Case No: 9LE91091
Neutral Citation Number: [2011] EWHC 38 (QB)

IN THE HIGH COURT
QUEEN’S BENCH DIVISION
AT NOTTINGHAM COUNTY COURT
60 Canal Street
Nottingham 
Nottinghamshire
England 
NG1 7EJ

Date: 18th January 2011 

Before:

THE HONOURABLE MRS JUSTICE SLADE DBE
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Between:

	Brodie McCoy
(A Minor by her Mother and Litigation Friend Joanne Jones)	Claimant	
	- and -		
	East Midlands Strategic Health Authority	Defendant	

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William Edis QC (instructed by Wilson Browne LLP) for the Claimant
Stuart Brown QC (instructed by Kennedys) for the Defendant

Hearing dates: 16th-19th November 2010
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Judgment
Mrs Justice Slade: 
1.	The Claimant, Brodie McCoy is 17 years of age having been born on 22nd March 1993 at 39 weeks gestation. She was born in poor condition at birth and has been left with brain damage. Brodie suffers from diplegic cerebral palsy (a brain injury that has an effect on contralateral limbs) which affects her legs, her mobility and her balance. She also has learning difficulties. Brodie claims damages for clinical negligence in failing to carry out a further cardiotocograph scan on 17th March 1993 when she was at 37 weeks gestation. She can pursue her claim by reason of the Congenital Disabilities (Civil Liability) Act 1976 Section 1. The hearing before me is to determine liability: negligence and causation.
Relevant Facts
2.	On 17th March 1993 at 38 weeks gestation Ms Jones, Brodie’s mother, complained of reduced fetal movements. She was advised to attend Kettering General Hospital for monitoring. The following facts were agreed between the parties:
i)	It was correct to admit Ms Jones to hospital on 17th March 1993 as reduced fetal movements are a risk factor for fetal wellbeing;
ii)	Entirely properly, an attempt was made to assess fetal wellbeing by way of a cardiotocograph (‘CTG’) trace;
iii)	That trace lasted some 58 minutes, running from 14.25 to 15.23 hrs;
iv)	Before Ms Jones was discharged the CTG was reviewed (in accordance with hospital policy) by a Staff Grade Obstetrician, Dr Lukshumeyah;
v)	He concluded that the trace was “satisfactory” and signed the CTG to that effect (on its far left margin). There is no other note as to what he made of it or what considerations he had in mind, for example the presence or absence of decelerations or accelerations;
Dr Lukshumeyah sent Ms Jones home with a kick chart to record fetal movements.
3.	It was common ground that: 
i)	Brodie’s birth weight was 2.88 kg which is on the 10th centile for gestational age and gender;
ii)	Her head size was 34cm, which is on the 50th centile for gestational age and gender;
iii)	She was in poor condition at birth, with Apgar scores of 5 at 1 minute, 7 at 3 minutes and 9 at 5 minutes.  (Apgar scores are a means of assessing the condition of a baby at birth.  Five different factors are measured, each being given a score of 0, 1 or 2. The perfect score is therefore 10);
iv)	There was nothing in her mother’s antenatal history to indicate that this was a high risk pregnancy, nor is any criticism made of her antenatal care, which was shared between hospital and GP;
4.	The parties were agreed that a suspicious or pathological CTG scan be an indication of hypoxia. Hypoxia is a pathological deprivation of adequate oxygen supply. It was contended by William Edis QC on behalf of the Claimant that Dr Lukshumeyah negligently interpreted the trace of the scan carried out on 17th March 1993 as ‘satisfactory’ and the scan should have been continued or a further scan undertaken. 
5.	Although it was agreed that the trace showed some reassuring features it was contended on behalf of the Claimant that a proper consideration of the CTG trace would have led to its classification as ‘suspicious’ or not ‘satisfactory’. If the trace had been properly interpreted further CTG scanning would have been carried out later on 17th March. It was contended by Mr Edis that further CTG scanning would have been likely to have shown a similar worrying or a worse fetal heart pattern. It would not have shown a better pattern as it was agreed that by 17th March 1993 the mother’s placenta was failing. Mr Edis contended that if the repeated CTG trace was suspicious, steps would have been taken to bring about early delivery on 18th March whether by induced labour or more likely by caesarean section. If Brodie had been delivered on 18th March 1993 her brain damage would have been avoided. 
