OUTER HOUSE, COURT OF SESSION |
|
|
OPINION OF T.G. COUTTS sitting as a Temporary Judge in the cause CATHERINE GALLAGHER Pursuer; against LANARKSHIRE HEALTH BOARD Defenders: ________________ |
Pursuer: Haddow Q.C., D. M. Campbell; Gray Muirhead, W.S. (for Bell Russell & Co., Airdrie)
Defenders: Stewart Q.C., Arthurson; Ian Crerar, Solicitor Scottish Health Service Central Legal Office
13 June 2001
[1] The pursuer sues as guardian of her son Adam, her first born. She was given 22 February 1989 as an estimated date of delivery. Adam was born on 28 February 1989 after caesarean section. The pursuer was small in stature, the baby was noted as "large", but the progress of her pregnancy was uneventful. She was admitted to the maternity unit of Bellshill Hospital at 4.10am on 28 February 1989. She had been having contractions from 11.00pm on 27 February 1989 and had had a "show". Adam unfortunately suffers from the effects of a bilateral stroke, i.e. injury by cerebral infarction in both hemispheres of his brain. Although serious, the effects upon him are not catastrophic.
The pursuer's case
[2] The sequence of events in relation to the pursuer's labour is discussed below. The pursuer avers that Adam was diagnosed as having hypoxic ischaemic encephalopathy, that he had suffered from lack of oxygen shortly before birth and that he suffered a neonatal stroke with consequent permanent brain damage. The pursuer's case, as pled, was that the injury to Adam was caused by the fault and negligence of the defenders' medical staff. However, that was refined to one accusation of medical negligence against Dr Miriam Deeny. She was the registrar involved with the pursuer's labour but only during her shift which was between 8.30am and 1.00pm. It can thus be seen that Dr Deeny was neither responsible for the early stage of the pursuer's admission, nor for the important latter stage when Adam was born. In essence, the case pled against Dr Deeny was that she failed to take steps either to proceed directly to a caesarean section at 11.15am or to obtain a foetal scalp blood sample in order to exclude hypoxia as a cause for foetal distress before permitting the pursuer's labour to continue.
[3] A disconnected averment for the pursuer appears at p.12B as follows: "He had suffered from a lack of oxygen shortly before birth. He suffered permanent brain damage. An MRI scan was taken on 1 November 1999. This suggests that Adam suffered a bilateral neonatal stroke occasioned probably by thrombosis or arterial spasm."
The defenders' case on pleadings
[4] It was averred that Adam was not severely asphyxiated at birth but that the insult to his brain was sustained prior to the onset of labour. There are several potential causes of intrauterine insult; in the vast majority of such cases the precise cause cannot be ascertained and no intervention would have altered the outcome. As a result of evidence, to which no objection was taken, the defenders answered the pursuer's call at p.7B to specify what they maintained caused the insult to Adam's brain, which on hypothesis is claimed to have occurred prior to the onset of labour. Their contention is that Adam suffered a stroke as a result of placental embolism prior to birth.
The witnesses
[5] The only non-medical witnesses were the pursuer and her husband. Their evidence did not assist in the resolution of the medical problems which faced the court at the conclusion of the proof. Reports were produced from, and oral evidence was led from Dr Douglas Somerville Mack, FRCOG, Consultant in Obstetrics and Gynaecology at the Glasgow University Hospital NHS Trust; from Dr Norman Reid Clifford Roberton, who retired from practice as a paediatrician in 1993, a Senior Fellow of the Royal College of Paediatricians and Child Health who has frequently given evidence in medico-legal cases since 1979; from Dr Philip Anslow, Consultant Neuro Radiologist, based at the Radcliffe Family Hospital, Oxford, who gave a report dated 6 November 1999 on the MRI scans of Adam. The court also heard evidence from Dr Deeny and Dr Susan Baillie, who were the registrars in charge of the pursuer during labour in 1989, Dr Baillie having taken over duties from Dr Deeny on the day of Adam's birth. Both of these doctors are now consultants, Dr Deeny at Stobhill and Dr Baillie in Middlesborough. It should be noted at this stage that no criticism whatsoever of Dr Baillie's conduct in relation to Adam's birth was made. The other witnesses were (1) Dr Helen Purdie McEwan, who retired in 2000 from the post of Consultant Obstetrician and Gynaecologist at the Glasgow Royal Maternity Hospital, a post which she held from 1972. Her professional qualifications are FRCOG, FRCS Glasgow, FRCP Edinburgh. (2) Dr Robert Charles McWilliam, Fellow of the Royal College of Paediatrics and Child Health, Consultant Paediatric Neurologist in the Fraser of Allander Neuro Sciences Unit, Royal Hospital for Sick Children, Glasgow. He attained the status of Consultant Physician in 1985 with special responsibilities in neonatal intensive care. The quality and complexity of the evidence given by these distinguished witnesses caused the court to order extension of the Notes of Evidence before delivering an opinion.
