Hearne v The Royal Marsden Hospital NHS Foundation Trust

The Claimant Mark Hearne claims damages for clinical negligence arising out of his treatment at The Royal Marsden Hospital, Sutton after admission on 28^th June 2010 for management of epigastric/abdominal pain following a first cycle of adjuvant chemotherapy. Whilst in hospital on 2 July 2010 the Claimant suffered a pulmonary embolism.

Damages are agreed subject to breach of duty and causation. Limited admissions have been made as to breach of duty. It is accepted by the Defendant both that it should have carried out a Venous Thromboembolism (VTE) risk assessment by 29.6.10, and that it should have provided anti-embolic compression stockings. All other allegations of breach of duty and causation are in issue.

The Claimant, aged 59, developed bladder cancer in May 2010 for which he underwent a transurethral resection on 21.5.10 followed by a first cycle of neoadjuvant chemotherapy on 24.6.10. He was discharged home the following day. When he returned home he began to feel very unwell, with stomach pain and a feeling of sickness. He was in such pain that he spent most of the day immobile on the couch. The pain persisted and got worse.

The Claimant was admitted to the Hospital on 28.6.10 and whilst it was noted on arrival that he was ambulant, his evidence, and that of Mrs Hearne, who drove him to hospital was that she fetched a wheelchair and wheeled him in to the hospital. He was able to transfer from the chair to the bed.

The notes of the admitting doctor at 22.00 record complaints of a 3 day history of abdominal pain, mainly in the epigastrium but also spreading down to the lateral abdominal wall bilaterally. The pain was noted as getting worse, then settling, although not completely. It was noted that he had had a peptic ulcer in 1976 which had been treated. A further note records no DVT. The doctor’s impression was of colicky abdominal pain due to a number of possible causes.: in order in the notes, chemotherapy induced, an illegible reason, a GI ulcer, which is followed by the word “unlikely” in brackets. An abdominal X-ray was performed that night and identified constipation.

The following morning on 29.6.10, Mr Hearne was reviewed at 09.00 by Dr Crane who noted that the pain had moved from being epigastric, and was now over the low abdomen, although on examination tenderness was worse over the epigastrium and LIF. The Claimant’s fluid intake the previous day was noted as was a history of being prone to constipation. Tests were carried out and there was raised urea of 8.6. An xray showed the bowel was not impressively overloaded. A rectal examination showed there was no blood or malaena. Dr Crane’s diagnosis was constipation secondary to dehydration and he prescribed Movicol, more fluids and a change of pain killers. There is no mention in the notes of any consideration of heparinisation.

At 10.30, the Claimant was assessed by Dr Welsh, Specialist Registrar, but the notes were completed by Dr Crane. In a relatively short note. Dr Welsh is recorded as diagnosing chemotherapy-induced constipation with dehydration. The note records “ consider OGD”.

A letter was sent the same day by Dr Crane to Dr Andreyev, a Consultant Gastroenterologist requesting an OGD – endoscopy. I will return to the contents of the letter. It appears to have been sent some time after 13.07, by fax indicating it was Urgent. There is a manuscript note of Urgent on the copy of the letter in evidence, and a fax was sent by the endoscopy unit to the Robert Tiffany ward in which the Claimant was receiving treatment at 16.35 indicating that the endoscopy would be carried out at 11 am on 30^th, the next day.

The Claimant was seen by Dr Crane at 9.00 . Mr Hearne reported increased pain from his abdomen, which he described as being similar to pain in the peptic ulcer felt previously. He reported a short lived epistaxis – nosebleed, that morning and Dr Crane reported “ FBC, clotting sent this am.”. Dr Crane noted the Claimant was going for an OGD and then “R/V on return”.

The endoscopy was performed at the Defendant’s Fulham Road site. The report was written up and timed at 13.28. Investigation identified a moderate sliding hiatus hernia, a number of small antral erosions and mild erythematous duodenitis with several small erosions believed to be most typical of non-steroidal anti-inflammatory medication use. The recommendation was to alter the Claimant’s medication.. The results of further tests were to be provided on 1^st..

