Marcus v Medway Primary Care Trust & Anor [2010] EWHC 1888 (QB)

Case No HQ08X01154[2010] EWHC 1888 (QB)
IN THE HIGH COURT OF JUSTICE
QUEEN'S BENCH DIVISION
Venue Royal Courts of Justice, Strand, London, WC2A 2LLDate Thursday, 22 nd July 2010
Before
ANDREW EDIS, Q.C.(Sitting as a Deputy Judge of the Queens Bench Division)
Between
Sebastian MarcusClaimantMedway Primary Care TrustDefendants(2) Dr Ashiq Hussain
Eliot Woolf (instructed by Gadsby Wicks) for ClaimantAlexander Hutton (instructed by Barlow Lyde and Gilbert) for First DefendantRichard Partridge (instructed by Berrymans Lace Mawer) for Second DefendantHearing Hearing dates: 12 th 14 th 15 th and 16 th July 2010
JudgmentAndrew Edis, Q.C. sitting as a Deputy Judge of the Queens Bench Division :
[1]The Claimant, Sebastian Marcus, suffered cruel misfortune in the first half of 2005 when he was 31 years old. He contracted a very unusual condition for a man of his age, namely the occlusion of the arteries of his left lower leg. The cause of this, I find, was embolisation from a lesion in the abdominal aorta which may have been the result of his smoking habit. This conclusion was advanced by Dr. Ashleigh, consultant interventional radiologist who gave expert evidence in this case, and supported, with less certainty, by the three vascular surgeons who gave expert evidence. It is based on the appearance on the angiogram performed on 13th May 2005 to which I shall come later. These occlusions caused ischaemia in the foot which caused very severe pain and resulted in the below knee amputation of the left lower limb on 20th June 2005. In fairness to the doctors who saw him while this condition was developing, two of whom have admitted breach of their duty of care to him, I should record that this presentation is so unusual that specialists who serve a large population area told me that they might see no more than 2 or 3 cases a year. The First Defendant’s employee diagnosed ischaemia, but failed to take the appropriate steps thereafter. The Second Defendant failed to diagnose ischaemia at any time on the three occasions when he saw him. Ischaemia occurs when the perfusion of tissue is inadequate at rest, denying oxygen to the muscles and causing very acute pain. If uncorrected it may lead to tissue death and amputation of the affected area. I attempt to explain other anatomical and clinical language at paragraphs 8 and 9 below.[2]No allegation is made in these proceedings about the treatment which was provided to him at the time of the amputation, or at any time after his admission to the Medway Maritime Hospital on 12th May 2005. The Claimant’s case is that between them the Defendants saw him on 4 dates during April 2005 and that their negligent failure to secure earlier intervention by a vascular surgeon caused delay which resulted in the loss of the lower part of his left leg. The First Defendant, through its employee Dr. Ruth Thom, a General Practitioner working in the Same Day Treatment Centre (SDTC) saw him first, on the 6th April 2005. The Second Defendant, who was acting as a locum in the Claimant’s own GP practice, saw him on the 14th, 21st and 28th April.[3]The Second Defendant admitted in its Defence on the 1st December 2008 that “immediate referral to a hospital for a vascular assessment was required” on each of the three dates on which he examined the Claimant. No such referral occurred. The First Defendant served a Defence on 12th November 2008 denying breach of duty, but, by a letter sent on 7th July 2010, 2 working days before the start of the trial, has now made an admission in the following terms:- “The First Defendant admits paragraph 26(i) of the Particulars of Claim, save that, in relation to sub-paragraph (e) thereof, it avers that it is probable that there was no malleolus (posterior tibial) pulse present at that time. Further, the First Defendant admits that its servants or agents should, as a consequence and as a minimum acceptable treatment in the circumstances, have ensured that the Claimant consulted his GP with a recommendation for urgent referral for vascular assessment, in accordance with the agreed answers to Question 1 of the Joint Statement of GP experts dated July 2010.”[4]On the first day of the trial I was informed by counsel that they had agreed quantum. Therefore, the only issue which I am required to resolve is causation. There are three possible outcomes to the determination of this issue, which I shall further define at paragraph 5 below. They are i) The blood supply to the limb might have been entirely restored, resulting in a normal left leg, or perhaps with some symptoms. This is the Claimant’s pleaded case. ii) The process may have been arrested by earlier anti-coagulant therapy at a time when a viable supply to the left lower leg was being achieved by collateral vessels. This would have resulted in a permanently symptomatic lower limb but the amputation would have been avoided. This arose from the exploration by Mr. Hutton, for the First Defendant, with Mr. Collin, the Claimant’s expert, of the hypothesis that the occlusion may have been at ankle level rather than in the foot, or higher up above the ankle. The Claimant’s case had been that the occlusion was higher up, and the Defendants’ case was (and is) that it was lower down below the ankle, namely in the foot. Mr. Hutton was exploring a new hypothesis which Mr. Collin told me he regarded as tenable. It was reasonable therefore for Mr. Woolf to explore