6.	Stuart Brown QC for the Defendant contended that Dr Lukshumeyah was not negligent in regarding the trace as satisfactory. Even if he were negligent in regarding the trace as satisfactory his failure in that regard did not cause the injury suffered by Brodie. On a balance of probabilities a further scan on 17th March 1993 would not have led to a decision to intervene to deliver Brodie earlier than 22nd March 1993. 
7.	There was agreement between the medical experts as follows:
i)	The damage to Brodie was caused by chronic partial hypoxia;
ii)	The hypoxia was caused by a failure in the placenta;
iii)	The placenta has two main functions:
a)	To provide nutrition to the foetus,
b)	To provide for an exchange of gases – oxygen in and carbon dioxide out.
iv)	When a placenta is failing, nutrition is provided to the brain in favour of the body. A disproportion in the centiles of head circumference and body weight is an indication of a failing placenta;
v)	When a placenta is failing, oxygen continues to be supplied in favour of nutrition;
vi)	Hypoxia can be sustained by a foetus without causing damage. Contractions in the course of birth can inflict pressure on the placenta causing hypoxia without damage resulting;
vii)	Brodie was undamaged on 17th March 1993. It is likely that damage was caused to her brain after 17th March and before her mother’s admission to hospital on 21st March 1993. 
viii)	The degree of Brodie’s disability indicated that damage only started to occur at some time after 17th March 1993. She was highly unlikely to have sustained damage by 18th March 1993.
8.	The issues for me to decide are:
i)	What were the relevant features of the CTG trace, in particular how many and at what time are decelerations shown;
ii)	Did Dr Lukshumeyah act negligently in categorising the CTG trace as ‘satisfactory’;
iii)	Had a further scan been carried out on 17th March 1993, on a balance of probabilities would it have led to delivery before hypoxia caused brain damage to Brodie.
The Evidence
9.	Ms Jones, Brodie’s mother gave evidence. Evidence was given by Dr Lukshumeyah and Midwife Pearson who attended Ms Jones at the hospital on 17th March 1993. The following expert evidence was given by their reports and in person: consultant obstetricians, Mr Jarvis for the Claimant and Mr Porter for the Defendant; Consultant Neonatologist, Professor Weindling, for the Claimant and Dr Thomas, Consultant Paediatric Neurologist, for the Defendant. In addition to their reports, the notes of meetings of the experts who gave evidence were produced as were the reports and minutes of a meeting of two neuroradiologists, Dr Kendall for the Claimant and Dr Forbes for the Defendant. They were not called to give evidence as they were in agreement that the radiological evidence supported the opinion that the cause of the Claimant’s difficulties was chronic partial hypoxia. 
10.	Included in the written material before the court were relevant extracts from the literature referred to by the obstetricians. The CTG trace was considered at length. 	
The trace
11.	Relevant to assessing a CTG trace are the baseline level of the fetal heart rate, the variability in the baseline heart rate, fetal movements and the existence of accelerations and decelerations. 
12.	The position of both Mr Jarvis and of Mr Porter changed over time. Mr Jarvis as to the significance of the reduced baseline activity for forty minutes and both Mr Jarvis and Mr Porter as to the number of decelerations. Both experts agreed that the baseline heart rate was satisfactory. The trace showed a variability of less than 5 bpm from 14.25 to 14.52. From the notes of the joint meeting between the obstetricians on 31st August 2010 it appears that at first Mr Jarvis considered that in the presence of decelerations this was too long to indicate fetal sleep. Mr Porter, however considered that this duration of reduced variability was perfectly consistent with fetal sleep. In cross-examination Mr Jarvis conceded that his previous opinion was in error; a period of reduced baseline variability of 40 minutes was perfectly consistent with fetal sleep. 
13.	The vertical lines at the top of the trace indicate Ms Jones’ detection of fetal movements at times during the scan. There are a number of vertical lines starting on the heart baseline of the trace which are said to be artefacts. Artefactual readings are those that appear to represent the fetal heart but do not do so. 
14.	The trace shows four accelerations. These are contained in six minutes of the trace (15.05, 15.06, 15.08-09 and 15.11). Accelerations are transient increases in fetal heart rate of 15 bpm or more above the baseline and lasting at least 15 seconds. 
