Cooper & Anor v Royal Berkshire NHS Foundation Trust

Christian Cooper (“the claimant”) is 46 years of age (DOB 7.10.68). On 21^st March 2000 she gave birth to her first child, Max, who weighed 2.69kg at 40 weeks. During the course of his vaginal delivery there was some retention of the placenta which required manual removal. Therefore when the claimant gave birth to her second child, Aimee, who weighed 3.23kg at 39 weeks on 28^th April 2004, she elected to do so by caesarean section.

Later on that year, the claimant again became pregnant. She was by then 36 years of age and of normal weight, with a BMI of 24.05kg/m2. The claimant was under the care of Miss Siddall at the Royal Berkshire Hospital and attended 13 antenatal visits at the hospital between the 12^th and 40^th weeks of her pregnancy. During these visits it was noted that there was no hypertension, no persisting proteinuria and no glycosuria. Miss Siddall saw her on three of these occasions, at the 15^th, 26^th and 39^th week, and it is evident that discussions took place between the claimant and Miss Siddall as to the mode of delivery which was to take place. The significance of this is that although it is perfectly possible for vaginal delivery to take place after a previous caesarean section, it carries with it a risk that, during the course of the subsequent delivery, a traumatic rupture of the previous surgical scar can occur with potentially serious consequences for the health of the mother and the baby. In the event, the claimant chose to give birth to her third child by vaginal delivery.

At about 21.30 on 13^th July 2005 the claimant attended at the hospital, together with her partner Julian Harrington. The claimant had by then reached the 41^st and 4^th day of her pregnancy, and vaginal examination confirmed the likelihood of early labour signs.

By 1.00 on 14^th July 2005 the claimant was asking for assistance, she was in severe abdominal pain, and the medical records show that there was a concern that the claimant had suffered either a placental abruption or a uterine rupture. At 1.15 fetal bradychardia was noted and the claimant was transferred to theatre where, at 1.27, during the course of a caesarean section, it was found that a uterine rupture had taken place and consequently the baby, Gene, and the placenta had entered the peritoneal cavity. These complications were managed, albeit during the course of the procedure the claimant lost 1lt of blood which was replaced by way of a transfusion.

Gene had a birth weight of 3.67kg. Sadly however he was by then in a poor condition due to a hypoxic period during his birth and, despite continuous hospital care, died on 4^th June of 2007.

Over the course of the following few days the claimant remained in hospital where her condition was monitored and she received medical care. Her partner Julian Harrington remained with her during this time.

At 3.00 on 14^th July 2005 her blood pressure was noted to be 122/75 and as a result of the events which had taken place, 5000 units of Heparin was prescribed to be provided to her twice daily. The first dose of 5000 units being provided to the claimant at 22.00.

On the following day 15^th July 2005 the medical records noted that the claimant appeared to be making a reasonable recovery, albeit no Heparin appears to have been provided to her.

On 16^th July 2005 the claimant’s blood pressure was noted to be 120/92. A dose of 5000 units of Heparin was provided to her at 13.15. and it may well be that a further dose was provided to her later that evening.

On 17^th July 2005 it was noted that the claimant was complaining of having suffered from chills over the previous couple of nights, a matter which is confirmed by Julian Harrington in his witness statement dated 10^th April 2014. It was noted that she had a slightly raised temperature and was pyrexial. Blood samples were cultured and subsequently an intravenous antibiotic was administered to her. The claimant was provided with a single dose of 5000 units of Heparin at 18.45.

At 9.00 on 18^th July 2005 the claimant’s blood pressure was noted to be 110/75. She was feeling low and was subsequently provided with two blood transfusions. At 18.00 her blood pressure was noted to be 120/70 and slightly later she was noted to be feeling better. No Heparin appears to have been provided to her that day.

At 4.00 on 19^th July 2005 the claimant’s blood pressure was noted to be 142/94. She was noted to have been vomiting and was complaining that she had been experiencing a headache over the previous 4 hours; the pain reaching from the front of her head to the back of her neck where it was more intense. In his witness statement Julian Harrington stated that the claimant had in fact been suffering from headaches over the previous few days, a matter which he had also mentioned in the interview conducted with him for the purposes of the subsequent internal review. However, he states that the claimant told him that the headache on 19^th July was significantly worse than the previous ones, and Codeine Phosphate was provided to her.

The claimant’s blood pressure was checked at 6.00 and 10.00 and was noted to be 135/90 and 125/90 respectively. At this latter time it was noted that the claimant had again vomited. At 10.45 it was noted that the claimant’s headache was better, a matter confirmed by Julian Harrington, and her blood pressure was noted to be 130/90. This level was recorded at both 13.00 and 14.00. There were concerns that the claimant might be suffering from pre-eclampsia and the Senior House Officer, Dr Hubert, attended at 14.40 in order to take blood samples from her for analysis. According to Dr Hubert’s witness statement dated 3^rd August 2005, the claimant told her that she did not have a headache and was able to converse with her whilst sat on the bed. After obtaining the blood samples, Dr Hubert left the claimant’s room in order to label the samples.

However, when Dr Hubert returned to the claimant’s room a few minutes later at 14.45/47 she found the claimant lying face down on the floor, her skin tone was mottled blue, she had saliva around her mouth and had urinated on the floor. Immediate emergency treatment was afforded to the claimant whilst she was on the floor which included cardiopulmonary resuscitation and oxygenation through an Ambu-bag. When the crash team arrived a few minutes later at 14.55 they found that the claimant was in asystole. She was intubated and provided with adrenaline. Ventricular fibrillation was administered and sinus rhythm was restored. In view of the suspicion of eclampsia, she was provided with intravenous Magnesium Sulphate.

The claimant was taken to the intensive care unit and en route underwent a CT scan at 16.01, which was reported as normal. The claimant’s care at the unit was undertaken by Dr Atul Kapila, Consultant in Intensive Care Medicine. She was admitted at 16.19 where her Glasgow Coma Score was recorded as being the lowest 3, and at 17.45 she began convulsing. The claimant was examined by the neurology team and a differential diagnosis was made, namely: a hypoxic brain injury with subsequent seizures; eclampsia with fit and subsequent collapse and cardiac arrest, or; a central nervous system infection. In due course a lumbar puncture was administered which excluded the latter possible diagnosis. Thereafter the claimant remained on artificial respiration.

Tragically, as a result of the period during which the claimant had no cardiac output she has suffered irreversible hypoxic neurological damage. The claimant has never regained consciousness, and in the intervening years she has remained minimally responsive and under continual medical care.

Understandably, since these events took place, the claimant’s family have been concerned to know not only the cause of her cardiac arrest, but also whether her present condition could have been avoided. An internal review of the medical care provided to the claimant has taken place and its findings include the following observations,

“In TP’s (Dr Tim Parke, Divisional Director of Clinical Support Services) view the most likely cause remains a seizure, possibly pre-eclampsia. However, the presentation would be delayed and very atypical, and RP (Mr Rick Porter, Consultant Obstetrician) did not think this likely. His personal view was that the most likely diagnosis is of a central (cerebral) venous thrombosis, which subsequently resolved.”

Civil proceedings

An action has been commenced on behalf of the claimant for the recovery damages for personal injury, loss and damage from the Royal Berkshire NHS Foundation Trust (“the defendant”). In these proceedings it is alleged that the claimant’s cardiac arrest and consequent hypoxic neurological damage was caused by the occurrence of a cerebral venous thrombosis (“CVT”) on 19^th July 2005, and that in turn this was caused or materially contributed to by the defendant’s negligence. Firstly, by the lack of provision of ante-natal advice to the claimant of the risk of uterine rupture occurring during the course of vaginal delivery by a woman who has previously undergone a caesarean section, and its possible detrimental consequences for the baby and the mother; it being alleged that had such advice been provided to the claimant, she would have heeded it, elected to have a caesarean section and thereby avoided the trauma surrounding the uterine rupture which caused or materially contributed to the occurrence of the CVT. Secondly, by the lack of consistent post-natal provision of Heparin, which caused or materially contributed to the occurrence of the CVT.