[6] It is to be noted that a report by Dr Paul Galea, written in 1993, produced by the pursuer, which had attributed the problems which Adam faced to hypoxic ischaemic encephalopathy was spoken about but not spoken to in evidence. It was stated by senior counsel for the pursuer in submissions that there was "no evidential basis" for his report. It has, however, not been without significance, both in the litigation and the matter of the opinion evidence which was both written and spoken to.
Available medical records
[7] The doctors who gave evidence, in formulating their opinions, depended upon the various medical records which were extant. Neither Dr Deeny nor Dr Baillie had any specific recollection of the labour but Dr Deeny claimed (543C) that it was in her nature to make quite systematic notes. Dr Deeny (543E) recalled having been told by Dr Baillie that there had been a need for an emergency section and that the baby was sick. She expected that she would have thought back over the events of the late morning to see whether she felt there was anything she had missed, but could not recall having so felt.
[8] Accordingly, the available records are the nursing notes and the notes made by the midwives and doctors in attendance from time to time. A document known as a partogram is extant; it contains certain recordings made by a midwife at intervals of time about matters which could be important and gives, in particular, the foetal heart rate. That document was essentially a snapshot of matters existing at the time of recording. There would also have been a CTG. That records the foetal heart by means of an external apparatus. Notes were made about its content. The actual CTG tracing appears to have been missing since 1992. No fault was involved and this was not a situation in which the absence of the trace was founded upon by either party in order to seek to raise any inferences. Its disappearance was, of course, regretted by the experts who gave evidence, not because it would have provided a complete answer to the problems in this case, but because it would have provided valuable additional evidence for consideration. All the principal consultants was able to affirm that they were in a position to formulate a satisfactory view of events based on the available medical records.
[9] The following two sections are my findings in fact on the evidence.
Events in hospital prior to Adam's birth
[10] When the pursuer was admitted her blood pressure was elevated at 145/105. She was experiencing regular contractions about every three to four minutes. The cervix was 5cms dilated. The membranes surrounding the baby were intact. At 5.50am an epidural anaesthetic was administered. A foetal heart tracing was instituted about 6.00am. At 7.15am the foetal heart rate was recorded as 170/180 beats per minute and the CTG was assessed at 7.30am as "reactive tracing normal baseline with decelerations on two occasions". At 7.30am a vaginal examination revealed that the cervix was fully effaced and 5cms dilated. The waters surrounding the baby were breached. This released meconium stained liquor. The pursuer thereafter was given Syntocinon, a drug with the property of increasing the frequency of uterine contractions. At 8.30am the foetal heart rate baseline was recorded as 145 beats per minute with decelerations to 120 beats per minute. At 11.15am vaginal examination revealed the cervix to be 8cms dilated and Dr Deeny identified hyper-stimulation of the uterus. She discontinued the Syntocinon. Her note in this regard, which was the subject of much discussion, reads thus "CTG poor tracing technically?. Uterine hypertonus." The note records the findings on vaginal examination, carefully noting the presence of a misleading suprapubic fat pad and then reads:
"Recording - hyperstimulation therefore could be iatrogenic foetal hypoxia Plan stop Syntocinon r/v in 15 minutes."
No review was noted at 12.00 o'clock but the contractions were then described in the notes by a member of the nursing staff. At 12.40pm. Dr Deeny noted "uterus contracting 6 and 10 spontaneously. CTG has recovered variability and is no longer pathological." There was no entry by Dr Deeny in the notes between 11.15 and 12.40. The only other entries were those of a nurse at 12.00 o'clock and 12.15. Certain entries were however also made in the partogram between those times.
[11] By 1.00pm there were shallow early decelerations. At 2.15pm, as recorded, the arresting uterine tone remained high. The cervix was fully dilated by 2.45pm and the pursuer started to push at 3.45pm. By 4.00pm a decision was made by Dr Baillie, then in control, to carry out a forceps delivery; this failed because the blades could not be applied successfully. The decision was taken to progress to caesarean section. This was delayed for twenty minutes while venous access was obtained to facilitate anaesthetic procedures. Previously at 3.40pm there was foetal tachycardia of 170 to 180 recorded in the nursing notes, although that does not appear on the partogram. At 3.50pm there were late decelerations to 120. There is no further record of the foetal heart until 4.25pm when it was 160. The meconium became thicker and was described as fresh until 4.11pm. Adam was born at 4.46pm.