in re-examination what implications for causation that possibility might have. He did this without objection and Mr. Collin told me that in that event, if there was simply a blockage at the ankle and anti-coagulant therapy had been provided before the blockages higher up, then the leg might have been saved by the preservation of the status quo at that stage. Professor McCollum, the expert vascular surgeon called by the First Defendants, agreed that there was a window in which anti-coagulant therapy would have had this effect. He said that the window was from mid-March to 6th April. Mr. Brearley, the expert vascular surgeon called by the Second Defendant, thought it possible that at a very early stage anti-coagulant therapy might have had this effect, but he was less confident of the outcome than either of his colleagues. The evidence therefore exists for me to consider this un-pleaded third possibility, even though it was not foreshadowed in any expert report served prior to trial. I shall do so. iii) If I find that the Claimant’s left lower leg was at all material times destined for amputation, then the Claimant can still recover damages for pain and suffering, because he was denied appropriate analgesia by the negligence of the Defendants for the period between 14th April 2005 and 12th May 2005 (28 days). For reasons which appear below, the Second Defendant is responsible for the whole of this period, and the First Defendant responsible for the time between 20th April 2005 and 12th May 2005 (22 days). I have not been asked to apportion liability between them. Although not formally conceded on behalf of the Defendants, in my judgment there can be no answer at least to this element of the claim, and the Claimant will be entitled, at least, to general damages on this basis. It follows from their admissions that they were negligent in failing to secure the referral of the Claimant to a vascular surgeon that they caused him to be denied proper treatment for a period of time. Much of this treatment may have been doomed to failure, but the use of appropriate analgesia in hospital while it was being attempted would have alleviated the symptoms. This Claimant did therefore suffer avoidable pain caused by the admitted fault of the Defendants. I shall not deal with this aspect of the claim further, but will assess the damages recoverable on this basis at the end of this judgment since they either form part of the claim or all of it. The Issue[5]For reasons which I address in paragraph 6 below, the issue on causation is as follows:- a) What was the latest date when intervention by a vascular surgeon would have saved the Claimant’s leg? b) If that date is a date before the 14th April 2005, the claim on this basis fails. c) If that date is a date after the 14th April but before 20th April then the claim succeeds against only the Second Defendant. d) If that date is after 20th April then the claim succeeds against both Defendants. No submissions have yet been made to me about apportionment of liability between them as joint tortfeasors. a) What was the latest date at which anti-coagulation medication would have preserved a compromised supply to the left lower limb, and prevented further embolisation? b) If that date is a date before the 14th April 2005, the claim on this basis fails. c) If that date is a date after the 14th April but before 20th April then the claim succeeds against only the Second Defendant. d) If that date is after 20th April then the claim succeeds against both Defendants. Again, no submissions have yet been made to me about apportionment of liability between them as joint tortfeasors.[6]Before proceeding further, I should explain why the critical dates identified above are different so that the date is later for the First Defendant than it is for the Second Defendant, even though the First Defendant saw the Claimant first. The First Defendant contends that a proper course for Dr. Thom to adopt on 6th April 2005 was to ensure that the Claimant was seen by his own GP as a matter of urgency, with the signs of vascular compromise which she had detected being specifically drawn to the attention of the GP. The GP would then have referred the Claimant to a vascular surgeon. It would not have been negligent for that referral to be an urgent referral but not an emergency referral. The difference is that an emergency referral would be seen on the same day, but an urgent referral might not be seen for over a week. Thus the relevant date for establishing liability against the First Defendant is not 6th April 2005, but a later date. It is common ground that a referral by the GP as an urgent, but not an emergency case, would probably have resulted in the Claimant being seen by a vascular surgeon no earlier than the 20th April 2005. Professor McCollum, the expert who gave evidence on behalf of the First Defendant prepared a supplemental Expert Report dealing with this issue which was disclosed on the first day of the trial and dated 8th July 2010. No objection on the ground of late service, or non-compliance with directions, was made and I heard the evidence. In it, he sought to extend the date for the First Defendant still further by suggesting that it might take a further week to admit the Claimant after he had been seen by a vascular surgeon. For reasons which I will give when I deal with the expert evidence below, I reject this evidence. The critical date, therefore, for the First Defendant is