The action has been defended. The defendant denies that there was any lack of reasonable ante-natal medical care or, in the event of such ante-natal or admitted post-natal lack of care, that it was causative of the claimant’s cardiac arrest. Firstly, it is alleged that appropriate ante-natal advice was provided by Miss Siddall, and that the claimant, knowing of the risk of uterine rupture and its consequences, elected vaginal delivery of her third child. Secondly, that even if such advice had not been provided, although it concedes that the trauma of a uterine rupture may have materially contributed to the occurrence of a CVT, the defendant denies that the claimant suffered from this condition on 19^th July 2005; rather she suffered from post-partum eclampsia (“PPE”) which was unaffected by the trauma. Thirdly, although it admitted that the lack of consistent post-natal provision of Heparin amounted to a lack of reasonable medical care, this also was not causative of the claimant’s cardiac arrest. Although it concedes that it may have materially contributed to the occurrence of a CVT, the defendant denies that the claimant suffered from this condition, and the PPE which she suffered was unaffected by any lack of post-natal provision of Heparin.

As it is conceded by the defendant that the lack of consistent post-natal provision of Heparin amounted to a lack of reasonable medical care of the claimant and, that if the cause of her cardiac arrest and consequential hypoxic neurological damage was a CVT, the admitted negligence would have been causative of her current condition, it is agreed that there is no purpose to be served in dealing with that aspect of the evidence relating to the ante-natal advice provided to the claimant by the defendant. Furthermore it is agreed that although there are other possible causes for the cardiac arrest and consequential hypoxic neurological damage suffered by the claimant on 19^th July 2005, these are sufficiently unlikely to have been responsible; such that the only two differential causes are likely to have been the claimant suffering either a CVT or PPE. In these circumstances it is agreed that the single issue which requires to be determined in relation to liability, is whether the claimant is able to establish to the civil standard of proof that the cause of the claimant’s cardiac arrest was a CVT.

The written evidence in this case has included medical reports from a number of experts in their respective fields.

On behalf of the claimant I have been provided with the following reports: Mr Mark Waterstone, Consultant Obstetrician and Gynaecologist, dated June 2014; Dr David Williams, Consultant Obstetric Physician, dated June 2014; Dr Brian Kendall, Consultant Neuroradiologist, dated June 2014, and; Professor David Chadwick, Emeritus Professor of Neurology, dated June 2014.

On behalf of the defendant, I have been provided with the following reports: Mr Derek Tuffnell, Consultant Gynaecologist and Obstetrician, dated June 2014; Dr Alexander Pirie, Consultant and Honorary Senior Clinical Lecturer in Obstetric and Maternal Medicine, dated June 2014; Dr Wellesley Forbes, Consultant Neuroradiologist, dated June 2014, and; Dr Guy Sawle, Consultant Neurologist, dated June 2014.

In addition I have been provided with the following joint reports: Mr Mark Waterstone and Mr Derek Tuffnell, dated 1^st December 2014; Dr David Williams and Dr Alexander Pirie, dated 22^nd December 2014; Dr Brian Kendall and Dr Wellesley Forbes, dated 10^th December 2014 and; Professor David Chadwick and Dr Guy Sawle, dated 9^th December 2014.

In his initial medical report, Mr Mark Waterstone provided his opinion upon the adequacy of medical care, in relation to both the requirement for the provision of ante-natal advice as to the risk of uterine rupture occurring during vaginal delivery after a previous caesarean section, and the lack of consistent post-natal provision of Heparin. He stated that if there was a lack of such ante-natal advice, then this would be evidence of a lack of reasonable medical care, as would the inconsistent post-natal provision of Heparin. However he did not provide any opinion upon the issue of the differential diagnosis between the occurrence of a CVT and PPE.

On the other hand, whilst Mr Tuffnell provided similar opinions upon the adequacy of the two aspects of medical care, he also provided an opinion upon the likely cause of the claimant’s cardiac arrest in these terms,

“The cause of the collapse in this case is difficult to identify with certainty. However, it does seem as though there was a seizure associated with the collapse and there had been an elevation of the blood pressure just before the collapse occurred. Therefore on the balance of probability this is more likely to be an eclamptic seizure and collapse than it is to be a collapse due to any other cause.”

In their joint report the two doctors were asked for their opinion as to the most probable cause of the claimant’s collapse on 19^th July 2005. Mr Waterstone stated that this was a matter which ought to be answered by other experts in the case, but,

“Nevertheless, I am able to state that the absence of any evidence of pre-eclampsia within 48 hours of the collapse makes the probability that this was due to eclampsia very low.”

However Mr Tuffnell maintained his originally expressed opinion and explained that,

“Whatever the cause of death in this case it was due to an extremely uncommon cause. The blood pressure was elevated before the seizure and this is consistent with that seizure being due to eclampsia, which can be associated with cardiac arrest. In the absence of any features of any other condition this uncommon cause of death (eclampsia) is more likely than the other much rarer causes.”

In his initial report, Dr David Williams noted that the father of the claimant’s second and third child was one and the same individual, namely Julian Harrington. In these circumstances he stated that research showed that the risk of the claimant suffering from pre-eclampsia when pregnant with her third child was 1%. Of those who suffer from pre-eclampsia, the condition only develops into eclampsia in 1% of women. Moreover, only 20% will suffer post- partum eclampsia after the first 24 hours post-partum.

He stated that pre-eclampsia is usually associated with poor placental function, such that the majority of women with the condition will have children with a poor birth weight. Moreover it is only in 20% of cases where a woman has an eclamptic seizure that there is an absence of hypertension. In contrast in this case, not only did the claimant give birth on 3 successive occasions to babies with a normal birth weight, including Gene, but apart from some mild to moderate diastolic hypertension in the period leading up to the seizure, the claimant had normal systolic blood pressure.

In these circumstances Dr Williams was of the opinion that it was “….very unlikely that the cause of her presumed post partum seizure was post partum eclampsia.”

In contrast he considered that a CVT was the most likely diagnosis. He stated that between 25 – 30% of all CVTs (both men and women) occur in relation to pregnancy, most commonly post-partum. The reason being that a woman’s blood is more thrombotic during this period, and in the present case this pro-clotting factor would have been increased due to the loss of blood during the emergency caesarean section; hence the need to provide a thromboprophylaxis like Heparin, which was not provided to the claimant. The risk of a CVT would have been enhanced by the pyrexia which the claimant suffered during the post-partum period, and her mild hypertension is compatible with a CVT as opposed to pre-eclampsia. Moreover, the most common presenting symptom for a CVT is a headache, which the claimant suffered in the post partum-period, and a grand mal seizure occurs in 20 – 35% of those suffering from a CVT. Dr Williams accepted that there was no evidence on the CT scan of matters which would support the occurrence of a CVT. However he observed that the absence of such evidence does not necessarily negative the occurrence of such an event.

In these circumstances he was of the opinion that had the claimant been provided with the prescribed course of post-partum Heparin, it is likely that she would not have suffered a CVT and therefore would not have suffered from the seizure leading to the cardiac arrest and consequential hypoxic neurological damage.

In his initial report Dr Pirie described his approach to differential diagnosis and stressed the importance of having regard to both the correlation between the known features and symptoms relating to the individual, as compared with the characteristics of the conditions being considered, and the relative prevalence of those conditions within the relevant parts of the population.

He listed the relevant features and symptoms which had been exhibited by the claimant in the post-partum period as follows: a period of 5 days following an emergency c-section for a ruptured uterus; headache of intermittent severity; the onset of mild hypertension; sudden maternal collapse; seizure; cardiac arrest; a successful cardiovascular resuscitation with chronic neurological damage and the normal results of subsequent tests such as a CT scan, lumbar puncture, 12 lead ECG and blood tests. He concluded that all of these features and symptoms fitted the possible diagnosis of a CVT and PPE, and that none of the features or symptoms positively refuted either of them.

