Raggett, The Executors of the Estate of v Kings College Hospital NHS Foundation Trust & Ors

This is a claim for personal injuries loss and damage brought on behalf of the estate of the late John Raggett deceased, pursuant to the provisions of the Law Reform (Miscellaneous Provisions) Act 1934.

There are six defendants to this action, although two of them have played no part in this trial. The Claimants and the First Defendant reached terms prior to the commencement of the trial and the Fourth Defendant, against whom a default judgement was obtained some time ago, has not appeared.

In summary, this is a clinical negligence claim, which is concerned with the above knee amputation, which the deceased underwent surgically on 8 March 2011. It is alleged that the Second Third Fifth and Sixth Defendants were negligent in their treatment of the deceased, as a consequence of which he was required to undergo the amputation and suffer further loss and damage. Originally, there had been a claim brought against the First Defendant under the Fatal Accidents Act, but this claim has been compromised prior to the commencement of this trial.

There will be eight sections to this Judgment:

John Raggett was born in December 1948 and died in July 2014. He had had a successful business career. As a young man, he had been fit and healthy. In 1985, when he was 36 years old, he suffered a sudden stroke when he was playing squash. As a result, he suffered some left-sided weakness, of which he made light. Following carotid endarterectomy in 1985 and revisional surgery in 1987, he suffered some recurrent blurring of vision. In 1994 he suffered a further stroke resulting in significant left-sided hemiplegia. In 1998 and in 2008 he had fusion operations to 2 toes on the left foot. It is common ground that he was an arteriopath, a prime candidate for peripheral artery disease.

He had retired from work, aged 41 years, in 1990. In 2008 he gave up driving because of concerns about his vision. By this time, he was significantly disabled but was able to mobilise independently, using a walking stick.

Things came to a head in the summer of 2010. On 31 August, he attended his GP, complaining of painful toes in the left foot. On 29 September he again visited the GP, this time complaining of left hip pain. On 2 October, he was seen by an out of hours GP, complaining of pain behind the left heel (8/83-4; 8/249a). On 8 October he was again seen by an out of hours doctor, presenting with a history of left foot pain for one week. Walking was painful, the heel was tender, but there was no swelling. A diagnosis of Achilles tendonitis was made; this was confirmed by his own GP, a week later. The GP referred him to Mr Franklin, the Second Defendant, “for pain control and investigation”. He was admitted to the Sloane Hospital (Fifth Defendant) on the afternoon of the 22 October 2010 and was reviewed by the Registered Medical Officer (RMO) that evening and also on the following day.

Mr Franklin saw the deceased at midday on 23 October. His diagnosis was that he was suffering from neuropathic pain: he referred Mr Raggett by telephone to Dr Hanna, the Sixth Defendant, a consultant pain specialist. Dr Hanna also considered the pain to be neuropathic. Over the next few days, the Second and Sixth Defendants saw Mr Raggett on more than one occasion. He underwent a diagnostic sympathectomy on 28 October and was discharged home on 29 October. Mr Franklin next saw Mr Raggett as an outpatient on 2 November. There were further consultations with Mr Franklin (at a different hospital) on 23 November and with Dr Hanna on 26 November. He also had an MRI scan at this time.

In very broad summary, it is alleged that Mr Franklin and Dr Hanna were both negligent in their treatment of the Deceased over this period; that they failed to diagnose or consider the possibility that the pain was vascular, to make proper investigation or to refer Mr Raggett for vascular opinion. It will, of course, be necessary for me to consider all of this in much greater detail, when I come to consider the negligence issues.

Resuming the background history: Mr Raggett remained in intense pain in late November and wanted a second opinion. On 29 November his GP referred him to the Third Defendant, Dr Hussain a Consultant Rheumatologist. Coincidentally at this time he was admitted to the Princess Royal University Hospital (PRUH the First Defendant) for urgent treatment of asthma and chest infection. On 4 December he was transferred to the care of a Consultant Respiratory Physician back at the Sloane Hospital. On 7 December there was an MRI scan of the left foot; the radiologist suggested the possibility of plantar fasciitis. Although still an in-patient, Mr Raggett saw the Third Defendant in the outpatient department on 9 December. Dr Hussain confirmed a diagnosis of plantar fasciitis and provided a steroid/local anaesthetic injection. The deceased was discharged home on 13 December. He was reviewed by Dr Hussain on 23 December and referred for ultrasound investigation.

The allegations of negligence against Dr Hussain broadly mirror those against Mr Franklin and Dr Hanna: that he failed to consider the possibility of a vascular cause for the pain and to make proper investigation.

The ultrasound scan took place on 6 January 2011 and Dr Hussain referred the deceased to the Fourth Defendant Mr Houshian, a Consultant Orthopaedic Surgeon.

As Mr Houshian has taken no part in this trial (and I have no decisions to make in respect of his contribution to events) I can deal with this part of the history with even more brevity. On 7 January the Deceased was re-admitted to Sloane Hospital and Mr Houshian undertook a surgical debridement of the left heel. He was discharged on the following day but attended appointments later in the month for dressings and re-dressings.

Allegations of negligence are also made against the Fifth Defendant. The deceased had been a patient at the Sloane Hospital on various occasions between October 2010 and January 2011. In a nutshell it is said that nursing notes were inadequate; negligently so.

I do not need to rehearse the history over the next few weeks except to note that the Deceased was again admitted to the PRUH. He was then transferred for intermediate care at the Orpington Hospital where, in due course, an ischaemic left foot was diagnosed. He was transferred back to the PRUH and then (on 1 March 2011) to St Thomas’ Hospital for vascular assessment. In very broad summary (again I will need to return to this in much greater detail later in this Judgment) CT angiogram study revealedwidespread arterial disease in both legs. Different surgical procedures were tried before an above knee amputation of the left leg was performed on 8 March.

Mr Raggett died on 22 July 2014. His death was attributed to pulmonary oedema due to myocardial fibrosis and coronary artery disease with contributions from hypertension and cerebrovascular disease.

I have to determine whether the Second, Third, Fifth and Sixth Defendants were negligent. I need also to consider causation, it being said, on behalf of all Defendants, that the leg was already “doomed” that is to say compromised to such an extent that an earlier correct diagnosis would have made no difference. There are other issues which may arise; for example whether the amputation may have been delayed by an earlier diagnosis and, if so, by how long.

First, however, I propose to consider what we have called the mechanism of the injury. This is an issue which has been hotly contested.

The mechanism whereby Mr Raggett suffered the arterial damage leading to ischaemia and amputation has been the subject of fierce debate between the vascular experts. With the benefit of hindsight, I am not at-all sure that the resolution of this issue is of the greatest significance. It has been submitted that this part of the evidence may help to inform my assessment of the experts and assist in determining (for example) the more important decision which I have to make: to what extent, if at-all, the leg could have been saved; whether, if a proper diagnosis had been made earlier, an immediate amputation would have been necessary, in any event. I propose to deal with the mechanism of injury at this early stage in my Judgment.

Each of the parties was permitted to instruct a vascular surgical expert. I heard from three of them; Professor Andrew Bradbury on behalf of the Claimant, Professor Jonathan Beard on behalf of the Second Defendant and Mr Stephen Brearley on behalf of the third and sixth defendants. I also received the written evidence of Mr Coleridge-Smith, who had been instructed on behalf of the first defendant, and of Professor Sir Peter Bell (5th Defendant). The defence experts spoke with one voice. Professor Bradbury was alone in expressing a different opinion as to the mechanism.

The dispute may be summarised in this way. It is common ground that Mr Raggett was suffering from ischaemic pain from the outset; that is to say from when he first started to complain of pain in the left foot in late August 2010. Professor Bradbury gave evidence that, in his opinion, the most likely mechanism of ischaemia was athero-embolism from proximal, probably iliac artery disease. Small pieces of blood clot and atheroma, which had formed in the iliac arteries, had broken off and travelled down the leg (‘embolisation’) to cause blockages in the small arteries in the foot, leading to ischaemic pain and discolouration. Professor Beard and all the other vascular surgeons disagreed. The undoubted extensive blockages in the arteries were the consequence of atherosclerotic peripheral artery disease (PAD). They all believed that athero-embolism was not a credible cause.

