded in writing until 1992, it was a very firm one. The policy was to administer cortico-steroids (i.e. betamethasone) and the associated tocolytic treatment (i.e. ritodrine or indomethacin: as to which, see below), but only once the patient had been diagnosed as being in actual premature labour (“preterm labour”) and not before. I accept that, from its inception, this policy was regularly discussed at the many perinatal meetings attended by Mr Davies-Humphreys and his colleagues and consideration was given to the question whether cortico-steroids should be administered at an earlier stage than when the diagnosis of actual preterm labour was made. However, every time the matter was discussed it was decided to maintain the existing policy of administering cortico-steroids only once a diagnosis of actual preterm labour had been made.

Mr Davies-Humphreys explained that the reasons that he and his team adopted and maintained a policy of giving cortico-steroids only to those women in whom actual preterm labour had been diagnosed, as opposed to being possible or likely, were:

Prior to 1989, the use of cortico-steroids in women in actual or threatened preterm labour was uncommon (see the obstetric experts’ agreed answer to Question 1 of the Defendant’s agenda) and there were concerns about possible adverse side effects. However, “Effective Care in Pregnancy and Childbirth” edited by Iain Chalmers et al (hereafter “Chalmers’ “Effective Care””) was published in 1989. This was soon followed by a paper written by Patricia Crowley, Iain Chalmers and Marc Keirse entitled “The effects of corticosteroid administration before preterm delivery: an overview of the evidence from controlled trials”, which was published in January 1990 in the British Journal of Obstetrics and Gynaecology (hereafter “Crowley 1990”). Both publications provided powerful evidence in support of the case for the appropriate administration of antenatal cortico-steroids in cases of premature delivery and it is clear that their publication marked the beginning of a sea-change in the profession’s overall approach to the use of these drugs in cases of preterm labour and delivery in order to address and reduce the significant risk of neonatal respiratory distress syndrome in premature babies (“RDS”). I should add that I accept Mr Walkinshaw’s evidence that, in the circumstances, it was reasonable for the profession to take up to 2 years from 1990 to change its approach in response to Crowley 1990. It is therefore helpful to quote the following passages from the texts of both publications.

In Chalmers’ “Effective Care” the relevant conclusions are expressed as follows (see pages 761-2):

“6 Conclusions

6.1

Implications for current practice

This overview of randomised trials provides ample evidence that antenatal treatment with 24 mg betemethasone, or 24 mg dexamethasone, or 2 g hydrocortisone is associated with a significant reduction in the risks of neonatal respiratory distress. This reduction is of the order of 40 to 60 per cent and is independent of gender. Furthermore, the benefit of antenatal corticosteroids appears to apply to babies born at all gestational ages at which respiratory distress syndrome may occur. While the greatest benefits are seen in babies delivered more than 24 hours and less than 7 days after commencement of therapy, babies delivered before or after this optimum period also appear to benefit. This reduction in the risk of respiratory distress is accompanied by reductions in periventricular haemorrhage and necrotizing enterocolitis. This in turn results in a reduced mortality rate and in a reduction of the cost and duration of neonatal care.

These benefits are achieved without any detectable increase in the risk of maternal, fetal, or neonatal infection, even in the presence of prolonged rupture of the membranes. Antenatal corticosteroid therapy does not increase the risk of stillbirth.

6.2

Implications for future research

The benefits of antenatal corticosteroids have been established. No further trials are necessary with the exception of certain specific situations (such as pre-eclampsia) or to establish other dosages or routes of administration. Specifically, a trial to establish the correct dose of drugs to use in multiple pregnancy would be helpful. …”

In Crowley 1990, the authors’ summary was expressed in the following terms:

“Summary. Continuing differences of opinion among obstetricians and neonatalogists about the place of corticosteroid administration before preterm delivery have prompted us to carry out a systematic review of the relevant controlled trials using methods designed to minimize systemic and random error. Data from 12 controlled trials, involving over 3000 participants, show that corticosteroids reduce the occurrence of respiratory distress syndrome overall and in all the subgroups of trial participants that we examined. This reduction in respiratory morbidity was associated with reductions in the risk of intraventricular haemorrhage, necrotizing enterocolitis and neonatal death. There is no strong evidence suggesting adverse effects of corticosteroids. The risks of fetal and neonatal infection may be raised if they are administered after prolonged rupture of the membranes, but this possibility is not substantiated by the results of the trials. The available data on long-term follow-up suggest that the short-term beneficial effects of corticosteroids may be reflected in reduced neurological morbidity in the longer term.”

The discussion section of Crowley 1990 contains the following passages:

“Discussion

This overview of radomized trials of antenatal corticosteroid administration … has shown that corticosteroid administration leads to statistically and clinically significant reductions in neonatal morbidity and mortality, and that these are very unlikely to be outweighed by unwanted effects of these drugs … Overall, the reduction in the odds of neonatal respiratory morbidity is of the order of 40 – 60%. Further, the beneficial effects of antenatal corticosteroids appear to apply to babies born at all gestational ages at which respiratory distress syndrome may occur, and regardless of whether or not there has been prelabour rupture of the membranes. Although babies born 24 h and 7 days after beginning steroid administration may well benefit most from prophylaxis, the evidence suggests that babies born outside this optimum period can also benefit. There is no evidence to support the view that the gender of the baby modifies these effects. Indeed, we have been unable to identify any subgroup of babies at risk of respiratory morbidity for which thee are data to justify a conclusion that corticosteroids have no beneficial effect.

The clear-cut reduction in the risk of respiratory distress is, as far as we can judge from the admittedly limited data available, accompanied by reductions in periventricular haemorrhage and necrotizing enterocolitis. All of this results in a reduced early neonatal mortality rate and reductions in the duration, and thus the costs, of hospital neonatal care.

…

A number of possible short-term and long-term risks of antenatal corticosteroid administration have been considered. … The immunosuppressive effects of corticosteroids could result in an increased susceptibility to fetal, neonatal or maternal infection, or to a delay in its recognition. Over the 11 years following the introduction of corticosteroids for fetal lung maturation in England and Wales, there were two maternal deaths from septicaemia associated with their use. … It is these two deaths that underlie the opposition of some British obstetricians to the use of corticosteroids for fetal lung maturation.

In the presence of intact membranes, there is no clear evidence of an increase in the risk of maternal, fetal or neonatal infection. In the presence of prolonged rupture of the membranes, the absolute risk of fetal and neonatal infection may be greater, but again, controlled trials provide no strong evidence that corticosteroids increase this risk. …

…

It is important to recognize that the neonatal respiratory distress syndrome is common in infants of mothers with pre-eclampsia delivered pre-term: for example, it affected 36% of babies of women with pregnancy-induced hypertension in the placebo arm of the Collaborative Group trial … In the light of the available data, it would seem reasonable to use corticosteroids to reduce this considerable neonatal morbidity, provided the commitment to early delivery implied by corticosteroid treatment is carried through. Those obstetricians who remain uncertain that the demonstrable advantages of this policy would be outweighed by possible disadvantages in hypertensive women, or in other circumstances, should collaborate in further ramdomized trials to provide evidence on which to base their practice more firmly.”

It is important to note that in 14 out of 15 pre-1991 controlled trials, twelve of which provided the data for the Crowley 1990 paper, the participants were women who were all expected to deliver preterm as the result of either spontaneous preterm labour, pre-labour/premature rupture of the membranes or elective pre-term delivery: see the Schedule of Qualifying Criteria in the Cortico-Steroid Trials attached to Mr de Navarro’s written opening note. In only one of the trials (the 1981 US Steroid Trial) was the qualifying criteria expressed in terms inconsistent with the incidence of actual preterm labour, i.e. “Hospital admission with high risk of pre-term delivery”, with no definition of what constituted “high risk.” As Mr de Navarro observed and subject to what was meant by “high risk” in the 1981 US trial, none of the trials was concerned with “threatened preterm labour and it was common ground that Mrs Cowley’s condition on 15^th April 1991 would not have satisfied the qualifying criteria of 14 out of 15 of the trials.