He then proceeded to observe that the prevalence of PPE is far commoner than CVTs by an order of at least two magnitudes, and on that basis alone would make the former diagnosis more likely than the latter. Although earlier in his report he had observed that during the ante-natal period in the present case neither the blood pressure nor urinalyses recordings disclosed evidence indicative of the existence of pre-eclampsia, he stated that there were factors which would favour a diagnosis of PPE over that of a CVT. Firstly, he considered that although a CVT can occur and fail to show features which are evident on a CT scan, where the thrombus is large enough to cause maternal collapse this is likely to show up on a CT scan. Secondly, if the post-partum headache was due to a CVT then he would have expected it to have steadily worsened after its initial onset, rather than as in this case, been intermittent and resolving.

In their joint report the two doctors agreed that whereas the lack of consistent post-natal provision of Heparin would have had no causative effect on the occurrence of PPE, it would have been likely to have reduced the risk of the claimant suffering a CVT.

They agreed that although there was a wide spectrum of possible diagnoses in this case, the most likely were PPE or a CVT.

In so far as the differential diagnosis is concerned, they agreed that the most significant factors favouring a diagnosis of PPE are: a headache; episodic post natal diastolic hypertension; the lack of signs on the CT scan and the relative prevalence of PPE over CVT in the general population, as opposed to the individual risk in the present case. This latter caveat being in parenthesis. Whereas the most significant factors tending against such a diagnosis are: the lack of any pre-eclampsia with the previous births; the lack of ante natal pre-eclampsia in this pregnancy and the fact that Gene was well developed at birth.

On the other hand the most significant factors favouring a diagnosis of a CVT are: the traumatic caesarean section; the significant loss of blood during the birth; the strong inflammatory response and the absence of regular thromboprophylaxis. Whereas the most significant factors tending against such a diagnosis are: the relative rarity of CVT compared to PPE and the lack of any sign of a CVT on the CT scan, albeit that it is acknowledged that the scan may have missed a CVT.

In his initial report Dr Kendall noted that the CT scan had been made without an injection of intravenous contrast medium and is imaged on bone and soft tissue windows. He noted that no abnormality is shown on the image, and in particular there was no evidence of any abnormal density within the intracranial vessels which may be present in intracranial thrombosis, and no evidence of any ischaemic or haemorrhagic damage, or brain swelling. However he observed that although the CT scan provided no evidence in support of the occurrence of a CVT, such scans missed cranial sinovenous thrombosis in up to 40% of cases. Moreover, a conventional CT scan performed less than 90 minutes after the occurrence of a cardiac arrest sufficient in length to cause brain damage, would be too early to show evidence of the ischaemic damage. In these circumstances he did not consider that the results of the CT scan favoured the diagnosis of PPE.

Dr Forbes, in his initial report, agreed that the CT scan shows normal appearances, and in particular there is no evidence of intracranial haemorrhage, infarction, brain swelling or mass lesion. He was of the opinion that the results of the CT scan rendered a diagnosis of a CVT unsustainable in that in his opinion the presence of a cerebral thrombus of the magnitude required to cause a severe encephalopathic illness would have shown signs on the scan of either the thrombus itself or an infarction, together with brain swelling.

In their joint report the two doctors retain their opposing opinions, albeit that Dr Kendall considered that the more likely diagnosis was that of a CVT.

It would appear that Professor Chadwick’s initial report was commissioned in order to provide an opinion upon the nature of and recoverability from the hypoxic brain damage which the claimant suffered on 19^th July 2005. The nature being profound and its duration likely to be permanent. He explained that he had considerable uncertainty as to the mechanisms leading to the hypoxic ischaemic brain injury and, that if a primary cardiac cause could be excluded in favour of a sudden seizure, he would be stepping outside his field of expertise to suggest that this was more probably caused by a venous sinus thrombosis than another cause. He stated that the post-partum period is associated with brain pathologies which increase the risk of acute symptomatic seizures including both PPE and CVTs. In this regard he agreed that symptoms such as headaches, neck stiffness and vomiting would be consistent with both such causes. He stated that CT imaging provides very poor sensitivity to identify intracranial changes, and at the time when the CT scan was taken it would not be able to identify the changes that would have become evident later of severe hypoxic brain injury.

Dr Sawle did not consider himself so constrained by his area of expertise. He agreed that the two most likely explanations for the claimant’s cardiac arrest were either PPE or a CVT. He considered that there was only one factor which “weakly supports” the latter diagnosis, namely that the cardiac arrest occurred on the 5^th day after the birth. The significance of this being that whereas this fitted within the window of time which research described as being associated with the occurrence of a CVT, only a relatively small minority of cases of PPE occurred at that point.

However, there were in his opinion a number of factors which favoured the diagnosis of PPE. Firstly, he considered that it was extremely rare for a seizure to cause a cardiac arrest. He stated that as research showed that it was necessary for a CVT to precipitate a seizure in order to cause a subsequent cardiac arrest, whereas PPE may cause a cardiac arrest either indirectly through a seizure or directly by the PPE itself, this made it more likely that a cardiac arrest would be caused by PPE, because there were two possible mechanisms by which this condition may cause the cardiac arrest, rather than the one rare cause in the case of a CVT. Secondly, research shows that where seizures occur to obstetric patients, those are more frequently of the focal variety rather than the generalised variety, and that it is only the latter type of seizure which is capable of giving rise to cardiac arrest. Thirdly, it would be rare for a focal seizure to occur without other neurological symptoms, besides headaches and vomiting, being present, such as aphasia, confusion, somnolence, limb weakness or visual loss. Indeed in the present case, the claimant had reported a lessening in the degree of pain associated with her headache. In contrast it is not unusual for PPE to occur after a short period increasing blood pressure, followed by a seizure, without any other neurological symptoms being present. Fourthly, a generalised seizure would have resulted in a haemorrhagic infarction or a major degree of venous blockage and raised pressure, both of which he understood are likely to lead to visible changes on a CT scan.

In their joint report the two doctors largely maintained the views which they expressed in their initial reports. Albeit they agreed that if the cause of the claimant’s cardiac arrest had been a CVT, then this is likely to have shown changes of venous infarction on the CT scan. Moreover, the absence of any preceding focal neurological symptoms reduces the probability that the cause of the cardiac arrest was due to a CVT.

At trial oral evidence was provided by Julian Harrington, Dr Kapila, Dr Williams, Dr Pirie, Dr Kendall, Dr Forbes, Professor Chadwick and Dr Sawle.

Julian Harrington’s recollection of the claimant’s post natal condition was that she was largely immobile, and suffered from headaches and chills. The latter symptom being experienced despite her room being particularly warm. He accepted that the medical notes appeared to suggest that the claimant had left her room to visit Gene on the 14^th July. However, his recollection was that only he had visited his son that day, and that the claimant had only left her room once on the 18^th July when she was taken in a wheelchair to visit Gene. He accepted, as the medical notes appeared to suggest, that the claimant had only had chills over a couple of days. However, despite there only being one mention of a headache in the medical notes on the 19^th July, he recalled the claimant complaining of headaches throughout the post natal period, albeit she told him that her headache was significantly worse on the 19^th July.

Dr Kapila said that it was necessary for a preliminary differential diagnosis to be determined in order to inform him as to the appropriate treatment that should be provided to the claimant whilst she was in the intensive care unit. In making that determination he was reliant upon the history of events with which he had been provided, the results of his examination and the opinions of others, including the neurologist Dr Khan. He said that as the claimant had been provided with Magnesium Sulphate after the seizure, he maintained its provision to her because of the possible diagnosis of eclampsia. Moreover, although a subsequent lumbar puncture had shown the claimant’s cerebral spinal fluid to be clear, after discussing the matter with the microbiologist, Dr Iyer, it was decided to provide antiviral medication to the claimant as a precaution. He said that the lumbar puncture had also shown an intra cranial pressure reading of 21cm, which he considered was towards the upper end of the normal range of between 5 and 25cm, and which may have been due to the convulsions which she had exhibited earlier. He acknowledged that a normal CT scan result did not necessarily exclude the occurrence of a CVT. However because of the reported normal CT result, he did not consider a CVT as one of the differential diagnoses in this case. However he accepted that it would be rare for eclampsia to occur 5 days post partum.