This debate needs to begin with the findings of the treating physicians who investigated and treated Mr Raggett in March 2011. A Doppler (blood flow) study had been undertaken on 23 February which had failed to detect any signals in the arteries at ankle level and it was this which prompted the decision that vascular assessment was required. On 1 March, following admission to the PRUH, no pulses below the femoral level could be detected; a diagnosis of left leg ischaemia was made and, as already noted, Mr Raggett was transferred to St Thomas’ Hospital. An urgent CT angiogram (CTA) showed an occlusion of the left external iliac artery. On 3 March reconstruction of the external iliac artery was attempted by angioplasty and stent. This was successful to begin with. It was found that there was also a long occlusion of the superficial femoral artery (SFA) continuing down into the above knee popliteal artery, which would also require repair; but there was a patent common femoral artery (CFA) albeit of small calibre (likely due to under filling because of the proximal occlusion). A review of the CTA also showed an occlusion of the proximal popliteal artery. There was fixed flexion of the knee, and a deep ulcer on the heel. An attempt was made at angioplasty of the SFA, which was unsuccessful; by this time there was a thrombus formation in the iliac stent. Although there was consideration of a by-pass, and there was a scan to look for a suitable vein, by 7 March there were such adverse factors that the decision was taken that the leg was not salvageable and the amputation was performed the next day. The adverse factors included the lack of run off, the fixed flexion and the extensive tissue loss.

The experts were all able to review the findings made at that time – the radiological reports to be read in conjunction with the images and the findings of the vascular team on 3and 4 March (the temporarily successful stenting and the attempted angioplasty of the SFA). I can find no significant distinction between the opinions of all vascular experts upon the interpretation of these images. In addition to the occlusions, there was stenosis of the left profunda femoris artery and disease of the distal profunda. More proximal arteries were under-filled and this continued to be the case even after the successful stenting. All were calcified and diseased. In the result, there was no arterial run-off into the foot.

It was Professor Beard’s opinion, supported by all other Defence experts, that there was no need to look for any further explanation for the extensive arterial blockages. There was chronic advanced PAD and the severe pain suffered by Mr Raggett over the period of 6 months could only be explained by blockages in the arteries in the more proximal parts of the leg, preventing run-off into the foot. There was absolutely no need to postulate some other process.

It is of note that it was late in the day that Professor Bradbury reached his singular opinion on causation. In his original report, he had reached the same conclusion as his colleagues. However, a short time before the arranged joint meeting of the vascular experts, a new piece of information had come to light from the disclosed material. This was the clinical note from the out of hours GP, who, as noted in section 1 above, had seen Mr Raggett on 8 October. The doctor had noted; “circulation fine, dorsalis pedis present” (8/249c-d). This was important evidence. If there was indeed a pulse, the cause of Mr Raggett’s condition could not be simply explained by PAD.

It was this information, coming to light late in the day, which caused Professor Bradbury to review his opinion. The Defence experts all expressed the firm opinion that the GP had not in fact detected a pulse. Pedal pulses are notoriously difficult to palpate. Research papers have been written which show that doctors frequently get it wrong, that there is a high percentage of so-called “false positives”. It was the Defence case that the GP had obtained a false positive.

But it went further than that. In his witness statement (and in the witness box) Mr Franklin stated that he too had tested the pedal pulses on 23 October 2010 and had found them to be present. Remarkably, he made no clinical note to that effect; indeed he made no note at-all of his examination. In fact, he did not claim to have an independent recollection of testing the pedal pulses but he relied on what he said was his normal practice. He put it this way:

“In line with my usual practice, I am certain I palpated the pedal pulses on both his feet and judged them to be present. Had this not been the case I would have requested an urgent vascular opinion.”

Professor Bradbury had, in effect, based his opinion on two separate and independent pieces of evidence from two different doctors, a few days apart, of a palpable pulse. He thought it unlikely that two doctors, independently and in quick succession, could make the same mistake, notwithstanding that it was a mistake that was often made.

The experts also agreed about one further thing (Professors Bradbury and Beard readily; Mr Brearley after some prevarication). If the pedal pulses were truly present, the only explanation (unlikely though the Defence experts thought it to be) was athero-embolism. If they were false positives, then the straightforward cause was the chronic and slowly advancing PAD.

I have to say that I found both Professor Bradbury and Professor Beard to be impressive and highly expert witnesses doing their best to assist the court. There were some genuine differences of opinion, of course, and there are a number of issues on which I have to make a decision whether to adopt the opinion of one rather than the other. But they were both witnesses upon whom I feel confident to rely. I was less impressed by Mr Brearley. However, on this issue, I have reached the firm conclusion that the first and obvious explanation is the correct one: that Mr Raggett had chronic advanced PAD and that this was responsible for the arterial blockages. I reach this conclusion for a number of reasons. First and foremost, I just do not accept that Mr Franklin did find a positive pedal pulse on 23 October. In my judgment, he did not do the test. I will need to deal with this in more detail when I come to consider breach of duty. I found Mr Franklin to be an unimpressive witness with, I regret to say, a slapdash attitude to his practice of medicine. This was exemplified by his wholly inadequate note taking. He did not consider possible vascular cause. I am satisfied that it never crossed his mind; and he did not do the test. In his case, this was not a false positive; he simply did not do the test. It also appears to me that the chronic PAD seen in March 2011 is a full and likely explanation of the many arterial blockages and consequent ischaemia. Without the two claimed successful palpations of the pedal pulse, this issue would never have arisen. The condition was extremely well advanced by March 2011 with obliteration of proximal arteries, loss of tissue and so on. Whilst it may be impossible to judge the exact picture, if images had been taken 6 months earlier, this is a slowly developing condition and would already have been well advanced at that stage. Apart from the claimed finding of a pedal pulse, there is nothing to point to athero-embolism as a likely cause; and Professor Bradbury agreed this. I make the three findings: (i) that the GP’s finding was of a false positive; (ii) Mr Franklin did not test; and (iii) the cause of the ischaemia was atherosclerotic PAD.

Mr Franklin saw the deceased on five separate occasions. He was the first of the defendants to examine Mr Raggett. The first three examinations may be taken together; 23, 24 and 26 October 2010.

Mr Raggett was admitted to the Sloane hospital (Fifth Defendant) on the afternoon of 22 October having been referred to Mr Franklin by his General Practitioner for investigation of left foot pain “for pain control and investigation”. He was immediately reviewed by the Registered Medical Officer (RMO) Dr Diana and was seen again on the following morning (9/532; 9/542; 9/543). Dr Diana’s notes are instructive. “Left leg pain under knee, started a month ago; during last night patient hit his leg on bedside - pain was increased after that and left ankle started to swollen (sic).” At 8:30 on 23 October: “During last night … atrocious pain in his left leg despite paracetamol …” And at 10:45 Dr Diana noted that there was still pain.

Mr Franklin saw the deceased at midday. Most remarkably, he made no clinical note of this consultation. Nevertheless, in his witness statement (taken in the usual way as his evidence in chief) Mr Franklin claimed a good memory of the consultation. In fact his recollection of events, which contains much detail, is remarkable, given that he made no clinical note and his only near contemporaneous record was a letter, which he wrote some days later and was of limited value as an aide memoire. He said he could recall a telephone call from the GP informing him that Mr Raggett had fallen at home and was in much pain. He told me that he would have read the clinical notes already made, by which he could only mean the notes made by Dr Diana. The detail continues:

“I remember this consultation well. He was exhibiting the classical physical sign of diffuse left sided limbs from dense long-term paralysis (hemiplegia) from a stroke, which had occurred many years earlier. He could barely move his left arm and held it in a fixed position. He had restricted movements in his left leg and could not walk. His left foot was swollen and a discoloured purple colour. In terms of the history I elicited, Mr Raggett told me he had been suffering severe pain in the left foot and leg for a number of weeks and that he had recently had a fall, which had made the pain in his left foot worse. He told me he had been in atrocious pain overnight but that this had improved. He did not report any symptoms of claudication (pain or cramping) in the lower leg whilst walking or any pain whilst resting at night.”

Mr Franklin also purported to recall that Mr Raggett was displaying severe hyperalgesic pain over the left heel and lower leg; there was no delay in capillary refill, no coolness to touch as well as two palpable pedal pulses (witness statement 4/1068-9). There is support for some of this detail in Mr Franklin’s letter, some days later (08.11.10) to Dr Gupta, the deceased’s GP (8/216): “he was in severe pain and his left foot was swollen as well as discoloured”. Mr Franklin diagnosed neuropathic pain and referred Mr Raggett by telephone to Dr Hanna, the Sixth Defendant, a consultant pain specialist.

I will need to consider, in due course, whether I accept that recollection, unsupported as it is by any contemporaneous record. It is remarkable for its detail.

Mr Franklin told me that he was aware of the medical history, including the two strokes suffered by the deceased at a relatively young age. This would, in any event, have been obvious from the left sided hemiplegia. He says that he was aware that Mr Raggett was a prime candidate for vascular disease and accepted the description “arteriopath”. He also accepted, when questioned, that it was essential that he should exclude the possibility of a vascular cause for the pain. As already noted, he claimed that he tested the pedal pulses on both feet and found them to be present. Thus, he said, he was able to exclude a vascular cause. It is common ground that, if he did test the pedal pulses, and, if he judged them to be present, he may be exonerated of negligence on 23 October. I have already dealt with this very briefly earlier in this Judgment. For a variety of reasons, I do not accept that he did palpate the pedal pulses. I will explain my decision in due course.

