Carter v Basildon & Thurrock University Hospitals NHS Foundation Trust

On 30 September 2002 Elaine Carter gave birth to a baby boy, Bradley, at Basildon Hospital. Bradley was about 8 weeks premature. This was two days before her 20^th birthday.

Bradley was admitted to the Special Care Baby Unit (SCBU) and Mrs Carter was allowed home the following day. Each day thereafter she and her husband visited Bradley until 7 October when Mrs Carter felt too unwell to attend. Whilst her husband was visiting Bradley that evening Mrs Carter was taken seriously ill and eventually transported by ambulance to Basildon Hospital where she died at about midday on 9 October.

She died only one week after her 20^th birthday. She saw Bradley only on a few occasions before her death. He will never know her. She left behind another son, Jamie, who was nearly 3 when she died.

Earlier in the year she gave birth to a daughter, Holly, who was stillborn.

Stating the facts in that bald manner indicates the nature of the personal and family tragedy that lies in the background to this case.

Not surprisingly, Mr Carter took his wife’s death very badly, but with the particular assistance of his mother, Mrs Peggy Carter, the boys were cared for in exemplary fashion both immediately after Mrs Carter’s untimely death and thereafter. Mrs Carter senior already had the responsibility of the care of the two young children of her daughter, but she took on this extra burden with remarkable vigour and commitment.

Fortunately, with the passage of time, Mr Carter met someone else whom he married last year, some four years after his wife’s death.

In circumstances to which I will refer in more detail shortly, it is now not disputed that Mrs Carter received negligent treatment by a doctor at Basildon Hospital on the evening of 6 October. The primary issue in the case is whether, had that negligence not occurred, her emerging and developing serious condition would have been arrested and her death prevented.

The case advanced on behalf of Mr Carter and the two boys (who seek damages under the Fatal Accidents Act) is that earlier identification of the serious and developing problem and its proper treatment would have prevented Mrs Carter’s death and that she would have survived intact. The case advanced on behalf of the Defendant hospital is that nothing could have been done to prevent her death and that the negligence, whilst regrettable, made no difference.

Mrs Carter died from the effects of a cerebral venous thrombosis (CVT) or, more accurately, a cerebral venous sinus thrombosis (CVST). It is a comparatively rare form of stroke that can present itself against a number of aetiological backgrounds. One such background is the puerperium – the period of about 6 weeks following childbirth when the various changes that occurred during pregnancy revert to the non-pregnant status. At the time that Mrs Carter’s CVST developed she was, of course, in the early stages of the puerperium.

As its name implies, CVST involves the formation of blood clots that affect certain veins in the brain. The veins, of course, carry blood back to the heart and, at its simplest, the existence of a CVST impedes the ability of the cerebral venous system to drain blood from the brain.

The relevant venous anatomy of the brain is illustrated in a diagram from a review article by Stam entitled ‘Thrombosis of the Cerebral Veins and Sinuses’ in the New England Journal of Medicine (April 2005) reproduced in Dr Hardie’s Supplementary Report. I take the liberty of reproducing it here:

The sagittal sinuses and cortical veins represent the superficial cerebral venous system. The other veins, illustrated above the level of the jugular veins, represent the deep cerebral venous system. It is into the jugular veins that these two systems drain.

As indicated in paragraph 11 and as the diagram tends to confirm, if these veins become constricted by blood clots, the natural drainage system will be compromised. As the effect of clotting increases, the volume of blood remaining within the brain will increase. This, plus associated impairment of the absorption of cerebro-spinal fluid (CSF), leads to back pressure. Intracranial pressure rises and other consequences, including generalised brain swelling and haemorrhage occur. The most serious consequence of increased brain swelling is that brain substance extends downwards into the foramen magnum (the large hole at the base of the skull through which the extension of the spinal cord passes). This results in compression of the brain stem, leading to death. The process is called ‘coning’.

In the sequence of events beginning with the initial clotting and ending with coning (if it occurs), the patient will display various symptoms depending on the location, mechanism and intensity of the thrombus development. There is, however, no clearly established pattern for the development of the symptoms and the presentation of the clinical signs. By way of example, in the review article from which the illustration in paragraph 12 above was taken the author states that “[the] symptoms and clinical course are highly variable.” Dr Stam continues thus:

“To understand the symptoms and signs of sinus thrombosis, two different mechanisms should be distinguished: thrombosis of the cerebral veins, with local effects caused by venous obstruction, and thrombosis of the major sinuses…, which causes intracranial hypertension. In the majority of patients, these two processes occur simultaneously.”

In a recent (February 2007) review article by Dr Marie-Germaine Bousser and Dr José Ferro (both leading figures in this field), the authors comment on the “remarkable diversity of [the] clinical symptoms” of CVT. I will not quote the passage entitled “Clinical aspects” in full, but the general picture is summarised in this extract:

“CVT presents with a remarkably wide spectrum of signs and modes of onset, thus mimicking numerous other disorders. The most common symptoms and signs are headache, seizures, focal neurological deficits, altered consciousness, and papilloedema, which can present in isolation or in association with other symptoms.”

That article also contains the proposition that “[when] the deep cerebral venous system is occluded, the clinical picture is usually more severe with coma, mental troubles, and motor deficits, which are usually bilateral.” That proposition has a resonance with what the experts have said in this case. Whilst there is a difference between them about when there was involvement of the deep cerebral venous system in Mrs Carter’s case, there was no dispute that once significant clotting occurs in that system a patient’s condition is likely to deteriorate quickly.

I mention the variety of presentations for this reason: one part of my task in this case is to make findings about how Mrs Carter’s symptoms evolved. In some situations it is possible to have regard to what is known and accepted about the evolution about a particular condition as a means of informing the fact-finding exercise. However, here, where there is no clearly definable pattern of presentation, I am left with doing my best to evaluate various strands of evidence to reach the probable picture.

As will be apparent from paragraph 16 above, one of the most common symptoms is that of headache. There is no doubt that Mrs Carter was complaining of headaches in the period before her death. One issue I have to address is when those headaches started.

There is no doubt that the first actual complaint by Mrs Carter to her husband was at about 22.30 on the evening of 5 October when they returned home having spent the day with Bradley at the SCBU. It is, of course, unlikely that it was precisely at that moment that the headaches emerged, but there is inevitably no direct evidence available now as to when they started. The nearest one can get to reliable evidence is the note made by a student midwife at about 16.30 on the evening of 6 October, when Mrs Carter attended Cedar Ward at Basildon Hospital for a post-natal check. She (the student midwife) recorded Mrs Carter, who was very tearful and vomited whilst with the midwife, as complaining of “headaches in the mornings”. There is no doubt that Mrs Carter was the source of the information that underlay the making of that note. All the other notes to which my attention was drawn reflected information conveyed to the relevant medical staff by others, most probably by Mr Carter whose information about headaches was as indicated above.