It can therefore be seen that the main benefits to be derived from administering appropriate antenatal cortico-steroid medication in cases of premature labour is that it renders less likely that the baby will develop respiratory distress syndrome (“RDS”) in the neonatal period and it also reduces the risk of periventricular haemorrhage (“PVH”). On this aspect of the matter there was no issue between the two obstetric expert witnesses who gave evidence in this case (Mr Gerald Joseph Jarvis – “Mr Jarvis” – on behalf of the Claimant and Mr Walkinshaw on behalf of the Defendant). However, it is important to note that in 1991 there was no authoritative (or any) guidance as to when the antenatal cortico-steroids should be administered to the patient – either from Chalmers, Crowley, the Royal College of Obstetricians and Gynaecologists (“RCOG”) or anyone else. Nor was there any express recommendation in 1991 that cortico-steroids should be administered in cases of threatened preterm labour. It was not until 1996 that RCOG issued the following guidance:

“ANTENATAL CORTICOSTEROIDS TO PREVENT

RESPIRATORY DISTRESS SYNDROME

1.

INTRODUCTION

Respiratory distress syndrome (RDS) affects 40-50% of babies born before 32 weeks. Evidence has been available since 1972 that the administration of corticosteroids prior to preterm delivery reduces the incidence of RDS. However, the use of antenatal corticosteroid therapy has been hesitant. An audit of preterm babies born in district general hospitals at a gestational age of less than 31 weeks in 1992 revealed that only 35% had antenatal exposure to corticosteroid therapy.

2.

EFFECTIVENESS

A meta-analysis of fifteen randomised controlled trials indicates that antenatal corticosteroid therapy reduces the incidence of RDS. There is an associated reduction in the risk of neonatal death and intraventricular haemorrhage. The efficacy of neonatal surfactant therapy is enhanced by antenatal exposure to corticosteroids. There is evidence of a benefit in all major sub-groups of preterm babies irrespective or race or gender.

…

TREATMENT DELIVERY INTERVAL

The effect of treatment is optimal if the baby is delivered more than 24 hours and less than seven days after the start of treatment. However, there is a trend toward a benefit in babies delivered before and after the optimal treatment interval has elapsed.

…

3.

REPEATED DOSES

It is important to emphasise that all evidence concerning safety and immediate and long-term side effects is derived from the randomized trials where a single course of treatment was administered. There are no randomized trials of repeated doses of antenatal corticosteroid therapy. The practice of repeating the course of treatment weekly has arisen in cases where the risk or preterm delivery persists or recurs following the initial treatment. The theoretical risks of this approach include some long-term effects on cognitive or neurological development that did not occur in the randomized trials which dealt with single courses of treatment only. …

…

6.

INDICATIONS FOR ANTENATAL CORTICOSTEROID THERAPY

Every effort should be made to initiate antenatal corticosteroid therapy in women between 24 and 36 weeks’ gestation with any of the following:

Threatened preterm labour

Antepartum haemorrhage

Preterm rupture of the membranes

Any condition requiring elective preterm delivery. …”

It is to be noted that the RCOG guidance does not say what is meant by “threatened preterm labour” and it was common ground that there is no generally accepted definition of that condition in the profession.

As is apparent from their curricula vitae, both the obstetric experts are very distinguished. Mr Jarvis was Consultant in Obstetrics and Gynaecology at St James’ University Hospital in Leeds from 1981 to 2002. In 2002 he retired from NHS practice and ceased practising as a Consultant Obstetrician. However, he continues to practice as Consultant in Gynaecology at The BUPA Hospital in Leeds. Urinary gynaecology was and remains Mr Jarvis’ primary specialisation. Mr Walkinshaw is a consultant obstetrician and is currently the Consultant in Maternal and Fetal Medicine at the Liverpool Women’s Hospital (formerly the Liverpool Maternity Hospital), having been appointed to that post in 1989.

From 1989/1990 onwards, Mr Walkinshaw has played a prominent part in promoting the use of antenatal cortico-steroids in order to achieve the foregoing benefits and I accept his evidence with regard to the benefits in question and the appropriate timing of the treatment, as summarised in paragraphs 5.14 and 5.15 of his expert’s report (and see also paragraphs 22 to 24 of Mr Jarvis’ report, which are to the same general effect):

“5.14

The use of steroids with delivery between 24 hours and 7 days after administration of the first dose reduces the odds of RDS by about 62% according to the Cochrane review last updated in 1996. In numerical terms 87 of 346 (25.1%) babies not achieving this will develop RDS compared with 44 of 382 (11.5%) who did receive full dose and deliver in this time interval. Delivery within 24 hours of the first dose reduced the rate of RDS by 30% (57 of 176 compared with 46 of 176).

5.15

It also reduces the risk of Periventricular haemorrhage by 52% using ultrasound diagnosis. Where steroids were not used then 26% of infants will have an intraventricular haemorrhage, whereas if steroids are given then 15.7% will have this complication. Long-term morbidity is reduced by 38% from 8% to 5.7% by the use of steroids.”

For his part, Mr Davies-Humphreys quite rightly accepted that, in order to achieve the maximum beneficial effect, the cortico-steroids should be administered at least 24 hours (but not longer than 7 days) before delivery of the premature baby. Appropriate tocolytic medication (i.e. ritodrine or indomethacin) was therefore routinely administered in conjunction with the betamethasone in order to try and extend the pregnancy by stopping contractions temporarily, thus delaying delivery sufficiently to bring it within the 24-hour to 7-day window required to achieve the maximum beneficial effect. Mr Davies-Humphreys readily acknowledged that the tocolytic treatment did not always work and was only successful in achieving the desired minimum 24 hour period between administration of the cortico-steroids and delivery in about 50% of cases involving treatment in accordance with the hospital’s pre-term labour policy (i.e. upon diagnosis of actual pre-term labour and not before). It was common ground that, once labour has commenced, it is most likely to be less than 24 hours in duration if allowed to progress naturally and the extent to which it will be extended by tocolytic medication will depend upon the effectiveness or otherwise of the tocolytic agents administered (see the obstetric experts’ agreed answers to question 3 of the Claimant’s Agenda).

It is clear from the medical literature to which I was referred and the evidence of both obstetric expert witnesses (in particular that of Mr Walkinshaw) that, as a fact, the hospital’s premature labour policy fell within the range of policies that were applied by obstetricians in 1991, which appear to have ranged from no use of cortico-steroids at all to their liberal use in any case where premature labour was possible and I accept Mr de Navarro’s submission to that effect: see paragraph 4 of his written closing note. It is perhaps worth noting that, if anything, the hospital appears to have been somewhat ahead of the game by adopting the policy it did as early as 1987.

As I have already stated (see paragraph 17 above), having regard to what she found when she carried out her examination of Mrs Cowley on 15^th April 1991, Dr Fishwick was right to conclude that Mrs Cowley was not then in actual or active preterm labour. Again, this much was common ground. For there to be actual preterm labour “the cervix should be at least 2 cm dilated and changing in some way with time”: see the obstetric experts’ agreed answer to question 7 of the Defendant’s agenda. Furthermore, in the course of his evidence, Mr Jarvis readily accepted that Mrs Cowley was clearly not in active premature labour when Dr Fishwick examined her during the late afternoon of the 15^th April 1991.

It is important to note that, having correctly concluded that Mrs Cowley was not in actual preterm labour, Dr Fishwick then consciously applied the hospital’s premature labour policy. This meant that Mrs Cowley was not treated with cortico-steroids (nor, for that matter, with any tocolytic medication). As Dr Fishwick said in evidence (according to my note of her cross-examination):

“My diagnosis was that she [Mrs Cowley] was not in labour. I was very junior and I followed routine departmental management policy. Betamethasone was not administered without a diagnosis of labour. So betamethasone would not have been considered in the light of my findings and diagnosis. But with 2 previous premature deliveries I decided to admit her for observation.”

Mr Jarvis also readily accepted in the course of cross-examination that, in treating Mrs Cowley as she did on 15^th April, Dr Fishwick was acting entirely in accordance with the hospital’s premature labour policy. Given that the essence of the Claimant’s case on breach of duty is that betamethasone should have been administered to Mrs Cowley following her admission in the late afternoon of 15^th April 1991, rather than in the evening of the 16^th April (see paragraph 2 of Mr Francis’ written skeleton argument), a crucial issue relating to breach of duty in this case is whether the hospital’s premature labour policy was within the range of policies an obstetric unit could reasonably have had in 1991: see paragraph 2(a) of Mr de Navarro’s written closing note.

The “Kardex” nursing record shows that, shortly before Mrs Cowley was transferred to Ward 34, a dipstick urine test was carried out and no abnormality was detected. Although not a conclusive test for urinary tract infection, the dipstick test did show that there was no protein in the urine and established that a urinary tract infection was very unlikely. As I have already stated, Mrs Cowley was admitted to Ward 34 at 1740. At the time of admission the foetal heart rate was regular, Mrs Cowley appeared to be “not bothered” and the required midstream urine sample was duly taken.