Events after birth
[12] Adam was very floppy at birth and gagged when suction was applied to the airways. He weighed 4.04kg; had a head circumference of 36cm; was given at one minute an apgar score of 1 for heart rate which came up to 7 at 5 minutes in response to bag and mask resuscitation. He was noted to be very flat and was transferred to the neonatal unit by which time he was rigid and had clenched hands. There was caput with moulding. He was offered a bottle and took 40ml of dextrose at 7.00pm.
[13] The apgar score has a maximum of 10. It is a quick scoring system which involves looking, observing and listening to the heart rate of babies as soon as they are one minute of age to assess the requirement for resuscitation. The five minute apgar score is to assess the initial response to what measures have been taken within the first few minutes. The maximum score is 10. 9 is considered normal at one minute.
[14] The apgar annotations indicate that Adam lost points on neurological functions but that his systemic function was assessed as being perfectly adequate. At that point there was positive evidence of the health of the baby, but some neurological abnormality, (McWilliam 675). There was no acidaemia, which occurs before permanent tissue damage. There was found to be normal kidney function, normal liver function and within a few moments of birth normal heart function. The heart was visualised on an x-ray taken to ascertain the placement of an endo-tracheal tube and the heart appearance was normal. The records contain many biochemistry reports and all were within normal limits. The haematological parameters were also within normal limits.
[15] Adam was admitted to the neonatal ward at or just after 5.00pm on 28 February. He sucked dextrose well at 7.00pm. There was a feed at 10.00pm via his gastric tube. He took a small feed at fifteen minutes past midnight and at 3.00am was fed and it is noted "sucked feed well". There was generalised twitching of right side with eyes fixed and staring at about 3.00am with generalised twitching of ten minutes, "right side worse".
[16] On admission to the neonatal ward it was noted "baby very flat, tense, back very rigid, hands clenched". At 5.45am Adam was "making cycling movements" and by 6.00am on 1 March, thirteen hours after birth, it was noted that Adam was unsettled overnight with regular episodes of fitting and opisthotonus, (which is arching of the back). The fits and associated apnoeic attacks with cyanosis became sufficiently severe for Adam to be intubated and ventilated. An ultra sound scan revealed that he had cerebral oedema. He was given mannitol for the oedema. By 2 March 1989 the fitting had resolved. By the second week of March 1989 Adam was feeding well and he was allowed home on 15 March. On long term follow-up Adam was averred as having virtually normal intelligence but he has an asymmetrical cerebral palsy which affects, mainly, his left side; to an extent this affects his speech. An MR scan carried out on 2/11/99 shows bilateral changes of cerebral ischaemia affecting primarily the right hemisphere with some less severe involvement of the left frontal lobe.
Competing theories for causation of the bilateral stroke
[17] (a) The pursuer contends on pleadings that there was a neonatal stroke occasioned by thrombosis or arterial spasm as a result of trauma during labour.
[18] (b) The defenders' theory is that Adam suffered a stroke occasioned by placental embolism before onset of labour or, at any event, before the time of 11.15am on 28 February 1989.
[19] (c) The defenders also contend that the cause of the bilateral stroke cannot be established or ascertained on the available evidence.
(a)
[20] There was no evidence of arterial spasm. That suggestion was departed from in cross-examination by Dr Roberton. Dr Roberton also confined the time involved to the period of one to two hours after birth. Dr Roberton accepted that a stroke before labour was possible on the features in the present case, but said that, if the stroke was before delivery, then he would not have expected the apgar to be so good. He further said that the stroke before delivery was not consistent with feeding well in the period starting after birth. There was, said Mr Haddow for the pursuer, sufficient evidence by Dr Roberton to establish a balance of probabilities that the course of events was as he suggested.