The Claimant returned to the Sutton site at approximately 16.30 and was seen by Dr Crane at 17.10. Dr Crane recorded that the Claimant vomited on the way to and from the Fulham Road, and that he had amnesia of events. He set out the findings of the report, which had by that time been received. He instituted the proposed drug regime. There is no mention of heparinisation.

The Claimant was reviewed by Dr Crane at 9.50 am and the pain, now epigastric, remained severe. The Claimant vomited during examination. Dr Crane’s impression was that he had known mild gastritis/duodenitis, but was remarkably tender. He queried whether there was a UTI and asked for repeat tests and a monitoring of fluid balance. At a further review with Dr Hateca at 11.45, the Claimant reported feeling much better., pain improved, but still in the epigastrium building up over a couple of hours. Chemotherapy was postponed for the nausea to settle.

On 1.7.10, the clinical records state that the Claimant was fitted with thigh length stockings at 13.00. This is disputed by Mr and Mrs Hearne. There is no narrative mention of this in the nursing or doctors’ notes at this time.

At 1300 the Claimant was seen again by Dr.Crane and reported feeling much improved. The pain had settled and he was for chemotherapy, although there was mild epigastric tenderness.

However, at 17.40 he collapsed and subsequently was diagnosed with a pulmonary embolism which was confirmed on CT scan. There is a note at about 18.40 which says “ his TEDS stocking on. No evidence of DVT”. He was commenced on therapeutic LMWH and admitted to the coronary care unit, following which he was discharged home on 5.7.10.

On10.9.10, the Claimant was admitted for surgery and underwent a cystoprostatectomy. In order to prevent further pulmonary embolism, inferior vena cava filters were inserted pre-operatively. Unfortunately, he developed chronic occlusion of the filters resulting in bilateral leg swelling on 27.9.10 due to extensive DVT.

It is agreed that the test to be applied is that in Bolam v Friern Hospital Management Committee [1957] 1 WLR 583 at 587:

It is further agreed that the Bolam test was qualifiedin Bolitho v City and Hackney Health Authority [1997] UKHL 46; [1998] AC 232 where .Lord Brown Wilkinson stated:

I have also been referred toC v North Cumbria University Hospitals NHS Trust [2014] EWHC 61 at [25] where Green J summarised the principles to be drawn and applied from Bolam and Bolitho.

There are two relevant sets of Guidelines, the NICE Guidelines published in January 2010 which are applicable across all disciplines, and the Royal Marsden’s own Guidelines.

The NICE Guidlelines provide as follows

The risk factors for VTE present in Box 1 were that the Claimant had been admitted as a patient receiving cancer treatment, he was 59, not 60, his mother had died aged 80 of a pulmonary embolism, he was dehydrated on arrival. He had been relatively immobile prior to admission and because of the pain he was suffering might have been expected to have reduced mobility over the next few days. He should, following this Guidance, have been assessed on admission and then after 24 hours. He had none of the factors in Box 2.

The Royal Marsden Hospital Guidelines (RHM) provide

The Claimant had a history of peptic ulcer in 1976, some 34 years earlier, but no other contra-indications for heparin.

The central issues are:

I turn to consider the evidence in relation to the aspects of breach of duty which are not admitted and in doing so firstly consider the evidence as to whether the Claimant had and/or complained about pain in his left calf in the days prior to the embolism.

Mr Hearne’s evidence prior to trial was that he informed the nursing staff on several occasions about pain in his calf. He said that a nurse looked at the calf, felt it and that it was hot. Nothing further was done about it. In evidence he frankly admitted that his memory was poor - no criticism of him for that - and he thought on reflection that it must only have been once he mentioned it. He was reliant on his wife during the course of his evidence, looking to her for reassurance and confirmation. Mrs Hearne also said that the pain in calf was mentioned to the nursing staff. Of significance she told the court that she had had a number of DVTs herself, but that when her husband complained of pain in the calf, this had not rung a bell with her. Mr Hearne had been in hospital a month previously, during which he had had TED stockings and prophylaxis. Mrs Hearne reproached herself for not realising the significance of the pain and not insisting on further consideration of it.