Dr Williams has a special interest and experience in pre-eclampsia, his research team being focused upon understanding the aetiology of the disorder. He explained that the cause of pre-eclampsia is currently understood to be associated with the placenta, and that when the condition occurs it is often discovered that the placenta is not properly embedded within the womb. Its classic characteristics are those of hypertension and proteinuria within the mother, and the babies of mothers suffering from pre-eclampsia are often found to be growth restricted. In the majority of cases the condition is monitored and it is only if the risk of hypertension is sufficiently serious that medical intervention is necessary. Ultimately, during the ante-natal period, the only cure for the condition is delivery of the baby, and a careful balance may have to be struck between the relative risks of the continuation of the condition to the mother, as opposed to that of premature birth to the baby. However, on occasions the condition may develop into eclampsia, which is characterised by a seizure within the mother’s brain. Dr Williams said that this is most likely to occur in the peri-partum and immediate 24 hour post-partum period, when the blood supply is diverted away from the placenta and back to the mother. However, its cause is unclear.

Dr Williams referred to the research literature and in particular to Professor Redman’s 1994 survey of “Eclampsia in the United Kingdom”, where eclampsia was described in the introduction as being, “….the occurrence of convulsions in association with the signs and symptoms of pre-eclampsia.” Its definition for the purposes of the research being, “…the occurrence of convulsions during pregnancy or in the first 10 days postpartum with at least two of the following features within 24 hours after the convulsions: hypertension ……proteinuria …….thrombocytopenia…….or an increased plasma aspartate transaminase concentration….” The national incidence of eclampsia was found to be 4.9 cases in 10 000 maternities. It was found that 75% of first seizures occurred in hospital, of which 38% developed before hypertension and proteinuria had been documented. Moreover, 18% of those suffering eclampsia did so during the intra-partum period, whilst 44% of those suffering eclampsia did so during the post-partum period. In relation to this latter group, 88% suffered eclampsia within the first 48 hours post-partum.

This research was updated in 2005 by Professor Knight in “Eclampsia in the United Kingdom 2005”. This followed the widespread introduction of Magnesium Sulphate for the treatment of eclampsia and severe pre-eclampsia, albeit 99% of those surveyed had only been given Magnesium Sulphate after their first convulsion. It found that the national incidence of eclampsia had reduced to 2.7 cases in 10 000 births. Moreover, 19% of those suffering eclampsia did so during the intra-partum period, whilst 36% suffering eclampsia did so during the post-partum period.

In the intervening period Dr Tuffnell and others had published the results of a relatively small research study of “Outcomes of Severe Pre-eclampsia/Eclampsia in Yorkshire 1999/2003” which found that 24 of the post-natal cases of those suffering from eclampsia occurred within 24 hours of delivery, whilst 1 occurred at two days and another at 5 days post-natal.

Dr Williams readily acknowledged that the incidence of eclampsia within the population is more than that of CVTs. The estimated annual incidence of the latter being described in Dr Stam’s review article in The New England Journal of Medicine, “Thrombosis of the Cerebral Veins and Sinuses”, as 3 – 4 cases per million of population, albeit with 75% of those cases being female. It was noted in the article that “A prothrombotic risk factor or a direct cause is identified in about 85% of patients with sinus thrombosis”, and that, “The frequency of peripartum and post-partum sinus thrombosis is about 12 cases per 100 000 deliveries…..” Moreover, the symptoms and clinical course of the disorder are described as being “…highly variable.” In relation to CT scanning the article noted that it, “……is a useful technique for the initial examination, to rule out other acute cerebral disorders and to show venous infarcts or hemorrhages, but its results can also be entirely normal.”

Dr Williams acknowledged that of those mothers who developed a post-partum CVT, not all would go on to develop a seizure. Moreover, the confidential enquiry into maternal mortality, “Saving Mothers’ Lives” published in 2011, showed that during the relevant period in only 8 cases per 100 000 maternities was a CVT recorded as the direct cause of death. He acknowledged that post-partum eclampsia may occur beyond the 48 hour post natal period, as exemplified in the single case study reported in volume 331 of the British Medical Journal, “Postpartum Eclampsia of Late Onset”. Albeit that in the latter case Dr Williams considered, given the symptoms described, it was likely that the mother was also suffering from posterior reversible encephalopathy syndrome.

Overall, Dr Williams was of the opinion that in the present case due to the timing of the seizure, namely 5 days post-partum, it was likely that the risk of the occurrence of PPE as opposed to a CVT was on a par. He based this not only upon his own experience, but also noted that although there was clear research evidence showing a significant fall in the incidence of PPE after the initial 48 hour post partum period, there was no such data available for the incidence of CVTs. Moreover the guidance issued by the Royal College of Obstetricians and Gynaecologists, “Reducing the Risk of Thrombosis and Embolism during Pregnancy and the Puerperium”, pointed out that a woman will remain at the highest risk of suffering a thrombotic event during the first week post-partum, such that the provision of thromboprophylaxis for only a 3 – 5 day period my be insufficient, and recommends that it should be provided over a minimum period of 7 days post-partum. It was for this reason that when he answered question 7 of the joint report, he had required the addition of the caveat, that although the incidence of PPE as opposed to a CVT in the population as a whole favoured the former rather than the latter explanation, the individual risk in the present case did not do so.

Dr Williams acknowledged that in the light of the lumbar puncture results, which showed that the claimant’s intra-cranial pressure was within normal limits, it was likely that if a CVT had occurred, it had initially caused a localised focal seizure which had then progressed into a more generalised one. Therefore the headache which had been recorded in the medical notes on the 19^th July was not one which was caused by any raised intra-cranial pressure, a matter which he had overlooked in his initial report. However, he pointed out that there was in any event a strong association between the incidence of headaches and CVTs. Moreover where, as in the present case, a relatively small venous blood clot may have occurred leading to only a partial blockage, the nature and strength of the resulting headache caused by the backing up of blood may well be less severe than would otherwise he the case. In this regard he observed from the medical notes in this case that the headache appeared to have become less intense if not resolved with the use of analgesics. He agreed that vomiting is a sign which was consistent with a diagnosis of both PPE and a CVT.

Dr Williams agreed that the lack of any sign of focal damage on the CT scan was a factor which tended against the diagnosis of a CVT. However, he pointed out not only that both the literature and other experts in the case suggested that negative scans may occur despite the occurrence of a CVT, but that he had himself been involved in a case when a CT had failed to disclose the occurrence of an acute CVT, which was shown to have occurred on more sensitive MRI imaging. He agreed that the claimant had been recorded as suffering from some hypertension, albeit it was not particularly severe. The normal systolic range, being between 90 and140, whilst the normal diastolic range, being between 60 and 90.

In conclusion, he remained of the opinion that the most likely diagnosis in this case was a CVT, and that it was very unlikely that the seizure was due to the occurrence of PPE. In regard to the latter opinion, he confirmed that the most important factors against a diagnosis of PPE were the history of well developed babies, the lack of any pre-eclampsia either previously or in the course of the most recent pregnancy and post-partum period, and the timing of the seizure being 5 days post-partum. In this regard, although he acknowledged that Gene had been born slightly past term, he had been the largest baby born to date to the claimant and could in no sense be classed as growth-restricted. Dr Williams maintained that the most important factors in favour of the occurrence of a CVT included, the post thrombotic condition of the claimant in the post-partum period, the blood loss resulting from acute uterine rupture, the traumatic caesarean section and the lack of consistent post-natal provision of Heparin. He said that the claimant’s immobility would also be likely to increase the risk of a CVT, as would any dehydration resulting from the temperature of her room in general, her previous pyrexial condition and the more recent vomiting.

Dr Pirie has considerable experience in acute obstetric care, working within a very large and busy maternity department. He said that he had seen a large number of mothers with eclampsia and, over the last 26 years, has seen about 5 cases of the condition occurring beyond the initial 48 hour post-partum period. He has also seen a number of cases of CVT. He agreed with Dr Williams that eclampsia is characterised by the occurrence of a seizure, and that it is likely that the claimant suffered a seizure in this case, leading to a cardiac arrest and the resultant hypoxic brain injury. Therefore the real issue in the case is whether the seizure was caused by PPE or a CVT.

He said that the three most important factors why he considered that the most likely diagnosis in this case was that of PPE, was firstly because of the relative prevalence of eclampsia as opposed to CVTs within the community. Secondly, the normal result of the CT scan, and thirdly the intermittent nature of the clinical presentation.