the date on which the Claimant would have been seen by a vascular surgeon had Dr. Thom referred him to his GP in the way in which she should have done, namely the 20th April 2010. I have misgivings about the agreement between the Claimant and the First Defendant that a responsible body of GPs seeing the Claimant on 6th April 2005 and in the week of the 11th April 2005 would have decided not to refer him as an emergency, for the following reasons:- i) I have received evidence from Mr. Collin, with whom Professor McCollum, Mr. Brearley and Dr. Ashleigh agree on this issue, that thrombolysis accompanied by thrombo-embolectomy if necessary is the treatment of choice for recently occurring blockages in the arteries, and that up to 3 weeks after the blockage it is likely to succeed. Between 3 weeks and 6 weeks it is likely to fail. After 6 weeks it is bound to fail. This is important evidence which I shall take into account in reaching my conclusions but will not repeat. ii) Neither Dr. Thom on 6th April nor a GP examining Mr. Marcus after a referral by Dr. Thom some days later could have known when exactly any blockage had occurred. They could not therefore have known that it would make no difference to the outcome to allow a delay of over a fortnight in the case of Dr. Thom, or a further week in the case of the Claimant’s own GP to whom she had referred him, before the Claimant was seen by a vascular surgeon. Indeed a delay of such a length might easily mean that treatment which was likely to be successful became unsuccessful. iii) There is a tension between the position of the Second Defendant, who accepts that immediate referral to a vascular surgeon was required on 14th April 2005, and that of the First Defendant which I describe above. This tension is made more striking by the fact that the GP to whom these different expectations are applied may well have been the same doctor. In other words, Dr. Hussain himself accepts that he ought to have referred the Claimant as an emergency case on 14th April 2005 but the Claimant and the Medway PCT are agreed that he would not have been negligent had he decided to refer as an urgent case thus allowing a further week or so to pass by before a vascular surgeon saw Mr. Marcus. iv) There is no evidence that anything changed during the week of the 11th April which would justify a finding that Dr. Hussain would not have been negligent in referring the Claimant as an urgent case on 11th, 12th or 13th April but negligent in taking that course on 14th April. v) For the reasons set out at (i) and (ii) above, I consider it possible that the position adopted by the Second Defendant properly reflects the duty of a GP examining the Claimant in the first week or two of April 2005, and that the position agreed between the Claimant and the First Defendant may be too favourable to the First Defendant. Because it is an agreed position I have heard no evidence which could explain or justify the agreed position and I make no finding on it, but I think it right to record my doubts about it. vi) The approach which the Court is required to take therefore lacks logical consistency between defendants. This is a consequence of the different positions they have adopted on advice during this litigation and is not of the Court’s making. They cannot therefore complain about it. From the Claimant’s point of view it makes no difference unless I hold that if he had seen a vascular surgeon between 6th April 2005 and 14th April his leg would have been saved, but that after that date it was doomed. vii) Therefore, the critical date for the Second Defendant is 14th April 2005 and that for the First Defendant (who saw him first) is the 20th April. The Facts[7]This has been a remarkable case in that there have been several notable changes of position and also important developments during the oral evidence given by the experts. I have heard detailed technical expert evidence from witnesses of great distinction. I shall try to avoid burdening this judgment with technicality except where it is necessary to do so in order to explain my conclusions. I shall not rehearse all the oral expert evidence which I heard, but it should not be concluded from this that I have failed to understand that evidence or failed to have regard to it. Some medical background[8]Anatomy:- The case concerns the left lower limb, and the supply of blood to it. This is achieved in the normal state by the Superior Femoral Artery (SFA) which passes through the thigh. At the knee this becomes the Popliteal Artery after it passes through the adductor canal. At this point, the Popliteal Artery runs behind the knee. Below the knee, the Popliteal Artery divides into the Anterior Tibial Artery (ATA) and the Tibio-peroneal stem. Below that, there is a further division into the Posterior Tibial Artery (PTA) and the Peroneal Artery. The ATA, the PTA and the Peroneal Artery are the three named arteries which pass through the calf, into the ankle and then the foot. The ATA becomes the dorsalis pedis artery in the foot. The PTA and the Peroneal Artery rejoin each other and supply the plantar arch. The ATA, the PTA and the Peroneal Artery have been referred to as the “calf arteries” and the “crural arteries”. In addition to the named arteries, the lower limb also has collateral vessels which supply the final distribution of blood and which are also capable of developing so as to enable a continued supply when the main named artery is blocked. In a healthy limb, through which the heart is pumping blood normally, there will be pulses at the posterior tibial (or malleolus) and the dorsalis pedis which, if accurately palpated, will reveal the presence of flowing blood. Where blockages occur due to blood clotting, these clots are called thrombi if they have occurred at the site of the blockage, or emboli if they have formed elsewhere but been carried to the point of the blockage by the circulation of the blood. In this case, the blockage will occur where the embolus encounters a bifurcation of the vessels or where the vessel narrows for some other reason so that the embolus is too large to continue its travel.