I find that it is unlikely that the pain was mentioned to the nursing staff as suggested. Mr Hearne was suffering from acute pain in his abdomen and that was overriding concern over any other pain he may have felt. Overall I conclude that it is more likely than not that after the PE, as noted in the notes, Mr and Mrs Hearne mentioned it for the first time. I consider that Mr Hearne’s memory of this is affected by Mrs Hearne’s anxiety and feelings that more could have been done. She should not reproach herself. Nonetheless, no mention was made to staff during this period.

I also find that Mr Hearne was suffering from some pain in his calf for some days prior to the PE, although it is not clear how many. I will return to this in dealing with issues of causation.

It is common ground that if here were no breach until 1 July, it would have been too late to prevent the PE. I start with the factual evidence, then medical literature and expert opinion.

Dr Welsh gave evidence. Although it had been conceded by the Defendant that a VTE should have been carried out by 29 June, he was reluctant to accept that no assessment had taken place. He said that an assessment could be informal and not noted, and maintained that he would have considered heparin on 29 June. The note of his ward round was completed by Dr Crane, and Dr Welsh was critical of the brevity of the note, which he concluded was a as a result of Dr Crane coming to the bottom of the page and running out of paper.

Dr Welsh said that the letter to Dr Andreyev, also written by Dr Crane, was a more complete summary of his assessment at the time. The relevant parts of the letter are as follows

“He has.....a vague history of peptic ulcer disease managed by the GP many years ago and which is treated with omeprazole .

He was mildly dehydrated with a urea of 8.6, creatinine 79. His amylase was very slightly raised at 137.

He has been reviewed by the registrars on our team today ( Dr Liam Welsh and Dr Charlie Comins) who found that an OGD is indicated to rule out a flare of a peptic ulcer causing his symptoms and also to complete GI screening in view of his uncommon histology on biopsy. We are treating him for constipation and giving rehydration fluids. His blood counts are currently normal but will be expected to fall with chemotherapy and so an OGD sooner rather than later would be desirable from this point of view...”

Dr Welsh said that the letter showed his concern about bleeding, in particular the raised urea and amylase. The upper GI symptoms may have had some connection with Mr Hearne’s cancer, and therefore cancer had to be excluded as a cause of the pain in his stomach. Dr Welsh agreed that the focus was on the acute symptoms, and that the notes do not demonstrate that that the risk of DVT was a being considered. He conceded that the letter to Dr Andreyev could have been clearer in indicating that one of the purposes of the endoscopy was to rule out bleeding, as a contra-indication for heparin.

Dr Welsh was not aware of the NICE Guidelines at the time, but knew of the internal RMH Guidelines, which he thought were in two documents and over-complex. It was routine to consider heparinisation in the case of cancer patients who had, as a group, an elevated risk above the general population, and he would have done so. In this case, in his view the balance of risk was clear cut. On the basis of the evidence available to him on 29 June, the risk of bleeding was in excess of the risk of developing DVT. Mr Hearne had epigastric pain with raised urea and amylase, which was best explained as secondary to peptic ulcer disease.

Dr Crane did not give evidence. His notes indicate that prior to Dr Welsh being involved, he thought that the pain was caused by constipation secondary to dehydration. Neither his notes of Dr Welsh’s ward round nor the letter to Dr Andreyev refer to bleeding or consideration of heparinisation. Once the endoscopy results came back, Dr Crane’s view, as expressed in a later discharge letter to Dr Ferguson, was that the endoscopy ruled out “active ulceration”. This is consistent with his notes which referred to mild gastritis/duodenitis and considered an alternative cause of the pain to be a possible UTI (urinary tract infection.