At one stage, it appeared to be suggested that, because the GP had referred Mr Raggett to an orthopaedic surgeon, Mr Franklin would be entitled to seek an orthopaedic cause and would not be required to explore the possibility of vascular disease. Insofar as that suggestion may have been tentatively advanced, it may now be dismissed. Both orthopaedic experts, Mr Ross (Claimant) and Mr Crawshaw (Defendant) – as well as Mr Franklin himself – accepted that the duty upon an orthopaedic surgeon, in the circumstances, was to consider all possible diagnoses, including the possibility of a vascular ischaemic cause for the pain. And, of course, it is Mr Franklin’s case that he did consider the possibility of vascular disease, that he tested the pedal pulses, and thereby excluded it.

Do I accept that evidence? There are, I am afraid, a number of remarkable facts about Mr Franklin. First and foremost, there is nothing in the notes to say that he did make this important positive finding. The first inkling that one could have, that the pedal pulses were tested, was when Mr Franklin signed his witness statement. He had to rely solely on memory and upon what he says would have been his normal practice. More remarkably, there is no note at all of this first examination. Not a single written note in the medical records. The only remotely contemporaneous record of that examination is to be found in the letter, dated 8th November, some ten days later (8/216) and which makes no reference to pedal pulses or that ischaemia/vascular disease had been considered and excluded.

It was also clear to me that Mr Franklin had failed to read carefully the note, taken earlier that day, by Dr Diana the RMO. This set out the recent history, which included that the pain, of which Mr Raggett was complaining, had developed over four weeks, albeit that it had been exacerbated by recent trauma. Mr Franklin’s initial diagnosis (of trauma induced pain) did not tally with that history. He did not consider that there was any need for any further investigation; all that was required was pain relief. And it was in those circumstances that he referred the deceased to Dr Hanna.

There is another curious feature, which I find disturbing. In his witness statement, Mr Franklin stated (again without the benefit of any note in the records) that, on his later examination on 23rd November, he had again tested the pedal pulses and found them to be present. That witness statement was signed in the usual way and with the usual caution. It was not until the opening written submissions were made that it emerged that Mr Franklin had reflected and now “remembered” that he had not in fact tested the pedal pulses on that later date! This is quite incredible evidence. Equally incredible, I fear, is the submission, made on his behalf, that this volte-face in some way increased his credibility and the quality of his evidence.

I am sorry to have to say that I have reached the very firm conclusion that I am unable to accept his evidence upon this and many other issues. I am entirely satisfied that he did not test the pedal pulses on either occasion. It may also be noted that Dr Hanna, who saw Mr Raggett later on 23October, gave evidence that the pain was so bad that it would have been cruel – indeed “inhumane” – for Mr Raggett to have the pedal pulses tested and he (Dr Hanna) did not do so.

Mr Franklin’s claim that he did so on the first occasion was necessary to his defence; his change of mind on the second occasion was not because he had had a moment on the road to Damascus and remembered, many months after he signed his statement, that he had not after all tested the pulses. And, as ever, there was nothing in his notes to assist him. I spent some time watching Mr Franklin carefully when he gave evidence and, I am afraid that I judged him to be wholly unreliable. I am satisfied that from the outset he adopted a very casual, even cavalier, approach to Mr Raggett’s case. He never considered vascular disease; it never crossed his mind. His carefree attitude is reflected in the lack of any written note from him on the 23rd; and the most cursory notes thereafter.

In the course of final submissions, I indicated to Mr Horne QC that, although I found Mr Franklin to be an unreliable witness, I would not take the view that he had been deliberately dishonest. Only he knows how far he deliberately tailored his evidence to suit his case. In my judgment, there was a considerable amount of wishful thinking and I suspect he may have persuaded himself that he could remember more than was in fact the case. I am not at-all sure that Mr Franklin had acquainted himself with the background, nor that he was in any way alerted by Mr Raggett’s hemiplegia to the fact that he was an arteriopath. Nor am I sure that, when he made his witness statement, he had anything more than the haziest recollection of this consultation.

There are other reasons why I am unable to rely upon Mr Franklin’s evidence. If he had excluded vascular or ischaemic causes, he would surely have said so in the notes or, failing that, in the letter to Dr Gupta. He did neither. In re-examination he said that he would have spoken to Dr Hanna at the time, probably on the telephone; he would have (my emphasis) told Dr Hanna that the pedal pulses were palpable. Dr Hanna did not remember such a conversation. That conversation, of course, did not happen. This was another example of Mr Franklin’s approach to his evidence. There was nothing in his witness statement about it. It was a self-serving answer given on a whim.

I am afraid that Mr Franklin’s memory of the condition of the foot, at the time of his various examinations, was selective. I regret to say that I cannot fully accept his descriptions of the state of the foot. Where a clinician (Dr Diana for example) or a nurse has recorded colour, temperature or swelling in the foot, I am obviously able to accept the evidence. Where the Defendant has made a contemporaneous note, I also accept it – albeit that there are few indeed. But I am not prepared, in the absence of any independent evidence, to accept the unsupported evidence of the Second Defendant as to the condition of the foot. He purports to have an independent memory; but in my judgment, his evidence has been tailored, consciously or unconsciously, to support a defence that all the signs pointed to a neuropathic cause for the pain. He found it difficult to accept that he had not even considered a vascular cause; but I find, on an overwhelming balance of probabilities, that he did not.

Thus I am entirely satisfied that he was negligent from the outset, it being conceded that, if (as I find) he failed to palpate the pedal pulse, that failure amounted to negligence. It is of note that it is now submitted on his behalf that he was mistaken in finding the pulse; there was in fact no pulse and his finding was a “false positive”. It may also be said (albeit with the gift of hindsight) that it is now known that there was in fact a diagnosable vascular cause. In making this finding of negligence, I do not need to distinguish between the three October dates. He should have considered vascular causes and eliminated them. If he had indeed tested the pedal pulses, he would, on the balance of probabilities, have found that they were absent, albeit that there was scope for a false positive. He should then have referred the deceased for proper vascular investigation.

The case against Mr Franklin does not end there. He saw Mr Raggett again on 2November 2010. In his letter of 8 November (to which I have already referred and which covered the whole period from 23 October to 2 November) Mr Franklin wrote that “the swelling has resolved and with it there has been improvement in the skin colour”. In my judgment, having heard what Mrs Raggett had to say (that the foot remained swollen and was a strange colour) any improvement was extremely modest.

Of more significance, Mr Raggett’s pain continued to get worse to the point where he returned of his own volition for an appointment with Mr Franklin on 23 November. Mr Franklin found exquisite tenderness on palpation of the Achilles tendon and he referred him for an expedited appointment with Dr Hanna; also for an MRI scan. Although Mr Franklin’s clinical note is cursory, it is clear that Mr Raggett was in severe pain indeed. Dr Hanna saw him three days later and Dr Hanna’s clinical note (of 26 November reads):

“Severe pain affecting the left lower limb for 6/ 52. Over the last 3/ 52 pain is unbearable. O/Ehyperalgesia over the heel +++ and leg ++. Allodynia over the whole lower limb. Diagnosis severe neuropathic pain with secondary ischaemia. Plan regulate pain control.” (9/543)

It may also be noted that Dr Hanna wrote to the GP (8/222) saying that the pain had been “out of control” since Mr Raggett left the Sloane Hospital (that is to say for the preceding three weeks). Dr Hanna booked a follow-up appointment and increased the dosages of analgesic.

It is therefore clear that, when Mr Raggett attended upon Mr Franklin on 23 November, his pain was very severe indeed. It was described, 3 days later, as being “out of control” and “unbearable”; it was so severe that Mr Raggett had sought a further appointment ahead of his follow-up appointment and it should have been clear that the original treatment was not working. Mr Franklin had originally said in his witness statement that he had again checked the pedal pulses on this occasion. But he now says that he did not.

I now need to consider the evidence of the two orthopaedic expert witnesses: Mr Ross, called on behalf of the Claimant, and Mr Crawshaw on behalf of the Second Defendant. It was Mr Ross’s opinion that the recurrence of pain of such severity should have alerted Mr Franklin to the possibility that the original diagnosis was wrong. In cross-examination: “… having excluded trauma and apparently having had little response to the treatment of neuropathic pain, it does raise the question in an arteriopath whether ischaemia was there present …” and, in response to the question; “How necessary would it be to take the pedal pulses?” “Well, I think it is mandatory”.