The definition of a deceleration
15.	Dr Lukshumeyah gave evidence that he was working to the FIGO classification and interpretation of CTG traces. FIGO (International Federation of Gynaecology and Obstetrics) guidelines in place in 1993 gave the following definitions in FIGO News 1987: 
“2.4 Decelerations. Transient episode of slowing of fetal heart rate below the baseline level of more than 15 beats/min and lasting 10 seconds or more.”
Donald Gibb in Fetal Monitoring in Practice 1992 (‘Gibb’) at page 30 writes:
“A deceleration is defined when the FHR decelerates by more than 15 bpm from the baseline for more than 15 seconds.”
It was agreed by the experts that the accepted definition of a deceleration is one of more than 15 bpm lasting for more than 15 rather than 10 seconds. 
16.	The trace shows three possible decelerations: D1 at 14.54, a decline of about 25 bpm for about 15 seconds, D2 at 15.12, a decline of 25 bpm for 30 seconds and D3 at 15.21, a decline of 30 bpm or more for at least 15 seconds.
D2
17.	The experts were agreed that D2 at 15.12 was a deceleration. It showed a drop from 140 bpm of 25 bpm and returned to baseline after 30 seconds. The nadir of the deceleration is missing on the trace. 
D3
18.	At the conclusion of the oral evidence, both Mr Jarvis and Mr Porter were agreed that D3 was a deceleration. Both regarded the sloping downward trace at 15.21 as the start of a deceleration. Midwife Pearson switched off the CTG soon afterwards and the trace stops at 15.23. 
19.	Mr Jarvis considered that a dot on the end of the trace showed the resting point of the trace pen as the machine was switched off. He was of the opinion that there was no record of when the heart returned to the baseline. The trace showed a deceleration of more than 15 seconds, the time between the start of the deceleration and the end of the trace.
20.	Mr Porter considered that the dots at 150 bpm at the end of the trace recorded the heart rate returning to the baseline. If this were the correct interpretation of the trace the heart rate would have been below the baseline for 15 seconds and so would be on the cusp for classification as a deceleration. 
21.	Midwife Pearson said in evidence that she would have heard the fetal heart beat after she had switched off the CTG machine. Therefore she was satisfied that the heart rate was satisfactory. She would have noticed if it was not. 
22.	Whether Mr Porter or Mr Jarvis is right about their interpretation of the dot or dots at the baseline at the end of the trace, D3 is a deceleration. The experts agree that the trace shows that the heart rate was below the baseline for 15 seconds on Mr Porter’s analysis and more than 15 seconds on Mr Jarvis’ account. Midwife Pearson’s evidence of hearing a heartbeat after the trace stopped recording cannot be relied upon as evidence that the fetal heart rate had returned to the baseline. She made no record at the time, did not refer to it in her statement and raised it in her oral evidence seventeen years after the event. In any event she could not be expected to be able to distinguish without measurement between a heart rate of 150 bpm and one below that.
D1
23.	The experts were not shown the original print out of the CTG trace when they produced their reports. Before seeing the original trace, Mr Porter considered that D1 was ‘artefactual’, a false reading which can be caused by loss of contact with the mother. When Mr Porter and Mr Jarvis were shown the original trace in the course of giving their evidence, they both could see that the heavy vertical line at 14.54 which descended below the baseline was in fact two parallel lines. They agreed that the parallel lines or at least one of them was artefactual. They agreed that the line to the left which descended at a slight angle was probably or could have been a true descent marking the start of a deceleration. However Mr Porter considered that the ‘squiggle’ starting at 14.53 to the left of the point where the parallel lines later rejoined the baseline was probably the resumption of the record of the heartbeat which by then had returned to the baseline. 
24.	Thus even if the line on the left marked a true descent whether the return to the baseline was recorded by the squiggle or one of the parallel lines, the period the fetal heart rate was below the baseline was less than 15 seconds and therefore was not to be classified as a deceleration. 
Conclusion on decelerations
25.	On the evidence outlined above I hold that the CTG trace records two decelerations, one of 30 seconds at 15.12 and one of at least 15 seconds starting at 15.21. 
26.	The period of variability of the baseline below 5 bpm was of such a length as not to give rise to concern. It was consistent with a period of fetal sleep. The baseline heart rate was satisfactory. 
27.	There were seventeen fetal movements recorded by the mother one of which coincided with D2.
28.	There were four accelerations which occurred before D2. There were no accelerations between D2 and D3.
Did Dr Lukshumeyah act negligently in regarding the CTG as satisfactory and in not carrying out further monitoring?