Mrs Cowley appears to have slept well during the night of 15^th/16^th April and felt well in the morning. I accept Mr Walkinshaw’s following assessment of the position (see paragraph 6.6 of his report): “… Mrs Cowley’s symptoms settled and she slept through the night. Therefore the period of observation did not flag any indication for change in practice.” Although she had continued to experience abdominal tightenings at regular intervals through the night, they had been pain free and she was unable to say how often they had occurred. Mrs Cowley’s condition on the morning of 16^th April was duly noted in the Kardex record in the following terms: “16/4/91 Slept well. Feels well. No further contraction pains just normal Braxton Hicks. No further show …” The foetal heart rate was heard to be regular and foetal movement was felt. However, as Mr Davies-Humphreys observed in paragraph 7 of his witness statement (correctly, in my view), there was no indication at this stage that labour had commenced or was imminent.

Mrs Cowley continued to experience abdominal tightenings at regular intervals throughout the morning and into the afternoon of 16^th April. However, these remained pain-free until quite late in the afternoon when she again began to experience pain at the same time as each tightening. As the result of her complaining about the renewed pain, Mrs Cowley was seen and examined by another Senior Senior House Officer, Dr Charlotte Porter (“Dr Porter”), who is now a Consultant in Reproductive and Sexual Health Care.

The time of Dr Porter’s attendance and examination is not recorded, but it appears to have taken place shortly before 4 pm (see the timing of the first administration of ritodrine and indomethacin as recorded in the Kardex and Drugs records).

I accept Dr Porter’s evidence with regard to her attendance on and examination of Mrs Cowley that afternoon: see paragraphs 4 and 5 of her witness statement, which are in the following terms:

“4.

I first saw Mrs Cowley on 16^th April 1991. She was 28 weeks gestation, in her fourth pregnancy, having had two previous premature labours, one at 35 weeks and one at 33 weeks. I have recorded in my Notes that in her first pregnancy, Mrs Cowley niggled into labour, but in the second pregnancy had a placental abruption which precipitated labour. My recollection is that at the time routine re-assessment of women presumed to be at risk of premature delivery was to undertake a speculum examination to avoid the introduction of infection and at this examination it was seen that there had been cervical change and that consequently this lady was at risk of premature delivery.

5.

I prescribed Indomethacin to be given rectally and for oral Ritodrine to be given in a 10 milligram dose 2 hourly. Both these drugs are tocolytic agents. I also prescribed a cortico-steroid, Betamethasone. I did so in accordance with the policy in force at the time.”

In her clinical notes, Dr Porter recorded that when Mrs Cowley had been examined the previous day her cervix had been considered to be a “multips os”: i.e. not dilated or indicative of labour. However, Dr Porter’s speculum examination showed the cervix to be 2 cms dilated and the membranes bulging, hence her decision that Mrs Cowley was at such risk of premature delivery as to make appropriate the administration of tocolytic agents in conjunction with betamethasone, i.e. that Mrs Cowley was by then, to all intents, in preterm labour. No criticism is made of that decision and the records show that the onset of labour was timed at 1530 on 16^th April.

The records also show that the tocolytic agents were first administered in accordance with Dr Porter’s prescription at 4 pm, but the betamethasone was not administered until 6 pm. As I understand it, there is no medical reason that prevents the administration of cortico-steroids within a short time of the tocolytic medication and there appears to be no specific explanation for the apparent delay in the administration of the betamethasone in this case. There is no suggestion that this apparent short period of delay in itself constituted a breach of duty. It was Mr Jarvis’ view that the timing of the betamethasone showed “rather a relaxed approach”. However, Mr Davies-Humphreys said that although the tocolytic agents and the steroids should be administered within a reasonable time of each other, it would be reasonable to give the steroids within an hour or two of the diagnosis of labour.

At the same time as she recorded the administration of the betamethasone (i.e. at 1800), the midwife noted that a regular foetal heart rate was heard and continued her note in the following terms: “Baby active. Having occasional tightenings between Braxton Hicks [contractions]. Will inform us if she gets any different.”

At 2000, the midwife noted a red vaginal loss and stronger but irregular contractions. A CTG was commenced which showed regular uterine activity. Dr Porter was informed and she had Mrs Cowley transferred to the delivery suite. I accept her account of what happened, which is in the following terms (see paragraphs 6 to 8 of her witness statement):

“6.

Later in the same day [i.e. 16^th April 1991], I was asked to review Mrs Cowley as she had had a small vaginal bleed. This was particularly concerning in view of her history of a previous pregnancy placental abruption. There was some concern about the fetal welfare, at this time, but the CTG was repositioned and there was no immediate concern with regard to performing an imminent delivery.

7.

In view of the bleed, the lady was transferred to the Delivery Suite as further prolongation of the pregnancy in a lady who was bleeding would be inappropriate. An ultrasound scan was performed to confirm the presenting part and a further speculum examination done which showed bulging membranes.

8.

Vaginal examination performed following this showed the cervix was fully dilated and the Paediatricians and Consultant on call were informed prior to awaiting spontaneous vaginal delivery.”

At 2115, there was a further small vaginal bleed (recorded as 40 ml) whilst Mrs Cowley was in the delivery suite. The ultrasound scan confirmed a cephalic presentation. Mrs Cowley progressed in labour, the amniotic membranes ruptured spontaneously at 2334 and Jamie was born by normal vaginal delivery at 2338. According to Mr Walkinshaw, the intrapartum CTG was entirely normal. The placenta delivered at 2345 and there was evidence of marginal placental abruption at delivery.

Mr Francis made it clear that no criticism is made of the treatment given immediately prior to and during delivery, nor did he criticise the neonatal care that Jamie subsequently received. As I have already indicated, the essential complaint is that there was a negligent failure to administer betamethasone to Mrs Cowley immediately following her admission on the afternoon of the 15^th April, rather than on the afternoon of the 16th. It is important to note that the Defendant is not criticised for any failure to administer tocolytic agents on the 15^th April. Mr Jarvis readily acknowledged that tocolytic agents do not provide any prophylactic benefit and that, therefore, it would be good practice to administer tocolytic medication during painful contractions and to cease their administration if the contractions become painless. He then went on to state: “I therefore consider that the way the tocolytic agents were used in this case cannot be criticised”.

It was therefore common ground that, on any view of the events of the afternoon of 15^th April, it would not have been appropriate to continue or commence the administration of tocolytic agents once Mrs Cowley’s tightenings became pain free during the afternoon of the 15^th April and, as I have already indicated, it is very probable that this occurred shortly before Dr Fishwick’s examination. In my view, the fact that it is common ground that Dr Fishwick was right not to initiate any tocolytic medication on 15^th April itself provides significant support for the suggestion that she did not act negligently, by the standards of the profession in 1991, in failing to administer cortico-steroids to Mrs Cowley that afternoon. I accept the evidence of Mr Walkinshaw that, in 1991, the use of cortico-steroids was inextricably linked to the use of tocolysis. In effect, if treatment with the latter was appropriate it was the trigger for the former. In Mr Walkinshaw’s Liverpool unit, the policy in 1991 was not to give antenatal cortico-steroids without also giving appropriate tocolytic treatment. The tocolytic agents that were used were very dangerous. They could cause maternal death and could affect the baby’s circulation before birth and it was established medical practice that the doctor did not expose the mother or baby to these drugs (i.e. the tocolytic agents) unnecessarily. Accordingly, in the ordinary way tocolytic treatment was only given when preterm labour had been diagnosed or where there was a very real threat that preterm labour was imminent: see, for example, the qualifying criteria for Mr Walkinshaw’s Liverpool unit (see paragraph 64 below).

Although the neonatal care that Jamie received is not criticised, it is necessary to summarise its main features and Jamie’s progress because of their relevance to the issue of causation. The essential details are not in dispute and are conveniently set out in paragraphs 5 to 24 of the report prepared by Professor John Stephen Wyatt (“Professor Wyatt”), the expert paediatric witness who gave evidence on behalf of the Claimant, as follows:

“5.

Jamie’s birthweight was 1.24 kg. … At birth Jamie was blue and floppy, the heart rate was approximately 60 bpm and there was no respiratory effort. The Agpar score at one minute was 2.

6.

At 2 minutes he was transferred to the Special Care Baby Unit, and … a tube was inserted into the trachea. Adrenaline … was given via the endotracheal tube. The heart rate rose to 90 bpm at 4 minutes of age and to 170 bpm at 6 minutes …. The Agpar score at 5 minutes … was 6. He became pink in colour at 8 minutes … and the Agpar score at 10 minutes … was 8. Mechanical ventilation was commenced … An intravenous dextrose infusion was commenced.