That note (made, as I have said, on the evening of 6 October) would suggest that she had suffered from headaches (in the plural) on more than one morning. Mr Carter was aware that his wife was still complaining of a headache on that morning (the morning of 6 October) and it follows that, if the note is correct and if what Mrs Carter told the midwife was correct, she would have suffered from headaches at least on the morning of 5 October, if not on previous mornings.

As to the accuracy of the note, it was made, as I have already indicated, by a student midwife who was being supervised by a more experienced midwife. That more experienced midwife countersigned the note indicating, as it seems to me, that she was happy that it reflected an accurate record of what Mrs Carter said. Indeed I have noted the statement made by Midwife McGowan, contained within the trial bundle, in which she states that Mrs Carter “said that she had been experiencing headaches in the mornings”. No reason has been advanced as to why Mrs Carter should have given exaggerated information about her condition. Indeed, if it be the case (as was to be the Defendant’s case if breach of duty had remained in issue) that she did not want to remain in hospital over that night, there might have been a temptation to underplay her symptoms. Furthermore, she may not have attached that much significance to them which may explain why she did not mention a headache to her husband until the evening of 5 October. At all events, it seems to me that the clear inference, at least on the balance of probabilities, is that Mrs Carter had experienced headaches from at least the morning of 5 October and possibly before that. That, therefore, is the finding I make.

As I have indicated, my conclusion is that Mrs Carter was experiencing headaches no later than the morning of 5 October and possibly before that. They had not necessarily reached an intensity that would have caused her to be alarmed or to mention them to her husband. However, as we now know, they would have been the first signs of her emerging and developing CVST. What other signs or symptoms emerged and when?

During 5 October Mrs Carter spent virtually the whole day at the SCBU. According to Mr Carter, they were there from 08.00 and arrived home at about 22.30. The notes do not seem to indicate that she had a post-natal check that day (such checks having been carried out on the preceding days). Whilst she probably experienced a headache at times during that day, there is no evidence of any other particular problem that day. The inference to draw, it seems to me, is that she was fully orientated during that day.

As we know, by that evening her headache was such as to prompt her to comment about it to her husband. The following morning she said her headache was no better. A new symptom was a feeling of nausea – and indeed, according to Mr Carter, she did vomit once before leaving for the hospital. She did not eat or drink during the day and by the time she saw the student midwife and Midwife McGowan she was noted to be “very tearful” and, as previously recorded, complaining of “headaches in the mornings”. She was noted to be “vomiting at present”. Dr Dina, whose examination and conduct has been called into question by the obstetric experts, noted that she was complaining of “headache”, but also noted that she was “anxious” and “crying”.

By this time, therefore, the evidence points to the conclusion that, in addition to a continuing headache, she had vomited on at least a couple of occasions and was plainly feeling generally unwell and distressed. She was, however, orientated and capable of expressing herself clearly.

It does have to be borne in mind, of course, that irrespective of how she was feeling physically at this time, she would have been worried about Bradley, who was still in the SCBU, and doubtless had her other son, who remained at home, on her mind as well. This was still only a few days after the premature birth of Bradley.

If one stopped at this point the picture, in layman’s terms, is of someone who started feeling unwell some 36 hours or so previously who was gradually feeling less well. There was no obviously dramatic downturn. The prescription of Co-codamol is consistent with the complaint of headache.

At the conclusion of such examination as was conducted by Dr Dina, Mr Carter said in his witness statement that his wife (who had been curled up on the bed) had difficulty in moving and getting up off the bed. He said that she was unsteady on her feet and that he took most of her weight in trying to support her. He helped her to the lift, he said. When they got out of the lift Mrs Carter vomited again. He said that she was having difficulty walking such that he “buzzed the labour ward for a wheelchair”. In the event, they got into the car without having had the assistance of a wheelchair. The car was driven by Mrs Carter’s mother and they went home, Mrs Carter feeling better by lying down in the car.

Had the issue of breach of duty been contested, the version of events concerning Mrs Carter’s inability to get up unaided would have been challenged: Dr Dina and Midwife McGowan both took issue with this. In the event, of course, I have not heard their evidence to assist on this issue. Mr Timothy Meakin, for the Defendant, did not challenge Mr Carter’s evidence (doubtless perceiving that it might assist his case on causation) about this part of the chronology. However, I do not consider that that binds me to accept it without question. According to Mr Carter, both later that evening and on the following day at about midday, Mrs Carter was apparently able to get up unaided from her bed and go to the toilet. On 7 October at about midday she got herself downstairs to the settee. Had there been some significant and irrevocable deterioration in her condition on the evening of the 6 October it is difficult to believe that she would have been able to do this on the morning of 7 October. The evening of 6 October would have been the end of a long, tiring and anxious day for Mrs Carter and it would not be surprising that she was feeling distinctly unwell and weak then. A further factor is that it is common experience that a close family member who perceives that a close relative has received an unsympathetic reception from a medical professional will persuade him or herself that the presenting condition was more serious than in fact it was. All these various factors have probably been in play here and I am inclined to think, and so hold, that there had certainly been some progression in what was undoubtedly a developing CVST by that evening, but that it did not represent a dramatic or significant deterioration in her condition.