In relation to the relative incidence of the two conditions, Dr Pirie said that in the main he based his opinion upon his own experience, rather than upon the results of research in the academic literature. Indeed he was part of a new movement away from reliance upon such research and preferred the value of evidence based medicine. That evidence being largely informed by experience, rather than the results of academic research. Having said that, prior to having written his report he had read the relevant academic literature.

It was against this background that he acknowledged that in his initial report he had neither mentioned the relative decline in the incidence of PPE after the initial 48 hour post-partum period, nor had he mentioned the results of research into the frequency of peri-partum and post-partum sinus thrombosis referred to in the review article in the New England Journal of Medicine. In relation to the former point, he didn’t consider it to be of relevance, because although he acknowledged that there was a significant decline, there was no research results as to the extent of that decline after the expiry of the initial 48 post-partum period. In relation to the latter point, he said that the academic study upon which the figure mentioned in the New England Journal of Medicine was based was commercially sponsored and therefore likely to be skewed for its own purposes. He also acknowledged that where, at paragraph 11.15 of his own report, he had mentioned the reported incidence of CVTs as being around “6 per million maternities” this was a typographical error and ought to have made it clear that the incidence was “6 per million of the population.”

Dr Pirie maintained his opinion that the relative incidence of the occurrence of PPE as opposed to a CVT, meant that the former event was more likely to have occurred than the latter one. However he acknowledged that the relative rarity of the occurrence of PPE after the expiry of the initial 48 hour post partum-period, caused the differential between the incidence of the occurrence of PPE as opposed to a CVT to be significantly less than if the seizure had occurred within the initial 48 hour post partum period.

In relation to the absence of signs of a CVT on the CT scan, Dr Pirie stated that he was reliant upon the opinions of the neuroradiologists as to the significance of this matter in the context of this case.

In relation to the intermittent nature of the clinical presentation, Dr Pirie stated that in his experience of individuals who have complained of a headache prior to the occurrence of a stroke, the nature of the headache is such that it would not be relieved by analgesics, but would become progressively worse. In that regard he referred to the descriptions of the types of headaches described in the confidential enquiry in relation to maternal mortality.

Dr Pirie accepted that in his initial report he had not mentioned the factors which he had agreed in the joint report were ones which tended against a diagnosis of PPE. He explained that this was because he did not believe that they had a strong countervailing effect. There is still a significant risk of a woman suffering from pre-eclampsia where she had not suffered from the condition in a previous pregnancy. Moreover he considered that the claimant had a history of small babies, her first child being below the first centile and one can never know a baby’s growth potential.

Dr Pirie agreed that he had accepted in the joint report that the lack of consistent post-natal provision of Heparin was a significant factor favouring a diagnosis of a CVT. However he said that it was only of relatively minor significance, because in his opinion it was unclear as to whether its provision did reduce the risk of the occurrence of a CVT, as opposed to a deep vein thrombosis. He was referred to the confidential enquiry into maternal mortality which appeared to indicate that the increased use of thromboprophylaxis may have reduced the incidence of deaths from CVTs, and agreed that this appeared to be the situation. Indeed he assumed that its provision did decrease the risk of the occurrence of a CVT.

Dr Pirie was also referred to the definition of eclampsia in Professor Redmond’s survey, and accepted that the claimant’s post seizure test results did not fulfil the necessary criteria. However, this was not a matter which he considered necessary to mention in his original report, because not only was this only a research definition, but it is accepted that it is possible for PPE to occur in the absence of the fulfilment of such criteria, as indicated in the survey by Dr Tuffnell and others. He agreed that the relatively mild level of hypertension recorded in this case was not one which necessarily indicated that PPE had occurred.

Dr Kendall said that on its own a negative CT scan, like the one in the present case, cannot be determinative of the appropriate diagnosis, as both disorders can occur without signs being recorded on a CT scan. He agreed that Drs Shroff and deVeber’s article, “Sinovenous Thrombosis in Children”, suggested that conventional CT techniques missed the presence of a CVT in 16 – 40% in children and adults, such that it underestimates, “….. both the extent of sinus involvement and the presence and extent of venous infarcts.” However, his own experience was nearer to that suggested in “Diagnosis and Management of Cerebral Venous Thrombosis” by Dr Saposnik and others, that on plain CT, abnormality is only shown in about 30% of cases of CVTs. However, he agreed that if the CVT had caused a thrombus in a cortical vein, as was posited in this case, then it is more likely than not that this would have been seen on a CT scan. He said that the occurrence of PPE may be seen on a CT scan, but agreed that more often than not there will be no signs of it. He said that from a neuroradiological perspective he is unable to provide an opinion as to the likelihood of the occurrence of a CVT as opposed to PPE in this case. However, he preferred the clinical opinion of Dr Williams to that of Dr Pirie.

Dr Forbes said that as a CT scan is more likely to record signs of a CVT than PPE, he favoured the latter diagnosis in this case. This being upon the basis that if a CVT had caused a thrombus in a cortical vein, then it is more likely than not that it would have been recorded on the CT scan, whereas if PPE had occurred, then it is more likely than not that it would not have been recorded on the CT scan. He said that he had glanced through Dr Sidhom and other’s article on “Cerebral Venous Thrombosis: Clinical Feature, Risk Factors, and Long-term Outcome in a Tunisian Cohort”, in which it was suggested that although CT scans are normal in up to 30% of CVT cases, their own cohort provided normal scans in about 46% of such cases, but had not read Dr Saposnik and others’ paper. He said that he didn’t consider it of importance to have read the academic literature as he had based his opinion upon his own clinical experience. He said that the Dr Sidhom’s cohort was extremely small and that his own experience of missed CVTs on CT scans was more in line with that suggested in Drs Shroff and deVeber’s article. Dr Forbes acknowledged that some of the observations in his original report, and in particular the strength of his opinion against a diagnosis of a CVT, was based upon a misunderstanding of the claimant’s case, namely that the CVT had been the direct cause of the cardiac arrest/hypoxic damage. However, now that he appreciated the posited mechanism of the occurrence of a relatively small blood clot in a cortical vein causing focal ischaemic damage/seizure progressing to a general seizure, he concluded that although it is perfectly possible that a CVT had occurred in this case, on the balance of probabilities he would still have expected to have seen signs of it recorded on the CT scan.

Professor Chadwick said that it was common ground that the claimant’s hypoxic brain injury had been caused by her having suffered a cardiac arrest, and his understanding was that, if a direct cardiac cause could be excluded, then the most likely cause of the cardiac arrest was the incidence of a seizure caused either by PPE or a CVT. He said that in either case, in order for the seizure to have caused the cardiac arrest, it would have had to have been a generalised seizure, which not only may have affected the muscles of the body, but must also have affected the autonomic parts of the brain which regulate the function of the heart and lungs. He said that this type of seizure may occur either directly, or indirectly through the rapid development of a focal seizure. He said that the latter type of seizure may be caused by a thrombus in the cortical veins and although this may not be recorded on a CT scan, one would expect to see some evidence of it.

He agreed that it was a rare event for PPE or a CVT to cause a generalised seizure, and that this made the diagnosis very difficult. He considered the diagnosis to be outwith the expertise of a neurologist and deferred to the opinions of Dr Williams and Dr Pirie. He was referred to Dr Cantu and Barinagarrementaria’s review article on “Cerebral Venous Thrombosis associated with Pregnancy and Puerperium”, as to the incidence of seizures following CVTs. However it was his opinion that the relevant table was not Table 2 which referred to presenting symptoms, but Table 3 which referred to the neurological findings in CVTs, where general seizures had been found to occur in 26.9% of cases. He agreed that the results of the lumbar puncture showed that the intra cranial pressure was within normal limits, albeit towards the upper end of the scale.

