Commentary
This case is primarily of interest to obstetricians, illustrating the court’s approach to the disputed interpretation of cardiotocographic evidence. There were no midwifery issues as such, but it may be of some interest to midwifery experts. The general learning points speak for themselves without reading the summary.
Learning points
General
Obstetrics
The case
The claimant is now aged 25 years old having been born on 14 October 1998. She brought this action for damages for personal injury arising from the alleged negligent delay in her delivery by the medical and nursing staff of the Doncaster Royal Infirmary between 28 September 1998 and 14 October 1998.
Background
The claimant was Julie Woods' first child. Mrs Woods attended her general practitioner on 19 February 1998 when the pregnancy was confirmed, and she was given a hospital booking appointment for 4 March 1998. Mrs Woods attended the hospital for routine appointments. Traces of sugar were identified in her urine in April, and it was recorded that she should undergo a glucose tolerance test at 28 weeks' gestation. On 5 June Mrs Woods attended the hospital feeling unwell since the previous day and complained of feeling nauseous, lightheaded and with intermittent cramping pain in her lower abdomen. It was noted that she was not complaining of pain on arrival at hospital but reported a watery discharge since yesterday. A speculum examination was performed which demonstrated a white discharge. Swabs were normal. She attended hospital again on 1 September 1998 querying whether she had experienced a spontaneous discharge of the membranes.
On 28 September 1998 Mrs Woods self-referred to hospital. The pregnancy was 39 weeks' gestation. At 19.45 it was noted that she had a history of "? leaking" since midday and having felt contractions that morning. Foetal heart monitoring using a cardiotocograph (CTG) was started at 19.42 and ran for around 100 minutes ("the first trace"). Shortly after the CTG started the midwife recorded that the foetal heart was 160 – 175 bpm and that the senior house officer, Dr Joynes, had been informed.
At 20.10, Mrs Woods was assessed by Dr Joynes who recorded in the clinical notes:
"Slight leakage – egg cup full
Some low abdo pain – 10 hr ago. Not now or since
On speculum: os closed, some white discharge
Triple swabs
Nitrazine negative
CTG – uterine contractions??
Baseline – 165 BTBV"
Dr Joynes recorded that the trace was to be reviewed by the senior SHO, Dr Samy. Dr Samy then recorded that "CTG shows tachycardia around 160 bpm but good variability. Keep on CTG for longer and review."
At 21.00 the midwife recorded: "foetal heart remains 160 – 170, foetal heart down to 150, Dr Samy informed. To remain on CTG recording. Dr Samy will come to see her later."
At 21.30 hours it was noted that Dr Samy had reviewed the first trace. The foetal heart rate was noted to be 155 – 160 bpm. He advised that Mrs Wood remain in hospital and have a repeat CTG in one hour's time.
By 22.40 Mrs Woods' care had been taken over by Midwife Sly. She made the following entry in the records: "CTG recommenced. F(oetal) H(eart) baseline 140 bpm. Accelerations were noted. No decelerations. Baby active. To be reviewed by Dr Samy."
The CTG referred to by Midwife Sly above ("the second trace") had been started at around 22.30. It ran for a total of around 33 minutes. Dr Samy reviewed Mrs Woods at or around 23.00. He made the following note:
"Reviewed (after being on CTG showing foetal movements). Foetal movements (++) felt by patient and shown on monitor. CTG baseline 140 bpm (in between movements). Variability 5 – 10 bpm. Accelerations repeated with movements (giving the impression of tachycardia but baseline between movements 140 bpm). Therefore, reactive trace. Maternal contractions shown on monitor but not felt by patient ?Braxton Hicks. Therefore, allowed home. Reassured. TCI [to come in] if feels contractions or reduced foetal movement."
The claimant attended hospital again on 6 October 1998 when she saw Dr Samy. The pregnancy was term plus one day. Dr Samy recorded the presentation (which was cephalic), maternal weight and blood pressure and checked the urine. He noted that Mrs Wood should come in for induction of labour to take place on 19 October 1998. The clinical record makes no reference to any inquiry or discussion concerning foetal movements.
Overnight 13/14 October, Mrs Woods attended the hospital with a history of regular contractions. She was assessed at 02.15 when a history of contractions 1 in 5 since 02.00 was noted. It was noted that she had had a show on Friday but did not have spontaneous rupture of the membranes. A CTG was started at 02.16 which showed a baseline of 140 bpm but reduced variability down to 2/3 beats per minute. The CTG ran continuously until 05.00. At 03.20. Dr Ibrahim examined Mrs Woods, reviewed the trace, and discussed care with Dr Barekat who agreed that the membranes should be ruptured with further observation of the CTG trace. Mrs Woods' membranes were ruptured at 04.15 and Dr Barekat reviewed her at 04.40, noting the presence of thick meconium liquor and a flat trace with no variability at all since admission at 02.15 and a baseline of 140 – 145 bpm. He noted that there were no accelerations, decelerations, shallow variable. A foetal blood sample to assess foetal wellbeing was not feasible and Dr Barekat advised delivery by caesarean section.