On the evidence I conclude that it is most likely that neither Dr Welsh nor Dr Crane considered heparinisation on 29^th June or thereafter. Consequently, they did not carry out any balancing between the risks of DVT and PE and the only contra- indication for heparinisation, active bleeding or a risk of bleeding. They were concentrating on finding the cause of the acute pain Mr Hearne was suffering, and the notes show that concern. I do not accept that the letter to Dr Andreyev shows concern over bleeding in the context of consideration of heparinisation. Whilst supported to some extent by Dr Plowman, and to a lesser extent by Dr Baglin, Dr Welsh’s insistence that the letter should be viewed in that way is untenable when seen in the context of the notes overall, both before or after the endoscopy. His blaming of Dr Crane for deficiencies in the notes and letter in this respect pre-supposes he both considered heparin, and informed Dr Crane of his views. If Dr Crane had been told by a more senior doctor, and asked to write to the gastroenterologist with that in mind, it is likely it would have been at least clear, if not prominent in the notes and letter. Further, if he was still concerned after the endoscopy about mild duodenitis and small antral erosions contraindicating heparin because he thought they were a risk of bleeding he would have said so in his note at 1710 on 30^th June.

It is significant that after Dr Crane relegated the possibility of a peptic ulcer further down the list of causes for the pain, heparin was still not being considered, as evidenced by the Notes, even though Mr Hearne had been relatively immobile for some days. He was in fact never prescribed in the 5 days prior to the PE in the evening of 2 July.

Expert evidence was given by oncologists Professor Taylor and Dr Plowman, by vascular consultants Mr Coleridge- Smith and Mr Brearley, and by haematologists Dr Keeling and Dr Baglin.

As a preliminary point Mr Woolf submitted on behalf of the Defendant that Mr Coleridge Smith’s evidence as to breach of duty should be discounted entirely on a number of grounds. Firstly, his expertise is as a vascular consultant not an oncologist, and although he may have some interest in DVTs, his work in this area was over 20 years ago, and academic rather than practical. His papers, set out in his full CV, are therefore of little relevance to the issues in this case. Further, since the late 1980s he has not held a Consultant position within an NHS hospital which brings him into contact with patients on a regular basis. His evidence was based on a reading of the literature, which was not a proper basis for expressing opinions on other disciplines. Mr Brearley had declined to give such evidence, feeling he was not qualified to express a view about a discipline outside his own.

Whilst as Mr Dyer submitted for the Claimant, the NICE Guidelines do apply to all disciplines, it was accepted by all experts that they are Guidelines, and do not exclude the need for the exercise of clinical judgment in individual cases. I accept the point that Mr Coleridge Smith’s lack of experience specifically with oncology patients – whose risks as a group of developing DVT are raised above those of non-cancer patients – and lack of recent experience of making such decisions within an NHS hospital detract from the strength of his evidence. As Green J said in C ( above) at paragraph 25(vi)

“In the context of allegations of clinical negligence in an NHS setting particular weight may be accorded to an expert with a lengthy experience in the NHS. Such a person expressing an opinion about normal clinical conditions will be doing so with firsthand knowledge of the environment that medical professionals work under within the NHS and with a broad range of experience of the issue in dispute. This does not mean to say that an expert with a lesser level of NHS experience necessarily lacks the same degree of competence; but I do accept that lengthy experience within the NHS is a matter of significance. By the same token an expert who retired 10 years ago and whose retirement is spent expressing expert opinions may turn out to be far removed from the fray and much more likely to form an opinion divorced from current practical reality”

I therefore find both vascular consultants evidence on the issues of breach of duty to be of little assistance at all, a view expressed by Mr Brearley himself.