7.

A capillary blood gas sample at one hour [was taken and analysed] … Chest X-ray at one hour … showed appearances compatible with respiratory distress syndrome (RDS) … An umbilical artery catheter was inserted. Blood cultures were taken and subsequently no growth of organisms was detected. At two hours … an arterial blood gas sample [was taken and analysed] … Antibiotic treatment with penicillin and neticillin was commenced and ethamsylate was given (to reduce the risk of intracranial bleeding). Vitamin K was given. A first dose of surfactant was given via the endotracheal tube. …

8.

Over the following hours, Jamie’s condition was stable although he continued to require a high inspired oxygen concentration … On 17 April a second dose of surfactant was given via the endotracheal tube. The tube was changed for one of larger diameter and Jamie apparently tolerated this procedure well. At 1600 on the same day the medical records note that Jamie’s blood gas values were deteriorating. A continuing deterioration was noted in his condition subsequently, with a progressive decrease of oxygen saturation, increase in arterial carbon dioxide tension and cyanosis. There was no improvement following adjustment of the ventilation settings. Albumin … was given intravenously. A repeat X-ray showed severe respiratory distress syndrome with pulmonary interstitial emphysema. At 1645 the oxygen saturation was below 50% despite an inspired oxygen concentration of 100% and a peak inspiratory pressure of 35 cm. …

9.

The arterial oxygen saturation continued to decrease and it was decided to change the endotracheal tube. … It was decided to use a 2.5 size tube. The tube insertion was successful and Jamie recovered slowly. Oxygen saturation improved for a short time but started then to decrease again. At 1815 it was decided to insert a larger endotracheal tube since there was an air leak with the smaller tube size. However, despite this there was a further deterioration in the respiratory function with increasing cyanosis and increasing arterial carbon dioxide tension despite maximal ventilatory settings. A chest x-ray showed changes consistent with severe respiratory distress syndrome, pulmonary interstitial emphysema and pulmonary haemorrhage. Jamie’s parents were informed of the critical nature of his condition, and he remained acutely unwell over the next few hours.

10.

At 0200 on 18 April a 3^rd dose of surfactant was given. The oxygen saturation improved over the following hours. … On the following day Jamie’s condition improved somewhat. A repeat chest X-ray showed increased shadowing within the right lung. … The plasma bilirubin concentration was moderately elevated …

11.

On 20 April the peak ventilator pressure was reduced … but the inspired oxygen concentration remained high and Jamie was unstable on handling. … A cranial ultrasound scan was performed … and this was reported to show a “grade 2” bleed on the left and a “grade 2-3 bleed” on the right. (… grade 2 was equivalent to intraventricular haemorrhage and grade 3 indicated a haemorrhagic lesion within the brain … tissue). No major abnormalities of blood pressure were recorded.

12.

On 21 April Jamie developed a mild metabolic acidosis and elevated carbon dioxide tension. The endotracheal tube was changed. A repeat chest x-ray showed a slight improvement, with both lungs expanded. On examination there was no significant abnormality. On 22 April a systolic heart murmur was noted and a persistent ductus arteriosus was suspected. Phototherapy for jaundice was continued. Intravenous nutrition was commenced. On 23 April some skin breakdown on the neck was noted. On 25^th April Indomethacin was started for treatment of persistent ductus arteriosus. A chest X-ray on the following day showed resolving pulmonary interstitial emphysema.

13.

On 29 April the endotracheal tube was changed and in the following hours Jamie’s ventilation improved. An abnormal heart sound (gallop rhythm suggestive of heart failure) was heard and frumeside was given. Jamie’s condition deteriorated overnight and he required 100% oxygen for an hour. His temperature was elevated at 38.8 degrees C and blood cultures were taken. These subsequently showed a growth of Gram positive cocci in all bottles, but this was interpreted as probably insignificant. Antibiotic treatment therapy was started. A repeat cranial ultrasound scan on 30 April showed a resolving grade 2 haemorrhage bilaterally and some ventricular dilatation, more on the left than on the right. The peak bilirubin concentration recorded for the entire admission was [moderately elevated] on 30 April and following treatment with phototherapy the bilirubin level declined rapidly [to an acceptable level] …

14.

Over the following days Jamie’s condition gradually improved. Dexamethasone was started as treatment for bronchopulmonary dysplasia (chronic lung disease). On 7 May at 2015 Jamie suddenly deteriorated with a marked drop in oxygen saturation. The endotracheal tube was removed and an initial attempt at reintubation was unsuccessful. Jamie did not respond to bag and mask ventilation and during this procedure Jamie became bradycardic and external heart massage was commenced. A further endotracheal tube was inserted. Adrenaline was given via the tube and intravenously. Calcium gluconate, glucose, plasma and bicarbonate were also given. A prolonged period of external cardiac massage was required and the heart rare and oxygen saturation improved around 2035 pm. A chest x-ray was performed. Blood was obtained on aspiration of the endotracheal tube. … Jamie was ventilated with 100% oxygen at peak pressure of 27 cm.

15.

Over the following days Jamie’s condition improved slightly. A repeat ultrasound scan of the brain showed resolving grade II haemorrhage bilaterally, with possibly parenchymal involvement on the right, but no enlargement of the ventricles.

16.

On 14 May Jamie was seen by a cardiologist who diagnosed a clinically significant patent ductus arteriosus. Surgical ligation of the ductus arteriosus was recommended. On 17 May Jamie was transferred to Alder Hey Hospital for ligation of ductus. The procedure was performed without difficulty and the post-operative course was uncomplicated. Jamie was transferred back to Countess of Chester Hospital on the same day.

17.

Following this Jamie remained ventilator dependent for a number of weeks. Repeated chest X-rays showed findings consistent with bronchopulmonary dysplasia.

18.

On 2 June a further episode of infection occurred. Blood culture grew Acinetobacter organisms. A lumbar puncture showed clear cerebrospinal fluid. Antibiotic treatment was given and Jamie improved. A repeat cranial ultrasound scan on 7 June showed a resolved grade II haemorrhage bilaterally and moderate enlargement of the lateral ventricles.

19.

On 9 June the endotracheal tube was finally removed and Jamie was able to breathe spontaneously with oxygen given by nasal prongs. On 17 July the prolonged course of dexamethasone was stopped.

20.

In the following weeks there were repeated episodes of fever requiring treatment with antibiotics, an increased requirement of oxygen supply and feeding difficulties. It was decided to give a second course of dexamethasone which continued until November 1991.

21.

In October and November there were intermittent episodes of fever and a urinary tract infection was diagnosed. This was treated with trimethoprim. A renal ultrasound examination showed normal findings. A micturating cystourethrogram (MCU) performed in 1992 showed bilateral reflux but no hydronephosis. On 22 October at a corrected age of about 3 months post term the head circumference was 38 cm and the weight was 3.72 kg. On 1 December Respiratory Syncitial Virus infection was diagnosed and Jamie was treated with ribovarin.

22.

Jamie was eventually discharged from hospital on 23 December 1991 still requiring additional inspired oxygen. He was seen in the follow-up department and he required readmission to hospital on several occasions with urinary tract infection and exacerbations of chronic lung disease. In January 1992 “jerky movements” were observed. Infantile spasms were suspected but clinical observation and EEG showed no abnormality. Because of Jamie’s severe chronic lung disease supplemental oxygen at home was required for over 2 years.

23.

Subsequently it became sadly apparent that Jamie was developing signs of dyskinetic and spastic cerebral palsy affecting all four limbs with the legs more severely affected than the arms. The cerebral palsy has led to severe impairment of gross and fine motor function. In addition there was evidence of profound global developmental delay, severe hearing impairment and behavioural problems.

24.

On 29 April 1994, at an age of 3 years, a magnetic resonance imaging (MRI) brain scan was performed. … In summary, the scan was reported to show marked dilatation of the lateral ventricles, with marked loss of Periventricular white matter particularly around the trigones (angles) of the lateral ventricles. In addition, there was patchy high T2 signal in the Periventricular white matter. There was abnormal T2 signal in the left globus pallidus and possibly in the inferior right pallidus. The cerebral peduncles, pons and medulla were small. In summary there is evidence of brain injury in several different regions, including the white matter adjacent to the lateral ventricles and the grey matter in the centre of the brain at the site of the basal ganglia and brain stem.”