Mrs Woods was transferred to the operating theatre at 05.02. At 05.10 the foetal heart was auscultated and found to be 136 bpm. The claimant was delivered at 05.20 with the cord wrapped once around the neck. It was noted that there was thick meconium-stained liquor, and the placenta was gritty. The claimant was delivered in poor condition with poor respiratory effort and a heart rate of less than 100 bpm. Her birth weight was 3.046 kg. The claimant's Apgar scores included the value of 3 at 1 minute. Her upper airways were aspirated, and she was given oxygen via a facemask. Resuscitation improved her condition. An arterial blood gas sample taken from the umbilical artery was noted to have a pH value of 7.0. No base deficit was recorded. She was transferred to the Special Care Baby Unit at 05.45.
The claimant and her mother were discharged home on 21 October. The discharge summary recorded that the claimant was a post term baby born by emergency caesarean section after profound late decelerations and thick meconium staining had necessitated delivery.
Claimant’s case
The claimant's case focussed upon the obstetric management on 28 September 1998 when Mrs Woods attended the hospital complaining of a history of leaking per vaginum. The case, which was advanced by Mr John Hare, consultant obstetrician, was that the first trace demonstrated a tachycardia and two decelerations. The tachycardia should have led to the trace being classified as "non-reassuring" or "suspicious" and the decelerations should have been recognised as a "pathological" feature. The appropriate course was followed by Dr Samy however and repeat CTG monitoring was commenced. However, the second trace was not reassuring. The second trace was not normal. It was not possible to identify the baseline; there were no typical accelerations and for most of the trace the foetal heart was running at 150/160 (that is, a tachycardia). In the circumstances, it was alleged that the decision by Dr Samy to discharge Mrs Woods to be followed up routinely was unreasonable and a breach of duty. Instead, Mrs Woods should have been asked to come back into hospital and to undergo a further foetal heart monitoring, an assessment of liquor volume and an assessment of foetal size.
Had such a further assessment been undertaken, it was the claimant's case that the further CTG trace would not have been normal or reassuring. An assessment of amniotic fluid volume would have found the volume to be reduced and the claimant would have already been showing signs of growth retardation due to placental insufficiency with head and abdominal asymmetry. In combination, these features would have mandated delivery on or around 29 September. The pregnancy would by this stage be almost 40 weeks' gestation.
The claimant further asserted that Dr Samy ought reasonably to have questioned Mrs Woods concerning foetal movements when he saw her for routine antenatal care on 6 October. There is no note that he did so. Had he asked Mrs Woods about foetal movements he would have been told by her that they were reduced. This ought to have led to a decision to undertake a further period of foetal heart monitoring on or around 6 October. The trace would have been abnormal and a decision to deliver ought to have been made. By this stage, the pregnancy was just over 40 weeks' gestation (term plus 1 day).
Defendant’s case
The defendant denied breach of duty. The defendant's case which was advanced by Mr D, consultant obstetrician, was that the first trace was difficult to interpret. It was therefore prudent to admit Mrs Woods and wait for an hour or so before commencing a second monitoring of the foetal heart rate. The second trace was wholly reassuring. It demonstrated a baseline of 140 bpm with no decelerations and accelerations from that baseline which were synchronous with foetal movements as experienced by Mrs Woods and as registered by the tocograph. In the light of the normality of the second trace, it was appropriate to discharge Mrs Woods for routine ante-natal review.
The defendant submitted that, even if Mrs Woods had undergone further assessment on 28 or 29 September, those assessments would not have led to a decision to induce labour before 11 October 1998. The defendant denied that by 28/29 September the claimant was affected by placental insufficiency or suffering from intrauterine growth retardation. Any further monitoring on either the 28 or 29 September (or 6 October) would have been normal and reassuring. Liquor volume would have been normal, and the claimant's weight would have been within reasonable range. No action would have been indicated.
The issues to be decided
i) Judged by reference to the standards of the day, was Dr Samy's conclusion that the second trace was reassuring a reasonable conclusion in the sense that it was consistent with that of a reasonable body of obstetric opinion?
ii) If not, and further assessment was reasonably required, then what on the balance of probabilities would have been the outcome of further assessment on 28/29 September? Specifically, would it have led to a decision that labour should be induced and, if so, when should labour have been induced.
iii) Ought Dr Samy have asked Mrs Woods about foetal movements on 6 October and, if so, would the inquiry have led to the claimant's delivery on or around 6 October?