Dr Sawle agreed that of all of the possible diagnoses, PPE or a CVT were the most likely ones to have been responsible for having caused the claimant’s cardiac arrest. However in this case he favoured the diagnosis of PPE causing it either directly or indirectly through the occurrence of a seizure. He acknowledged that PPE appeared to be characterised by the occurrence of a seizure, but maintained his opinion that PPE may lead directly to a cardiac arrest without the occurrence of one. He conceded that this was a matter which was outwith his field of expertise, but said that this was his understanding of the literature including the description of cardiopulmonary arrest in Dr Barton and Sibsai’s article on “Acute Life-Threatening Emergencies in Preeclampsia – Eclampsia” and Table 4 of Dr Munro’s article on the “Management of Eclampsia in the Accident and Emergency Department”, albeit that when he was referred to and appreciated that the results recorded in Table 4 originated from Professor Redman’s study into eclampsia in the United Kingdom, he accepted that this did not appear to provide support for his thesis.

He accepted that the reference to the incidence of generalised seizures caused by a CVT in his original report relied on the results set out in Table 2 of Dr Cantu and Barinagarrementaria’s review article, which only referred to presenting symptoms. However, although he accepted, as Professor Chadwick had said, that it was possible for a CVT to have caused a focal seizure which developed into a general one and thereby caused the claimant’s cardiac arrest, he maintained that the occurrence of such a seizure was still a rare event.

He also accepted that the reference to the rarity of a person with a CVT presenting with a headache alone, as opposed to other neurological symptoms, in his original report was based, inter alia, upon the results set out in Table 1 of Dr Ferro and others’ article “Prognosis of Cerebral Vein and Dural Sinus Thrombosis” and Table 3 of Dr Cantu and Barinagarrementaria’s review article, neither of which were limited to presenting symptoms. He agreed that in fact none of the literature to which he had referred in this part of his original report founded the assertion that it would be extremely rare for a patient with a CVT to present only with a short history of headache, rather the literature showed that these were simply the type of symptoms which may be exhibited by a person with a focal seizure.

However he maintained his opinion that the normal result of the CT scan was a significant factor tending against the occurrence of a CVT.

Dr Sawle stated that the results of the lumbar puncture showed that the claimant’s intra-cranial pressure was within normal limits, albeit towards the upper end of the scale. However he accepted that even without any rise in intra-cranial pressure, the ischaemic damage caused by the presence of a small blood clot in the cortical veins could cause a headache, moreover that this may fluctuate depending upon her position. He acknowledged that the extent of his expertise did not allow him to provide an opinion as to the relative significance of the timing of the post-partum event, and therefore the reference in his original report to the weakness of the support to be gained from this feature in favour of a CVT should be excluded. However, from a neurological point of view he maintained that the occurrence of PPE was more likely than that of a CVT.

I remind myself of the helpful guidance provided by Stuart Smith LJ in Loveday v Renton & Wellcome Foundation Limited [1990] 1 Med LR 117, in relation to the court’s approach to the assessment of expert evidence,

“The mere expression of opinion or belief by a witness, however eminent…….does not suffice. The court has to evaluate the witness and the soundness of his opinion. Most importantly this involves an examination of the reasons given for his opinions and the extent to which they are supported by the evidence. The judge also has to decide what weight to attach to a witness’s opinion by examining the internal consistency and logic of his evidence; the care with which he considered the subject and presented his evidence; his precision and accuracy of thought as demonstrated by his answers; how he responds to searching and informed cross-examination and in particular the extent to which a witness faces up to and accepts the logic of a proposition put in cross-examination or is prepared to concede points that are seen to be correct; the extent to which a witness has conceived an opinion and is reluctant to re-examine it in the light of later evidence, or demonstrates a flexibility of mind which may involve changing or modifying opinions previously held; whether or not a witness is biased or lacks independence.”

Undoubtedly what took place on the 19^th July 2005 was a most unexpected event, and one which has caused a considerable amount of discussion and debate between the experts who have been instructed to provide their opinions as to its cause; none of whom have been able to provide certainty. However, this is not an atypical situation in contested civil proceedings arising out of alleged clinical negligence and, mindful as I am of the implicit invitation on the part of the defendant that because the matter is so fraught with difficulty I should on that basis resolve the proceedings in their favour, I consider that there is sufficient evidence in this case in order to allow me to reach a concluded view upon the issue which is determinative of liability in this case. In this regard I do not consider that the opinions expressed by the experts are in the main simply based upon which of the two diagnoses is the least likely, rather they have reached disparate opinions upon which is the most likely diagnosis in this case.

There is no dispute that the claimant’s current state of health is due to a hypoxic episode, caused by the claimant having suffered an asystolic cardiac arrest during the few minutes whilst she was alone in her hospital room on the afternoon of the 19^th July 2005. It is agreed that there is no evidence of any cardiac related condition which may have caused the arrest and, given the relevant surrounding circumstances, the two most likely causes of the arrest are either PPE or a CVT. Although at one stage or another there has been some variation as to the mechanism by which each of these disorders is likely to have caused the arrest, subject to the views of Dr Sawle, this now appears to be resolved.

In so far as PPE is concerned, this disorder is characterised by the occurrence of a seizure, and if this disorder was the cause of the claimant’s cardiac arrest, then it is the effect of a generalised seizure upon the autonomic parts of the brain, and in particular those regulating the functioning of the heart, which was the immediate cause of her cardiac arrest. PPE, being an obstetric event, is one in which the views of the obstetricians are likely to be most authoritative, and both Drs. Williams and Pirie agree that PPE is not diagnosed without the occurrence of a seizure. Moreover, in the authoritative study reported by Professor Redmond and others, eclampsia is defined in the introduction as being, “……the occurrence of convulsions…..”

Although I did not understand that Dr Sawle necessarily disagreed with this definition, he expressed the view, both in his original report and perhaps surprisingly maintained it in evidence, that PPE could cause a cardiac arrest either directly or indirectly through the mechanism of a seizure. This was not a view expressed by Professor Chadwick who, in relation to CVTs, stated that the occurrence of a generalised, as opposed to focal seizure, would be required in order to cause the relevant autonomic parts of the brain to be adversely affected, so as to cause a cardiac arrest. Dr Sawle accepted that the diagnosis of PPE was outwith his field of expertise and stated that his opinion was based upon certain aspects of the academic literature. In this regard I am afraid that I do not consider that the literature to which he referred supports his view. Although the articles variously stated that “Although rare, cardiopulmonary arrest can occur in association with these changes…...”, and cardiac arrest is one of the tabulated “Complications of eclampsia”, there is nothing within the articles to suggest that cardiac arrest is directly caused by the condition in the absence of a seizure, which is of course the fundamental pre-condition for its diagnosis. In these circumstances I consider that Dr Sawle is in error on this point, and I am satisfied that in order for either PPE, or indeed a CVT to have caused the claimant’s cardiac arrest, the mechanism by which this took place was the occurrence of a generalised seizure.

In so far as a CVT is concerned, the evidence of both Professor Chadwick and Dr Sawle was that this can cause a general seizure, either through a large thrombus causing a significant rise in the intra-cranial pressure, or from the development of a focal seizure caused by the occurrence of a smaller thrombus in the cortical veins. In either event the generalised seizure may in turn adversely affect the relevant autonomic parts of the brain, leading to a cardiac arrest. In the absence of any evidence of significantly raised intra cranial pressure, it was the latter event which Professor Chadwick considered was likely to have occurred in the present case.

In so far as the resolution of the differential diagnosis between PPE and a CVT is concerned, although both the neuroradiologists and the neurologists have valuable matters to contribute to the overall assessment, especially in relation to the possible diagnosis of a CVT, it seems to me that the most valuable assistance is to be gained from the views of the obstetric experts. However before turning to the evidence of Drs Williams and Pirie, it is convenient to deal with that of the other experts.

The most important contribution provided by the neuroradiologists is in relation to the likelihood of a CT scan detecting changes which may be caused during the occurrence of either or both of these disorders. Although in his original report Dr Forbes appeared to hold a strong view against the occurrence of a CVT, as he acknowledged in evidence, this was based upon a misunderstanding of the mechanism by which it was posited that the disorder had caused the claimant’s cardiac arrest. Once this misunderstanding had been resolved he accepted that despite the normal nature of the result of the CT scan, it was perfectly possible for a CVT to have occurred in this case, albeit that in his view it was more likely that PPE would result in a normal CT scan, whereas it was more likely that a CVT would result in an abnormal one.