So far as 7 October until about 18.30-19.00 is concerned, as I have already indicated, the balance of the evidence leads to the conclusion that she had slept until midday, but had got herself up to go to the toilet and had brought herself downstairs. She had been able to say that she did not want to eat and that her headache was the same. Mr Carter said that she “responded fine” and this seems to be consistent with the statement of Angela Carter to the ambulance service enquiry when she said that by the time she became concerned about Mrs Carter’s position at around about 20.30 hours she (Mrs Carter) “had not spoken for around two hours”, the implication being that until then she had been communicating satisfactorily. There is no specific evidence about the extent to which she was either awake or asleep on the settee between midday and about 18.30. Mr Meakin perfectly properly drew attention to the note to which I will refer again shortly in which Mr Carter’s account of what he told the staff on Cedar Ward on the evening of 7 October was recorded and suggested that it contradicts his oral evidence. The midwife noted that “the deceased woke late and then sat/lay on the settee at home, saying little and being apparently withdrawn.” The note was not exactly contemporaneous with the conversation (the note being made the following morning) and may not be wholly accurate. However, it seems to indicate that Mrs Carter, having got herself downstairs to the settee, varied her position from sitting to lying from time to time and that she spoke (albeit little) from time to time. I do not really think this undermines Mr Carter’s evidence. In my view, all I can infer, and I do infer, is that at times during that period she communicated both to her husband and to his sister in a way that did not cause either of them particular concern. They could not, for example, have thought that she was incoherent or significantly uncommunicative; that did not come until after about 18.30. It needs to be borne in mind that she was able to communicate her decision not to accompany her husband to see Bradley that evening, something which would presumably not have been decided upon until near the time of departure. Although I have noted suggestions in, for example, Dr Hardie’s report that Mr Carter left home at about 18.00 that evening, I do not think Mr Carter told me precisely when he left for the hospital and I am left to draw such inference as I can. The note prepared the following morning (after the dramatic events that took place overnight) by a midwife, to which I referred above, indicated that Mr Carter had contacted Cedar Ward at “approx. 19:00 hrs last night” to explain that Mrs Carter would not be attending for her post-natal check. He told me that he telephoned the hospital before he left home. Precise timings probably do not matter, but the inference to be drawn is that, whilst plainly unwell and not feeling up to going to the hospital, Mrs Carter was able to communicate satisfactorily at least until her husband (who was accompanied by Mrs Carter’s mother, Mrs Neville) left for the hospital. This was probably between 18.30 and 19.00.

I will return to the significance of these findings including that made in paragraph 22 (and to what occurred later in the evening of 7 October) below. I should now turn to the alleged (and admitted) negligence.

In paragraph 20 I referred to a post-natal check carried out by midwives at about 16.30 on 6 October. It is clear that the midwives felt that Mrs Carter ought to be seen by a doctor in the light of her presentation. That doctor was Dr Olufemi Dina, a Senior House Officer in Obstetrics and Gynaecology. It was his conduct that formed the focus of the allegations of negligence against the Trust.

The Particulars of Negligence were in the following terms, the “junior doctor” referred to being Dr Dina:

Notwithstanding those pleaded answers to the Claimant’s case, the Trust admitted the breach of duty allegations recorded in paragraph 33 above by letter dated 27 April 2007 which, I have been told, was sent by fax at shortly before 18.00 that evening – which, incidentally, was a Friday. It follows that the effective notice that breach of duty was admitted was exactly 21 days before the commencement of the trial. I do not say that critically: it will have been necessary for the Defendant’s advisers to consider the position in relation to breach of duty carefully in the light of the discussions between the obstetric experts that took place on 21 March, the agreed notes not being finally signed off until 26 March, those experts being critical of aspects of Dr Dina’s response to the situation that confronted him. It did, however, result in the discussions that took place between the neurologists and the neuroradiologists that took place on 26 March taking place against the background of a perceived continued dispute on the issue of breach of duty. That, I think, may have contributed to the flurry of expert activity on the issue of causation that took place in the run-up to the trial.

The effect of the admission of the allegations of negligence is that it is now accepted that Mrs Carter should have been admitted to hospital on the evening of 6 October for further assessment and observation. It is common ground between the obstetric experts that in that event she would have been seen by a medical registrar by 09.00 the following morning, 7 October. Dr Hardie and Professor Schapira, the neurologists for each party, were agreed that a competent neurologist would have been included CVST in the differential diagnosis that morning and that an urgent CT scan would have been indicated. Dr Molyneux and Dr Forbes, the neuroradiologists for each party, basing themselves at least in part on what was eventually shown on the CT scan carried out later, were agreed that a CT scan carried out that morning would have shown features of a significant increase in raised intracranial pressure with brain swelling and evidence of CVST, namely, thrombosis of cerebral veins. Since it is not known in which area of the cerebral venous system Mrs Carter's thrombosis began - i.e. in the more superficial or in the more deep venous structures – they agreed that it would not have been possible to identify the location of the CVST at that stage. However, they agreed that if the radiologist had been given CVST as part of the differential diagnosis, he or she would probably have agreed that the changes were at least consistent with and probably indicative of this diagnosis and even if there been no notification of CVST in the differential diagnosis, a competent radiologist would again have described the changes and have included some description of the thrombosis. Whilst Professor Schapira in the record of the joint discussion indicated his view that not to have administered Heparin “could be construed as reasonable practice”, he and Dr Hardie agreed that they would each have given Mrs Carter Heparin had CVST been diagnosed that morning, together with other supportive measures as appropriate including rehydration, control of any seizures and therapy to lower raised intracranial pressure. The case has proceeded on the assumption that Heparin would have been given and I have not been invited to consider a notional factual scenario in which it would not have been given. Indeed there was no contra-indication for Heparin in Mrs Carter’s case.

The essential issue is whether, had Mrs Carter been treated appropriately following a notional admission on the evening of 6 October, her death would have been avoided (Footnote: ¹).

For this purpose “appropriate treatment” means the administration of Heparin from about 13.00 on 7 October and any additional supportive measures that would have proved necessary including rehydration, control of any seizures and therapy to lower raised intracranial pressure. The main focus, however, for present purposes is the administration of Heparin.

Heparin is the well known anti-coagulant. It was common ground between the experts that Heparin acts very quickly once it is administered, something confirmed in the literature. It acts by arresting the formation of new thrombus, but does not operate to break down thrombus that has already formed. That process depends upon the body’s own thrombolytic mechanisms. Arresting the formation of new thrombus assists in preventing further development of thrombus in the cerebral venous system and also reduces the associated risk of pulmonary embolism.

Resolving this essential issue depends, of course, on what is known about the efficacy of Heparin in treating CVST generally and its likely impact in particular on Mrs Carter at the time it would have been administered had she been treated properly. Before endeavouring to answer those questions, I should complete the review of the events of 7 October that I began in paragraph 31 because they may have a bearing on the issue I have identified.

In paragraph 31 I dealt with how Mrs Carter appeared to her husband and to his sister during the day until about 18.30 – 19.00. As I indicated, at some time after 18.30 – 19.00 she became uncommunicative in a way that caused Angela Carter cause for concern. I have not received direct evidence from her, but it is not an issue that at 20.21 she telephoned the NHS Healthcall expressing concerns and that at 20.37 she spoke to a doctor who called her in response to her initial call telling the doctor that Mrs Carter was “unconscious”. It was agreed during that telephone conversation that efforts should be made to get her to A&E and as a result Angela Carter made a 999-call which resulted in an ambulance being sent at 20.43, arriving at 20.50.