Expert obstetric evidence for claimant
The claimant's expert was Mr John Hare. The following is a summary of the salient parts of his evidence.
The first trace ran for a period of around 102 minutes with the speed of recording of 1 cm per minute. On his review of the trace, it showed two abnormal features. A tachycardia and 2 decelerations.
For the majority of the trace the average baseline rate was 165 – 170 bpm. This rate was in excess of the internationally accepted 1985 FIGO (International Federation of Obstetrics and Gynaecology) Guideline which states that a foetal heart rate pattern is "suspicious" if the heart rate falls above 150 bpm. The evidence based clinical guideline concerning the use of electronic foetal monitoring published by the Royal College of Obstetricians and Gynaecologists defines a normal baseline heart rate as one which is running up to 160 bpm. However, Dr Donald Gibb, the author of Foetal Monitoring in Practice stated in the edition of the manual current in 1998 that "Priority should be given to the revised definition of normal baseline FHR, 110 – 150 bpm." Gibb continued: "any tracing with a baseline rate of greater than 150 bpm should be carefully scrutinised for other suspicious features." On either of these two definitions of the acceptable normal range for the foetal heart rate, the first trace demonstrated a tachycardia.
The two decelerations were timed at 20.30 and 21.00. The first deceleration lasted 6 to 7 minutes, the second deceleration was much shorter. In his report he said that the presence of the two decelerations meant that the trace should be classified as "pathological." In his oral evidence and in the joint note of his meeting with Mr D he described the trace as "non-reassuring with pathological features."
The second trace was of poor quality. In its current (that is, as at trial) condition significant sections of the trace were illegible having degraded over time. The court therefore used a copy of the trace which had been obtained by Mr Hare at the time of his initial reporting of the case in around 2019. The trace quality had degraded even by 2019, but some sections, in particular the earlier sections, of the trace remained legible.
The trace ran for around 32 minutes. Mr Hare described the trace as showing the foetal heart varying in rate between 140 bpm and 160 bpm. Most of the time the heart rate was running at a rate between 150 and 160 bpm. Critically, he observed that at no point could the baseline be determined. There was only one short section of around 3.5 minutes at the beginning of the trace where it was possible to see a flat section of trace and there the heart rate was around 140 bpm. 3 or so minutes was not a sufficient period during which to declare a baseline. In order to determine the baseline, a heart rate which is stable for 10 minutes or a minimum of 5 minutes was necessary. The FIGO Guidelines define the baseline as "the mean level of the fetal heart rate when this is stable, accelerations and decelerations being absent. It is determined over a time period of 5 or 10 min and expressed in beats/min (Bpm)". The RCOG Guidelines confirm that the baseline is determined over a time period of 5 or 10 minutes. In Mr Hare's opinion there were no typical accelerations or decelerations. Mrs Woods appeared to be recording frequent foetal movements and the trace was impossible to interpret.
Mr Hare said that it was unacceptable for Dr Samy to have concluded that the trace was reassuring. The second trace had been obtained for clarification purposes and it had not served that purpose. It was impossible to interpret, and the only safe course was to conclude that it was non-reassuring. He disagreed with Dr Samy's stated conclusion (in the clinical notes) that the trace was accelerative and reactive to foetal activity. First, he said that the trace was not long enough: it had not been allowed to continue until foetal activity had ceased so as to permit the identification of the true baseline. Mr Hare said that if the tachycardia was thought to be due to foetal activity, then, as foetal activity is finite, the trace would have permitted identification of the resting baseline had it been continued. Second, Mr Hare made the linked point that it should not have been assumed that the tachycardia was due to foetal movement. The first trace ran for 100 minutes which was, in his opinion, just too long to be explained by the foetus being in an active state.
Mr Hare therefore said that the only reasonable management was a repeat CTG and an assessment of foetal wellbeing using some of the elements of a biophysical profile. Much time was spent at trial discussing whether biophysical profiling was in use in 1998 or whether it was outdated. However, as Mr Hare had set out in the joint note, his position was that it was only elements of biophysical profiling which should have been used to obtain more information about the pregnancy. There ought to have been a further CTG, a measurement of liquor volume and an assessment of the size of the foetus including head circumference. Mr D agreed that these were reasonable further investigations if there was a concern over the condition of the foetus.