Mr Crawshaw’s evidence on this point was less than satisfactory. It relied upon an acceptance of every part of Mr Franklin’s detailed account; that he had taken the pedal pulses on an earlier occasion; that he had looked at the colour and temperature and the capillary return; and that he had excluded vascular cause at that earlier stage. To the suggestion put to him by Mr Kemp that it was unacceptable to omit an examination of the pedal pulses: “If someone is presenting with similar symptoms … I wouldn’t necessarily expect them to do so” (my emphasis).

I am afraid that I found Mr Crawshaw to be somewhat evasive; he often answered different questions to the ones he was asked. For example, when asked to say how long it would take to palpate for pedal pulses, he failed to answer the question four times. Only when pressed by me (three times) did he give a direct answer. I also found his answers upon the issue of Mr Franklin’s wholly inadequate note-taking to be unconvincing. I much preferred the evidence of Mr Ross. But, as I have already noted, Mr Crawshaw was basing his opinions on Mr Franklin’s evidence, much of which I do not accept. I have no doubt that a competent orthopaedic surgeon, faced with a patient with unbearable and out-of-control pain, and who was a known arteriopath, should have revisited the earlier diagnosis and, at the very least, should have palpated the pedal pulse. If I had not found him negligent from the outset, I would certainly find that he was negligent at the time of this re-presentation on 23 November.

I add only this. Out of deference to the detailed submissions of Mr Horne QC in his final written submissions (paragraphs 3.1 to 3.30) I note that these are based upon the assumption that Mr Franklin’s evidence is reliable and credible. Nor does it depend upon the expert evidence in view of my findings. At the risk of repetition: I am satisfied, on the very substantial balance of probabilities, that Mr Franklin failed to have any regard to the possibility, however remote, of a vascular/ischaemic cause for the pain. He did nothing to satisfy himself that it could be excluded because that possibility did not cross his mind.

The allegations of negligence against Dr Hanna, a consultant pain specialist, mirror those against Mr Franklin. This is hardly surprising as they effectively treated Mr Raggett in tandem. Dr Hanna saw Mr Raggett on 23, 25, 27 and 28 October (he had been seen by Mr Franklin on 23, 24 and 26th). Dr Hanna saw him for the final time on 26 November, three days after Mr Franklin had seen him. As with Mr Franklin, the October dates may be taken together.

When Dr Hanna first saw Mr Raggett on 23 October he made a contemporaneous clinical note (9/543). He recorded that there had been severe pain for the last six weeks, “unbearable during the last three weeks”. On examination, there was hyperalgesia over the heel and leg and allodynia across the foot. Dr Hanna then made a diagnosis of “severe neuropathic pain with secondary ischaemia” (my emphasis). In fact, the word “ischaemia” was virtually illegible in the note and was transcribed in Dr Hanna’s witness statement initially as “infection”; he later confirmed that he had written “ischaemia”. He did not consider the ischaemia to be of great relevance; in the witness box he said that there was almost always some ischaemia (effectively, as I understood him, at or near the surface of the skin) in cases of neuropathic pain. I will need to return to this. His plan was to regulate with pain control; drugs (gabapentin and amitriptyline) were prescribed.

In his witness statement (paragraph 13) Dr Hanna, who, like Mr Franklin claimed to have a good recollection of the consultation, gave more detail of his examination than disclosed by the clinical notes. He referred to:

“… classical signs of neuropathic dysfunction, in the form of severe allodynia affecting the heel, ankle and foot and the lower part of the leg as well as severe hyperalgesia in the same areas. There was obvious abnormal swelling around the ankle, heel and foot … he had patchy sensory loss which was in keeping with the neurological sequelae of a vascular stroke that had left Mr Raggett with a hemiplegia. I was struck by the extent of the swelling and the severity of the pain that Mr Raggett appeared to experience, even on mild touch (e.g. with a paintbrush)”.

Mr Raggett also suffered from disturbed sleep due to severe breakthrough pain at night. Based on all of this, Dr Hanna diagnosed (as already noted) "severe neuropathic pain with secondary ischaemia" in the clinical notes.

Dr Hanna’s witness statement has much more detail than the contemporaneous clinical note. Dr Hanna reached the conclusion that the pain was “classically” neuropathic in character. But he went further; it was his opinion that the pain was “the neurological sequelae of (the) vascular stroke … ”, that is to say, the stroke suffered by Mt Raggett many years earlier. In his witness statement (paragraph 14) Dr Hanna stated that he reached the conclusion that the history (and, I assume, his examination) pointed away from chronic critical ischaemia. He relied in part upon the absence of rest pain or intermittent claudication.

I need to say something about rest pain. As far as I can see, there is nothing in the clinical notes to indicate (from Dr Hanna, Mr Franklin or elsewhere) that Mr Raggett had reported that he did not suffer from rest pain. I find it surprising if that is indeed the case. Mrs Raggett was clear that, by this time, one of the main problems was pain on rest at night – that Mr Raggett tried to sleep with his leg hanging over the side of the bed and had long sleepless nights because of pain. Mr Raggett had also had a most painful night on the 23rd, as he reported to Dr Diana. I do wonder whether it is true that Mr Franklin and / or Dr Hanna had indeed elicited from Mr Raggett a history of lack of pain on rest.

On 25October, Dr Hanna saw the deceased again and recorded that he was much better. It is not surprising that there had been an improvement. It is agreed that, whatever the cause of the pain, the gabapentin and amitriptyline would have provided relief. The note also refers to the possibility of a clinical sympathectomy (9/544). In fact, this was an error; what was considered was a diagnostic sympathectomy and this was undertaken on 28 October. This also provided some temporary relief. Again (whatever the cause of the pain) this was unsurprising; it consisted of a simple block and local anaesthesia.

What is clear from Dr Hanna’s evidence is that, even now, he does not really accept that he was treating a patient with something more complex than neuropathic pain. What he claims to have seen at the time was a foot and lower leg with classical signs of neuropathic pain and that was and remained his diagnosis throughout. All experts agree that there was likely a neuropathic component. But this was a complex presentation and it is common ground that the pain was primarily ischaemic.

Before I review the evidence of the experts in pain medicine, I should note a number of further matters. Although Dr Hanna accepted that Mr Raggett was a high-risk patient to develop critical ischaemia, he did not consider it necessary to test the pedal pulses or to instigate (whether through Mr Franklin or otherwise) other investigations (e.g. Doppler flow study) to exclude pain of vascular origin. He said that it would have been “inhumane” to test the pedal pulses. But he was clear that he considered it to be unnecessary in any event. He had all he needed from his clinical examination; and, in his opinion, the pain was neuropathic.

In support of this diagnosis (neuropathic pain secondary to an earlier stroke) he said in evidence that there was a “new learning curve”; that it was now known that victims of a chronic or previous stroke could develop neuropathic pain at any time. It used to be thought that pain secondary to a stroke would likely emerge at an early stage or not at-all.

“ … But now, with extensive studies … that has changed. So (Mr Raggett’s presentation) fell within not just the believable sort of clinical picture but everything else, from the history, from the character of the pain, and from specific sensory examination, that the major dominant feature of Mr Raggett’s pain was neuropathic”.

Thus he said that he did not feel the need to institute vascular investigation. He had a diagnosis in which he had confidence. It is remarkable that, even now, he remains of the view that he was right; that it was neuropathic pain and that there was no vascular/ ischaemic cause.

I can now consider the expert evidence. Dr Karen Simpson, a Specialist in Anaesthesia and Pain Medicine, gave expert evidence on behalf of the Claimant. She was “stunned” to hear about the so-called new learning curve. It was just not true. It would be unusual in the extreme for neuropathic pain to develop spontaneously some 16 years after a stroke. It was not a likely diagnosis. It was a possible (but highly unlikely) diagnosis and a lot less likely than a vascular problem. Nor was there any literature to support Dr Hanna’s assertion that there had been new learning. Dr Charles Pither the Consultant Pain Specialist called on behalf of Mr Hanna agreed with Dr Simpson on this point.

“Q: do you accept in principle Dr Simpson’s evidence that it would be very unusual indeed for neuropathic pain related to stroke to come on 16 years after the stroke? A: Yes”

It is at this stage that I can return to Dr Hanna’s note of “severe neuropathic pain with secondary ischaemia”. Dr Hanna had explained that he did not consider there was any real significance in his using this word. He meant no more than that there was some inadequacy of blood supply to the skin; and this was something invariably seen where there was neuropathic pain. This, of course, was raised with the two experts. Both agreed that it was not a recognised term; nor was it something with which they could agree. Dr Pither agreed that “secondary Ischaemia” appeared to him to make no sense at-all, particularly as Dr Hanna had failed to investigate the cause of this supposed insufficiency of blood supply.