I need not dwell at length on what happened, but the ambulance crew took the (wholly erroneous) view that there was nothing intrinsically wrong. They interpreted Mrs Carter’s presentation (that she was looking at them but would not talk to them) as being attributable to “the old hormone disturbance”. They asked their control to make arrangements for a GP visit. They left shortly after this.

Simply for completeness, I should record that this episode became the subject of a detailed inquiry by the ambulance service, the outcome of which was the conclusion that the crew had delivered a level of care below acceptable professional standards. An apology was proffered subsequently.

The relevance of the episode for present purposes is merely that it confirms that by the time of the visit of the ambulance crew Mrs Carter was not communicating. Mr Carter told me that he was aware that one member of the ambulance crew telephoned Mrs Carter’s mother (who, as I have said, was with him at Basildon Hospital visiting Bradley) asking that she speak to Mrs Carter to try to get a response from her. I have not heard directly from Mrs Neville but I have no reason to doubt Mr Carter’s evidence that he was told by her that “she could not get any sense out of her.”

At that stage Mrs Carter was not fitting. However, within a little over an hour after the first ambulance crew’s departure at 21.34 she was and this prompted Angela Carter to call the ambulance service direct at 22.35. She told them that Mrs Carter was “now fitting”, she had wet herself and her eyes were rolling. Angela Carter described her as being “completely out of it”.

A second (and different) ambulance crew arrived shortly afterwards. They observed that Mrs Carter was indeed fitting and on arrival assessed her GCS (Glasgow Coma Scale) score as 8/15, with her eye opening being recorded as “nil” and her verbal response as “incomprehensible”. Arrangements were made for her transfer by ambulance to hospital where she arrived at 23.21. She was seen by a doctor at 23.30 and assessed to have a GCS score of 6/15, an assessment confirmed in other examinations carried out over the next hour or so.

For the purposes of the matters I have to consider, I need trace the chronology thereafter no further. Mrs Carter never regained consciousness, was assessed as brain-stem dead and, after consultations with the family about organ donation, she was taken off ventilator support on 9 October. The only matter that needs to be recorded is that a CT scan of Mrs Carter’s brain was taken in the early hours of 8 October and that scan has been the subject of consideration by the neuroradiological experts in this case. I will refer to that below.

In paragraph 30 I concluded that by the late evening of 6 October there had been some progression of the developing CVST, but that there had been no dramatic or significant deterioration. That she spent much of the next day asleep or resting on the settee, but was able to communicate until some time after 18.30, suggests that the gradual progression continued throughout 7 October with a very significant deterioration in a period of 2-3 hours that evening.

The experts accept that the evidence is consistent with a sudden deterioration in Mrs Carter’s condition during the evening of 7 October. In their joint statement they say this:

“… the cause of the sudden deterioration was as a result of the continuing extension of the thrombotic process with secondary haemorrhage, seizures and a further rise in intracranial pressure, which then led to cerebral herniation (“coning”).”

I described the process of coning in paragraph 14. Dr Hardie accepted that by 22.35 on 7 October the progress of the CVST was probably irreversible and that coning would have occurred by then. In paragraph 15 I drew attention to the sequence of events leading to coning and to the “highly variable” clinical course of CVST. I must turn to the expert views about what was occurring in Mrs Carter’s case from the morning of 7 October until coning occurred later that day, though it will be important to bear in mind throughout the uncertainties necessarily generated by the variety of presentations of CVST: see paragraph 18 above.

There are two elements considered by the experts from whom I have heard in their analysis of how Mrs Carter’s CVST developed, namely, the radiological evidence and the clinical course so far as it can be ascertained. I will deal with the radiological evidence first.

Dr Andrew Molyneux, a Consultant Neuroradiologist based at Frenchay Hospital, Bristol, reviewed the CT scan performed 01.20 on 8 October. His conclusion was as follows:

“… there is intracranial bleeding … [the] cause [of which] is thrombosis (clotting) of the veins draining from the deep part of the brain, namely this affects the straight sinus and the deep veins draining the brain. The sagittal sinus also shows evidence of thrombosis. This has resulted in venous infarction and haemorrhage in both basal ganglia, with swelling, secondary subarachnoid haemorrhage and intraventricular haemorrhage.”

Dr Molyneux is a clinical radiologist involved in the diagnostic management of patients with vascular and stroke-like conditions.

Dr Wellesley Forbes, a Consultant Neuroradiologist at Salford Hospital and the Senior Neuroradiologist at the Regional Neurosciences Centre at Hope Hospital, gave a detailed account of what he saw on that scan in his report and summarised his opinion as follows:

“The CT brain scan performed on 08/10/2002 shows evidence of established thrombosis of the deep cerebral venous structures with characteristic features of infarction of the deep grey matter structures, subarachnoid and intraventricular haemorrhage and brain swelling. In addition there was evidence of coning ....”

As will be apparent from that summary, Dr Forbes did not refer to the thrombosis in the sagittal sinus which is part of the superficial cerebral venous system (see paragraphs 12 and 13 above). In cross-examination he acknowledged that this was an omission.

The neuroradiologists have been invited to postulate how a CT scan carried out during the morning of 7 October would have presented. In their joint discussion on 26 March they agreed as follows:

“The neuroradiologists agreed that on the morning of 7 October a CT scan would have shown features of a significant increase in raised intracranial pressure with brain swelling and evidence of CVST, i.e. thrombosis of cerebral veins. It is not known in which area of the cerebral venous system [Mrs] Carter's thrombosis began, i.e. in the more superficial or in the more deep venous structures. Therefore it is not possible to identify the location of the CVST at this stage.”

In the letter of 23 April, to which I referred in paragraph 54, Dr Forbes expressed the opinion that “from a neuroradiology perspective the extent of the damage to Mrs Carter’s brain at 0900 hours on 7 October … was likely to have been serious and irreversible.” He was, therefore, suggesting that by the morning of 7 October, the CVST would have progressed to the extent of causing brain damage and revealing it radiologically. However, he retreated from this position during cross-examination and accepted that imaging carried out during that morning would probably not have revealed anything representing irreversible brain damage. In re-examination he said that the CT scan at that time “might” have shown evidence of damage to the thalami (the two masses of grey matter that relay sensory nerve impulses to the cerebral cortex which lie under or adjacent to the deep venous system), but accepted that he could not say that this was more than merely a possibility.