Mr Hare said that at birth, the claimant had intrauterine growth retardation ("IUGR") due to placental insufficiency and that this was the process which had led her to suffer a period of chronic damaging hypoxia in the days leading up to her delivery and accounted for the appearance of the CTG on 13/14 October 1998 and her condition following her delivery. He said that the process of IUGR due to placental insufficiency had started during the third trimester and was present on 28 September 1998. In his opinion, the features on the first trace were caused by a reduction in oxygen to the foetus due to reduced placental function. The oxygen reduction was not (in September 1998) brain damaging because the foetus was compensating for the reduction in oxygen by an increase in the heart rate.
It followed from Mr Hare's opinion on the underlying pathology that had the further investigations been undertaken on or around 28 September then: the further CTG trace would have been, at best, non-reassuring; the liquor volume would have been reduced and there would have been growth asymmetry with relative sparing of the head. On this basis, Mr Hare said that induction of labour would have been mandatory.
Mr Hare agreed that, given that the underlying cause for the trace features was placental insufficiency, then the appearance of the trace would not improve over time. Placental insufficiency is a deteriorating condition, and the trace would never go back to normality with a normal baseline and standard pattern. When it was put to him by counsel for the defendant that the second trace was an improvement on the first, he did not accept this. Although there were good variability and good foetal movements, he said that it was impossible to detect the baseline and so it was impossible to interpret the trace in the way that it had been by Dr Samy. Nor did he agree that, if his theory concerning the underlying cause of the trace features was correct, the claimant would not have survived until 14 October. He said that in his experience the rate of deterioration might be very slow and may vary as the pregnancy progresses. He drew the court's attention to the FIGO Guidelines which set out at [4.3]: "that the evolution of chronic foetal hypoxia is slow. In general, abnormal fetal heart rate patterns are observed over several weeks before ante partum foetal death." It was suggested to him that the FIGO Guidelines did not footnote the studies and evidence upon which they were based. Mr Hare said that the FIGO Guidelines were produced by 20 eminent scientists who would not have said this absent a good basis for doing so.
The abnormal features in the first trace and the absence of reassurance to be derived from the second trace were, said Mr Hare, complemented by other features of the pregnancy which, although individually did not require earlier delivery, either required further inquiry or supported the case for induction. Those features were: that Mrs Woods was taking Colofac for treatment of her irritable bowel syndrome, the possible rupture of the membranes on 1 September 1998; multiple episodes of glycosuria during pregnancy and the absence of a glucose tolerance test during the third trimester; her report that she had been unwell in the two weeks leading up to the 28 September with persistent vomiting.
The only further feature which was, to use his phrase a "standalone" indication for active management was the maternal history of lack of foetal movements. Mr Hare told me that Dr Samy should have asked Mrs Woods specifically about her perception of foetal movements on 6 October 1998. He should have noted down her response. If, as she asserts, she was sensing a reduction in foetal movements then this should have prompted a repeat CTG assessment. This would, in turn, have proved to be at best non-reassuring and would have led to further assessment and induction of labour.
Expert obstetric evidence for defendant
Mr D agreed that the first trace was not easy to interpret. The predominant feature of the trace was the heart rate. In his report he described the rate as being around 155 to 165 bpm with variability of around 10 bpm. He described the heart rate as falling "near the top of the normal range." In his evidence at trial, he said that the heart rate was 155 bpm – 170 bpm which was the upper limit of what is considered normal. He acknowledged that interpretation of any CTG when the baby is quite active was challenging. In his report he said that it had been noted that the baby was moving at this time. He described the clinicians as being cautious in deciding to repeat the CTG, but he clarified this in evidence by saying that, had the trace not been repeated, then he would have been disappointed. He noted however the normal variability which was a reassuring feature. As he put it, the clinicians were faced with a trace which could not be described as normal but was not of such concern that the clinician would wish to intervene. In his view therefore, Dr Samy did the correct thing by allowing the trace to run for a while but, when still unsure of it, the trace was discontinued for a while before it was re-started.
The purpose of the second trace was to check whether the foetal heart remained elevated. Mr D found the second trace to be clearly interpretable with a normal baseline of around 140 bpm. This was apparent from the first 3 or so blocks of the trace representing the first 3 or so minutes of monitoring. When challenged, Mr D did not agree that it was necessary to have 5 minutes (at least) of stable baseline in order to determine the true baseline. He said that when the RCOG referred to the need to have 5 or 10 minutes of stable baseline the authors were referring to the foetal heart rate in labour and not during the antenatal period. Provided that there were plenty of accelerations and good variability, it was not necessary to have an interrupted period of 5 minutes minimum to be confident of the true baseline.