I now turn to the question: Had a competent VTE assessment been carried out on 29^th June, what would have been the outcome? Evidence was given in this respect by oncologists and haematologists,

Professor Taylor and Dr Plowman had similar experience as oncologists, different approaches and views, but had reached significant agreement in the Joint Statement

Professor Taylor said that it would have been reasonable to leave the VTE assessment to the morning of 29^th June. He would not expect a junior doctor to be familiar with the NICE Guidelines at the time, but would have expected him to be familiar with his own hospital Guidelines. As the RHM Guideline provided that in a complicated case advice should be obtained from a Haematologist that should have been done in this case. In his view the presence of epigastric pain of uncertain cause and several risk factors made this a complicated case which justified this course of action.

Professor Taylor did not accept that the endoscopy was sought as consideration was being given to bleeding as a contra-indication for heparin, as the notes and letters gave no indication of it. He said that raised amylase was an indication of pancreatitis which was low on the list of causes for the pain in this case. It was reasonable to ask the advice of an expert in gastroenterology to assist with the cause of the pain, but that should not have been an alternative to referral to a haematologist.

In his report Professor Taylor said

“it would not have been regarded as negligent for an oncology team to consider that the presence of undiagnosed epigastric pain for which peptic ulceration was a diagnostic possibility constituted a risk of bleeding which would have swung the balance against the use of LMWH”;

Although he had agreed in the Joint Statement that peptic ulcer was high on the list of causes for pain, he qualified that and said it should have been significant rather than high. He said that the presence of risk complicated matters so that there should have been referral to a haematologist for specialist advice. He did not consider that the referral to the gastroenterologist in the terms in which it was put was an adequate substitute.

A VTE should have been done following the endoscopy, On a balance of probabilities he considered that following either or both of the NICE Guidelines and RHM Guideline heparin should a have been started on 29^th following a competent VTE. When the endoscopy results were known that would not have led to it being stopped.

Dr Plowman expressed the view that there was an active peptic ulcer and the letter to Dr.Andreyev made clear that bleeding was being considered. The ulcer was a contra- indication for heparin as there was a risk of bleeding, even if no actual bleeding. He did not accept that the endoscopy ruled out the presence of an ulcer as he considered there was little if any difference between erosions and a superficial ulcer. He agreed that had the NICE Guidelines been followed, on a balance of probabilities Mr Hearne would have been given heparin on 29^th June. However, as he put it “not on my watch”. His view was that but for the active peptic ulcer heparin would have been given, but if that was excluded there was no other contra- indication. He did into consider that this was a complicated case.

I found Professor Taylor to be thoughtful about his views, on occasion to the point of vagueness, On the contrary Dr Plowman was combative and had researched aspects of the case which had arisen whilst he had been listening to the evidence. On several occasions he sought to enter the fray and argue the Defendant’s case as if he were Counsel rather than an independent expert. Thus neither was an overwhelmingly impressive witness.

On the other hand, both haematologists were good witnesses, high in expertise and in their careful approach to the evidence in this case. They had considered medical literature on the issues, to which I will refer briefly, as in the end, there was very little disagreement between them on the import of the literature.

On issues of breach of duty, Dr Keeling’s view was that on 29 June there was no real indication that bleeding was being considered by the doctors in this case. There was no evidence of bleeding when the Claimant was admitted. The NICE literature found a 1.57% increased risk of major bleeding with LMWH which Dr Keeling considered low. ON the other hand Mr Hearne had a number of risk factors for DVT, and where there are multiple risk factors, this multiplies the risk , rather than increasing it by adding the factors together. In his opinion Mr Hearne was at very high risk of venous thrombosis. Dr Keelingreferred to NICE guidance which estimates that the effect of the use of LMWH reduces the risk of DVT by 53% and PE by 59% . Further meta- analysis estimates the reduction at 60%.

Der Keeling said that he received calls for advice regularly from other disciplines, but was very reliant upon the information which was given to him. If he had been told that there was a risk of peptic ulcer bleeding and asked if heparin should be held off for 24 hours, he would agree. But had the risk factors for DVT present in Mr Hearne’s case been included in the information as well he would have given heparin and believed most doctors would too. He agreed, however, that if Dr Baglin would not, that would be indicative that some people, although a minority, would not.