The applicable law. There was no dispute as to the principles of law that apply in this case. They are conveniently and succinctly set out in paragraph 10 of Mr de Navarro’s written opening note in the following terms:

“Issues of breach of duty fall to be decided by whether the Defendant’s obstetricians’ actions (or inaction) were within the range of practice of reasonably competent obstetricians in 1991 and/or whether the Defendant’s policy was within the range of policies that might properly have been adopted by reasonably competent obstetricians in 1991. If breach of duty is established, the issue on causation is what, absent breach of duty, would/should have happened and whether that would have on balance of probabilities avoided or materially reduced the damage. [Bolitho ~v~ City and Hackney HA (1988) AC 231 applying the test in Bolam ~v~ Friern Hospital Management Cmee (1957) 1 WLR 582]. It is for the Claimant to establish causation on balance of probabilities. Failing such proof, there is no claim for loss of a chance of a better outcome [Gregg ~v~ Scott (2005) UKHL 2].

Breach of Duty. As I have already indicated, the essence of the Claimant’s case on the issue of breach of duty, supported by the evidence of Mr Jarvis, is that betamethasone should have been administered to Mrs Cowley following her admission to the hospital in the late afternoon of 15^th April 1991, rather than in the evening of 16^th April 1991. Accordingly, much of the focus of this aspect of the case is upon the treatment given (or rather, not given) by Dr Fishwick when she saw and examined Mrs Cowley shortly after her admission to the labour suite. According to my note of his oral evidence in chief on 19^th October 2006, Mr Jarvis summarised his opinion on this aspect of the case in the following terms:

“In 1991 there was no justification for a policy that restricted the use of cortico-steroids in cases of threatened pre-term labour.

I am aware that there is literature showing that obstetricians were not using cortico-steroids as often as may be appropriate – but I have no knowledge of any reason for not using cortico-steroids in threatened pre-term labour. Any such practice was unreasonable in 1991.

Cortico-steroids should have been administered to Mrs Cowley on 15^th April. That should have been done at a stage when it was apparent that she was more likely to go into labour than she had been on 14^th April. In my view, that was the position when she was seen by Dr Fishwick on 15^th April. Against the background history of 2 premature deliveries, Mrs Cowley was experiencing contractions which were painful for some of the time. Although the cervix was not abnormal there had been a show of a blood-stained mucous plug. Putting these factors together, there was a likelihood of her going into premature labour and, therefore, she should have been given cortico-steroids on the 15^th April.”

However, as Mr de Navarro pointed out (see paragraph 1 of his written closing note), it is common ground that Dr Fishwick’s actions and treatment were entirely in accordance with the hospital’s premature labour policy, because Mrs Cowley was not in active preterm labour when Dr Fishwick saw and examined her on the 15^th April (see also paragraphs 32 and 33 above). Accordingly, I accept Mr de Navarro’s submission (see paragraph 2 of his written closing note) that the breach of duty issue in this particular case gives rise to the following two questions:

(1) Was the hospital’s policy within the reasonable range? I agree with Mr de Navarro that the correct approach to this question is as set out in the following passages in the speech of Lord Browne-Wilkinson in Bolitho (see pages 241G to 242B and 243A-E):

“[Mr Brennan] submitted that the judge had wrongly treated the Bolam test as requiring him to accept the views of one truthful body of expert professional advice even though he was unpersuaded of its logical force. He submitted that the judge was wrong in law in adopting that approach and that ultimately it was for the court, not for medical opinion, to decide what was the standard of care required of a professional in the circumstances of each particular case.

My Lords, I agree with these submissions to the extent that, in my view, the court is not bound to hold that a defendant doctor escapes liability for negligent treatment or diagnosis just because he leads evidence from a number of medical experts who are genuinely of opinion that the defendant’s treatment or diagnosis accorded with sound medical practice. In the Bolam case itself, McNair J. … stated that the defendant had to have acted in accordance with the practice accepted as proper by a “responsible body of medical men”. Later … he referred to “a standard practice recognised as proper by a competent reasonable body of opinion.” Again, in the passage which I have cited from Maynard’s case … Lord Scarman refers to a “respectable” body of professional opinion. The use of these adjectives – responsible, reasonable and respectable – all show that the court has to be satisfied that the exponents of the body of opinion relied upon can demonstrate that such opinion has a logical basis. In particular in cases involving, as they so often do, the weighing of risks against benefits, the judge before accepting a body of opinion as being responsible, reasonable or respectable, will need to be satisfied that, in forming their views, the experts have directed their minds to the question of comparative risks and benefits and have reached a defensible conclusion on the matter.

…

These decisions demonstrate that in cases of diagnosis and treatment there are cases where, despite a body of professional opinion sanctioning the defendant’s conduct, the defendant can properly held liable for negligence (I am not here considering questions of disclosure of risk). In my judgment that is because, in some cases, it cannot be demonstrated to the judge’s satisfaction that the body of opinion relied upon is reasonable or responsible. In the vast majority of cases the fact that distinguished experts in the field are of a particular opinion will demonstrate the reasonableness of that opinion. In particular, where there are questions of assessment of the relative risks and benefits of adopting a particular medical practice, a reasonable view necessarily presupposes that the relative risks and benefits have been weighed by the experts in forming their opinions. But if, in a rare case, it can be demonstrated that the professional opinion is not capable of withstanding logical analysis, the judge is entitled to hold that the body of opinion is not reasonable or responsible.

I emphasise that in my view it will very seldom be right for a judge to reach the conclusion that views genuinely held by a competent medical expert are unreasonable. The assessment of medical risks and benefits is a matter of clinical judgment which a judge would not normally be able to make without expert evidence. As the quotation from Lord Scarman makes clear, it would be wrong to allow such assessment to deteriorate into seeking to persuade the judge to prefer one of two views both of which are capable of being logically supported. It is only where a judge can be satisfied that the body of expert opinion cannot be logically supported at all that such opinion will not provide the benchmark by reference to which the defendant’s conduct falls to be assessed.”

In presenting his argument that the failure to administer cortico-steroids to Mrs Cowley on admission on 15^th April constituted a breach of the duty of care owed to her by the hospital, Mr Francis submitted that: (i) In 1991, it would have been indefensible to have a policy of not giving antenatal cortico-steroids at all, (ii) in 1991, any competent policy/practitioner should have accepted the need to give cortico-steroids to women at risk of preterm delivery in 1 to 7 days; (iii) one group of women to whom cortico-steroids had to be given to ensure that they were administered within the optimum time frame were those at real risk of imminent preterm labour, and (iv) on 15^th April 1991, Mrs Cowley presented with such a risk, was at real risk of imminent preterm labour and should have been given appropriate antenatal cortico-steroid treatment on 15^thApril. It was Mr Francis’ submission that the failure to do so was the result of the hospital’s premature labour policy which (it was submitted) was unreasonably restricted and had led to no real consideration of the critical question whether, in the light of her previous history and presenting symptoms, Mrs Cowley was likely to deliver within 1 to 7 days of admission. Mr Francis submitted that, in Mrs Cowley’s case, if Dr Fishwick had not been constrained by the hospital’s policy of administering cortico-steroids only once there had been a diagnosis of actual preterm labour, she would have been free to consider whether Mrs Cowley was in a condition of threatened preterm labour and/or whether there was a significant risk of delivery being imminent.

In effect, it was Mr Francis’ submission that if Dr Fishwick had been free to consider the matter in that way, the only reasonable conclusion she could have reached would have been that there was a significant risk of imminent delivery and that cortico-steroids should be administered to Mrs Cowley without delay, in order to ensure that they were given within the optimum time frame. I should say at once that I am not persuaded that there was any discernable risk of “imminent (my emphasis) delivery” on the afternoon of 15^th April. By the time Dr Fishwick saw Mrs Cowley, the pain associated with her tightenings/contractions had ceased, treatment with tocolytic agents was therefore no longer appropriate, the tightenings/contractions were occurring at intervals of about 10 minutes and were not observed on examination and there was no sign of any cervical change. The earlier “show” was not, of itself, diagnostic of the onset of labour and I accept Dr Fishwick’s evidence (supported, as it is, by the evidence of Mr Walkinshaw) that there was nothing in her findings to suggest that labour would take place within the week. In my view, the conclusion that Dr Fishwick reached (i.e. in view of Mrs Cowley’s history of two previous premature deliveries, to admit her for observation and reassessment) was entirely reasonable in the circumstances.

Mr Francis nevertheless submitted that Mr Jarvis had presented consistent, logically based evidence in support of the Claimant’s case on breach of duty and that his evidence should be preferred to that of Mr Walkinshaw.