Mr D said that following the initial period of baseline heart rate there were then a number of accelerations which coincided with foetal activity. Foetal activity was recorded in two ways on the trace. First, by Mrs Woods pressing a button when she felt the foetus move which generated an ink mark on the paper trace. Second, by the tocograph recording foetal movement when detected (although Mr D acknowledged that this was not a particularly robust tool). Although some of the ink markings were faint, he was confident that the foetal heart rate was accelerating in response to foetal movements. As he put it, in the first section of the trace there were multiple foetal heart movements and multiple accelerations in association with the foetal activity.
The other key feature of the trace, and aid to its interpretation, was that beat-to-beat variability was maintained throughout. Mr D said that in the "hierarchy of reassurance" the most reassuring feature is the presence of accelerations, but that normal variability is the second most reassuring feature. He told counsel for the defendant that a tachycardia with normal variability was in his experience almost always caused by the baby moving and that whilst he could not rule out that a persistent tachycardia with normal variability may be due to hypoxia, this would be very surprising. It was not, he said, something which he had ever seen in his career.
Mr D said that Dr Samy's note suggested that he had thought carefully about the trace and had reached the correct conclusion. It was the conclusion which he shared. The second trace was healthy, and the heart rate was reacting to foetal movements. He did not accept that the active phase usually lasted only 20 minutes or so. All babies have quiet and active phases, and some will move more than others during active periods. He said that it was quite appropriate to review the first trace in the light of the second trace and to reinterpret it. On this basis it was a safe conclusion that the elevated heart rate apparent on the first trace was a response to foetal activity and the so-called decelerations were not true decelerations but were a return to the true baseline of around 140 bpm. He referred the court to the edition of "Foetal Monitoring in Practice" by Donald Gibb and S. Arulkumaran which was current in 1998 which referred to difficulties in assessing the baseline heart rate of an active foetus. The authors state: "Persistent accelerations may lead to confusion such that some traces have been termed "pseudodistress" patterns. When the fetus is very active it may show so many accelerations that it is misinterpreted as tachycardia with decelerations. This situation can arise in the antenatal period or in labour." This was, exactly, the assessment made by Dr Samy and which he endorsed.
Mr D said that he would not have interpreted the first trace as showing a deceleration. He said that interpretation of CTG traces is all about pattern recognition and the two dips in the foetal heart trace did not, to him, look like decelerations. They were the wrong shape and if they had been true decelerations in conjunction with a true tachycardia then he would have expected them to be associated with loss of variability. Furthermore, a deceleration lasting several minutes (as postulated by Mr Hare) would have been a late feature of placental insufficiency. Two things followed from this. First, the only correct management would have been immediate delivery (rather than further investigations) and second, the claimant would not have survived until 14 October 1998.
Mr D accepted that if contrary to his opinion, the clinician ought to have sought further information then an assessment of foetal weight, liquor volume and a further CTG would be a reasonable investigation to undertake. He did not accept however that the claimant was suffering from IUGR in September 1998. He said that babies affected by IUGR fall into two groups. In addition to those which are affected by placental insufficiency in the third trimester or earlier, there is a group of babies who suffer from what he described as "late onset" IUGR. That group will have reasonably normal growth but towards the end of pregnancy the placenta begins to start failing and those foetuses tend to deteriorate over a few days and that process of deterioration is more rapid. He said that in September 1998 the liquor volume would have been assessed as normal; the trace would have been normal, and the foetal weight would have been assessed as within the normal range. In these circumstances, there would have been no indication to induce labour before Mrs Woods was well past term.
Mr D agreed that, on 6 October 1998, he would have expected Dr Samy as a matter of routine to ask Mrs Wood about reduced foetal movements and he would have expected a competent clinician to make a note of the outcome of that inquiry. He told the court however that notetaking in 1998 was not as diligent. He agreed that if there had been a complaint of reduced foetal movements then Dr Samy ought to have undertaken another CTG. He did not accept that a further CTG on 6 October would have been abnormal.
Expert midwifery evidence
The evidence of the midwives was of doubtful relevance. There were no criticisms of the midwifery management, and it was common ground that the midwives acted reasonably by, at all times, escalating their concerns to the obstetric team.
Findings
The judge referred to some aspects of Mr D's evidence which she found to be problematic.
As Mr D acknowledged, his report of 2023 had been prepared by him without a recent review of the second trace. In his covering letter to the report dated 7 June 2023 he wrote: "I have completely redrafted my report because the case that is being put now is different to the case that we dealt with in 2007. However, my interpretation of the CTG is based upon the interpretation I made at that time on 28 September 1998. I do not seem to have another copy…I have based this report upon my previous interpretation of the CTG…" The judge assumed that the reference to 28 September 1998 was an error and that he meant, in 2007. When asked about the preparation of his report in court he said that he might have had a copy of the second trace, but it was not legible. This was not what he said in his covering letter though. Whatever the problem, he confirmed that he had imported into his July 2023 report that section of the report from 2007 which set out his interpretation then of the second trace.