[9]The medical procedures:- I have heard detailed evidence about angiography, which is an imaging technique by which dye is introduced into the blood vessels to show the flow on x-ray, by a process which is described is “opacification”. This is performed by a radiologist. The radiologist may also introduce wires into the vessels which will guide catheters so that Tissue Plasminogen Activator (tPA) can be infused at the site of a blockage. This is called thrombolysis and is designed to dissolve the clot. This drug therapy has been described as “clot-busting drugs” in evidence. If that does not work, a surgical procedure called thrombo-embolectomy is performed in which a catheter is introduced into the artery carrying a balloon. The balloon is inflated and withdrawn, and in a successful procedure the clot is withdrawn by it. Anti-coagulant drugs are also given, whose purpose is to prevent further clotting of the blood, as opposed to the dissolution of clots which have already formed. The Claimant’s History[10]I shall start with an overview and then move to detail. The Claimant began to feel pain in his foot at some point before he attended his General Practitioner on 24th March 2005. At 02.51am on 6th April 2005 he attended the Accident Centre of the Medway Maritime Hospital with a “foot problem”. He was referred to the Same Day Treatment Centre and seen later that morning by Nurse Anna Gazes who referred her to Dr. Thom. Dr. Thom felt that there was ischaemia, but not critical ischaemia, and referred the Claimant for an x-ray to exclude a fracture as the source of the pain. She referred the Claimant to his own GP, but failed to refer to her findings of ischaemia in her letter of referral. Those important clinical findings were not therefore taken into account by either of the GPs who saw the Claimant on 4 occasions between 6th April 2005 and the time when he attended a podiatrist on 12th May who immediately diagnosed ischaemia and rightly decided that an immediate referral to the Hospital was required. Dr. Hussain saw the Claimant three times, and Dr. Gopal saw him on the 4th such occasion. Neither doctor diagnosed ischaemia. I have not heard the issue of negligence, but I have heard evidence which suggests that the examinations and the note taking were both sub-standard on all these occasions.[11]There are therefore relevant clinical records on 6 occasions prior to the attendance of the Claimant upon the podiatrist on 12th May. After that attendance, he gave a history of his condition to a number of different people. The histories recorded in these clinical records are not consistent with each other, and are also inconsistent with his account given in his witness statement. The Claimant gave brief evidence orally dealing with his memory and his recollection of the development of symptoms. The evidence of the Claimant is regarded as of great importance by the Defendants. Mr. Woolf who appeared for the Claimant, on the other hand, and Mr. Collin who gave evidence on his behalf, invite me to reject his recollection of the times at which his symptoms developed, and to be guided only by the records.[12]The Claimant’s witness statement for these proceedings was dated 28th September 2009. However, an earlier version of it must have existed because the Particulars of Claim is in very similar terms and was served on 9th July 2008. According to his witness statement there was a progressive worsening of his symptoms between February 2005 and 6th April when he presented with a full constellation of symptoms of critical ischaemia. Until the admission made by the First Defendant on 7th July 2010, of course, he was seeking to prove breach of duty against Dr. Thom and it was in his interests on that issue to say that his symptoms were fully established. The interests of the First Defendant, of course, were the mirror image of that. In that phase of the litigation it was in their interests to say that his symptoms were subtle and that the course she took was therefore appropriate. Now each party has changed its position on the facts in the light of their interests on the causation issue. The Claimant wishes me to find that the symptoms were subtle so that his leg was still capable of being saved. The First Defendant wishes me to find that the symptoms were severe so that I reach the opposite conclusion and now contends that I should find that Dr. Thom was wrong in finding a weak pulse in the posterior tibial artery (PTA) at the ankle. The First Defendant has not felt inhibited in taking that course by the fact that its pleaded case is and has remained that there was such a pulse. I raised this matter on the first day of the trial and no application for permission to amend that Defence has been made. I am not invited to hold the First Defendant to