As far as 30^th June was concerned after the endoscopy results, because there was no peptic ulcer or lesions rather than erosions, there was no more than a risk of a risk of bleeding, and the cause of that was receiving treatment. Therefore there was no need to hold back heparin.

Dr Baglin said that he would not have expected to be contacted on a case like this which was not complicated. If he were called, and told there was severe epigastric pain and peptic ulcer was on the list of contra indications, he would consider not giving heparin to be reasonable, if the risk of DVT was not overwhelming. Dr Baglin did not consider Mr Hearne to be at the top of the high risk category. The fact of his mother dying of PE in her eighties would not worry him. The type of cancer Mr Hearne had was not a high risk for metastasis. Dr Baglin did not think that the previous history of peptic ulcer in this case was a factor he would have thought important. What was important was that there was severe epigastric pain.

Dr Baglin adopted Dr Keeling’s view that what he was told was crucial to any decision as to whether to give heparin or not. In this case, if he had been told that the pain was due to constipation and the effects of chemotherapy, he agreed that heparin could be given. But if there were no peptic ulcer, but a possible source of GI bleeding it would be reasonable not to do so. When he was asked about the admission note that the pain was unlikely to be caused by the peptic ulcer, he said that in that case it was so straightforward that he would not expect a call and heparin should be given. If there were no real worries about bleeding as a result of a peptic ulcer then any reasonable haematologist would have prescribed heparin on 29^th and would have fallen below the appropriate standard had they not done so. On the other hand , if there was real concern about the cause of the pain, even after the endoscopy on 30^th he would have considered it reasonable to withhold heparin, treat the condition and when the pain abated, give heparin.

In his report Dr Baglin expressed the view that heparin lowered the risk of developing DVT by less than 50%. He relied on a paper by De Nisio, a study of outpatients (ambulant patients) who were at a much lower risk of DVTs because of their mobility .In cross examination Dr Baglin agreed that the NICE study gave the best idea of the statistical likelihood of Mr Hearne developing DVT in hospital. He accepted that had Mr Hearne be heparinised it would have reduced the risk by more than 50%. Candidly, he accepted Dr Keeling’s analysis that the more risk factors a patient has, the risk is magnified overall, and that he had fallen in to a “type 2” error in his interpretation of the statistical data in underplaying the degree of reduction of risk by heparin and in his reference to the study of asymptomatic DVT.

Neither Dr Keeling nor Dr Baglin thought that TED stockings would have made any significant difference to the development of DVT, but if heparin was given, they should also have been provided, perhaps more in hope than expectation.

Having considered the evidence of the experts in the context of the factual evidence and the literature, I have come to the following conclusions.

Overall, I preferred the evidence of Professor Taylor to that of Dr Plowman, for the reasons previously given. In fairness to Dr Plowman, he appears to have initially thought he was being asked to provide a report into what happened in the latter stages of Mr Hearne’s treatment for the PE, rather than prior to it, and that might have affected his approach to the issues in this case. I also found the evidence of Dr Keeling to be more logical when considered against the statistical analysis in the literature. Whilst Dr Baglin gave ground on this issue and accepted flaws in his report and approach, Dr Keeling was clear from the outset, and to a large extent, Dr Baglin agreed with his views.