The Literature
29.	FIGO 
“Definition of antepartum fetal cardiograms
11.3 Normal patterns
11.3.1 Baseline heart rate between 110 and 150 beats/min.
11.3.2 Amplitude of heart rate variability between 5 and 25 beats/min.
11.3.3 Absence of decelerations except for sporadic, mild decelerations of very short duration.
11.3.4 Presence of two or more accelerations during a ten minute period.
…
11.4 Suspicious patterns
…
11.4.4 Absence of accelerations for more than 40 min.
11.4.5 Sporadic decelerations of any type unless severe.”
Severe decelerations (which these were not) would be classed as pathological.
Gibb
“The presence of two accelerations in a 20-minute trace is termed a reactive trace and is suggestive of a fetus in good health. ……in order to be described as non-reactive the trace should run for a period of at least 40 minutes during which two accelerations are not identified in any 20-minute period.”
Gibb at page 41 uses the analogy of a child playing with a ball to explain that  reduced baseline variability and then a flat baseline are indicative of increasing hypoxia. At page 66 he states that ‘accelerations are the hallmark of fetal health’.
30.	Turnbull’s Obstetrics 1989 (‘Turnbull’)
Turnbull writes at page 376:
“Decelerations of a transient nature are a frequent occurrence. The non-recurring early or mildly variable type, in association with uterine activity or fetal movement, are normally associated with normal fetal outcome (Kidd et al 1985a). Late and recurrent decelerations are of hypoxic origin (Perar et al 1980, Kidd et al 1985a).
…
Normal and abnormal antepartum fetal heart rate
A normal trace is one with a baseline of 120-160 beats/min with a variability of 5-25 beats/min, with at least two accelerations of an amplitude of 10-15 beats/min over a 15-20 minute interval. There should be no decelerations, except for an occasional sporadic mild variety.”
At page 377 he observes:
“Similarly, mild repeating decelerations in the presence of accelerations are suspicious signs requiring repeat tests to be performed. Minor deviations of baseline fetal heart rate and sinusoidal patterns require further evaluation to assess the worth of these patterns in diagnosing pathological fetal states. 
Fetal heart rate tracings showing marked reduction in variability and accelerations with isolated or recurrent decelerations should be regarded as abnormal.”
The Expert Evidence 
31.	In paragraph (28) of his report of 22nd March 2010 Mr Jarvis stated that the CTG was predominantly but not entirely worrying concerning fetal well being. 
32.	Mr Jarvis wrote:
 “The one thing that cannot be said is that the CTG was satisfactory and it would be totally inappropriate to send the patient away for several days. Given this CTG, which is predominantly but not entirely worrying concerning fetal well-being, especially fetal oxygenation, the only acceptable response was either to keep the patient in hospital and to continue with the CTG monitoring or to allow home but advise to return later that day for further CTG monitoring. If the same pattern continued, then it would have to be presumed that this baby was hypoxic and delivery would take place, almost certainly by caesarean section.”
At paragraph (29) he wrote:
“A failure to recognise the potential seriousness of the abnormalities on this CTG falls below the standard to be expected. It was not acceptable to allow Joanne Jones home without further assessment. That further assessment would be repeated cardiotocography with delivery if there were any deterioration.”
33.	In his oral evidence Mr Jarvis said ‘because of the decelerations I would have repeated the CTG.’ He said that the CTG was predominantly worrying. There were two or possibly three decelerations. He disagreed with the concept that there cannot be fetal hypoxia in the presence of accelerations. 
34.	As for the deceleration at the end of the trace, D3, Mr Jarvis said that it was unwise to assume that the heart rate would return to the baseline. One should check recovery. 
35.	From the note of the joint meeting of the obstetricians on 31st August 2010 it is clear that whilst Mr Jarvis considered the CTG to be suspicious, Mr Porter considered it to be reassuring. 
36.	Mr Porter gave evidence that he believed the CTG was satisfactory because of the accelerations and fetal movements. He said that a reasonable obstetrician would first concentrate on the positives. There were a sufficient number of accelerations to be reassuring. In addition, the deceleration at 15.12 was associated with a fetal movement. 