It seems to me that from a neuroradiological point of view, this was an opinion that was not wholly dissimilar to the one held by Dr Kendall, albeit that the latter expert approached the matter from a different perspective, suggesting that because of the significant number of instances in which a CVT may result in a normal CT scan, the result of the CT scan in this case didn’t favour the diagnosis of PPE. However he did acknowledge that more often than not PPE may result in a normal CT scan, whereas the effects of a thrombus of the cortical veins would be more likely to result in an abnormal scan. Although there was clearly a difference both in clinical experience and in the relevant academic literature as to the incidence of CVTs resulting in normal CT scans, taking into account the combined evidence of Drs Kendall and Forbes, I have reached the conclusion that in this case, whereas PPE is more likely to have resulted in a normal CT scan, a CVT is more likely to have resulted in an abnormal one. This is a matter, as the Consultant Neurologists agree, which requires to be taken into account when deciding the question of the differential diagnosis in this case.

It is apparent that Professor Chadwick remained of the opinion that from a neurological point of view, he was unable to provide an opinion as to the relative likelihood of the competing diagnoses, albeit that a CVT was more likely to result in an abnormal CT scan and the absence of preceding focal neurological symptoms reduced the probability of the occurrence of a CVT.

I have already mentioned the position of Dr Sawle in relation to his views on the mechanisms by which PPE may result in a cardiac arrest. The significance of my rejection of his opinion on that point, is that it is one of the four matters upon which he appears to have based his opinion that it is more likely that the claimant suffered PPE in this case. In this regard however I am afraid that I am similarly unable to accept his opinion in relation to two of the other matters upon which he relies.

It seems to me that Dr Sawle’s reliance upon the results of Table 2 of Dr Cantu and Barinagarrementaria’s review article, in order to seek to establish that it is much rarer for obstetric patients to suffer focal rather than general seizures is flawed. The title of Table 2 makes it abundantly clear that the results relate to presenting symptoms, such that the appropriate table is Table 3 from which it is apparent that there was only a modest increase in the number of such patients suffering from focal as opposed to generalised seizures. Moreover the number of obstetric patients suffering from generalised seizures after a CVT represented 26.9% of the total. Equally, as he eventually acknowledged in cross-examination, his reliance upon the academic literature to found the expression of his opinion that it would be “extremely rare” for a patient with a CVT to present only with a short history of headache was unwarranted. It is apparent that the academic literature to which he referred wasn’t limited to presenting symptoms, and simply listed the type of other neurological symptoms which may result from a focal seizure.

In these circumstances apart from the matters upon which Professor Chadwick concurred, it seems to me that much of the force of Dr Sawle’s opinion was dissipated. Moreover, it is of concern that he was providing an opinion outwith his area of expertise when he had sought to express a view upon the relative significance of the timing of the post-partum event.

I was impressed by an initial reading of Dr Pirie’s original report, informed as it appeared to be, by a very clear statistical bias in favour of the occurrence of PPE over CVTs. What I had not appreciated, until listening to Dr Pirie’s evidence in the course of the trial, was that not only was his opinion largely based upon his own clinical experience with little reference to the results of academic research, but that when this was considered, as he eventually acknowledged, a significantly different and less cogent picture emerged as to the bias in favour of the occurrence of PPE over a CVT in the particular circumstances of this case. I am afraid that by the conclusion of his evidence both this factor and some of the other contrasting matters which did not appear have been discussed in his report, led me to the conclusion that his opinions required to be scrutinised with particular care. In fairness to Dr Pirie, he did acknowledge at one point in his evidence, that having felt from the beginning that this was a case in which PPE had occurred, he may have become unconsciously biased and omitted matters in his report which ought to have been considered by him.

In contrast, not only did it become apparent during the course of Dr Williams’ evidence that he was an expert of the first calibre in his field, but, with the exception of the results of the lumbar puncture, he had weighed with conspicuous care all of the matters germane to the conclusions which he reached. The defendant has sought in closing submissions to criticise him for having omitted from his initial report express reference to the incidence of the occurrence of CVTs. In my judgement this criticism is unfounded as it is apparent that, when properly analysed in the light of the clinical findings in this case, it is unlikely that there is any material differential.

It is readily apparent both from clinical observations and from the results of academic research that there is a clear statistical bias in favour of the incidence of PPE over CVTs. However, that is a matter of generality and, as became clear, it is a matter which requires careful examination and assessment as to its effect upon the present case. In relation to PPE I am satisfied that due to the date upon which the claimant’s cardiac arrest occurred, and bearing in mind that 99% of the women who were included within the updated 2005 eclampsia survey by Professor Knight had not received magnesium sulphate prior to any seizure, the relevant incidence of eclampsia in general is 2.7 cases per 10 000 births. Moreover, although the overall incidence of CVT in the population as a whole may be 3 to 4 cases per million, it seems to me that the relevant figure relating to this case, where we are dealing with a post-partum event, is that referred to in Dr Stam’s review article, based upon the research article by Drs Lanska and Kryscio, “Risk Factors for Peripartum and Postpartum Stroke and Intracranial Venous Thrombosis”, namely that the frequency of peripartum and post partum sinus thrombosis is about 12 cases per 100 000 deliveries. The fact that this was commercially based research was not a matter which caused Dr Williams concern when he considered it, and I am unpersuaded of the validity of either Dr Pirie’s criticism of its suitability or that of the defendant in closing submissions. On the contrary, as the article makes clear, in contrast to some of the other research, this survey was based upon results from a large and varied cohort.

As I have observed even the use of these statistics provides a bias in general terms in favour of the incidence of the occurrence of PPE over CVTs, albeit one of around 2.7 cases as opposed to 1.2 cases per 10 000 respectively, rather than that set out in Dr Pirie’s original report. However, in order to properly understand the potential significance of these figures, I am satisfied like Dr Williams, and subsequently Dr Pirie, of the need to take properly into account the circumstances of the claimant’s case, and in particular in this regard the timing of the cardiac arrest, namely 5 days post partum. In this regard I consider that it is of considerable significance that Professor Redman’s survey found that the overwhelming majority of PPE, some 88%, occurred within the first 48 hours of the birth. A matter which is echoed in Dr Tuffnell and other’s subsequent research study in Yorkshire. In contrast there is no research based evidence of the fall-off in the incidence of CVTs post-partum. Indeed such relevant academic study that there is in relation to the condition, suggests that a woman will remain significantly prothrombotic throughout the first week post-partum, hence the recommendation of the Royal College of Obstetrician’s and Gynaecologists that thromboprophylaxis should be continued for a minimum of 7 days post-partum. In the event Dr Pirie acknowledged that, in the present case, the differential between the incidence of the occurrence of PPE as opposed to a CVT is significantly less than if the seizure had occurred within the initial 48 hours post-partum. On the other hand Dr Williams inclined to the view, as he alluded to in their joint report, that the risks of either event occurring in this case was on a par. It seems to me that the evidence upon which this latter opinion is held justifies this view. Moreover even if a differential does remain in favour of the incidence of PPE, it is so relatively insignificant as to carry little weight in the overall consideration of this case. In this regard I of course take into account that it is rare for a CVT to result in a seizure leading to a cardiac arrest, but so too is it relatively rare for PPE to lead to a cardiac arrest.

I turn then to consider the relevant clinical circumstances surrounding this case. The first one being the normal result of the CT scan which was undertaken after the occurrence of the cardiac arrest. This undoubtedly is a matter of relevance and one upon which all those involved have provided their various opinions. In the main and when properly analysed those opinions fall into two main camps, on the one hand it is suggested that this is a contra indication as to the occurrence of CVT and a positive indication as to the occurrence of PPE, whilst on the other that it is relatively neutral, neither supporting the occurrence of PPE nor militating against the occurrence of a CVT. I am inclined to the view that whilst undoubtedly the normal results recorded on the CT scan cannot support the occurrence of a CVT, and tends to undermine its occurrence, its ability to positively support the occurrence of PPE, whilst significant, requires to be balanced against both the incidence of normal CT scans after known CVTs, and the other relevant clinical circumstances of the case. In relation to the former, it seems to me that it is of relevance that not only is it the clinical experience of those carrying out such procedures, such as Dr Kendall, that the signs of a CVT are not infrequently unrecorded on a CT scan as opposed to more sensitive procedures, but as is pointed out in the relevant academic literature the results can be entirely normal in a significant number of cases,( Dr Stam’s article in The New England Journal of Medicine; Drs Shroff and deVeber’s article, and; Dr Saposnik and others’ article). A matter which both Drs Williams and Pirie acknowledged in their joint report.