In assessing the alleged negligence of Dr Hanna, the evidence of the experts is of importance. I can say at the outset that I found Dr Simpson to be a most impressive witness; Dr Pither less so. He had suggested that the Pain Specialist might not have the same diagnostic responsibilities as, for example, the Orthopaedic Surgeon. His role was to treat the pain; and this was particularly the case where, as here, Mr Franklin, who was responsible for his overall care, had referred Mr Raggett to him. Although that proposition was not formally abandoned, it was not really followed up. Dr Hanna himself accepted that he needed to make his own diagnosis and had done so. This was necessary in order that he could prescribe the correct drugs in the correct quantities. And Dr Pither himself, both in writing and orally in the witness box, gave evidence that there was a diagnostic duty. The pain specialist had to consider a vascular cause for the pain as part of his “diagnostic algorithm”.

The principal difference between the two experts was whether it was mandatory (Dr Simpson) for the ischaemia to be excluded by some independent determinative test; or whether (Dr Pither) simple consideration coupled with clinical examination was sufficient. In cross – examination, Dr Pither confirmed what he had said earlier: that he (Dr Hanna) had to consider a vascular cause for the pain “in his diagnostic algorithm which is going on in his head. It is not my view that he needed to formally implement tests to exclude it, but he would certainly have considered it…” This was consistent with what both experts had said in their joint statement; they had agreed that critical limb ischaemia should be considered within the differential diagnosis of any patient with severe neuropathic pain in the lower limb (questions 15; 35).

I have highlighted the words “any patient”, because Mr Raggett was not just “any patient”; he was a known arteriopath. Dr Hanna told me that he was aware that Mr Raggett was a prime candidate for vascular compromise and that, of all the possible diagnoses, this was potentially the most dangerous.

The crucial question for me is whether, in the circumstances of this case, a diagnosis based solely on clinical examination, was sufficient; or whether ischaemic pain should be excluded by something more. Would a body of competent Pain Specialists have considered it satisfactory for the diagnosis to be made, without more?

I need to consider carefully what the two experts said about this. Whereas Dr Pither expressed the opinion that there was no duty on Dr Hanna to go any further than consider vascular causes, Dr Simpson, said it was mandatory to exclude ischaemic pain by independent means: testing the pulses, Doppler flow studies or even by referral for specialist vascular opinion. This was particularly so in an arteriopath. There was another factor; the so-named “secondary ischaemia”. A discernable insufficiency of blood supply on the surface of the skin was not a normal finding and required investigation. Confidence in one’s own diagnosis was just not sufficient. It was Dr Simpson’s opinion that excluding a vascular cause for limb pain in a man with a history of stroke and cardiovascular problems is “very basic and standard medical practice”.

What did Dr Hanna himself have to say about this? When asked what he did to exclude a vascular cause he said:

“Since I did not consider the possibility of vascular critical ischaemia on the day, I didn’t take any further steps but to diagnose the pain mechanism involved for Mr Raggett”.

And then:

“Q: Dr Hanna, you have in front of you a patient who is at very high risk of vascular disease. You identify neuropathic pain, which of course is the pain management you want to get under control. Are you saying that you took no steps whatsoever to consider even whether this high-risk patient in fact had neuropathic pain because of underlying vascular disease?

A: I admit so.”

Mr Kemp, on behalf of the Claimant submitted that these answers were sufficient to underpin a finding of negligence, even if Dr Pither’s evidence were preferred. He had agreed that there was a duty to consider possible vascular cause, but with no obligation “to formally implement tests to exclude it”. These answers amounted to an admission by Dr Hanna that he did not even “consider the possibility of vascular critical ischaemia”. I am not sure that Dr Hanna meant to make the full concession that he had not even considered vascular causes. I took him to mean that the exclusion of vascular causes was inherent in his confident diagnosis of straightforward neuropathic pain; that so “classical” were the signs that it was unnecessary to go further. I will have to decide whether or not that is correct.

There are thus two crucial questions for me: (i) did Dr Hanna consider the possibility of vascular critical ischaemia as part of the diagnostic process? (ii) If he did, can I accept Dr Pither’s evidence that it was not necessary to exclude vascular causes by some separate independent means over and above mere clinical examination? As to the second of those questions, and at the risk of repetition: would a body of competent pain specialists have considered it satisfactory for the diagnosis to be made, without any further tests for possible vascular cause?

Before I answer those questions, I should return to the history. After the diagnostic sympathectomy on 28 October Mr Raggett was discharged home. He returned for a follow-up appointment with Mr Franklin on 2 November (9/528).

On 23 November Mr Raggett returned to see Mr Franklin earlier than had been intended, because he was still experiencing intense pain. As noted earlier in this Judgment, Mr Franklin sent him for an MRI scan and for an expedited appointment with Dr Hanna. He saw Dr Hanna on 26 November. This, of course, was an opportunity for the diagnosis to be reconsidered. On this occasion, 26 November, Dr Hanna did not revisit his original diagnosis. He prescribed increased doses of gabapentin and amitriptyline and made a follow up appointment for six weeks time. Dr Hanna wrote to the GP saying that the pain had been “unbearable” and “out of control.”

Dealing with the appointment on 26 November, Dr Hanna described “a long and detailed discussion on the possible mechanisms and best method to control his pain” (my emphasis). He confirmed that his diagnosis had not changed. His clinical note read:

"I reviewed Mr Raggett in today's Outpatient Clinic accompanied by his wife. I believe the situation has been really out of control since he left the Sloane Hospital. (I) had a very long discussion with him and his wife about the nature of his pain and the best way forward. I have explained to him that normal painkillers including Morphine are not particularly effective in central neuropathic pain and what we have to rely on is central medications such as Gabapentin and Amitriptyline…

I do not think Dr Hanna was asked about these detailed discussions, nor about the “possible mechanisms” which were discussed. I find these detailed discussions to be somewhat surprising given that, so far as Dr Hanna was concerned, there was only ever one mechanism. Also, when he was giving oral evidence, Dr Hanna volunteered that, on this occasion, he did not even examine the foot. Mr Raggett’s shoe and sock remained on.

I have reached the conclusion that vascular causes never entered Dr Hanna’s mind. This just did not form a part of his so-named “diagnostic algorithm”. On that finding, he was clearly negligent.

But, if I were wrong about that, I have to decide whether he should have gone further and sought to exclude vascular causes by Doppler studies, taking the pedal pulse or other means. I have reached the conclusion that any competent pain specialist would have done so and I much prefer the evidence of Dr Simpson on this issue. I judged that Dr Pither – who was required to make numbers of concessions – was much less secure in his opinion. In my judgment, Dr Simpson’s evidence was plain good sense. It was just not acceptable to fail to consider and seek to exclude vascular causes in this known arteriopath. It was not acceptable in October; even more so in November. By this later date, it was clear that the treatment was not working. Mr Raggett had returned for more help because of the unbearable pain. In those circumstances, it was surely imperative to re-visit the original diagnosis. That was certainly Dr Simpson’s opinion. It was necessary to examine the foot – particularly as there had been an apparent lack of blood supply to the skin at the time of his first examination.

I have to say that I detected that Dr Pither felt some embarrassment in attempting to support Dr Hanna on this. He made a number of concessions including (i) that, a failure to test the pedal pulses should have “set in train some other things”; and (ii) that an examination of the foot would have been informative, given that there had been three or more intervening weeks during which time Mr Raggett’s pain had got worse.

In deference to Mr Davidson’s attractive submissions, I should note that I agree with him (as did Dr Simpson) that Dr Hanna’s diagnosis was one that a body of reasonable pain specialists could have reached; that his treatment with gabapentin and amitriptyline was acceptable; and that the diagnostic sympathectomy was a proper procedure, properly carried out. But this was almost beside the point. Dr Hanna’s failing was in not excluding vascular causes as an adjunct to this treatment. Doctors frequently make confident diagnoses. But it is standard practice to call for blood tests, or a CT scan, or an X-ray to exclude more serious (albeit remote) possibilities. So here it was imperative for Dr Hanna to exclude ischaemic pain. However confident (and reasonable) his diagnosis, more serious and more remote possibilities should be considered and excluded. I find that Dr Hanna was negligent from the outset.

The allegations of negligence against Dr Hussain, a consultant rheumatologist, are effectively the same as those made against Mr Franklin and Dr Hanna. It is alleged that he too failed to consider or diagnose ischaemic pain. For reasons which will become clear, this section of my Judgment can be briefer than the previous two.