its pleaded case by the Claimant, and I shall return to the significance of this pleading later. In this unedifying state of affairs I must do my best to make findings of fact on the balance of probabilities relying on the clinical records, the statements of the Claimant and Dr. Thom, and on such parts of the expert evidence as enable me to judge what the Claimant’s signs and symptoms were likely to be at different times. Dr. Thom did not give evidence. She was to be called by the First Defendant who served a witness statement from her. The exigencies of litigation having made her evidence inconvenient to them, they decided not to call her and now invite me to find that she was wrong in some important respects. The Claimant, also motivated by the exigencies of litigation, has now put in her witness statement as hearsay evidence in support of his case. That statement essentially proves the accuracy of her clinical records from the 6th April 2005. I bear in mind in assessing the weight of that statement, and of all the clinical records from April 2005, that they represent material supplied by doctors who were admittedly acting negligently at the time. This is relevant to the weight which I can attach to them.[13]There are important differences between the Claimant’s witness statement and the clinical records and it is necessary for me to decide which represent the progress of his condition more accurately. His oral evidence was to the effect that he has a very poor memory and that he was not really sure when the pain became so severe that he started to relieve it by hanging his leg off the bed. This is a classic symptom of limb threatening ischaemia. When the tissue is warm the chemical changes which are caused by ischaemia occur more quickly and patients find that some relief is obtained by cooling it, by removing it from the bed. At one point he told me that he began to do this when he started to use crutches but at another point he said that it was weeks before that. I have said that he was not able to give the doctors an entirely consistent history of his condition in April 2005, which is one reason why they fell in to error. Since that time his difficulties have been compounded by his traumatic event in losing his leg, and his job. Time has also passed and I find that at this point he is quite unable to tell me reliably when any particular symptom first developed. I do not know when the first version of his witness statement was drawn up, but whenever it was, this inability to recall accurately the symptomatic progress of his condition had already set in. I find that I am unable to place any weight on the parts of that document which attempt to date the development of the different symptoms. This finding is reinforced by a history taken by Professor McCollum on 10th July 2009. He elicited a different account from the Claimant’s witness statement, and one which was, in some respects, more consistent with the contemporaneous records. I shall interpolate these different accounts into a review of the records and other factual evidence below. The Statements and Records[14]The Claimant’s witness statement says at paragraph 4:- “in about February 2005 I started to feel pain on the underside of my left foot which gradually worsened and caused me to limp. The foot became noticeably colder than my right foot. Over the subsequent few weeks this worsened to the point that when I put it into warm water it made it more painful. When it reached the stage when depressing the clutch in my car to drive to work became too painful I decided to go and check it out. I made an appointment to see my GP but was seen by a locum Dr Mongalee and he prescribed me painkillers for a painful foot”.[15]The Claimant told Professor McCollum in July 2009 that “... he started to get pain in his left foot when exercising in February 2005. This was sufficient to cause him to limp, his foot felt cold. He had no pain in the calf (he did not have calf claudication). By March this pain was more severe and occurred at rest and when weight bearing. His left foot was so painful that he thought he may have broken a bone.” I have underlined the words “and occurred at rest” because they are highly significant. The experts agree that rest pain is a clear symptom of ischaemia caused by the occlusion of arteries supplying the foot. It does not indicate the location of the occlusion. There is a dispute about how many of the crural arteries need to be blocked in order to cause symptoms: Mr. Collin says that blockage of two crural arteries will have this effect, while Professor McCollum and Mr. Brearley say that all three vessels would have to be blocked, because any one of them is capable of supplying an adequate blood supply to the foot, such as to mean that the occlusions will be asymptomatic.[16]On the 24th March 2005, the Claimant saw the locum GP who noted: “Painful lt foot. T. Diclofenac 40 1 TDS (28)”.[17]The Claimant says in paragraph 5 of his witness statement:
“Over the next two weeks the foot continued to worsen. At some point it became too painful to put my foot on the bed at night so I had to sleep with it dangling outside the bed. Even then I was only getting about two hours sleep at a time and the pain would wake me. The foot was painful both when walking and at rest. I thought maybe I had broken a bone so I went to Accident and Emergency at Medway Maritime Hospital on 6th April 2005. It was about two o’clock in the morning...”