Professor Schapira did venture a view about the likely radiological appearance of the scan taken in the morning of 7 October in his oral evidence, but that view had not surfaced in the joint statement and I think he would defer to the views of neuroradiologists on this kind of issue. At the end of the day, of course, the radiological appearance of the brain is merely one piece of the evidence of its condition at the time it is taken and since no CT scan was taken during the morning of 7 October, what would have been shown if one had been taken is at best informed speculation. What I take from the evidence of Dr Molyneux and Dr Forbes, bearing in mind the concessions that the latter made, is that from their perspective they were not able to say definitely that the deep venous structures had become significantly affected by thrombus development by that time, nor that it was probable. The highest that Dr Forbes could put it was that it was possible, though he appeared to accept the existence of a factor (namely, Mrs Carter’s ability, despite plainly feeling very unwell, to get up and come downstairs) that tended to undermine the possibility.

Doing the best I can on this material, I conclude, on the balance of probabilities, that whilst there may have been some thrombus development in the deep venous system by the morning of 7 October (which would be consistent with the simultaneous processes referred to in the quotation in paragraph 15 above and possibly with the presumed presence of papilloedema: see paragraph 60 below), it had not developed to the stage of significant occlusion. That did not occur until the evening. Had there been significant involvement earlier in the day, I do not think that Mrs Carter would have been able to get herself up and then bring herself downstairs when she did which, as a matter of fact, I find that she did.

That conclusion addresses the question of whether the progression of Mrs Carter’s CVST had reached the stage of significant deep venous involvement by the morning of 7 October. Dr Molyneux and Dr Forbes had agreed (see paragraph 55 above) that a CT scan that morning would have “shown features of a significant increase in raised intracranial pressure”. Dr Hardie and Professor Schapira had agreed that her neurological condition that morning would have “included headache, drowsiness and papilloedema”, all of which are well recognised symptoms of raised intracranial pressure.

Papilloedema is the expression used to describe swelling of the optic disc caused by raised intracranial pressure. Whilst the postulated presence of papilloedema that morning is a matter for consideration in respect of Mrs Carter’s chances of survival if properly treated (see paragraph 83 below), it does not of itself indicate anything more than the existence of raised intracranial pressure. Professor Schapira would say, as I understood him, that his prediction of its existence at about this time would be a function of the “relatively rapid” rate of progression of Mrs Carter’s CVST and, together with Dr Forbes, “an indication of probable involvement of the deep venous system at [that] stage”. Dr Hardie, on the other hand, saw it as something that would have been demonstrated at that time as part of her “slow” deterioration. At all events, they are agreed that it would have been present on the morning of 7 October and, accordingly, I find, on the balance of probabilities, that it would have been.

As to the suggestion that the postulated presence of papilloedema indicated “probable” involvement of the deep venous system, I am unable to accept that proposition in quite such clear terms. A review of the extensive literature with which I have been provided does not assign the symptom of papilloedema only to those cases where deep cerebral venous system involvement is established. Indeed the Table that I shall annex as Appendix 1 to this judgment (to which I will refer in paragraph 83 below) shows papilloedema as a sign where there is no evidence of deep cerebral venous involvement. I am, as I have indicated, prepared to say that it is possible that there was some deep cerebral venous involvement on the morning of 7 October, but it would, if present, have not been to a significant degree.

I have already alluded to the sudden and dramatic change in Mrs Carter’s status between some time after 18.30-19.00 and 20.30 that evening and to the agreed position of the experts in relation to what caused it in paragraph 50 above. There can be little doubt, bearing in mind what the CT scan a few hours later showed and the well-established effect of significant occlusion of the deep cerebral veins (see paragraph 17 above), that the deep cerebral veins had indeed become significantly occluded during that period of an hour and half or so.

An issue arose as to whether the progression towards this occlusion was substantially a linear process or one which proceeded at a moderate linear rate and then “cascaded” exponentially towards the end. Dr Hardie drew this distinction and characterised Professor Schapira’s approach as favouring the former and he (Dr Hardie) the latter. I am not sure that Professor Schapira necessarily accepted the distinction but it did, I think, broadly reflect the difference between them. Professor Schapira’s position is that the evolution of Mrs Carter’s CVST was rapid and that it escalated quickly to its effective end-point over a period of about 48 hours. Dr Hardie’s view was that the overall progress was slower, but that there was eventually a sudden deterioration which occurred in effect exponentially.

From a layman’s perspective, Dr Hardie’s description fits the symptomatic progression in Mrs Carter’s case, as I have found it to have been, more closely than does a rapid and steady movement towards the end-point of coning. The difficulty I have with accepting it as necessarily the pathophysiological pattern of events is that one would have expected it to have become identified by now as the usual pattern in most cases – or one of the most usual patterns. However, the extensive literature does not support this: there just seems to be no recognised pattern of presentation.

It is for similar reasons that I cannot accept Dr Molyneux’s construction of what happened as necessarily having occurred in this case. I do not use the word “superficially” in any pejorative sense, but his analysis was superficially very attractive. He suggested that the thrombus started in the superficial sinus, causing swelling and raised intracranial pressure, which led to Mrs Carter’s symptoms before the significant deterioration. He characterised the pathological process as progressive but the serious occlusion of the deep venous system did not occur until there was a major obstruction at the confluence of the superior sagittal sinus, the straight sinus and the transverse sinuses (see illustration at paragraph 12). When that occurred, in his construction of events, there would have been rapid involvement of the deep venous system with the serious consequences already identified.

The difficulty with this analysis is that there is no clearly defined pattern of presentation of CVST that can be correlated to the pace and place of thrombus development. It is, of course, a plausible explanation (as Dr Forbes accepted) and indeed it could be said to fit the symptomatic pattern here. But, as Dr Forbes observed, in my view correctly, the pattern fits another plausible explanation (consistent with what Dr Stam recorded: see paragraph 15 above), namely, that more than one vein was involved from the outset.

I have to say that it is, in my view, impossible to conclude, even on the balance of probabilities, what the pathophysiological sequence was in this case. All one can say (and indeed I do so conclude) is that in the evening of 7 October there was a marked change in the symptomatic pattern (which had been broadly stable during the day) which was consistent, and only consistent, with the final total, or near total, occlusion of the deep cerebral venous system which then led to the subsequent terminal events. The crucial issue is whether earlier intervention would have avoided that occlusion whatever the precise pathophysiological sequence may have been that led to it. It is to that issue that I now turn.