On any assessment, this was wholly unsatisfactory. In 2007 when the section of the report concerning the second trace had been written, the second trace was not the subject of criticism. By 2021 when the case was issued however, the second trace was the focus of the claim. A better and more legible copy of the second trace was available. Even if the copy retained by the defendant had degraded, the claimant's team was in possession of a copy which had been made by Mr Hare before the trace had deteriorated badly. It was unclear whether it was sent to Mr D. If it was then it did not appear that he reviewed it before the meeting with Mr Hare. In the joint expert minute, he observed that his "consideration of the CTG has to be based upon my first review of this case which happened in 2007. The current available copy of the CTG actually has no heart rate visible, so I can only rely on my opinion at that earlier time. I cannot review it." In fact, a better copy of the second trace formed part of Mr Hare's report. Although the later part of the trace remained difficult, if not impossible, to interpret, it was possible to identify (although perhaps not clearly) the heart rate, the variability and the ink markings associated with foetal activity in the earlier sections. The second trace appeared within the body of Mr Hare's report (rather than as an appendix). It was difficult to see how, had Mr Hare's report been considered by Mr D, he could have missed the copy of the second trace.
There were some other parts of Mr D's evidence which were concerning. In the section of his report which considered the first trace, he set out that it had been noted that the baby was moving at the time of the trace. There was however no such reference in the notes. His report referred to there being no history of continuing leakage and/or leakage on the day of attendance. This statement had to be seen in the context of a documented report from Mrs Woods of leakage, indeed on the basis of the midwifery note, this was the presenting complaint and the reason for the self-referral. Mr D explained that this was clumsy wording and that he was intending to convey that there had been no further leakage following admission but, as counsel put to him, this was not in fact what he wrote in the report.
Both of the points above were small points. But in conjunction with the circumstances in which the report was put together by Mr D they went to create an unfavourable picture. The judge was reluctantly driven to the conclusion that, in this case, Mr D's preparation had lacked the attention to detail which the case demanded. Predictably, it led to matters being raised for the first time in evidence (not having featured in his report or expert meeting and not having been put in cross examination) in circumstances when it was impossible to know whether Mr D had thought about these things beforehand (but not set them out in writing) or whether they were occurring to him for the first time in the witness box. He relied on little, if any, literature even when he was challenging the use of Guidelines (for example, FIGO/RCOG and the need for 5 minutes minimum of stable baseline). Whilst the judge understood that in his oral evidence, he might have been trying to convey the reality of practice in a busy but competent antenatal ward, she regretted to say that the overall impression was of a rather casual approach to the issues in the litigation. As counsel highlighted, this was in stark contrast to Mr Hare who gave the impression of having considered the issues in the case with real care and who provided thoughtful and measured responses to the questions posed.
Conclusions
The first issue was whether the second trace was sufficiently reassuring to justify discharging Mrs Woods back to routine antenatal care. The first trace demonstrated throughout its course a heart rate in excess of the normal baseline. Even if the appropriate upper limit of normal was 160 bpm, the claimant's heart rate exceeded this value. The heart rate was not, as Mr D suggested, towards the "upper limit of what is considered normal." It was over the limit of what is or should have been considered normal and by some margin. Although the reason for the tachycardia may not have been known prospectively the heart rate was undoubtedly tachycardic and had continued to be so for almost 100 minutes.
She did not accept Mr D's opinion that the tachycardia should have been considered a feature of limited concern due to the retained beat to beat variability. His evidence was that tachycardia with retained beat to beat variability was almost always due to foetal activity rather than hypoxia and that whilst he could not rule anything out, in his career he had never encountered such a feature. As counsel for the claimant acknowledged, this statement was later qualified to an extent when Mr D remarked that foetal activity was the cause in the "vast majority of situations." The point did not feature in Mr D's report. It was not mentioned in the joint expert note nor was it put directly to Mr Hare in cross examination.
Mr D's interpretation of a tachycardia with retained variability as being almost always, or in the vast majority of situations, due to foetal activity was an overstatement. The RCOG define a tachycardia as a non-reassuring feature. The FIGO classify its presence as suspicious. Neither definition discriminates between a tachycardia with or without retained beat to beat variability. Dr Gibb's manual sets out that a very active foetus may show so many confluent accelerations that it is misinterpreted as a tachycardia with decelerations. It makes the point that if beat to beat variability is maintained then the trace will not generally represent an hypoxic foetus. But the manual also counsels that "any tracing with a baseline rate of greater than 150 bpm should be carefully scrutinised for other suspicious features." In these circumstances she accepted the claimant's case that it would be unsafe to assume that a tachycardia with retained variability was due to foetal activity.