If this is right, it means that all the symptoms of limb threatening ischaemia which were ever present were present by this date. The only sign which ever developed later was the finding of gangrene in the big toe, first seen on 12th May 2005.[18]The notes from that A&E attendance show his arrival at 02.51 on the morning of 6th April 2005, his complaint was “foot problem” and the triage notes state, “pain and coldness left foot 7/12 [7 months] since motor bike accident”. “Immediate nursing care given: None Given, Tetanus covered, SDTC 10.15.” The SDTC is the Same Day Treatment Centre, and the First Defendant is responsible for the SDTC. Thus he was given no treatment in A&E but a decision was made that his painful and cold left foot should be assessed in the SDTC later that morning. It will be noted that this history is different from the witness statement which dates the onset of symptoms to February 2005. The Claimant did have a motorcycle accident, but it is agreed by all experts that this was irrelevant to the development of his ischaemia and was a red herring which may have misled the doctors who saw the Claimant in April 2005. He must have said this to the Nurse on triage, and he must therefore have thought that he had been suffering from symptoms in the left foot for about 7 months. Clearly, though, he was also saying that they had got much worse recently, because he presented at 02.51am at Accident and Emergency which itself implies that things were much more difficult for him to tolerate than they had been.[19]The SDTC is staffed by nurses and GPs and is designed for those who do not need hospital treatment but nevertheless need to be seen the same day. The Claimant attended the SDTC as arranged. He was noted to have arrived at 10.03 and he was triaged by Nurse Anna Gazes who noted the history:
“pain and coldness in left foot since motor bike accident, September 04 had motorcycle accident left leg was dragged along – has noticed foot increased pain to left foot and it has been blue or very pale and cold. Increased pain on walking has to stop let pain ease and then walk again. Smokes roll ups. Taken NSAID [non-steroid anti-inflammatory drug] from GP 2/52 [2 weeks] ago PMH [past medical history]: ingrowing toe nail Medication none Allergies none known.”
Again, I have underlined the critical words. To say that pain increases on walking implies that it is present, at a lower level, when not walking. In this context, this means that there was some “rest pain”, the significance of which I deal with above. Further the complaint is of pain in the foot and not the calf. This appears to me to be a description of foot claudication, which is a rare condition. Claudication is a condition in which the compromised blood supply to muscles causes symptoms when those muscles are exercised, which increases their need for blood tenfold. When the muscles are rested, the symptoms resolve. The perfusion of the tissue is adequate at rest, but not when exercised. Inadequate perfusion of tissue at rest causes ischaemia. This Note therefore records some rest pain, which worsened on exercise. This implies that there was a severely compromised supply to the foot. Calf claudication is much more common, but there is no recorded complaint of pain in the leg, as opposed to the foot, at any time until the Claimant was seen in Hospital on 12th May 2005. PMH [past medical history]: ingrowing toe nail Medication none Allergies none known.” Then under “examination” Nurse Gazes noted some signs which she had noted because she was suspicious of ischaemia as the cause of the problem. She noted:
“Capillary refill >2 [more than 2 seconds] to toes of left foot

All toes very red, cold to touch, some dusky areas of skin”

All toes very red, cold to touch, some dusky areas of skin” Nurse Gazes referred the Claimant to the doctor. Of all those involved in the care of the Claimant prior to his arrival at the hospital on 12th May 2005 only she and the podiatrist he saw on that day can be commended on their performance of their functions. Neither, of course, is a qualified doctor. The records of 6th April 2005 continue:
“S/B [seen by] Dr Thom. No Critical Ischaemia Has tenderness to 4th and 5th metatarsal. Given form for x-ray of left foot to exclude fractures for review by own GP re x-ray result and vascular compromise to left foot. Advised to contact again if worsens or not resolving.”