The crucial issue as I have described it in paragraphs 38-41 and 68 can be refined further. The question is whether, on the balance of probabilities, the administration of Heparin from about 13.00 on 7 October, in association with any other supportive treatment (see paragraph 39), would have arrested the development of Mrs Carter’s CVST such that the occlusion that occurred between about 18.30-19.00 and 20.30 would not have occurred.

I described the agreed effect of Heparin in paragraph 40 and will not repeat it. Given its relatively immediate impact in terms of stopping the creation of new thrombus, one would think that as soon as it takes effect in a pathological process that otherwise would lead to deep cerebral venous occlusion, its administration ought inevitably to prevent such an occlusion from occurring several hours later. Unfortunately, the position does not seem to be quite as simple as that although the logic behind the administration of Heparin (which Professor Schapira accepted) is something that will have to be taken into account in the final analysis.

In their review article, to which I referred in paragraph 16, Drs Bousser and Ferro, having mentioned the diversity of the presentation of CVT, went on to say this:

“…furthermore, a cause cannot be found in about 15% of cases, the individual outcome may still be difficult to predict, and the disorder may occasionally worsen despite anticoagulation.”

That part of the introduction to their article indicates that there are cases where anticoagulation does not prevent the continued progression of condition. That yields a clue to the debate between Professor Schapira and Dr Hardie in this case. I will deal with that debate below, but it is worth highlighting the areas of agreement before looking at the areas of disagreement.

Studies over recent years have shown that the vast majority of those shown to have CVT survive. In their review article (see paragraphs 16-17 above) Bousser and Ferro say this:

“CVT is now typically recognised as a non-septic disorder with various clinical presentations and a usually favourable outcome, with mortality well below 10%.” (Emphasis added)

Mr Meakin has accepted that 87% with CVST survive. I think that his acceptance of that figure is derived from the ICVST study (see paragraph 76 below) where the “death and dependency rate” (i.e. the proportion of those who died or were significantly dependent because of long-term disability) was 13.6%. However, 87% also represents the survival rate of those in the ICVST study who were shown to have thrombosis of the deep cerebral venous system (see Canhão et al, 2005) which, of course, is what was ultimately demonstrated to be the situation in Mrs Carter’s case.

Whilst the vast majority of those with CVST (and indeed those who have thrombosis of the deep cerebral venous system) survive, it is equally clear that a small minority do not. The general trend established by these statistics (see per Lord Nicholls of Birkenhead in Gregg -v- Scott [2005] 2 AC 176, paragraph 28) is one of survival; but, notwithstanding that proposition, the burden is on the Claimant to establish that, with proper and timely treatment, Mrs Carter would more probably than not have been a survivor rather than a non-survivor.

I have not received any evidence from a medical statistician. Dr Hardie and Professor Schapira have each assisted me with their informed appreciation of the conclusions to be drawn from the statistical material available and I am grateful to each of them for doing so. However, whatever role the concepts of absolute risk reduction, relative risk reduction and the odds ratio may have in other cases, I do not think that, save in one particular area, my decision in this case is going to be assisted by endeavouring to make findings on those matters. In my view, the decision, albeit not a straightforward one, can be made without significant recourse to those considerations. There are one or two statistical considerations of importance, but they are only part of the material I need to consider.

I mentioned the ICVST study in paragraph 73 and I should say a little more about it because it represents an important body of recent learning about CVST. ‘ICVST’ stands for the International Study on Cerebral Venous and Dural Sinus Thrombosis. It was a prospective multinational observational study that involved consecutive patients aged greater than 15 years with symptomatic CVT. Those included in the study became included within it between May 1998 and May 2001 and were followed up from diagnosis to 31 December 2002. A total of 624 adult cases became included in the study from 89 centres in 21 countries. The diagnosis of CVT had to be confirmed by, inter alia, conventional angiography, CT venography or MRI scanning that embraced venous consequences.

The median delay from onset of symptoms to admission to hospital was 4 days. This means that half of the 624 patients (312) came within the category of those whose admission to hospital took place within 4 days of the onset of symptoms. The median delay from onset of symptoms to diagnosis was 7 days.

The patients were defined as displaying an acute clinical course if the period between the onset of symptoms and diagnosis was less than 48 hours, sub-acute if the period was between 48 hours and 30 days and chronic if greater than 30 days. The numbers (and proportions) in these categories were 232 (37.2%), 346 (55.5%) and 45 (7.2%) respectively. It is important to note that over 80% of the series received intravenous Heparin or subcutaneous low-molecular-weight Heparin in therapeutic dosages during what was called “the acute phase”.

The results of the study and the implications of those results were reported and commented on by various members of the Steering Committee and the Coordinating Office of the ICVST. These included Drs Bousser, Ferro, Stam and Canhão.

I will return to certain of those commentaries below, but I should pause to determine where Mrs Carter would have been in this classification. Professor Schapira took the position that her symptoms started with the complaint of headache in the late evening of 5 October and that her status was to all intents and purposes irretrievable 48 hours later. To that extent he would have assigned her to the acute category. Indeed he described her case as “most unusual” and said that the rapidity of the progression of her CVST was at “the extreme short end” of the ICVST spectrum. In one of his reports he had said that her “clinical presentation for CVST was extremely unusual in its very short duration from onset of symptoms to death” and that this “exceptionally rapid evolution…implied an unusually aggressive acceleration progression of events initiated by her CVST.”

Having done my best to evaluate the course of her symptoms, I have concluded that Mrs Carter suffered headaches from at least the morning of 5 October and possibly longer: see paragraph 22 above. This would extend the period relied upon by Professor Schapira by at least 12 hours. If one took the end point of the period that is relevant for this purpose as when the diagnosis ought to have been made (say, about midday on 7 October), the period of 48 hours would have been exceeded, albeit not by much.

It is, in my view, clear that Mrs Carter’s CVST did progress relatively rapidly. However, I cannot accept that it was “extremely unusual” in the rapidity of its evolution. Mr Taylor makes a fair point, in my judgment, when he says that Mrs Carter’s case fell somewhere in the middle of the group of 312 patients whose admission to hospital took place within 4 days of the onset of symptoms. At all events, whilst I am prepared to say that there was relatively rapid progression of the CVST here, it cannot fairly be described as exceptionally rapid given the information emerging from the ICVST study.