Dr Hussain saw Mr Raggett for the first time on 9 December 2010. Mr Raggett had seen Dr Hanna on 26 November and was dissatisfied with the treatment he was receiving. His pain was intensifying. By 29 November he had asked his GP for a second opinion. It is unfortunate that the GP did not refer him to a vascular specialist; he sent him to Dr Hussain. There is a referral letter (10/1026) which contained; “the pain is usually when he is standing up, therefore he cannot bear weight and occasional pain with rest.”

In the meantime he was admitted to PRUH suffering from unrelated respiratory problems and was transferred to the BMI Sloane Hospital (Fifth Defendant). An MRI scan of the left lower leg was performed on 7 December. This showed oedema at the anterior Achilles tendon, which was noted as intact. There was high signal relating to the plantar fascia and a provisional diagnosis of plantar fasciitis was made

When Mr Raggett saw Dr Hussain on 9 December 2010, he was in considerable discomfort. It was Dr Hussain’s evidence that there was a separate area of skin thickening on the medial and inner aspect of the left foot and that Mr Raggett was complaining of focal pain over the left heel. He also said that there was no surrounding erythema. Dr Hussain then confirmed the diagnosis of plantar fasciitis. He thought that this might be a result of inflammation of the fascia caused by an altered gait consequent upon the left sided hemiplegia.

Dr Hussain provided an injection of steroid and local anaesthetic (lignocaine and depomedrone). Not surprisingly, this provided swift relief. Dr Hussain wrote:

“ … This gentleman has had a previous left-sided stroke and examination … reveals areas of skin thickening on the medial and inner aspects of his left foot. Simple palpation of the heel elicited extreme pain and hypersensitivity. There is no evidence of ulcer or breakdown in the skin. I would think that the underlying cause for his extreme discomfort, which he describes as walking on glass, is due to plantar fasciitis. I therefore injected the heel using a medial approach with 2ml of 2% lidocaine and 10mg of Depomedrone, cortisone injection. The local anaesthetic provided immediate relief. I have not made any further appointments to review the situation however l will contact him to chart progress."

On 23 December Dr Hussain saw Mr Raggett for the second time. He made a note that he only had residual symptoms of his plantar fasciitis. He was given colchicine and an ultrasound scan was organised. This was undertaken on 6 January 2011. It showed subcutaneous oedema but no definite indication of any problem with either the Achilles tendon or plantar fascia. As Mr Raggett was still suffering from persistent pain, Dr Hussain referred him to Mr Shirzad Houshian (the absent Fourth Defendant) for possible surgical intervention. That was the end of Dr Hussain’s involvement.

The principal allegation of negligence is, once again, the failure to consider and exclude a vascular ischaemic diagnosis. Expert evidence was from Consultant Rheumatologists Dr Armstrong (Claimant) and Dr Huskisson (Defendant). Dr Huskisson considered that the diagnosis of plantar fasciitis was a reasonable one, that Mr Raggett was actually suffering from plantar fasciitis and that the injection given on 9 December was reasonable. Dr Huskisson expressed the opinion that he did not think that “Mr Raggett’s symptoms were due to vascular insufficiency when he saw Dr Hussain”: nor did he think that if Dr Hussain had “identified the arterial problem it would have made any difference to the treatment or the outcome”. I find that he was wrong in both those matters. First, it was the firm opinion of the vascular experts that, from the outset (that is to say when Mr Raggett first saw Mr Franklin) he was suffering from critical ischaemia of the left lower leg. Indeed, in the joint report, Dr Huskisson accepted that “in retrospect” Mr Raggett’s foot was likely to have been ischaemic. Second, if arterial disease had been identified, it must follow that the attempts to save the leg would have commenced immediately, and long before March 2011. Whether or not the leg could have been saved at that time is a matter for the vascular experts.

The two experts differed on a number of matters; whether plantar fasciitis was a correct or reasonable diagnosis; whether the injection was appropriate treatment; whether the injection technique was adequate; whether it was or may have been a cause or trigger for the infection which later became manifest; and whether the administration of colchicine was an appropriate treatment.

I do not consider that it is necessary for me to resolve any of these matters. The crucial question was and remains this: if Dr Hussain knew (as he clearly did) that Mr Raggett had a left sided hemiplegia, why did he not investigate the possibility of vascular insufficiency and was it negligent of him to fail to do so? On behalf of the Claimant, it is submitted (in respect of Dr Hussain as with the other Defendants) that there was a particular need to exclude the possibility because of the likely serious consequences if the diagnosis was missed.

In answering this question, I can start with Dr Hussain’s evidence that he was aware that Mr Raggett had had two strokes and was hemiplegic and was therefore a high-risk candidate for vascular disease; also with the expert’s joint report and the several agreed matters:

Dr Hussain accepted that he did not check the pedal pulses, nor did he take a peripheral vascular history. If he had done so, he would have learned much more than he now says he knew: that there had been uncontrolled pain, escalating over a period of more than a month in spite of increasing medication aimed at pain control; pain at night; the sympathectomy and so on.

It had been Dr Huskisson’s evidence that Dr Hussain’s examination had been “appropriate”. However, when cross-examined he had to concede that it was not.

“Q. Given you now accept that he didn’t do two things that you say were mandatory, you can’t possibly say that his examination was appropriate can you? A. I think the conclusion of his examination was correct and appropriate. How he arrived at it may not have been ideal… I am satisfied that he satisfied himself that the foot was not ischaemic … and therefore what he did was entirely correct.”

The difficulty, however, is that the foot was ischaemic. Thus, as it seems to me, insofar as Dr Hussain may have “satisfied” himself that the foot was not ischaemic, he was wrong. And, as Dr Huskisson had to accept, he had reached that wrong conclusion by a “not ideal” route. In fact it was by a route, which avoided the mandatory requirements of testing the pedal pulses and taking a full history.

I fear that Dr Huskisson had founded his initial report on his belief (set out earlier in this Judgment) that the foot was in fact not ischaemic at the time. That has turned out (albeit with the benefit of hindsight) to be incorrect. It is just illogical for Dr Huskisson to continue to try to maintain that the Defendant had (i) failed to do things which were mandatory (ii) reached a conclusion which is now known to be wrong; but (iii) reached a conclusion that was “correct and appropriate”, and given treatment which was “entirely correct”.

In my judgment, Dr Hussain deprived himself of the tools whereby he could reach a truly correct conclusion. If he had taken that full history and tested the pedal pulses, he could not (without further negligence) have failed to consider vascular ischaemic causes and put in train a proper course of inquiry and treatment. I find that he was negligent.

Many, indeed most, of the allegations of negligence against BMI Healthcare (Sloane Hospital) have not been pursued. Mr Raggett was an inpatient at the hospital between 22 and 29 October and between 4 and 13 December. In summary, the remaining allegations are concerned with a failure of the nursing staff in record keeping and / or a failure to make reports to the medical staff that Mr Raggett was in pain and requiring analgesia. It has been submitted that the provision from nurses to clinicians (whether by keeping up to date accurate records or by oral reporting) is essential in the overall management of a patient.

During the October period, Mr Raggett was seen at least once on every single day by either Mr Franklin or Dr Hanna, in fact a total of eight times. He was fully able to describe how he felt, the nature of his pain, how he had slept, and so on. One of the main allegations was that Mr Franklin had not been told on 28 October, the day before Mr Raggett was discharged that he was recorded in the notes as suffering from pain assessed as high, that is to say a score of 3 on the charts. In a manful cross examination of Mr Franklin, Mr Kemp attempted to elicit (i) that Mr Franklin would have expected to be told and (ii) that, if he had known of this, he might have revisited his “approach” to the case. It was clear to me that Mr Franklin was reluctant to agree.

Mr Kemp had more success with the expert witnesses. Both Mr Ross and Mr Crawshaw would have wanted reports to be made. They would also have expected full notes (charting the pain on an hourly basis and so on) so that they had an up to date record to inform them as they planned their treatment.

It is really common ground that the nursing notes and record keeping during this period were to some limited extent either inaccurate or incomplete. And Mr Kemp relies upon admissions made by Ms Johnson, the Fifth Defendant’s nursing expert as to the inadequacy of the notes and the oral reporting.

I do not propose to deal with this at any length because I have reached the firm conclusion that any failure – negligent or not – did not make any causal contribution to the failure of any of the other Defendants to consider a vascular cause for Mr Raggett’s extreme pain. If the notes had been 100% accurate and if the nurses had made a point of making constant and repeated oral reports of Mr Raggett’s pain cycle, nothing would have changed. As Miss Gollop QC submitted, all three of the doctors had a full picture of Mr Raggett’s pain. They relied upon his own reporting. He was, after all, in hospital for the very purpose of getting to grips with his severe pain. He was able to articulate his problems to the doctors. And insofar as (for example) Mr Franklin was eventually and reluctantly persuaded to agree that he “might” have revisited his diagnosis, I do not for one moment accept that he would have been prompted to take any different course, to consider any different cause for the pain, or to act in any way differently from the way in which he did act. The same applies to Dr Hanna.