[20]The x-ray request form was signed by Dr Thom and stated:
“X ray Lt foot + metatarsals Clinical details: - Motorcycle accidents 6m ago, Injury to Lt foot – C/O – pain in 4th and 5th metatarsals - And dorsum of foot - Colour getting blue intermittently - O/E – poor capillary refill >2s - Weak Lt malleolus pulse - Pinkish foot – cool? - ? Exclude # [fracture] - Some ischaemia”
I have underlined the record of the weak left malleolus pulse because that is a highly significant entry. If that was a genuine pulse, then there was as at 6th April 2005 a patent artery (the PTA) supplying the foot. If it was not, then there was not. The significance of this record has been the subject of dispute by the expert witnesses, and I shall return to it below. Clinical details: C/O – pain in 4th and 5th metatarsals

Clinical details:

[21]The x-ray was subsequently reported on 8th April 2005 as having normal appearances of the left foot.[22]The GP was also sent brief details of the Claimant’s attendance at A&E earlier on 6th April 2005. These details conspicuously failed to pass on the details of Dr. Thom’s examination, which are recorded only on the x-ray request form and were overlooked for this reason by Mr. Collin until quite recently. The referral letter says only “Diagnosis: Disorder of foot (left)”.[23]The Claimant next saw the Second Defendant GP on 14th April 2005 who noted on the computer:
“Inflammation of scar on the left foot due to IGTN [ingrowing toe nail] and infected blister”
Flucloxacillin [an antibiotic] and Diclofenac [a painkiller] were prescribed. In the handwritten notes for that day it was noted:
“Cellulitis of left foot And hot – has infected IGTN [ingrowing toe nail]”
. This note suggests that Dr. Hussain did examine the foot. He had not been alerted to the signs of ischaemia noted by Dr. Thom, but they were still there for him to see. It is common ground that ischaemic limbs are prone to infection, and the Claimant may have had an ingrowing toenail. He probably did not have cellulitis, and this may have been a misinterpretation of the redness and swelling which would be a sign of “sunset foot”, a term used by Professor McCollum which describes both the colour of a severely ischaemic foot and, he said, its future. Professor McCollum told me that the finding of cellulitis (an infection in the foot) is a mistake which GPs often make when confronted with a red foot. In fact the Claimant was suffering from ischaemia, one effect of which is to make the foot appear red. This is counter-intuitive, and can confuse clinicians who lack experience of this condition. I consider it to be important that it was on this day that the Claimant was first signed off work. He had an active job, such that he cannot do it now with his prosthesis, which he described as “parking ships”. It required him to move around the quayside with agility. He told me that he had been working up to this time. Although he also told me that he did not work a full week in that job, the fact that he was able to work until 14th April 2005 without any description of difficulties in doing so is an objective fact against which I must measure the various contentions as to his likely level of symptoms at this time.[24]On 21st April 2005 the Claimant attended the Second Defendant again when the latter made no entry in the computer records but did so in the handwritten records:
“Med 3 [sick certificate] one week

Athlete’s foot – Canesten HC [treatment for athlete’s foot] see SOS [return again when needed].”

This finding is very hard to understand. I have not heard from Dr. Hussain about how he reached it. All the experts agreed that this was a very inadequate examination and diagnosis. Athlete’s foot is a condition of the skin which causes itching. This man was in very severe pain. There can be no doubt that this was a negligent assessment of his condition, but it is not even explicable by negligence unless the Claimant, at that point, was not showing obvious signs of very severe pain in his foot. If that is so, it accords with the history elicited by Professor McCollum set out below. Athlete’s foot – Canesten HC [treatment for athlete’s foot] see SOS [return again when needed].”[25]The Claimant told Professor McCollum in July 2009 that “...it was around the third week in April when his left foot became so severely painful that he started to hang his foot out of bed. He could not leave his foot in bed as the pain was even more severe.” The Professor commented that these symptoms are typical of ischaemic rest pain. The significance of this piece of evidence may be considerable given that the critical date for the First Defendant is the 20th April 2005 and for the Second Defendant the 14th April. The Claimant was describing a noticeable change in his condition to Professor McCollum and attributing it to a time after he saw the First Defendants. In one sense therefore this was an admission against his interest. Although I have no real confidence in his dating this change to the third week in April, I think it reasonable to conclude that he did recollect a deterioration in his condition which occurred after he saw Dr. Thom, and after he first saw Dr. Hussain, and fairly close to the time when he presented at the hospital.[26]On 28th April 2005 the Claimant attended the Second Defendant again when it was noted: (1) Computer:
“Ingrowing great toe nail condition is the same. I have referred him to pods and orthopods mr. Hammer”; (2) Handwritten: “Kicked the stuff on the floor. Got worse – Eryth [erythromycin]... Co-dydramol. Refer pods and orthopaedic surgeon. Med 2, 7 days.”