Having given the matter much anxious thought I have come to the conclusion that I do not accept Mr Francis’ submission that the hospital acted in breach of duty in failing to administer cortico-steroids on the afternoon of 15^th April 1991, rather than on the afternoon of 16^th April and I do not accept that Mr Jarvis’ evidence should be preferred to that of Mr Walkinshaw. This is not a case of a hospital which pursued a policy of not administering antenatal cortico-steroids at all. The hospital’s policy was to administer cortico-steroid therapy, but only after actual/active preterm labour was diagnosed and Dr Fishwick’s actions were entirely in accordance with that policy. As I have already stated, Mr Walkinshaw is a very distinguished obstetrician who has been a leading proponent of the antenatal use of cortico-steroids since 1989/90. Mr Walkinshaw was emphatic in stating that he considered the hospital’s premature labour policy to be a reasonable policy (both in 1991 and now). It is also clear and I entirely accept that Mr Walkinshaw genuinely believes that to be the case.

It is very important to stress that the hospital’s premature labour policy did not preclude the administration of cortico-steroids, but it is and was very specific as to the timing of their administration, i.e. only after actual preterm labour has been diagnosed and not before. As I have already indicated (see paragraph 26 above), neither Chalmers’ “Effective Care” nor Crowley 1990 gave any guidance as to when the antenatal cortico-steroids should be administered and it was not until 1996 that RCOG issued its guidance. I accept Mr de Navarro’s submission that it is not a question of which policy the court thinks best but whether the policy in question has a logical basis. Applying the principles enunciated in Bolitho (supra), in the “vast majority of cases” the fact that a distinguished expert in the field (i.e. in this case, Mr Walkinshaw) considered the policy a reasonable one will be determinative. “It will very seldom be right for a Judge to conclude that views genuinely held by a competent medical expert are unreasonable” because the assessment of medical risks and benefits is primarily a matter of clinical judgment. It is only in a rare case when a judge can be persuaded that the expert opinion cannot be logically supported at all and that the expert opinion can be disregarded. I am firmly of the opinion that this is not such a case.

I therefore turn to summarise my reasons for concluding, as I do, that the hospital’s premature labour policy did (and does) have a logical basis and that in consequence Mr Walkinshaw’s opinion is logically supported and cannot be disregarded.

In 1991, as I have already observed, it was common ground that there was no authoritative (or any) guidance as to when antenatal cortico-steroids should be administered, nor was there any express recommendation that they should be administered in cases of “threatened” preterm labour. I therefore accept Mr Walkinshaw’s evidence that, in those circumstances, the qualifying criteria for the trials that provided the data for Crowley 1990 make a reasonable starting point for deciding the appropriate timing of antenatal steroid therapy, because the trials showed that the babies of mothers who met the qualifying criteria benefited from the treatment. There was no other scientifically based information available to demonstrate what other group or groups of women/babies could or would benefit from such treatment.

Apart from the 1981 US steroid trial (where “high risk of preterm delivery” is not defined) all the trials involved women who were in actual preterm labour or who had experienced premature/pre-labour rupture of the membranes (“PROM”) or who were to have elective preterm delivery – and it is common ground that elective and PROM cases will deliver within 7 days. It is clear (and Mr Jarvis agreed) that Mrs Cowley would not have qualified for 14 out 15 of the pre-1991 trials and the hospital’s premature labour policy was consistent with the qualifying criteria for all the Crowley 1990 trials apart from (possibly) the 1981 US steroid trial.

Although Mr Jarvis emphatically stated that, in 1991, his own unit at St James’ University Hospital did have a written policy that provided for the administration of cortico-steroids to women who were considered to be at significant risk of preterm delivery (i.e. in a state of “threatened preterm labour”), he was unable to produce a copy of any such policy. However, after making appropriate enquiries overnight, he did produce a copy of St James’ written policy for the management of “Pre-Term Labour With Intact Membranes”. The policy is an extract from a loose-leaf publication and commences with the definition “Preterm labour is defined as the onset of labour [my emphasis] before the 37^th week of gestation. The policy dates from about 1994 (“the St James’ 1994 policy”) and there is no reason to believe that the equivalent policy in 1991 was any different. Under the heading “Management” the policy continues in the following terms: “The obstetric registrar on call must be notified and he/she will make a decision on whether labour has commenced [my emphasis] based on frequency and duration of contractions, abdominal palpation of presenting part, vaginal assessment of cervix and relationship of presenting part to the ischial spines.

It is clear from a full reading of the St James’ 1994 policy that the subsequent management of the preterm labour, including treatment with appropriate tocolytic medication and the administration of cortico-steroids, is entirely predicated on the basis of the obstetric registrar’s diagnosis that the preterm “labour has commenced”. Accordingly, as Mr de Navarro observed, the St James’ 1994 policy was, for all practical purposes, on all fours with the hospital’s premature labour policy. It did not purport to nor did it deal with a condition of “threatened” preterm labour.

Although Mr Jarvis emphasised that he was confident that, in 1991, St James also had a written policy headed “Cortico-Steroids” that did reflect his views with regard to the need to administer antenatal cortico-steroids to women who were at significant risk of going into preterm labour (i.e. cases of “threatened” preterm labour), I consider it to be significant that there is no mention (by cross reference or by any other means) of any such policy in the St James’ 1994 policy, which is expressly stated to be for the management of preterm labour and which policy, like the hospital’s, commences with the need for a decision to be made as to whether labour has commenced. I am satisfied that, if this policy (i.e. the St James 1994 policy) had been applied by Dr Fishwick on the afternoon of 15^th April 1991, her actions and treatment would have been the same as they were and they would have involved a correct application of that policy.

Not only is the hospital’s premature labour policy entirely consistent with St James’ 1994 policy, but it also accords with the approach recommended by McNamara and Vintzileos in Chapter 11 of the 1997 major text book on Preterm Labor (sic) (“McNamara and Vintzileos”), from which it is convenient to quote the following passages:

“The inaccurate diagnosis of preterm labor has been a major obstacle to improving care, as nearly half of the women treated are not a true preterm labour. Meta-analysis of randomized controlled trials has indicated that 47 percent of mothers randomized to placebo deliver at term.

DEFINITIONS

Preterm labor is defined clinically as progressive cervical dilatation and/or effacement with regular uterine contractions prior to the completion of 37 weeks gestation …

DIAGNOSIS

The clinical diagnosis of true preterm labor has traditionally been based on the presence of uterine contractions and cervical changes. …

Our clinical approach to preterm labor is summarized in Table 11-2. To prevent unnecessary drug therapy with potential adverse side effects, certain criteria should be adhered to before diagnosing preterm labor. These criteria involve gestational age assessment, uterine contractions, membrane status, and cervical assessment.

Table 11-2. Clinical Questions in Preterm Labor

1 Is it a true or false labor?

2 Is there a need for immediate delivery?

3 Are there any contraindications to tocolysis?

4 Is there a treatable cause or causes present?

…

UTERINE CONTRACTIONS

…

Experience has shown that the rate of error in diagnosing preterm labor based on uterine contractions alone is 50 percent or more. … Frequency, regularity, or discomfort from contractions does not always reliably distinguish true preterm labor from false labor, nor does the period of time over which the contractions persist.

…

MEMBRANE STATUS

If the membranes are ruptured in association with regular contractions, preterm labor is diagnosed. If the membranes are intact, cervical changes must be present in association with regular uterine contractions to diagnose preterm labor.

CERVICAL STATUS

Cervical changes have also been studied as predictors of preterm labor. …

…

Therefore, if the membranes are intact, cervical dilatation of at least 2 cm or effacement of at lease 80 percent is required to diagnose preterm labor. …

INITIAL EVALUATION AND MANAGEMENT

The objectives of management of preterm labor include minimization of perinatal morbidity and mortality and preservation of maternal health. In each individual case, the risk of continuing the pregnancy versus those of preterm delivery must be carefully considered. Since preterm delivery remains the major cause of perinatal morbidity and mortality, this condition should be managed by experienced personnel. Since these cases may present at any time, experienced personnel should be readily available. It is essential that all delivery units have written guidelines. The protocol outline in Figure 11-1 is an example. …”

Figure 11-1 in McNamara and Vintzileos takes the form of a flow chart with a starting point of “Threatened Preterm Labor”. If the patient is found to be in “advanced labor” or there is “fetal distress” the protocol proceeds to delivery. If no cervical change is found, the patient is observed. This is expanded upon in the text, as follows: “True preterm labor is preceded by a prodomal phase that may be reversible following simple non-specific measures. Patients with intact membranes who present with little or no cervical change should be observed on bed rest, avoiding the supine position.” If there is cervical change, an expression which clearly refers to progressive dilatation/effacement of the cervix, the protocol then proceeds to “Diagnostic Workup”, leading to appropriate treatment, including tocolysis and cortico-steroid therapy. For all practical purposes, the McNamara and Vintzileos protocol is the same as both the hospital’s premature labour policy and the St James’ 1994 policy. I have no hesitation in accepting Mr Walkinshaw’s evidence that the McNamara and Vintzileos protocol falls within the range of accepted views both then and today.