In spite of Mr Kemp’s attractive submissions, I am far from satisfied that there was frank negligence. Ms Heaps, the Claimant’s nursing expert agreed with Miss Gollop that the records were broadly adequate. But insofar as there was a failure (whether negligent or not) it made not the slightest difference. If there was an inadequacy in the records, neither Mr Franklin nor Dr Hanna was misled. There was no relevant aspect of Mr Raggett’s history or pain which was available to the nurses but not available to the doctors or known by them. Any inadequacy was, in my judgment, of no causative significance.

This is even more starkly illustrated when one looks at the second period of in-patient treatment. On 9 December Mr Raggett was an in-patient but was being treated for respiratory problems. He saw Dr Hussain in an out patient clinic within the hospital and Dr Hussain was not provided with the nursing notes. Nor would it have been normal practice for the notes to be provided for him. Here the criticism appears to be that the notes did not record the extreme pain with which he presented to Dr Hussain. But he went to the out patient clinic to tell Dr Hussain all about his pain. It is self evident that Dr Hussain would not have been assisted by a nursing note repeating that fact. And it is fatuous to suggest that the presence of such a note would have caused Dr Hussain to make a different diagnosis or offer different treatment.

In summary, as against this Defendant, I find that there is no causative link and that there is no need for me to give any careful consideration to whether there had been any breach of duty sufficient to give rise to a finding of negligence. The claim against BMI Healthcare is dismissed.

On behalf of the Second Defendant, Mr Horne QC has divided the issue of causation into two parts: factual causation and medical causation. In view of the fact that I have determined (i) that Mr Franklin did not palpate the pedal pulses and (ii) if he had done, he would have found them to be absent, factual causation ceases to be an issue. In either event (non palpation or absent pulses) he should have referred Mr Raggett for vascular investigation. The same applies (though in a slightly different way) to the other negligent Defendants.

So far as medical causation is concerned, I have to decide the extent of the loss and damage flowing from the various breaches of duty. What would have been the likely outcome, if the Second, Third and Sixth Defendants had not been negligent?

There is an agreed starting point. If the Second and / or Sixth Defendants had referred the deceased for vascular investigation, he would have been seen in early November; that is to say, approximately four months earlier than was in fact the case. It is the Defendants’ case that there would have been no difference in outcome at all; that the PAD was so advanced that the vascular surgeons would have made the same attempts to save the leg but with the same results. There may have been elective amputation earlier rather than later – but the life of the leg could not have been extended beyond March 8, in any event. To reach that conclusion, the Defence experts used the images and findings of March 1, 3 and 4 and assessed what would have been the picture four months earlier. It was the collective view of the Defendants’ vascular experts that, if those procedures had been undertaken four months earlier, there would have been very little difference in the findings. So deep seated was the disease that the arteries would have been in much the same condition In November 2010 as in March 2011 and the images would have been identical or nearly so.

Professor Bradbury, on the other hand, considered that there had been a significant advance in the condition over the intervening months. Relying upon his clinical experience, and having regard to the progression of signs and symptoms, the leg would have been salvaged and would likely have remained viable for some three to five years – probably until Mr Raggett’s untimely death.

Mr Horne, in submissions which were adopted by all Defendants, was extremely critical of Professor Bradbury. First (as I have already found) Professor Bradbury was wrong about the mechanics of the injury; this error, it is submitted, contaminated (my word) his opinion on likely outcome. It was not just the error; but his whole approach had been flawed. The court would have to determine what was the pattern of disease at the time that there should have been vascular referral (early November in the cases of the Second and Sixth Defendants; a later date in respect of Mr Hussain). When that had been determined, it would then be necessary to consider whether the leg would have been amenable to successful revascularisation. Professor Bradbury, he submits, has avoided providing his opinion on this question, except in the most general of ways. He did not, for example, enter properly into the debate about the likely pattern or extent of the disease, as it would have presented in November 2010. Nor had he seen all the images from March 2011. He had seen and considered the CT angiogram of 1 March as well as the angiogram of 3 March. That was clear from his initial report. But he had not viewed the angiogram of 4 March. In paragraph 75 of his report he had said that it was not possible to see the status of the popliteal artery or the crural arteries below the knee from the images. In fact, examination of the angiography of 4 March would have enabled him to do so. He had also provided drawings at the trial to illustrate the pathological process, but these necessarily omitted any reference to the angiogram of 4 March and the additional information which it provided. In fact, Professor Bradbury had not seen the images of 4 March, although he clearly knew that they existed and would be available to him. Thus he was much less well informed than the Defence experts who had all seen the full range of images. The criticism goes further. Professor Bradbury had caused frustration amongst his colleagues at the time of the joint meeting (in fact a telephone conference call) by failing to discuss the detail of the disease as revealed in the imaging. The Defendants’ experts wished to discuss the likely progress of the disease over the four months prior to March 2011 and to reach conclusions about notional images, if they had been taken in November 2011. But Professor Bradbury would not participate properly in that debate.

A further criticism was made. It was not until the beginning of the trial that he considered the images of 4 March and it is suggested that by the time he was being questioned about it, his opinions were too deeply entrenched to enable him to modify his opinion. He did, however, accept in cross-examination that Professor Beard’s interpretation of the angiogram of 4 March was correct. Mr Horne submitted; “that he left such a concession about the extent of the disease until so late in the evolution of his evidence is extremely regrettable; it raises real questions over his willingness to take account of evidence that is unhelpful to his case.”

I should say at the outset that I do not accept these criticisms of Professor Bradbury. Although he had not seen the final images, he was well aware (as is apparent from his report) of the fact that there was occlusion of the arteries at ankle level and across the foot arch. These images, when he looked at them, provided no surprises and looked just as he expected them to look. And of course he accepted Professor Beard’s “interpretation” which was no more than a simple pen and ink reproduction of what the angiogram imaging had shown.

On the other side of this coin, Mr Kemp has submitted that criticism can also be made of the Defence experts. For example, when they came to consider the mechanism of the injury, not a single one of them had referred to Mr Franklin’s evidence that he had (or “would have”) tested the pedal pulses on 23 October. This was a crucial piece of the evidence when assessing the mechanism of injury. If the pedal pulses had been truly palpable, there would have been only one possible mechanism, namely athero-embolism. Mr Kemp submitted that this was a major failing in their evidence.

None of this is particularly helpful. I formed the opinion that all of them were perfectly able to accommodate whatever new information came to light and to deal with it. And I also formed the view, in respect of each of them (certainly Professors Bradbury and Beard) that they were prepared to make appropriate concessions and to express honest opinions founded on the merits of the evidence and argument. None of them had become “entrenched” (to use Mr Horne’s word) to the point where he allowed his proper judgment to be impaired.

At the risk of repetition, I found Professors Bradbury and Beard to be impressive and reliable witnesses. I now have to weigh their evidence and to reach my own conclusions.

What does the March 2011 imaging show? As already mentioned Professor Beard provided me with a drawing summarising the state of the leg as shown on the imaging. The popliteal artery was occluded above the knee; but it was patent below the knee albeit diseased and calcified. Blood supply to the lower levels was by collaterals, by-passing the upper popliteal artery and superficial femoral artery. The peroneal and posterior tibial arteries were occluded, as (crucially) was the foot-arch. The anterior tibial artery was patent above the ankle but diseased and calcified. That of course was the picture in March 2011. Professors Bradbury and Beard agreed that the imaging did not provide clear evidence as to the availability of run-off. But Professor Beard was firmer in his opinion than Professor Bradbury that there was in fact no run-off. The leg was clearly incapable of salvage at this stage although, as we have seen, attempts were made.

If Professor Bradbury frustrated his colleagues as Mr Horne suggests, that is because he approached the task in a wholly different way. To iterate: the Defendant’s experts’ approach was to look at the March imaging and to try to recreate, in their own minds, what similar imaging would have disclosed some four months earlier. They reached the collective conclusion that the PAD was so far advanced and the development of the condition was so slow-moving that the life of the leg could not have been extended beyond March 2011. The process of creating the notional images for November 2010 involved little more than looking at the extent of the disease in March 2011 (how developed and severe it was) and using their experience to judge how it would have looked four months earlier. It was as simple (and difficult) as that.

Professor Bradbury did not wish to enter fully into that debate. His approach was to consider the condition of the leg and foot during the intervening period and to use that evidence to make a judgment about likely blood flow and arterial sufficiency in November 2010. He thought that the images of March 2011, whilst enormously informative, were of limited value in judging the state of the leg during the preceding four to six months. There would inevitably have been very significant atheroma present in November, but the progression of PAD, whilst slow, is highly variable. He disagreed with the suggestions (put to him by Mr Horne) that, if there had been noticeable progression of the condition over the four month period, that would have been atypical. The atheroma may look bad on imaging, but the importance is the effect it has on blood supply.