37.	Mr Porter believed that the decelerations recorded on the trace were overridden by the accelerations. Faced with the reactivity and fetal movements it was permissible not to do more. Once there were accelerations and fetal movements there was no need to carry on with the trace.
38.	Whilst at one stage Mr Porter said there cannot be hypoxia in the presence of accelerations, later in his evidence he replied ‘no’ to the question of whether the presence of accelerations rendered hypoxia impossible. 
39.	Mr Porter agreed that if Dr Lukshumeyah had not seen the dot at the end of the trace which Mr Porter regarded as indicating the fetal heart rate returning to normal, he should have continued the CTG. In response to the question from Mr Brown of what Dr Lukshumeyah should have done if he was unaware of either the dot or the return of the heart rate to normal Mr Porter said: 
“He should beyond doubt have continued the CTG.”
The attending practitioners
40.	Since the fetal heart rate showed insufficient variability at the start of the scan Midwife Pearson continued the CTG beyond the usual twenty minutes duration to derive further information and to get a good picture of the fetal heart. The fetal heart rate descended towards the end of the trace. She said that if the fetal heart rate had still been down after the CTG was turned off she would have turned the printer on again. She said that she heard the heartbeat after the printer was turned off but she did not include this in her statement. 
41.	Ms Pearson agreed that the descent in fetal heart rate at the end of the trace was potentially another deceleration. This would have been a second deceleration in ten minutes with no accelerations. Ms Pearson could not say why she switched the CTG off. Looking back she said that she should not have switched it off when she did. 
42.	In his oral evidence Dr Lukshumeyah could not remember why he did not re-start the trace. He would have changed his view of the trace – that it was satisfactory – if the third possible deceleration was a deceleration. He agreed that a second deceleration within a short time of a previous one was possibly a sign of hypoxia. 
43.	Looking at the situation with hindsight Dr Lukshumeyah agreed that it was unreasonable not to repeat the trace. The trace does not cost anything and it might pick up something significant. Under cross-examination he agreed that if the fetus was possibly compromised the mother should have been admitted to hospital on 17th March 1993 to repeat the CTG. He said that looking at the CTG now it passes the threshold of requiring a repeat. 
Discussion and conclusion on negligence
44.	It is for the Claimant to establish on a balance of probabilities that Dr Lukshumeyah acted negligently in deciding that the CTG scan was satisfactory. The legal test for establishing negligence in these circumstances is uncontroversial. It is summarised in paragraph 28 of the skeleton argument of Mr Edis as follows:
“A clinician (of any discipline) is not to be adjudged negligent if he has acted in a way considered reasonable by a reasonable body of his peers, provided always that the thinking that underpins his actions bears logical scrutiny, (Bolam/Bolitho).” (Bolam v Friern Hospital Management Committee [1957] 1 WLR 582, 586; Bolitho v City of Hackney Health Authority [1998] AC 232, 241)
45.	The parties are agreed that there has been no material change in the relevant medical knowledge between the date of the alleged negligence, March 1993, and today. All the literature relied upon was current in 1993. It was not suggested that the expert evidence did not represent the relevant state of knowledge and medical practice at the time of the alleged negligence. 
46.	Ms Jones was advised to go to hospital because she had detected reduced fetal movement. Appropriate action was taken to monitor the fetal heart rate by means of CTG monitoring. This is a cheap and non-invasive test which can identify fetal distress. Midwife Pearson’s action in continuing the CTG trace because of her concern over initial lack of baseline variability illustrates that if the trace is potentially worrying the proper course is to continue the trace. 
47.	Both Dr Lukshumeyah and Midwife Pearson said that with hindsight the trace should have continued or been re-started or Ms Jones admitted, if necessary after giving her an opportunity briefly to return home, for a further CTG later that day. However, as was pointed out by Mr Brown, their actions in 1993 are not to be judged by their own assessment made with the benefit of hindsight but by the facts known to them at the time. 