Canhão and others analysed the 27 cases of those in the ICVST study who died during their period of hospitalisation. I have reproduced Table 1 from their article in ‘Stroke’ in August 2005 as Appendix 1 to this judgment. The abbreviations used in the table are set out on the frontpiece of the Appendix. The purpose of their analysis was to try to find a predictive model of the patient likely to die during the acute phase. Mr Taylor has relied upon this table to demonstrate that, certainly at the time Mrs Carter ought to have been admitted to hospital (the evening of 6 October) and indeed by the following morning, she possessed none of the combinations of the “symptoms/signs until admission” demonstrated by the patients identified in the table. Professor Schapira, as I understood him, agreed that this was so and also that there was no better general indication of those likely to die during the acute period of CVST than the information contained within the table even though, it must be noted, the authors made it clear that “the individual time course is highly variable in venous stroke” which “partly explains why our predictive model has a low sensitivity.”

Professor Schapira, however, said that the known natural history of Mrs Carter’s CVST could not be ignored. It did lead to her death and, in his view, it would have done so even had Heparin been administered when it should have been. Whilst it might appear unattractive to point to the occurrence of death as evidence that it was going to happen in any event, I can see, and accept, that it is a factor that cannot be ignored in the retrospective analysis that is involved in deciding the issue of causation in this case. It is, sadly, part of the clinical history that cannot be ignored. Equally, however, it is, in my view, legitimate to consider what the general prospects of survival were, on the basis of the best information available, in the period leading up to the time when, but for the admitted negligence, the generally accepted “first-line therapy” (Footnote: ²) [Heparin] should have been administered.

Professor Schapira’s reference to the actual natural history in Mrs Carter’s case is understandable against the background of his clinical experience of CVST which he described in one of his reports as follows:

“Over the last 19 years as a consultant neurologist with regular responsibility for the acute neurology service for a population of 3 million, I have seen many patients with CVST. These are typically tragic cases like Mrs Carter: young women, many of whom are in the later stages of pregnancy or the early stages of the perium. Since the early 1990s it has been my routine practice to anticoagulate these patients. In my recollection most have survived and done well but others have progressed and died despite anticoagulation.”

I do not doubt that this is his genuine recollection of what has occurred in his clinical experience, but it does have to be set against other more cogently collated material in the various research papers. Mr Taylor argued with justification, in my view, that women who go on to develop CVST in the peripartum or puerperal situation are likely to have a good outcome. Dr Hardie had drawn attention to two particular studies in his Supplementary Report as follows:

“22.

Two large studies of stroke in pregnancy and the puerperium have been published in the last decade, both in 2000 in the journal Stroke.

23.

One was a retrospective analysis of more than 1.4 million deliveries in 17 States in the USA in 1993 and 1994, amongst which 183 cases of peri-partum stroke and 170 cases of peri-partum CVT were observed (Lanska & Kryscio, 2000). It was based on the US nationwide sample of 20% of all community hospital discharges in those two years. In contrast to the cases of arterial stroke, of which 29 (15.8%) died, none of the 170 CVT cases died.

24.

In another retrospective study (Jaigobin & Silver 2000) all cases admitted to the Toronto Hospital with stroke during pregnancy and the puerperium were identified over a period of more than 17 years. There were about 50,700 admissions for delivery during this period amongst which 13 arterial strokes and eight venous strokes (i.e. CVT) were identified, and there were no deaths. Seven of the eight venous strokes occurred post-partum.”

Professor Schapira did not challenge this analysis in his response to that report.

I need prolong this analysis no further. It seems to me that, viewed prospectively at the time she should have been admitted to hospital on 6 October, Mrs Carter would have been predicted as having an excellent prospect of survival. Indeed the only difference between then and when Heparin should have been commenced the following day was, as the experts agreed, that she would have developed papilloedema the following morning as a result of the raised intracranial pressure and would probably have been drowsy also. The evidence does not suggest that this, either in isolation or in association with headache, represents a predictor of death. I have found as a fact that until the evening of 7 October she was capable of communicating in a way that did not cause concern.

So what caused Mrs Carter to die despite the apparently optimistic prospective position even up to midday or thereabouts on 7 October? Was it simply the natural history of her CVST which ran, as it were, against the run of general experience? Was she one of the small minority destined to die irrespective of any treatment offered? Or was it the failure to administer Heparin from about 13.00 on 7 October?

Of the 27 deaths considered by Canhão and others (see paragraph 83 above), 25 of those who died had been treated with Heparin – “a similar proportion compared with those who survived.” Mr Meakin submits that this is a critical matter and establishes that Heparin does not prevent the death of those whose cases were serious enough to have died without treatment. I agree that it (and indeed material from other papers) evidences the proposition that there are cases where even the timely administration of the “first-line therapy” for CVST makes no difference. I do not think that that has been in issue. But there seems to me to be a risk, if the proposition is pursued too far, of the complacent response that in every case where there is a death from the direct effects of CVST in the absence of Heparin that its administration would have made no difference. Plainly, as Mr Meakin has forcefully submitted, it is important to look at each individual case of CVST albeit in the context of what is known about the general trend of such cases.

Mr Taylor was justified in his submission that Mrs Carter did not fit the symptomatic pattern of the 27 in the ICVST study who died. There is also no evidence of anything else about her physical makeup that would suggest that she was in a vulnerable category. Indeed, she was young and fit – and indeed, of course female which itself puts the general CVS victim in a better prognostic category (see Ferro and others, March 2004). Given my finding that the onset of her symptoms, though relatively rapid, did not mark her out as being in some exceptionally unusual category, and bearing those prognostic factors in mind, the question “is it more likely than not that she would have survived if properly treated?” is to be answered affirmatively.

She did not receive proper treatment in the form of Heparin therapy for a period of about 5 – 6 hours before the significant change in her condition in the evening of 7 October. It is said on behalf of the Defendant that since the benefit of Heparin has not been proven in the generality of cases I should not hold that it would have made a difference in this case.

Although the literature has been subjected to close scrutiny by both Dr Hardie and Professor Schapira, and indeed by Mr Taylor and Mr Meakin, there is no issue that the efficacy of Heparin in the context of treatment for CVST has not been proven to the 95% confidence level. That is the level of statistical significance habitually used in the medical world to exclude the possibility that when something occurs it does so by chance rather than by reference to some assumed state of affairs: see generally Loveday -v- Renton and Another [1990] 1 Med LR 117 and Temple -v- South Manchester Health Authority [2002] EWCA Civ 1406. In some situations (see, e.g., Temple -v- South Manchester Health Authority) the 95% confidence level is equated with proof to the “standard of scientific proof” although Stuart-Smith LJ in Loveday -v- Renton said that there was no “generally accepted” scientific standard. At all events, it is plain from those cases (and was not disputed in this case) that a court, when applying the civil burden of proof, is not bound by propositions that need to be established to that level of proof for other purposes.