Having concluded that Dr Welsh and Dr Crane did not consider whether heparin should be given on 29^th, I reject Dr Welsh’s evidence that he did so. I consider that he has reconstructed with hindsight what he should have done, rather than what he actually did. I conclude that the likelihood, on a balance of probabilities, is that had Dr Welsh done so, he would have taken into account the RHM’s own Guidelines, if not the NICE Guidelines, and would have concluded that Mr Hearne was at a high risk of developing DVT. He would have still wished to exclude the possibility of a flare of peptic ulcer as a cause of the symptoms of pain and would have asked for an endoscopy. I accept that whilst Dr Crane may have thought that a flare of the peptic ulcer was unlikely, Dr Walsh was sufficiently concerned to order an endoscopy to exclude the possibility. I accept the evidence of Professor Taylor and Dr Plowman that a reasonable oncology team could have considered that the presence of undiagnosed epigastric pain for which peptic ulceration was a possibility constituted a risk of bleeding which would have swung the balance against the use of LMWH. The alternatives at that stage were to exclude that possibility prior to commencing heparin by awaiting the outcome of the endoscopy, or to follow the RHM Guideline and consult a haematologist.

I find that at the stage of the request for an endoscopy, peptic ulceration was considered a possible cause, the clear preference being for constipation combined with either dehydration or chemotherapy. There was no sign of any active bleeding. What was most of concern was the pain. I find also that Mr Welsh sought in evidence to play down Mr Hearne’s level of risk of developing DVT and that had a competent VTE been carried out, it would have concluded there was a high risk, even if not in the highest possible category. I bear in mind that awaiting the outcome of the endoscopy could be supported by a reasonable body of medical opinion, represented by Dr Plowman and Dr Beglin. Dr Keeling accepted that though a minority, some doctors would have held off giving heparin when in possession of the facts in this case.

However, as all the experts agreed, the decision depended very strongly on the information available, and the recognition and the balancing of competing risks, which were not static. The reasonableness of a decision to hold off giving heparin until the results of the endoscopy might depend on how long it took to get those results. Whilst they are Guidelines, and differ from the NICE guidelines, the RHM guidelines take into account the particular risk of a patient group with by definition higher risk of developing DVT, and more possibility of complication than in general. As Professor Taylor said, the reason for speaking to a haematologist is that he or she would have more experience in a wide range of situations arising in a number of specialisms rather than only in the context of cancer. There were a number of possible causes of the pain under consideration at the time. .

I find that on a balance of probabilities, (despite Dr Welsh’s evidence to the contrary, coming as is does after the event,) after a competent VTE , and having taken the decision to ask for an endoscopy, Dr Welsh or Dr Crane would have concluded that Mr Hearne was a high risk patient, and consulted a haematologist at the same time, to discuss the risks. If the effect of requiring assistance from a gastroenterologist to eliminate a possible cause of pain, was to hold up the otherwise strong case for heparinisation, there were sufficient complications to require consultation with a haematologist. Whilst the Guidelines are not mandatory, they represent good practice in a renowned cancer hospital and some good reason for departing from them would be required. Dr Plowman agreed that a consideration of the NICE Guidelines would have led to heparinisation, although not by him.

Dr Baglin did not consider this a complicated case, largely because had he been told the views expressed by both doctors in the Notes as to the likely cause of pain, and been led by their views, he would have said that heparin should have been started, and would have been surprised to have been asked at all. Absent a real concern about bleeding the indications for heparinisation were extremely strong.

I find on a balance of probabilities that had a competent VTE been carried out, and had Dr Welsh or Dr Crane consulted a haematologist as they should, setting out their views as expressed the notes, heparinisation would have been advised and commenced on 29^th June, subject to review on the outcome of the endoscopy. I reject the evidence that a responsible body of haematologists, presented with the facts of this case by doctors holding the views expressed in the Note,s would have considered the risks of bleeding outweighed the risks of DVT. On analysis, both Dr Keeling’s and Dr Baglin’s evidence was to the contrary.