48.	On the evidence of the experts and having regard to the literature I find that:
i)	Decelerations in fetal heart rate can indicate hypoxia;
ii)	As Mr Porter agreed, the presence of accelerations as well as decelerations does not eliminate the possibility of hypoxia in the fetus;
iii)	There was a deceleration of at least 25 bpm for 30 seconds starting at 15.12;
iv)	There was a second deceleration starting at 15.21. The trace does not clearly show when the heart rate returned to the baseline. The suggestion by Mr Porter that dots show a return to the baseline is a best guess on his part as is the hypothesis of Mr Jarvis that the marks indicate the pen of the trace returning to its resting position. There is no evidence that the obstetrician attending Ms Jones considered whether the trace showed that the heart rate had returned to the baseline before the recording ceased. There is no evidence that he noticed the dots at the end of the trace or if he did, that he considered how they should be interpreted. 
v)	I accept the opinion of Mr Porter that if Dr Lukshumeyah was unaware of either the dot at the end of the trace or consider whether there was evidence of a return of the fetal heart rate to normal he should ‘beyond doubt have continued the CTG’.
vi)	On a balance of probabilities I find that Dr Lukshumeyah was unaware of the dot or a return of the heart rate to normal. He made no contemporaneous note of his interpretation of a mark at the end of the trace the interpretation of which was unclear. In his statement for the purpose of these proceedings made seventeen years after the event Dr Lukshumeyah made no mention of the dot or whether the heart rate had returned to normal nor did he refer to these matters in his oral evidence. 
49.	When the trace terminated there had been two decelerations of the fetal heart rate without any intervening accelerations. It was not clear from the trace whether the fetal heart rate had returned to the baseline before the CTG was stopped. I have found that Dr Lukshumeyah did not know whether the heart rate had returned to normal. 
50.	In my judgment Dr Lukshumeyah acted negligently in describing the trace as ‘satisfactory’ and in failing to re-start the CTG or at least to admit Ms Jones after a few hours to carry out a further CTG scan when, as Mr Porter stated in evidence, it should have been continued. Since the end of the trace showed another deceleration within nine minutes of the start of a previous one, the trace should have been continued to ascertain whether and when the heart rate had returned to normal, whether there were further decelerations and whether the heart rate was indeed satisfactory. 
Causation
51.	Mr Edis contended that if a further CTG had been carried out on 17th March, on a balance of probabilities it would have been worse than or at best no better than the scan which was carried out between 14.25 and 15.23 on that day. This is because it is highly likely that the placenta had begun to fail by that time. It was agreed that once the placenta begins to fail it does not recover. 
52.	Mr Edis submitted that the CTG trace was suspicious. A repeat trace would have been suspicious or worse, namely pathological. With two suspicious traces or with worsening traces it was submitted that on a balance of probabilities a decision would have been taken to deliver the baby on 18th  March 1993. If that had occurred, Brodie would not have sustained damage.
53.	Mr Brown submitted that if the trace had been continued or a second trace carried out on 17th March the likelihood is that it would have been satisfactory. He submitted that the CTG carried out on 17th March 1993 had been properly categorised as satisfactory and a second carried out soon afterwards is likely to have been similar or not much worse. He contends that if hypoxia had been present on 17th or 18th March 1993 the damage to the baby would have been worse than it was. 
The expert evidence
The Obstetricians
54.	Mr Jarvis gave evidence that a discrepancy between head circumference which at 3-4cm at 39 weeks was on the 50th centile and body weight which at 2.88kg was on the 10th centile indicates placental dysfunction. The limited nutrition which is passed to the fetus goes to the brain in preference to the body. Professor Weindling described this as ‘brain sparing’. A failing placenta will lead to a deprivation in nutrition before failure of the gas exchange function of providing oxygen and removal of carbon dioxide. Mr Jarvis considered that hypoxia was present on 17th March 1993 as in his opinion the trace was suspicious. A suspicious trace with decelerations was indicative of the presence of hypoxia although it had not yet caused any damage. 
55.	In his report Mr Porter was not persuaded that a repeated CTG would have shown deterioration before labour began. He gave evidence that he was struck by the fact that Brodie did not suffer more significant damage if hypoxia had been present on 17th March 1993 and had progressed in a linear fashion up to the time of delivery on 22nd March 1993. 
56.	As to whether a CTG showing two or three decelerations in one hour would be regarded as suspicious Mr Porter pointed to an inconsistency in the FIGO classifications between paragraph 11.4.5 (suspicious) and paragraph 11.3.3 (normal) in that sporadic mild decelerations of very short duration according to paragraph 11.3.3 are not incompatible with a normal trace whereas paragraph 11.4.5 provides that sporadic decelerations of any type unless severe are signs of a suspicious heart rate pattern. The note of the experts meeting of 31st August 2010 records that Mr Porter considered the FIGO classification as suspicious were not met with one possible exception, the deceleration at 15.12 as to which he referred to the apparent inconsistency in the FIGO classification. 