In his written Closing Argument, Mr Taylor produced a detailed analysis of all the papers touching on the issue of efficacy of Heparin to support the proposition that “the overwhelming preponderance of opinion [is] that Heparin works.” He will forgive me if I do not set out his analysis in detail. For my part, I think I need go no further than to quote the analysis contained in the EFNS (European Federation of Neurological Societies) ‘Guidelines on the Treatment of Cerebral Venous and Sinus Thrombosis’ published in the European Journal of Neurology in 2006 (of which journal, incidentally, Professor Schapira is the Co-Chief Editor). The authors of the guideline include Einhaupl, Bousser, de Bruijn, Ferro and Stam. In their analysis they referred to two trials, one published by Einhaupl and others in ‘The Lancet’ in 1991 and the other by de Bruijn and Stam in ‘Stoke’ in 1999, and to the meta-analysis of those two trials by Stam, de Bruijn and another in 2002 (under the auspices of The Cochrane Collaboration). The EFNS guide said this:

“A meta-analysis of these two trials showed that the use of [anticoagulation] led to an absolute risk reduction in death or dependency of 13% (confidence interval -30 to +3%) with a relative risk reduction of 54%. Although this difference did not reach statistical significance both trials showed a consistent and clinicably meaningful trend in favour of [anticoagulation] and demonstrated the safety of anticoagulant therapy. Thus, data from controlled trials favoured the use of [anticoagulation] in patients with CVST because it may reduce the risk of fatal outcome and severe disability and does not promote [intracranial haemorrhage] at least in the small number of patients in the trials.”

The Cochrane Collaboration paper itself had concluded that anticoagulant therapy “was associated with a pooled relative risk of death of 0.33 (95% CI 0.08 – 1.21)” the effect of which, as Dr Hardie said, was that those who received Heparin risked death at one-third the level of those who did not – or, putting it the other way round, that those who did not receive Heparin were three times more likely to die than those who did. As I understood him, Professor Schapira did not challenge that statistical analysis, but pointed (perfectly fairly in my view) to the relatively small numbers in the cohorts considered.

The authors of the paper do comment that although “the estimated pooled risk reductions did not reach statistical significance, patients and doctors may be reluctant to embark on a new trial that involves a placebo group.” Translating that observation into the realities of scientific life means that it is very unlikely that there will ever be a research series carried out prospectively that will reveal to the 95% confidence limit whether Heparin does alter the outcome in these cases. As I observed during the hearing, given the perceived benefit of Heparin administration, it would almost certainly be regarded as unethical to develop a trial that involved some patients receiving Heparin and others not receiving it for the purposes of trying to see whether death or dependency is prevented by the administration of Heparin. The consequence of this is that if a court felt itself bound to act on evidence that demanded statistical cogency to a 95% confidence limit, no claimant negligently deprived of Heparin would ever succeed at the causation stage.

In Temple -v- South Manchester Health Authority, upon which I invited the assistance of both Counsel, the Claimant was unable to establish that the negligent treatment (the administration of a fluid infusion of incorrect salinity) caused the cerebral oedema that led to his disabilities. The Claimant’s experts had agreed with the Defendant’s expert that it was not possible to say whether the cerebral oedema would have been avoided by an infusion of different salinity, but they did so applying the 95% confidence limit. They suggested that had they applied the balance of probabilities test their answers would have been different. The Judge preferred the evidence of the Defendant’s expert who said that, even applying the balance of probabilities test, it was impossible to say whether a different strength infusion would have altered the outcome even though that other strength infusion would have been regarded as the strength of infusion of choice to deal with the situation with which the clinicians were presented.

In the present case Professor Schapira, who I think in this particular case had difficulty in readjusting his focus from the 95% confidence limit approach to the balance of probabilities test, adhered to his view that it could not be proved that Heparin makes any difference in any case and, in particular, that it would not have made any difference in this case because of the unusually aggressive nature of the development of Mrs Carter’s symptoms.

Dr Hardie, on the other hand, adhered to his view that, if treated at or about the time I have found that she should have been treated, on the balance of probabilities Mrs Carter would have survived and gone on to make a full recovery.

Whilst I have not found the issue an easy one, I broadly accept Dr Hardie’s approach, though I would summarise my conclusions in this way:

I think it is reasonable in those circumstances and against that background to hold and infer that Mrs Carter would more probably than not have survived had Heparin been administered at or about 13.00 on 7 October. She would have been spared the best part of 5 or 6 hours of continued thrombotic development (which would have added cumulatively to what had already occurred) during a period when, albeit feeling distinctly unwell, she was capable of communicating and would have received this treatment hours before the eventual total, or almost total, occlusion of her deep venous system.

On that basis, and for those reasons, the claim succeeds on the issue of causation.

Although I had received evidence and heard some submissions on the issue of damages during the trial, it was agreed during the closing submissions that the issue would await the result on causation. In the absence of agreement on the issue of quantum, I will entertain further argument about it, either in written or oral form, depending on the wishes of the parties.

As I have indicated, this is not an easy case. This judgment has been far more lengthy than I had intended when I embarked upon it. However, there has been a considerable body of literature to consider and there have been extensive written and oral submissions from both Counsel to whom I express my genuine appreciation for their assistance thus far. I am conscious that I have not addressed each matter they have raised. However, I have addressed those issues that have seemed to me to be of importance in reaching a decision on the central issue. I am grateful also to their respective Instructing Solicitors for collating much of the relevant documentation in the case in an electronic form and for supplying it to me in that form after the hearing was concluded.

Mental, MD indicates mental disorder; L, left; R, right; Hem, hemorrhagic; inf, infarct; SAH, subarachnoid haemorrhage; post, posterior; bilat, bilateral; SSS, superior sagittal sinus; SS, straight sinus; LS, lateral sinus; CV, cortical vein; DVS, deep cerebral venous system thrombosis; ALL, acute lymphotcytic leukaemia; LP, lumbar puncture; OC, oral contraceptive; APCr, activated protein C resistance; MEA, multiple endocrinopathy adenomatosis; ENT, ear-nose-throat infection; and MD, missing data