In my view, Mr Jarvis apparent insistence that, in effect, cortico-steroids should be administered in all cases of “threatened” preterm labour (provided the well established contra-indications of hypertension and/or prolonged rupture of the membranes are not present) and that any policy/protocol that failed (in 1991 and now) to provide for such treatment would be wrong necessarily meant that he rejected not only the hospital’s premature labour policy as too constrained, but also the McNamara and Vintzileos protocol for the same reason. I cannot accept Mr Jarvis evidence to that effect. On Mr Jarvis’ approach, the same criticism could also be made of the St James’ 1994 policy (unless there is some relevant applicable provision in the missing “Cortico-Steroid” policy – which I consider doubtful, given the absence of any cross reference). It is also worthy of note that the policy for the management of preterm labour practised by Mr Walkinshaw’s Liverpool unit defines “preterm labour” as “Uterine activity of 30-60 seconds duration occurring at least once in every 5-7 minutes, sufficient to cause distress, and/or evidence of cervical dilatation/effacement or progressive changes in the cervix.” Mr Jarvis’ view of what constitutes “threatened” preterm labour is clearly very wide, since it was his view that it included Mrs Cowley’s condition on the afternoon of the 15^th April, a condition that Mr Walkinshaw confirmed would not have qualified for treatment under his unit’s policy for the management of preterm labour. However, understandably, Mr Jarvis did not go as far as to suggest that the policy followed by Mr Walkinshaw’s Liverpool unit was unreasonable.

For his part, Mr Walkinshaw’s approach was to recognise and accept that there was a range of reasonable policies in 1991, of which the hospital’s premature labour policy was one. He described his Liverpool unit’s policy as a somewhat more liberal one than the hospital’s and falling somewhere between the hospital’s policy and Mr Jarvis’ approach. He confirmed that his unit’s definition of preterm labour (see the previous paragraph) covered cases that could be described as “threatened” preterm labour and he said that he would interpret the expression “threatened preterm labour” in the 1996 RCOG guidance in like terms. I accept his evidence to that effect. Mr Walkinshaw is a fulltime obstetrician, who is still in practice and is pre-eminent in his field. Far from concluding that Mr Walkinshaw’s views do not have a logical basis, it seems to me that they represent the entirely logical outcome of an overall approach to the issues that is both reasonable, well informed and the product of an enormous amount of experience. I reject Mr Francis’ submissions to the contrary effect.

In my view, a consideration of the various drawbacks/problems that exist and/or can arise as a result of the application of a policy such as that argued for by Mr Jarvis strongly support the conclusion that I have reached on this aspect of the matter. In this regard, it is interesting to note that although Mr Walkinshaw accepted that Mr Jarvis’ approach came within the range of policies that were reasonable, he made it clear that it was not one with which he agreed (mainly, as I understand it, because of its drawbacks, to which I now turn under two main headings).

(i) The unnecessary administration of drugs: It is common ground that there is a very high level of “false positives” in cases of “threatened” preterm labour – in roughly half the cases of “threatened” preterm labour the symptoms will resolve naturally and of those the majority will progress to full term or something closely approximating full term (although a significant minority will still go on and experience a preterm labour). Mr Jarvis’ approach therefore necessarily means that potentially harmful drugs will be administered to many patients who do not need them (i.e. the false positives who progress to full term).

I accept Mr de Navarro’s submission that, in the case of the cortico-steroid therapy, the published material does not wholly allay fears concerning the possible adverse side effects of infection and still birth. Although such concerns as may still exist on this score are not enough to justify a policy of total non-administration, I accept that it is reasonable to take them into account when considering whether to extend the administration of cortico-steroids to a large number of women who do not, in fact, need them (i.e. the “false positives” who progress to full term). That reasoning is all the more compelling in the case of tocolytic agents which, as already explained, are potentially very dangerous to both mother and child.

(ii) Risk of repeat doses/loss of protection: Mr Jarvis made it clear that he did not advocate repeat doses of the relevant medication. He said in terms “I do not advocate repeat doses. My approach involves the giving of only one dose, because there is no relevant evidence that repeated doses are safe” (see xx 19^th October). Mr Jarvis also readily accepted that, on his approach, the beneficial effect of the cortico-steroid therapy would be lost 7 days after administration and that this meant that if a patient went into premature labour after 7 days from administration, she would have no benefit from the cortico-steroid therapy she had received earlier. In those circumstances, the application of Mr Jarvis’ approach will have resulted in the patient either being exposed to the unacceptable risk of a repeat dose or of having no protection at all.

As Mr de Navarro pointed out, an obvious benefit of waiting until preterm labour has been diagnosed (as in the hospital’s policy) is that delivery will certainly be within 7 days and there is a high likelihood that tocolytic medication (particularly indomethacin) will buy the necessary time to bring the patient within the 24 hour to 7 day window (Mr Jarvis accepted an 80% success rate with indomethacin). Mr de Navarro therefore submitted that if (as is common ground), only one course of cortico-steroids is to be used, the ideal time to treat is, in effect, as close to the actual onset of labour as possible and the hospital’s “diagnosed preterm labour” policy is a reasonable example of such an approach. I agree with that submission.

In his evidence, Mr Jarvis argued that, if such an approach is adopted, it would mean that (as in Mrs Cowley’s case) the minimum 24 hours would not be achieved in a significant number of cases (even allowing for the 80% success rate for indomethacin). However, as Mr de Navarro pointed out, Mr Jarvis’ own approach means that there will be a significant number of patients who will be faced with the risk of repeat doses or no protection at all (see above), quite apart from all the patients who will have received this powerful medication without, in fact, actually requiring it. As Mr de Navarro succinctly put it: “There is slippage for a significant minority either way.”

I therefore agree with Mr de Navarro’s submission that the overwhelming weight of evidence demonstrates that the hospital’s premature labour policy is within the reasonable range of such policies. This case is one of the “vast majority of cases” referred to in Bolitho (supra). I accept the evidence of Mr Walkinshaw that the hospital’s policy was and is within the range of reasonable policies for the management of preterm labour. It follows that, since Dr Fishwick acted fully in accordance with the hospital’s premature labour policy in not administering betamethasone to Mrs Cowley when she examined and treated her on 15^th April 1991, she (and consequently the hospital) did not act in breach of duty for not having done so. This action must therefore fail for that reason.

(2) What if the Hospital’s policy was not reasonable? I now turn to consider briefly the second question by reference to which the issue of breach of duty can be considered (see paragraph 49 above). For these purposes, I will assume that the hospital’s premature labour policy was unreasonable, because it excluded and/or failed to make provision for the administration of antenatal cortico-steroid therapy in cases of “threatened” preterm labour.

As I have already indicated, there is no accepted definition of what is meant by “threatened” preterm labour and the expression is not defined in the 1996 RCOG guidance. However, I am satisfied that the “liberal” regime followed by Mr Walkinshaw’s Liverpool unit (see paragraph 64 above) extends to cases that are properly described as “threatened” preterm labour and that it provides an appropriate touchstone for the consideration of this question.

I accept Mr de Navarro’s submission that, on 15^th April 1991, Mrs Cowley was not in a condition of threatened imminent labour on any sensible definition of that expression (see paragraph 52 above). Accordingly, if the hospital’s policy had included appropriate provision for cases of “threatened” labour, instead of being limited to cases where actual labour had been diagnosed, I accept Mr de Navarro’s submission that, in the light of Dr Fishwick’s findings, cortico-steroid therapy would not have been administered to Mrs Cowley on 15^th April 1991 in any event. Furthermore, the position would have remained the same if there had been a reassessment on the 15^th April, because the pain had ceased that afternoon and did not reoccur until the afternoon of the 16^th April 1991.