57.	The experts agree that Brodie would have been in better condition had she been born earlier than 22.30pm on 21st March 1993, the time of Ms Jones’ admission to hospital, and was likely to have been undamaged on 18th March 1993. 
The Neonatologists
58.	The Claimant’s expert Professor Weindling, professor of perinatal medicine wrote in his report of 20th March 2010 that if the CTG had been continued, a deterioration in the fetal heart trace would have been recognised before permanent damage occurred. It would have been probable that the heart rate would have deteriorated after 17th March 1993. Professor Weindling explained that the nutritional effect of a failing placenta is felt before impaired gas exchange. Impaired gas exchange is the last part of placental function to fail. The degree of discrepancy between head circumference and body weight was indicative of placental failure starting before 17th March 1993, the date of the CTG. Professor Weindling wrote that:
“51. Although the fetal heart rate pattern on the CTG was abnormal, there were also periods of normal acceleration of the fetal heart rate. The implication of this observation is that it is likely that on 17/3/93 the fetus was still not seriously and permanently damaged by the on-going hypoxic ischaemia, and that the situation was still recoverable. Firstly, the first trace still showed elements of reactivity. Secondly, although the reason for doing the CTG was that Ms Jones had noticed diminished fetal movements, there were marks on the top line of the trace that were likely to have been made in response to fetal movements and which therefore indicated that fetal movements were still present. Thirdly, the trace was less abnormal than the heart rate trace on 21/3/93 and the inference from this observation is that there was deterioration between the two traces. The rate of deterioration was not necessarily smoothly progressive. 
52. The first CTG trace on 17/3/93 was sufficiently normal to be able to conclude that fetal autonomic control was still present and that it is therefore likely that Brodie was probably still neurologically intact. My conclusion from the above considerations is that it is probable that if delivery could have been effected at or close to this time, Brodie would have been either normal or very much less damaged than she is. 
…
58. I do not think it is possible to say when irreversible damage actually occurred but it was probably after 17/3/93 and before 21/3/93 when contractions began. On the balance of probability, if CTG recording had been continued, a deterioration in the fetal heart rate trace would have been recognised before permanent damage occurred.”
59.	Dr Thomas for the Defendant was of the opinion that Brodie suffered inter uterine hypoxic stress before her mother’s admission to hospital on 21st March 1993. As recorded at paragraph 61 of his report of 29th April 2010 he considered that injury was sustained in the 24-48 hours prior to birth.
60.	The notes of a meeting of the neonatologists/neurologists on 10th September 2010 recorded that the presence of nucleated blood cells in Brodie shortly after delivery indicated that she had suffered hypoxia which had been going on some time before birth. It was likely that brain damage occurred between the afternoon of 17th March and the evening of 21st March 1993. 
61.	In his oral evidence Professor Weindling explained that the fetal heart rate goes up in order to increase the supply of oxygen. When the rate slows the fetus becomes short of oxygen. 
62.	Professor Weindling agreed in cross-examination that if hypoxia had been going on for several days he would have expected Brodie to be in a much worse state. In his view the duration of the hypoxia could be limited safely to forty eight hours before delivery. 
63.	Professor Weindling explained that a decrease of fetal movement is an early warning sign of hypoxia.
64.	Dr Thomas did not consider that the degree of discrepancy between the centiles of Brodie’s body weight and the circumference of her head indicated hypoxia. He considered that it was more likely than not that damage was caused to Brodie by hypoxia 24 to forty 48 before her birth. He considered that it was implausible to suggest a deteriorating picture for several days beforehand. 
The Neuroradiologists
65.	Dr Kendall for the Claimant and Dr Forbes for the Defendant agree that the radiological evidence supports the agreed cause of the Claimant’s brain damage, chronic partial hypoxia.
Discussion and conclusion
66.	The answer to the question of whether continuing or resuming a CTG on 17th March 1993 would have led to a decision that Brodie should be delivered on 18th March depends upon whether on the balance of probabilities the further CTG would have been suspicious. 
67.	A suspicious further scan on 17th March 1993 would have indicated the possibility of hypoxia. Since in this case hypoxia would have been the only cause of a suspicious scan, the question of whether a further scan would have been suspicious depends upon whether hypoxia was present on 17th March 1993. 