In any event, an immediate review after receipt of the endoscopy was required. That was not in dispute. It is not clear when the results were available to Dr Crane. The results were available from Dr Andreyev from roughly midday on 30^th. They were not written into the notes by Dr Crane until his review in the early evening after Mr Hearne returned from the procedure which was carried out at the Fulham Road site. I find that having considered that the endoscopy should be carried out urgently, after a notional competent VTE balancing the risks and holding off heparin pending the results, those results should have been chased, and would have been available in had copy from shortly after Dr Andreyev typed them up on 30^th. Heparinisation could not have taken place at the hospital however, until Mr Hearne’s return at about 4.30, if it had not already been started

.I do not accept the evidence of Dr Plowman that at this stage there was still ulceration with a risk of bleeding which would outweigh the risks of DVT. It was not supported by any of the other experts. The nearest support came from Dr Baglin who considered that erosions could also be a cause for concern in the presence of severe pain. I conclude that as Dr Andreyev found and Dr Crane recorded there was mild epigastritis and duodenitis, with no active ulceration. I accept the evidence of Dr Keeling that at that stage the risk of bleeding had reduced to a risk of a risk. This would not have caused heparin to be stopped.

The consensus in the evidence of the experts was that risk of bleeding from a peptic ulcer was the only contra-indication to heparin within the Guidelines. If that risk was eliminated, or outweighed by the high risk of DVT then heparin ought to have been given. In this respect I reject the views of Dr Plowman and Dr Baglin to the extent that they sought to represent a body of opinion against commencing heparin in the light of the endoscopy results. There would be no logic once the one contra-indication was eliminated, in the absence of other evidence of bleeding or continuing risk of bleeding.

I therefore conclude that a failure to heparinise after the results of the endoscopy were available was also a breach of duty in this case.

In order to determine whether starting heparin would have made any difference to development of Mr Hearne’s DVT and PE, it is necessary to decide when it became proximal. Both Dr Baglin and Dr Keeling were agreed on the following

Dr Keelings evidence was that as Mr Hearne had a PE on 2^nd July, at some point before that the DVT must have become proximal before becoming a PE. It is difficult to say when that occurred because there is no entry in the notes between the admission note that there was no DVT on 28^th and the embolism on 2^nd July. It is likely that he had a proximal DVT the day before the embolism, on 1^st July. Prophylactic heparin would not have helped in that case. It probably would have helped prevent the embolism on 28^th June, but he was uncertain about the effects of prophylactic heparin on 30^tth, particularly if the claimant was symptomatic on that day.

Dr Baglin said that if a DVT does not propagate within 7 days, then it will not embolise. On a balance of probabilities, if there was an embolism on 2 July, it is more likely than not that for the preceding 5 days Mr Herne had a proximal DVT not confined to the calf. He considered it most likely that for the majority of the week before the embolism, the probability increasing through that week, Mr Herne had a proximal DVT. He said that DVT was probably proximal on 30^th, 3 days before the embolism.

It is common ground between Dr Keeling and Dr Baglin that on the balance of probabilities, had heparin been started on 29^th it is likely to have been effective in preventing the pulmonary embolism on 2 July.

As to the 30^th Mr Dyer submits that the effect of Dr Baglin’s evidence is that until half way through the week, which he calculates as the evening of 30^th June prophylactic dose heparin would, on a balance of probabilities, have prevented the embolism. He relies on Dr Keeling’s report in which he said that prophylactic heparin would still have been effective on 30^th.

Mr Woolf submits, and I accept, that on the basis of Dr Keeling’s evidence at trial, he cannot say whether prophylactic heparin would have been effective on 30^th or not. Dr Baglin considered that the DVT was probably proximal on 30^th, and Mr Dyer’s analysis of a midway point is unsupported by the weight of the evidence on this point. On this basis the claim would fail on causation if heparin was not started until 30^th June. However, that is not the case as heparin should have commenced on 29^th June.

In conclusion I find that the Defendant was in breach of duty in not administering prophylactic heparin to the Claimant on 29^th June, when on a balance of probabilities it would have prevented the pulmonary embolism which occurred. I also find that the Defendant was in breach of duty in not giving prophylactic heparin on 30^th June, when, on a balance of probabilities a prophylactic dose would not have been effective as the DVT was likely to have been proximal