Mr de Navarro made the uncontroversial point that an appropriate policy for the management of preterm labour is necessary in order to avoid abrogation to, whims of, and consequent variation in practice by, junior staff. He submitted that if a preterm labour policy is to include provision for the administration of cortico-steroid therapy in cases of “threatened” preterm labour, that expression should be clearly defined – as in the case of Mr Walkinshaw’s Liverpool unit. I agree with that submission and I also agree that it would be tantamount to perverse to suggest that the “liberal” regime of Mr Walkinshaw’s Liverpool unit is not wide enough to cover the appropriate management of cases of “threatened” preterm labour. As Mr de Navarro pointed out, under the Liverpool unit’s regime, Mrs Cowley would not have qualified for cortico-steroid therapy on 15^th April because, on admission, her uterine activity was no more than 1 in 10. Under the Liverpool regime, she would have been admitted for observation and by late afternoon she was no longer in pain and certainly not distressed.

Furthermore, I accept Mr Walkinshaw’s evidence that (ignoring cases of elective preterm delivery and premature/pre-labour rupture of the membranes) antenatal cortico-steroid therapy is generally only given in cases where labour is sufficiently threatened to justify tocolysis and, as I have already indicated, that was not the case on the 15^th April 1991 so far as Mrs Cowley was concerned (see paragraph 45 above). Having carried out her examination and made her findings (the accuracy of which I accept), Dr Fishwick exercised her clinical judgment. I am satisfied that, despite the history of two previous preterm deliveries and the “show” (as to which, I accept the points made by Mr de Navarro and summarised in paragraph 12(h) of his written closing note), Dr Fishwick’s conclusion that Mrs Cowley was not in a condition of “threatened” preterm labour when she examined and treated her on the 15^th April 1991 was both reasonable and correct (by any reasonable definition of that expression – i.e. by any definition equating to that of the Liverpool unit).

Overall Conclusion on Breach of Duty. Accordingly, my overall conclusion on the two questions that arise from the issue of breach of duty in this case is that the hospital’s premature labour policy was reasonable, but if it should have extended to include cases of “threatened” preterm labour Mrs Cowley would not have been given cortico-steroid therapy on 15^th April 1991 in any event.

It therefore follows that there was no breach of duty on the part of the Defendant as alleged or at all and, for that reason, this action fails and must be dismissed.

Causation. Having regard to the firm conclusion that I have reached in relation to the issue of breach of duty, I do not think it necessary to embark upon an equally exhaustive analysis of the issue of causation. In the circumstances, I consider that it is sufficient if I outline my reasons for concluding (as I do) that, if steroids had been administered on 15^th April 1991, the outcome in terms of Jamie’s brain damage and disability would have been materially better.

Professor Wyatt’s analysis of the “cascade” of events leading from Jamie’s preterm birth to seriously damaged neurological outcome was not disputed by Dr N. R. C. Roberton (“Dr Roberton”), the paediatric expert witness called by the Defence. In summary, the relevant chain of events includes the following (for a more detailed account, see paragraph 46 above): (i) Severe RDS; (ii) Episode of hypoxic ischaemia; (iii) Ventilation; (iv) Periventricular Leucomalacia (PVL)/Intraventricular Haemorrhage (IVH); (v) Chronic lung disease; (vi) Episodes of infection; (vii) Prolonged administration of Dexamethasone; (viii) Cardiac arrest; (ix) Further episode of hypoxic ischaemia; (x) Permanent damage to white matter; (xi) Long term disability.

As Mr de Navarro observed (see paragraph 15 of his written closing note), essentially this case is concerned with the causation of Jamie’s PVL, because it is common ground that this condition was responsible for causing the majority of Jamie’s brain damage (i.e. to the white matter) and that this did not result from the moderately elevated levels of bilirubin experienced by Jamie during the neonatal period.

Stated shortly, it was Professor Wyatt’s view that, if the antenatal cortico-steroids had been given on Mrs Cowley’s admission on 15^th April 1991, the outcome in terms of brain injury and disability would have been materially less severe because, by reducing the severity of Jamie’s RDS, this would have: (i) reduced the hypoxic ischaemia and in turn this would have (ii) reduced the severity of the chronic lung disease, which would have (iii) reduced, if not removed, the need for ventilation, (iv) reduced infection, (v) reduced, if not removed, the need for Dexamethasone, (vi) avoided the cardiac arrest and thus (vii) reduced the PVL, brain injury and associated disability (the “knock-on effect”). However, although Professor Wyatt was firmly of the view that the outcome would have been materially better, he very fairly acknowledged that it was impossible to quantify the amount of that benefit.

It was Mr de Navarro’s submission that the most that could be proved on the balance of probabilities is that there was a chance that the outcome for Jamie might have been better if Mrs Cowley had been given cortico-steroids on 15^th April and that this is insufficient to prove causation in this case.

Based on Dr Roberton’s evidence, which was essentially founded on statistical evidence (to which there was much reference), Mr de Navarro submitted that, at best, the statistics show that with steroids there is an increased chance of a reduction in RDS and improvement in long term outcome. He accepted that the statistical evidence relating to the antenatal use of steroids is supportive overall, but that the most impressive benefit is at 30 – 32 weeks gestation and that, “in relation to less than 28 weeks gestation it is much more questionable; the statistics at this gestation are less compelling” (see the evidence of Professor Wyatt in xx).

I accept Mr Francis’ submission that the key issue on this aspect of the case is whether the antenatal cortico-steroids would have reduced the severity of Jamie’s RDS if they had been administered on 15^th April, with the resulting “knock-on” beneficial effect. Accordingly, as Dr Roberton accepted in evidence, in my view the critical question on the issue of causation is whether Jamie’s RDS would have been rendered significantly (i.e. materially) less serious by corticosteroids having been administered 24 hours earlier than they were. I also agree that if it is proved on the balance of probabilities that the steroids would have materially reduced the severity of Jamie’s RDS, it is more likely than not that the severity of the outcome would also have been materially reduced as the result of the beneficial “knock-on” effect described by Professor Wyatt. In my view, this point can be dealt with very succinctly.

Dr Roberton accepted in cross examination that there was no threshold for the relevant beneficial effect of steroids based on gestational age. He agreed that there was a gradient with regard to the development of pneumocytes and thus the efficacy of steroids. He also agreed in cross examination that Jamie’s RDS was what caused his hypoxic ischaemia. When the agreed joint answer to question 6(a) of the Claimant’s agenda on Neonatal/Causation was then put to him, Dr Roberton said: “Point taken”. Question 6(a) was in the following terms: “Do you agree that antenatal steroids administered for more than 24 hours prior to the Claimant’s birth; (a) Would have reduced the extent of hypoxic ischaemia?” The agreed joint answer was short and to the point, namely “Agreed.” My note of his evidence at this point is as follows: “Having regard to the answer to question 6(a) of the joint statement, I now accept that the steroids would have had a material effect on the extent of Jamie’s hypoxic ischaemia. It would have been a small but nevertheless material effect.”

I accept Mr Francis’s submission that the expert clinical opinion of Professor Wyatt is strong evidence in support of the Claimant’s case on causation. Professor Wyatt’s conclusion, on his assessment of Jamie’s individual case, is that if the antenatal steroids had been given 24 hours earlier than they were, they would have materially reduced the severity of the RDS and thus the severity of the outcome, because of the beneficial “knock-on” effect summarised above.

In my view, Dr Roberton almost conceded that to be the case in that part of his evidence to which I have briefly referred in paragraph 87 above. I am therefore satisfied that, in this respect, Dr Roberton’s evidence was significantly supportive of Professor Wyatt’s opinion that the outcome for Jamie would have been materially better in terms of brain damage and disability – as opposed to going no further than supporting the suggestion that, having regard to the overall severity of his illness, at most Jamie lost the chance of a better outcome.

I accept Mr Francis’ submission that Dr Roberton’s original opinion essentially stands or falls on his view of the statistical evidence. However, he did not claim that the statistics prove there was no causal link, only that there is no evidence of “statistical significance”. On the other hand, Professor Wyatt (who is an expert of great distinction whose specialised area of research is into the cause of brain injury) carried out a detailed and comprehensive clinical assessment of Jamie’s individual case and came to a conclusion that was (as Dr Roberton very fairly accepted) biologically plausible. In my view, Professor Wyatt’s opinion is an entirely reasonable one in the circumstances of this case and I see no reason not to accept it.

Accordingly, on the issue of causation, I am satisfied that, if steroids had been administered to Mrs Cowley on 15^th April 1991, the outcome for Jamie in terms of brain damage and disability would have been materially better.

Conclusion. Although I am satisfied that the Claimant would have succeeded on the issue of causation, this claim fails on the issue of breach of duty for the reasons already given. Accordingly, this action must be and is hereby dismissed.