Of course much of the clinical presentation of the claimant leading up to her cardiac arrest and beyond is consistent with both diagnoses. However, it seems to me that there is here a preponderance of other significant factors which do, as Dr Williams suggests, positively support the likelihood of the occurrence of a CVT rather than PPE. The first of these is the significance of the fact that at the time when the cardiac arrest took place, the claimant was, as I have already observed, in a prothrombotic condition purely by reason of her post-natal status. Secondly, that condition was significantly enhanced by the occurrence of a number of subsidiary factors, including the uterine rupture, the emergency caesarean section, her pyrexial condition, her vomiting, relative immobility and the temperature of the room. In this regard I accept the evidence of Julian Harrington, that the temperature in the room was, as is not an uncommon and understandable in a hospital context, extremely warm, such that the claimant may well have been relatively dehydrated; a potentially prothrombotic factor. Thirdly, the lack of consistent provision of the post-natal thromboprophylaxis Heparin. In relation to this latter factor, having regard to the observations in the confidential enquiry into maternal mortality, I am not minded to accept the opinion of Dr Pirie that this factor is of little weight and prefer to accord it the significance which was accorded to it by Dr Williams.

I have not overlooked that two of the factors which both Drs Williams and Pirie agreed in their joint report were ones which significantly favoured the diagnosis of PPE were the headache suffered by the claimant and her hypertension.

As I understand the evidence the presence of a headache can be attributable to the existence of both PPE and a CVT. However Dr Pirie’s real point was as to the nature of the headache of which the claimant made complaint, being one that was intermittent and at least resolved with analgesics, as opposed to one which did not resolve and worsened. I consider that the evidence on this point is somewhat equivocal. In that whilst I accept both from Dr Pirie and the literature that a headache caused by a CVT is likely to be one which can be described as the worst one ever experienced and is unlikely to be resolved by the ingestion of simple analgesia, I note that the description in the literature doesn’t seek to distinguish between those cases in which such a headache is caused by a CVT causing raised intra cranial pressure, as opposed to a relatively small blood clot in the cortical veins. As I understand it from the evidence the former type of CVT would undoubtedly be likely to cause an extremely severe headache. However according to Dr Sawle and Dr Williams the latter type of CVT may also cause a headache of some degree, and Dr Sawle observed that headaches may fluctuate in intensity according to the position of the sufferer’s body. Moreover, I accept the evidence of Julian Harrington that not only had the claimant been suffering from intermittent headaches during her post natal period in hospital, but that in contrast the severity of the headache which she suffered on the 19^th July was significantly worse than any of the previous ones. In these circumstances and bearing in mind both the incidence of headaches being associated with CVTs and the mechanism by which it is now understood a CVT may have caused the cardiac arrest in this case, it seems to me that the presence of the type of headache which the claimant suffered on the 19^th July is not inconsistent with the occurrence of a CVT; it appears to be consistent with the occurrence of both conditions.

Moreover, the significance of the evidence of hypertension appears to have lost much of its potency. Not only is it clear from the evidence that the hypertension suffered by the claimant on the 19^th July was relatively mild in degree, but it was not one of the factors upon which Dr Pirie concentrated when advancing his opinion in favour of PPE, acknowledging as he did that it did not necessarily indicate the occurrence of PPE.

A point maintained by Dr Sawle was that if an initial focal seizure had taken place, then one may have expected the observation of other neurological signs, and none were recorded in this case. Although it is clear that much of the strength of this point also appears to have dissipated in the course of cross-examination, I am aware that Professor Chadwick had agreed in the joint report that from a neuroradiological point of view, the absence of such symptoms reduced the probability that the cause of the cardiac arrest was due to a CVT. Although he was not questioned about this aspect of his evidence, I note that he envisaged a fairly rapid development of the generalised seizure from the initial focal one. However, whether this is correct or not, it seems to me that the absence of any other observed neurological symptom is a matter which must be weighed in the balance, as a factor, albeit now one of limited weight against the occurrence of a CVT.

It is also necessary to bear in mind the matters which have been recognised from the outset by both Drs Williams and Pirie to be contra-indicators of the occurrence of PPE in this case. Namely, the lack of history of any pre-eclampsia or indeed eclampsia in either of the claimant’s previous pregnancies, the lack of evidence of any pre-eclampsia in her third pregnancy and the fact that Gene appears to have been a well developed baby. In this regard, I am not persuaded by Dr Pirie’s attempt to undermine the significance of these factors. Even if the complainant’s first baby was below the 1^st centile, there is no evidence that this had any association with an eclamptic condition. Moreover, although it may be that one can never know with certainty the full potential of a baby’s growth, and even bearing mind that Gene was past term, I accept the evidence of Dr Williams that in reality there is no evidence that Gene was a growth-restricted baby.

As I have already observed, the issue which requires to be determined in relation to liability, is whether the claimant has been able to establish that it is more likely than not that the cause of her cardiac arrest on the 19^th July 2005 was a CVT. In my judgment, and having considered the evidence with care, I am satisfied that she has been able to do so.

It is clear that at the outset of the trial the main focus of the defendant’s case was its submissions relating to the relative incidence of the occurrence of PPE over CVTs. However, I consider that when properly analysed and due regard is had to the timing of the cardiac arrest, the evidence does not support those submissions. If any differential in favour of the incidence of PPE exists, then in my judgement it is so relatively insignificant as to carry little weight in the overall consideration of this case. In the event however, for the reasons I have set out above, I am persuaded that at 5 days post partum it is unlikely that there is any differential.

It is therefore necessary to focus upon the competing significance of the various clinical findings in this case.

It seems to me that the combination of other significant factors, over and above those which are consistent with both diagnoses, which are likely to have been causative of a CVT, and the presence of significant contrary factors indicating the likely absence of PPE, is such that in my judgment it is more likely than not that the claimant suffered a CVT leading to her cardiac arrest and consequent hypoxic neurological damage on 19^th July 2005.

Although I appreciate that PPE can occur without a previous history or signs of pre-eclampsia and beyond the immediate 48 hour post natal period, not only does the evidence establish that this would have been a particularly unusual event, but set against the other significant factors which are likely to have been causative of a CVT, I accept the evidence of Dr Williams that it is unlikely that the claimant suffered PPE preceding her cardiac arrest, and instead it is likely that she suffered a CVT. Those other significant factors being the generally prothrombotic condition of the claimant, which was significantly increased by the effects of her traumatic delivery and post natal condition, together with the lack of consistent post natal provision of Heparin.

Moreover I do not consider that the other clinical findings, namely the headache, hypertension and lack of other neurological symptoms, are of such significance that, either alone or in combination, they materially alter my conclusion. Although the mechanism by which a CVT is likely to have caused a generalised seizure, namely from the development of a focal one, may well have caused other neurological symptoms, this was not inevitable. Moreover not only did Dr Pirie agree that the relatively mild degree of hypertension was not necessarily indicative of PPE, but according to both Dr Williams and Dr Sawle, the nature of the claimant’s headache was consistent with the development of a relatively small thrombus in the cortical veins.

I should make it clear that I have taken full account of the evidence that the normal result of the CT scan favours the occurrence of PPE rather than a CVT. The former disorder being more likely to be consistent with a normal result, whereas the latter disorder is more likely to be inconsistent with a normal result. However, it is clear that in itself this is not a determinative matter; at the very least there will be a significant minority of cases of CVTs where normal results will be recorded on the CT scans. In my judgement it is likely that this is one of those cases.

In these circumstances, I am satisfied on the balance of probabilities that on 19^th July 2005 the claimant suffered a CVT, leading to the development of a focal and then general seizure, which in turn caused her to suffer an asystolic cardiac arrest and consequential neurological damage.