It was also Professor Bradbury’s evidence that a limb which is in imminent danger will show external signs of ischaemia. He found it difficult to conceive that, if Mr Raggett had been investigated in early November 2010, the leg would have been lost. In Mr Raggett’s case, none of the doctors had noted any typical signs of ischaemia of such severity that loss of limb was imminent. Mr Franklin had described a discoloured and swollen foot. Dr Hanna said there was abnormal swelling of ankle heel and foot. And Dr Hussain described skin thickening on the medial and inner aspects of the foot. These were not classical signs of ischaemia and all three of those Defendants relied upon the fact that there was nothing visible to put them on obvious notice that this was an ischaemic leg. Insofar as clinical notes were made (including the nursing notes during Mr Raggett’s in patient care) there were no obvious signs of underlying vascular problems. The GPs who saw Mr Raggett in early October made notes which are similarly lacking in any such evidence; “heel looks normal and is not tender. No sign of infection along left foot and leg” (2/388) and “no redness and swelling” (Dr Borhan, the out of hours GP who tested the pedal pulses; 2/390). In short there is no evidence of obvious signs of ischaemia between early October and Christmas time (when Dr Hussain last saw Mr Raggett).

By February 2011 the limb was patently severely compromised. Clinical photographs were taken (4/942-5). These show a horribly swollen discoloured and ulcerated foot with substantial loss of tissue. In terms of external signs there had been an enormous change in a very short time. Looking at the foot at that stage, it would not be difficult for even the untrained eye to see that there was a problem with circulation. Also, by this time, Mr Raggett had developed a fixed flexion deformity at the knee. It was this, together with the probable loss of run-off and extensive loss of tissue, which persuaded the surgeons that there was no alternative to amputation.

In determining the viability of the leg at any given time, a crucial feature is run-off into the foot. If the remote arteries and foot arch are occluded, the only possible blood supply is by collateral routes. As Mr Kemp has submitted, if the notional imaging of October / September 2010 was, to all intents and purposes, the same as the actual March 2011 imaging, the foot must have been sustained and supplied by collaterals during that period with no visible deterioration. By the time the March images were made, the foot was ulcerated with loss of tissue, horribly discoloured and clearly deprived of blood supply. But between October and the early part of 2011 no one had detected any coldness in the foot or any of the other classical signs of an obviously ischaemic lower limb. This suggested that there was some limited blood supply into the lower part of the leg. If so, the limb could have been saved at that earlier stage. Clearly the blood supply was compromised and this was causing Mr Raggett’s extreme pain. But there could not have been total occlusion without classical signs, including tissue loss.

Professor Bradbury went further. The evidence suggested that there was no tissue loss until January 2011. And the fixed flexion deformity did not develop until February. Up to this point the only symptom was severe pain including (of significance) rest pain. It was his experience that a patient with advanced PAD and rest pain only was not in imminent danger of limb amputation. Only when there was tissue loss was the damage likely to be so acute that revascularisation would be impossible. It is also of note that arteries which are stenosed as to less than 70% may be revascularised. In Professor Bradbury’s opinion, the lack of any of the classical signs of ischaemia in the interim period meant that the arteries were not completely occluded, particularly at the extremity, that there was sufficient blood flow into the foot and an early referral would have permitted successful revascularisation. He told me that, in his opinion, the occlusion of the foot arch had occurred over the period October to January. If there had been total occlusion in October, there would have been much earlier loss of tissue as well as other classical signs of ischaemia.

I have reached the conclusion that I much prefer Professor Bradbury’s evidence upon this issue. One of the difficulties with the approach of Professor Beard and his other colleagues is that the only explanation for the appearance of the foot and leg over the period up to January 2011 is that the symptoms were not a reliable reflection of the underlying disease. I asked Professor Beard when, in his opinion, the leg would have been salvageable. My concern was this. If the imaging had been identical 4 months earlier (despite the foot being of near normal appearance and temperature) presumably it would have progressed very little over the preceding four months and the same things would be said then as now. Professor Beard’s reply:

“Well logically the earlier you treat – you pick somebody up with arterial disease, the more chance there is of them not having lost run-off. The key here is the lack of run-off in the foot. Everything else above it can, theoretically … be treated. But the point is you can’t bypass – if the blockage is in the foot, you can’t go past that blockage to revascularise the foot. So I can’t say when the foot run-off was lost because we have no images for that.”

In my Judgment, on the balance of probabilities, there was still run-off at all times prior to Christmas 2010 such that the leg could have been salvaged. I make it clear. The leg could have been saved if any one of the three negligent Defendants had referred Mr Raggett for vascular investigation.

I add this. In reaching that conclusion, I take account of the efforts made at St Thomas’s Hospital to save the leg. Clearly an expert vascular team considered that the leg might still be saved and for almost a week, they tried to save it. Two major surgical procedures were carried out and Mr Raggett underwent physiotherapy in order to try to reverse the fixed knee flexion. A vein map was sought to try to find a vein for by-pass surgery, albeit that this may have been a belt and braces approach taken before the full imaging had been completed. Mr Kemp makes the valid point that, if there were prospects of a successful procedure in March 2011, how much more likely that it would have worked some months earlier, prior to the loss of tissue and prior to the onset of the fixed flexion deformity.

I need to move on to the likely prognosis for a revascularised leg. Professor Bradbury has been consistent throughout on this issue. In his original report, at a time before he considered any mechanism other than PAD, he stated that the limb would have been successfully revascularised and would have survived. Both Professor Beard and Mr Brearley (as we have seen) believed that the leg could not have been saved. But, in their reports they went on to express an opinion as to likely length of survival, if the leg could have been saved. It may be noted that Mr Raggett had been reported to suffer fromanti-phospholid syndrome. Professor Beard stated:

“Even if revascularisation had been successful in salvaging the foot in the short term, the likelihood of medium to long-term limb salvage would have been compromised by his anti-phospholid syndrome (which was diagnosed in late March 2011 i.e. after the amputation). Anti-phospholid syndrome has been reported to increase the risk of failure of both endovascular and open arterial intervention and to cause more rapid progression of peripheral artery disease. On the balance of probability, the combination of the syndrome reduced mobility and continued smoking would have resulted in the need for an amputation within 1 to 2 years even if revascularisation had been successful ... The most powerful risk factor for arterial/ graft/ stent thrombosis would have been the anti-phospholid syndrome …”

Thus it was that Professor Beard thought that the reconstructed limb would have a life of one to two years. Mr Brearley’s prognosis was 2 to 3 years. I think I am correct in saying that the other two Defence experts had not expressed an opinion on this issue in their reports.

The question was raised for the joint meeting of the experts. Of course, it must be understood that all the Defendants’ experts adopted the primary position that the leg could not be saved. But in the alternative they stated (5/1253-4; q3); “(The four Defence experts) consider that angioplasty and stenting … might have delayed amputation of the deceased’s leg by up to six months”. This, of course represented a retreat by both Professor Beard and Mr Brearley. They explained their reasons for the change. They had discussed this in detail at their meeting and their colleagues had persuaded them that this was the correct estimate. Neither of them gave me any clinical reason for the change.

In fact the way the question had been asked by the lawyers (5/1253) did not permit of any particularisation above 12 months; Professor Bradbury gave his opinion that it would be in excess of 12 months. He has remained consistent and his figure is between 3 and 5 years.

Having decided that the leg could be saved, I am not prepared to hold that there would have been an early amputation. To begin with, I note that it is now agreed that Mr Raggett did not suffer from anti-phospholid syndrome as had originally been reported. This makes Professor Beard’s change of heart even more difficult to understand, given that he took this as an important factor in the assessment. I also adopt the approach of Longmore LJ in Keefe v Isle of Man Steam Packet Co Ltd. [2010] EWCA Civ 683. Where the lack of important evidence is a consequence of the Defendants’ breaches of duty the court should judge the Claimant’s case benevolently and the Defendants’ case critically.

In my Judgment, the revascularised leg would have survived for the period up to Mr Raggett’s death, a period of, say, 4 years from the autumn of 2010.

In the event, there will be judgment for the Claimant against the Second Third and Sixth Defendants; and there may also be judgment for the Fifth Defendant against the Claimant. I am told that the parties are likely to be able to agree damages, but, if not, I may make an order for the trial of the issue of quantum. I also imagine that apportionment will not be a problem in view of my findings. I would hope that, when this Judgment is handed down, I can be told what agreements have been reached and that a draft order will be available.

At the time of handing down, I will also deal with any other issues which are raised, including costs.