The first trace also demonstrated two episodes when the fetal heart rate dropped to around 140 – 150 bpm. Again, she was unable to accept Mr D's opinion that because beat to beat variability was maintained throughout the course of the episodes, they should not be classified as decelerations and otherwise treated as benign features. This interpretation did not fit with the textbooks which describe the presence of a deceleration as a non-reassuring feature but one which if associated with additional loss of variability would justify the classification pathological. Viewed prospectively, it was impossible to judge the cause of the deceleration and whether it was due to hypoxia or maternal position or for some other reason.
It followed that the judge accepted Mr Hare's evidence that the first trace had two apparently abnormal features, tachycardia, and decelerations, and that there was a need therefore for further information.
The second trace did not provide sufficient reassurance to justify allowing Mrs Woods to go home with routine antenatal follow up. There were a number of reasons for this conclusion.
i) The judge accepted Mr Hare's evidence that in order to determine a baseline heart rate, a minimum period of 5 minutes is required. Mr D asserted that the minimum requirement for 5 minutes stable heart rate was relevant only to traces in labour, but this caveat does not appear in the FIGO or RCOG Guidelines. On the second trace Mr D identified a block of no more than 3 or so minutes when the heart rate was stable at 140 bpm. Thereafter he identified a few episodes of a minute or so between accelerations when the rate was 140 bpm. She agreed with Mr Hare that the second trace was not capable of being interpreted as demonstrating a foetal heart rate baseline of 140 bpm.
ii) The judge accepted that the trace appeared to show accelerations in conjunction with periods of foetal activity. However, if the tachycardia were due to the foetus being in an active state, then the active state must have continued for an unusually long period of time. The first trace lasted around 100 minutes and was tachycardic throughout its course save for the two decelerations. Mr Hare stated that the active phase would not usually persist for longer than 20 minutes or so. Mrs Johnson said that she could not recall an active phase lasting for more than an hour and thought that around 30 minutes was the norm. Mr D did not give a timescale but indicated that he might have women on the antenatal ward for an hour or so with traces which are difficult to interpret. If the baby was active and variability maintained, then he would advise stopping the trace and starting it again. He said that the trace would come back normal. This of course was not what occurred in Mrs Woods' case where the trace did not come back normal. On the basis of this evidence as a whole, it did seem to her that if the tachycardia were to be explained by foetal activity, the active phase was very long indeed. It was a minimum of 1 hour and 40 minutes (subject to the short blocks of deceleration) followed by another period of around 30 minutes. This would assume that the baby was in a quiet phase between the two episodes of monitoring. If the baby was not in a quiet phase between the two episodes of monitoring, then the active phase continued from 19.45 when the first trace started until around 23.00 when the second trace was disconnected.
Dr Samy's decision to let Mrs Woods go home on 28 September was not a reasonable decision. Having determined correctly that the first trace could not be interpreted and that a further trace should be performed to assist in its interpretation, the further trace did not serve its intended purpose. The second trace did not provide the necessary reassurance for the reasons set out above. As Mr Hare put it, the active phase was finite. The trace should have been allowed to run on beyond the active phase in order that the true baseline could be established. Having determined that another trace should be obtained it was wholly illogical to stop the trace before the active phase was over.
The judge then turned to the question of the further investigations which ought to have been undertaken and the results of those investigations. In reality, there was no difference between Mr Hare and Mr D as to the types of further investigations. Mr Hare overstated matters in his report by referring to the need for biophysical profiling when, in effect, he was stating only that certain elements of the biophysical profile were required. Those elements were a further CTG, an assessment of liquor volume and an assessment of foetal growth. Mr D did not disagree that if the obstetrician wished for more information and was concerned about the possibility of growth retardation secondary to placental dysfunction then those investigations were appropriate.
The judge was satisfied that had those further investigations been performed they would have led to a decision to induce the labour on or around 29 September 1998. This was her thinking.
The logical starting point for determination of this issue was consideration of whether, in fact, the claimant was affected by IUGR due to placental dysfunction at birth. On this issue, it seemed to her that all of the evidence pointed one way. There was an asymmetry between the claimant's head circumference and her birth weight. There was relative head sparing and the head circumference was on 50th centile whilst her birthweight was (using Mr D's app) between the 9th and 25th centile. Both experts agreed that asymmetry is one of the features (or can be one of the features) of IUGR. The placenta was gritty, and the liquor was thick, and meconium stained. Both Mr Hare and Mr D said that a gritty placenta is or is usually caused by calcification due to it not functioning properly. The thick liquor was due to reduced liquor volume which was, in Mr Hare's opinion, an important pointer towards IUGR. Mr D accepted that thick meconium is commonly associated with reduced liquor which can be associated with IUGR due to reduced blood flow to the kidneys and so less liquor. Given all of these features, the judge found it likely that the claimant was affected by IUGR due to placental dysfunction at the time of her birth.