[21] Dr Roberton also drew the court's attention to, and to an extent relied upon, what he described in his report as "the relatively small literature on neonatal stroke" for his theory of an event which caused injury occurring neonatally. Dr McWilliam did not accept the theoretical basis said to be derived from the four learned articles referred to in the extensive reference to these documents in Dr Roberton's report and evidence. Of those, that of Professor Laura Ment, production 27/7 was the one upon which Dr Roberton founded most strongly. Professor Ment said in that article that the most common cause of cerebral infarction was perinatal asphyxia. However, in the article she also stated "although neonatal cerebral infarcts are reported to be caused by embolic or thrombotic effects, perinatal asphyxia, with its attending hypoxia and hypertension appears to be the most commonly determined reason for stroke in all the incidents in our series. In full term neonates the asphyxia was almost always an intra partum event". Dr Robertson's final position was that Dr Ment attributed all her cases to asphyxia and he pointed to the sentence "the most common cause of cerebral infarction in our series was perinatal asphyxia". Dr Roberton seemed to think that that was the same as attributing all her cases to asphyxia. In my view, that cannot be said. Dr Roberton at 456B stated that he had never suggested Adam was severely asphyxiated. He then went on to differ from Ment in that he disagreed with her view that the causative path from asphyxiated brain lesion did not involve embolic or thrombotic stroke. His own view is "most of them are thrombotic, not most, but the majority" (458E). When asked which distinctive criteria of birth asphyxia were satisfied in Adam's case, he responded "They haven't done the tests". He agreed that there was no evidence of metabolic acidosis. Dr Roberton postulated (p.473) that there were two pathways between an incident in the perinatal period and stroke. He said the pathway was not clear. If it were due to hypotension then that must occur prior to delivery. He went on to say that if it was the minor, or less severe degrees of asphyxia which triggers thrombosis or can cause spasm in the arteries, then that could happen in the first few hours after birth as the baby is still, as he put it, convalescing from what went on during the last few hours of labour. "Now I don't know", he said, "which applies in this case". "My hunch is that this baby clotted off the major branch of the cerebral vessels in the hour or two after delivery as a sequel of what had gone on before". On balance of probability, he contended, Adam's features at birth were not due to cerebral oedema.
[22] In his report, which he incorporated into his evidence without qualification at p.416, Dr Roberton said this: "On the basis of this literature, therefore, I believe that Adam Gallagher suffered a bilateral stroke as a sequel to the asphyxia which has been identified by the obstetric expert in this case as lasting for some hours prior to delivery". There was no such identification to the court and no lengthy asphyxia was spoken to by any witness. In his evidence in the court (424A) Dr Robertson said: "I think this birth asphyxia is a trigger for the thrombosis in this case". Dr McWilliam agreed (668D) that there was a mild degree of intra partum asphyxia. At 677 he stated that from the clinical state of the baby at birth he could rule out significant asphyxia for any period before birth.
(b)
[23] The defenders' contention that the stroke was caused by placental embolism prior to the onset of labour was, it was claimed, supported by the lack of evidence of severe asphyxia which was, in any event, negated by the clinical and biochemical evidence from birth through the early neonatal period. Arterial occlusion by embolism is a well documented cause of infarction, argued the defenders. Sources of emboli have most commonly included placental fragments. The risk of placental embolism increases with the duration of pregnancy; this was a 40-41 week pregnancy. The pattern of damage visualised on the MRI scan makes it likely that there was occlusion of one or more cerebral arteries by placental embolism. Dr Anslow, at the conclusion of cross-examination, said that he thought the likely scenario was that it was a placental embolism which gave rise to the event. He said that he thought it was possible that Adam had a clotting defect, triggered by hypoxia, which allowed this insult to happen. "If I were asked", he said, "which one is more likely than the other, I would say the former". The former cause i.e. placental embolism has nothing to do with hypoxia, it is a random event. It is plain therefore that Dr Anslow, on clear balance of probabilities, regarded placental embolism as the cause of the insult to Adam's brain. There is no evidence which is inconsistent with that hypothesis. Stroke by placental embolism cannot happen more than ten minutes after birth, said Dr McWilliam, and Dr McWilliam was very clear that with the feeding pattern recorded, there could not have been a stroke in that interval since birth (713). Further, said Dr McWilliam, had there been a neonatal stroke it must have been followed by a period of shock lasting at least six hours. There was no such event in the early neonatal period up until the onset of frank convulsions at birth plus thirteen hours (722).
(c)
[24] The theory of neonatal stroke is not established by the evidence on a balance of probabilities.
Conclusion on the above contentions
[25] From the above discussion it is apparent that there are two distinct bodies of reputable medical opinion which ascribe the bilateral stroke to different times and causes. Although I incline to the view that Dr McWilliam's and Dr Anslow's opinions are, on balance of probabilities, correct it is not necessary to go so far. It is sufficient for the defenders to maintain that the pursuer has not on a balance of probabilities proved that it was a neonatal stroke that caused the insult. Mr Haddow agreed that there was sufficient evidence proposed by Dr McWilliam to lead to his views being upheld and since I am not persuaded that they can be rejected, the pursuer must fail on this aspect of her case, and the defenders are entitled to absolvitor.