68.	The parties are agreed that the damage suffered by Brodie was caused by chronic partial hypoxia. This resulted from placental failure. 
69.	The parties are further agreed that it is likely that damage was suffered by Brodie from hypoxia after 18th March 1993 and before the admission of Ms Jones to hospital at 22.30pm on 21st March 1993. It is likely that the damage was suffered between forty eight to twenty four hours of her birth. 
70.	The parties are further agreed that once the placenta starts to fail it cannot recover. A further CTG trace could at best have shown a similar pattern to that at issue or a worse pattern. I therefore must assess on the evidence whether on a balance of probabilities a further trace would have been suspicious or worse. If the further trace had been properly regarded as normal no action to deliver the baby would have been taken. 
71.	The trace which was carried out on 17th March 1993 had the following reassuring features:
i)	The baseline fetal heart rate was satisfactory;
ii)	After a period probably attributable to fetal sleep the baseline variability and level was acceptable;
iii)	There were fetal movements;
iv)	There were accelerations. 
The only troubling feature of the trace was that there were two or possibly three decelerations. 
72.	I have found that Dr Lukshumeyah acted negligently in forming a view that the trace was satisfactory without clear evidence of whether and if so when the fetal heart rate returned to normal after a drop some 15 seconds before the CTG scan was switched off. 
73.	The experts gave evidence that the assessment of a CTG requires a consideration of the entire trace although this may be done in a few seconds. 
74.	I accept the evidence of Mr Porter that a reactive trace with fetal movements, baseline variability and accelerations is an indicator of fetal health. He pointed out the apparent internal inconsistency in the FIGO classification of decelerations in antepartum fetal CTGs. 
75.	It was said in evidence that there is no specified number, length or depth of deceleration which leads to categorisation of a trace as normal, suspicious or pathological. The trace has to be viewed as a whole. 
76.	The curtailed trace is insufficient evidence upon which to conclude that a continued or further trace would have been suspicious. There were two decelerations in the trace which was carried out which were concerning but there were a number of reassuring features. Overall the trace was reactive. The evidence was that a reactive trace with accelerations was a sign of fetal health although accelerations in themselves do not negate the presence of hypoxia. 
77.	The basis for the conclusion of Mr Jarvis that hypoxia was present on 17th March 1993 was twofold. The CTG trace carried out was suspicious because it contained two if not three decelerations. For the reasons given above the Claimant has not established on a balance of probabilities that the trace carried out on 17th March 1993 was suspicious. Nor has the Defendant established that it was normal. The trace should have been continued or repeated.
78.	The other basis for the opinion of Mr Jarvis that the fetus was suffering from hypoxia on 17th March 1993 is the disparity in the centiles of head circumference and body weight of Brodie at birth. It is said that the cause of this disparity, placental insufficiency, must have been in operation for some time and was therefore present on 17th March 1993. In my judgment on the evidence the disparity was a result of deprivation of nutrition as a result of placental insufficiency and is not an indicator of oxygen deprivation over a period of time. Accordingly, in my judgment, disparity in centiles of head circumference and body weight do not assist in determining whether hypoxia was present on 17th March 1993.
79.	Ms Jones had been sufficiently concerned about lack of fetal movement on 17th March 1993 to seek medical advice and to go to hospital for a CTG. She was discharged from hospital with a kick chart. I find it unlikely that she would not have contacted a doctor again if she had continued concern about lack of fetal movements. 
80.	I accept the evidence of Mr Porter that the degree of damage sustained by Brodie indicated that hypoxia was not present on 17th March 1993. I also note that Dr Thomas considered that it is implausible to suggest a deteriorating picture for several days before delivery. He considered that injury occurred between 24 and 48 hours before birth. This evidence accords with that of the Claimant’s impressive expert, Professor Weindling, who agreed that the duration of the hypoxia could be limited safely to 48 hours before delivery. 
81.	Accordingly I find on a balance of probabilities that the Claimant has not established that a second or resumed CTG on 17th March 1993 would have been suspicious or pathological so as to lead her obstetrician to decide that Ms Jones’ baby should be delivered on 18th March 1993 or at any time before 21st March 1993.
82.	The Claimant has not established that the negligence of Dr Lukshumeyah in failing to carry out a further trace on 17th March 1993 was the cause of the damage suffered by Brodie. 
83.	The claim is dismissed.