The next question was whether the claimant was affected by IUGR in September 1998 such that it would have been detected on further investigation on 28/29 September 1998, two weeks before her delivery and, on the claimant's case 11 or so days before her condition deteriorated and she began to sustain brain injury.
Mr Hare had explained the pathological process which he asserted was ongoing on 28/29 September. As a result of placental dysfunction, less oxygen reaches the foetal circulation and so the foetal heart beats faster to make up the deficit. For a period of time the deficit will be compensated and there will be no foetal brain damage. Once the heart is unable to compensate then brain tissue damage may occur. Mr Hare described the process as a slow one which may take place over a period of weeks. His experience suggested that on occasions it started at the beginning of the third trimester. The speed of the process he described was reflected in the FIGO Guidelines which set out that: "the main target of antepartum fetal heart monitoring is the detection of chronic fetal hypoxia related to chronic placental dysfunction… the evolution of chronic fetal hypoxia is slow. In general, abnormal fetal heart patterns are observed one or several weeks before antenatal death."
Mr Hare's case that loss of variability occurs only after the foetal heart is unable to compensate was reflected in Parer: "in the presence of normal FHR variability, no matter what other FHR patterns may be present, the foetus is not suffering cerebral tissue asphyxia because it has been able to successfully centralise the available oxygen and is thus physiologically compensated. In the presence of excessive asphyxia stress however as evidenced by severe periodic changes or prolonged bradycardia this compensation may break down and the foetus may have progressive central tissue asphyxia. In this case it is theorized that FHR variability decreased and eventually is lost."
Mr D's opinion that, had the trace demonstrated a tachycardia and decelerations, the claimant would not have survived until 14 October had to be seen in the light of the literature above. The trace features on 28 September were not due to foetal hypoxia. On Mr Hare's analysis, on 28 September, the foetal heart was still compensating adequately for the placental deficiency. Indeed, the two episodes of deceleration on the first trace may have been simply episodes when the fetal heart dipped due to maternal posture. The FIGO Guidelines and Parer supported Mr Hare's opinion of a process which is slow with trace deterioration and loss of variability taking place only once the foetal heart is no longer able to compensate for the placental insufficiency.
The defendant alleged an inconsistency in Mr Hare's evidence when in the joint statement he recorded: "As baseline variability was not impaired this pattern indicates that this was an early stage of foetal compromise. The foetus would have been receiving adequate oxygen for the health of the brain to be maintained, albeit by increasing the blood flow to the brain by an increase in the heart rate. It is perfectly feasible that this should continue for several days before damaging hypoxia developed." (judge’s emphasis). The point which Mr Hare was making in the joint report, as in his oral evidence and which was supported by the literature, was that the downward trajectory of the foetal heart's compensatory mechanism may be very slow when the underlying mechanism is placental dysfunction. Mr Hare referred to "several days"; the 20 authors of the FIGO Guidelines referred to "several weeks." The judge could see no inconsistency in Mr Hare's evidence and his evidence was supported by the literature.
The judge accepted Mr Hare's account of the underlying process which culminated in the claimant's delivery on 14 October with IUGR. Whilst noting that Mr D asserted that IUGR may be a "late stage" condition, there was no evidence in this case that it was so. The point was not raised in Mr D's report and not put to Mr Hare, and she had no literature or information on the topic. Mr Hare's clinical experience was that placental dysfunction can start relatively early in pregnancy and in his experience, it can start at the beginning of the third trimester. The judge accepted this evidence. Mr D acknowledged that the gritty placenta was not something which would "happen overnight," accepting that it indicated that the placenta had been sub optimal in the last week or two before delivery. This might have been be a small concession by Mr D, but it pointed in the direction of a process which had been ongoing since, even on his assessment, 14 days before delivery i.e., on or after 1 October.
The judge was therefore satisfied on the balance of probabilities that, had a longer CTG trace been undertaken on 28/29 September 1998, it would have continued to be abnormal as Mr Hare had said. It would have continued in this way without improvement until the foetal heart was ultimately unable to compensate for the oxygen deficit caused by the placental dysfunction. She also found that if a liquor volume assessment had been performed it would have demonstrated a lower-than-normal volume and that foetal assessment would have demonstrated the asymmetry which was apparent at her birth. The gestation was term, or near term. In these circumstances, she accepted that reasonable management mandated induction of labour on or around 29 September 1998.
Judgment was entered for the claimant.