Further contentions by the pursuer
[26] It was contended that if there had been a neonatal stroke, such was capable of being caused by the stress of the pursuer's labour; it was claimed that it was so caused. Further it was avoidable had there been a different management of labour. Dr Roberton thought that that was plainly so, founding upon Volpé's textbook. Dr Anslow stated that the scans were not typical of a stroke caused by the stress of labour, but he could not preclude a hypoxic event as a cause. Dr McWilliam accepted that a stroke was capable of being caused by the stress of labour, but that was not to be expected from the result here and significant asphyxia would have been required. In relation to the second aspect of these further contentions, i.e. whether the stroke was caused by that distress, I have indicated above that there was no bilateral stroke so that the question does not require answering. It is the same point which the views of Dr Roberton and Dr McWilliam differ upon, and although it may be a possibility, it is not, in my view, a probability that the stroke was caused by that stress. A different management of labour might possibly have made a difference, but the evidence on that matter is in an even worse state. No witness could say with any conviction that, on a balance of probabilities, different management of labour would have led to a different result. The critical timing was around 11.15 when Dr Deeny was involved. I deal with Dr Deeny's position later, but the high water mark of the position on that matter requires to be that an earlier caesarean section might have made a difference. There was no criticism made of Dr Baillie attempting to deliver the child vaginally by means of forceps when she did. Had caesarean section been of paramount importance, she was in a position to have so decided at any time after 1.00pm. Dr Mack's position was that the events at 11.15am as disclosed in the notes were such as to require a special type of monitoring. He was not, however, able to say that had such monitoring taken place the inevitable would have been caesarean section and that, demonstrably, is an end of that particular contention.
Alleged negligence on the part of Dr Deeny
[27] Let it be said at the outset that I reject the contention that Dr Deeny was negligent. That proposition was founded upon the note she made about the condition of the pursuer at 11.15 during her labour. Examination of the notes she made at the time indicates that she had in mind certain questions and that she embarked on a course of action to attempt to resolve them. Dr Mack is incorrect in his report of 12/10/93 and subsequently in suggesting that Dr Deeny had concluded that the over-stimulation could be causing foetal hypoxia. As I read her note, she was recording the question in her mind and to answer it, decided to stop the Syntocinon, which was stimulating the uterus, and to keep the matter under review. According to Dr McEwan, that could not be faulted. Dr Baillie was of a similar view. I agree. Dr Mack's view was that the conduct of the labour must be criticised when, given signs of possible foetal distress, no attempt was made to evaluate it. He agreed that evaluation, which he envisaged as foetal blood scalp sampling, would not necessarily have led to any different result. Dr Deeny did attempt an evaluation. She stopped the drug and she kept the matter under review. She did review at 12.40 where the CTG was noted by her as having recovered variability and being no longer pathological. Some criticism was made of the absence in the notes of any review having taken place within fifteen minutes, but that does not establish that there was no such review or observation. There was certainly no review by Dr Deeny noted, but she would not necessarily have required to do anything if matters had settled. It is known that there was continuous attendance by two midwives according to the pursuer's evidence, and the entries between 10.30 and 12.15 are by a staff midwife. The partogram records monitoring at that time. As counsel for the defenders put it, it cannot be inferred from the records that no monitoring took place, but even if it did not, there is no evidence that the absence of monitoring would have led to any different management in the pregnancy. Dr Mack was unable to say what, if anything, the foetal blood scalp sample would have disclosed and thus there is neither substance in his criticism of the management nor was it established that it was "universal practice in Scotland" as the pursuer avers, to do as he suggested. Dr McEwan and Dr Baillie both negated that assertion.
[28] It requires to be stated, however, that Dr Mack agreed that it was entirely reasonable to remove the cause of the potential problem before reassessing (276A) and further explains his position at 278C "I think she acted appropriately in stopping the Syntocinon. It may have been appropriate to review in fifteen minutes, but we don't appear to have that record, and that's where I feel her actions were out of keeping with normal standard practice." A view of that evidence might be that Dr Mack is merely saying that it would be negligent not to review in fifteen minutes and that that is the thrust of his criticism, not the failure to take a foetal scalp blood sample.
[29] Be that as it may, I am satisfied on the evidence of Dr Deeny, Dr Baillie and Dr McEwan that there is wholly insufficient evidence for me to assert that Dr Deeny's management fell below the standard of a reasonably competent registrar at the time in question.
Decision
[30] Since it is my view that the pursuer has failed to establish the essential factual basis for her case, i.e. that Adam suffered a bilateral neonatal stroke; that his bilateral stroke was the result of a thrombosis triggered by a lack of oxygen and that the management of the case, if different, would necessarily have led to a different result on the balance of probabilities. Finally, negligence on the part of the defenders not having been established, they are entitled to absolvitor. I shall therefore sustain the defenders' fourth and fifth pleas-in-law and repel the pursuer's pleas and grant decree of absolvitor.