It seems to me that this is some contemporaneous support for the proposition that the Claimant’s pain had become noticeably worse at this time. If nothing else it records something said by the Claimant at the time which relates to an incident which he now recalls, namely that there was an incident when he did kick some DIY materials which he had never got round to using. This is not the “third week in April”, but it refers to an incident between 21st and 28th April, and there is an approximate coincidence therefore between the history given to Professor McCollum and the contemporaneous records.[27]The Second Defendant’s letter of referral to the Orthopaedic Surgeon was dated 5th May 2005 (1 week after he had decided to send it) and stated that the Claimant was “suffering from cellulitis on his foot. He has been to hospital where he had an x-ray which was normal. He has been prescribed two courses of antibiotics which have not worked.”[28]The Claimant attended the surgery on the 5th May and was seen by Dr Gopal. Dr Gopal “O/E [on examination] infected toe C/o pain on the right foot (sic) O/E Poor circulation with ingrowing toe nail. Ref to Podiatrist at Dartford on request.” A referral to the Podiatrist was made by Dr Gopal and was also dated 5th May 2005 and stated “Pain and discolouration of Rt foot [sic]. Was treated with antibiotic for infected toe...” The handwritten note for that day says “Med 3 7 days. Wants Ref to podiatrist at Dartford”. It appears that the Claimant at this time was attending his GP every 7 days, perhaps because of his need for certificates for his work. He was not a regular attender at his GP in normal times and he appears to have been bearing considerable pain with some stoicism. This also may have misled the doctors about the gravity of his condition.[29]The Claimant was seen by the Podiatrist, Mr. Paul Chambers, on 12th May 2005 who recorded that the Claimant was ischaemic and said the following on his letter of immediate referral to the A&E:- “Query DVT [deep vein thrombosis] – DD Bergers [differential diagnosis Bergers disease which is a condition which involves ischaemia] Dorsalis Pedis absent, Posterior Tibial absent. Popliteal Biphasic (Doppler).”[30]The Claimant arrived in A&E at 15.36 on 12th May 2005 where it was noted on triage that his history was of “Left ischaemic foot pain being treated last 4 weeks with antibiotics” and refers to the podiatry letter. It is then noted that his left foot was discoloured and “feels cold.. ankle pulses +. Ref surgical”. Professor McCollum made the point that at this date there can have been no ankle pulses at all, and draws this to my attention as evidence of how common it is for false positive findings to be made by inexperienced doctors who think they can feel a pulse when there is none to feel. This note, interpreted in this way, would suggest that the doctor felt two false positives. It is suggested that this provides a valuable insight into Dr. Thom’s recorded palpation of a single pulse at the medial malleolus (ankle) on 6th April 2005. I do not accept that I should read the note this way. It is at least equally possible that what the doctor has recorded is “x” rather than a “+” sign. I accept that the note appears as “+” rather than “x”, but it seems more likely that the doctor was attempting to record an absence of pulses than a double false positive. This is reinforced by the fact that the doctor no doubt had the podiatrist’s letter of referral which recorded the absence of pulses and referred to the fact that the podiatrist had to some extent used a Doppler device in his examination. He would be less likely to make a false under-diagnosis knowing that a podiatrist with Doppler technology available to him had made a diagnosis. This is a small point, to which I attach little significance one way or the other.[31]In fact the Claimant was not referred directly to the surgeons, but to the SDTC again and triaged there at 17:08 by Nurse Finlayson who noted, inter alia:
“3/52 h/o L foot feeling cold to the touch, swelling, redness with blackened tip of big toe and discolouration of little toe. Patient states he has pain like electrical current shooting through L foot and into lower leg. No swelling or pain to l calf. Difficulty walking on limb [the note then accurately records the history of treatment by the GP in April]. PMH: RTA September 04 damaged L foot then. ... Works as shipping linesman. Lives alone. Mum has been helping with daily needs. O/E difficulty in walking in to CR L foot red, warm to the touch Blackened big toe with discolouration of toe nail Little toe small broken area and red Skin over foot dry

...Discussed and seen by Dr Rao, who referred patient to surgeons...”

This is an important note. For the first time, a clinician has recorded an observation that the Claimant had difficulty walking. The Claimant was clearly complaining of significant difficulty with daily living which required help from his mother. She records a complaint of pain in the leg, as well as the foot. She finds a red foot with gangrene. There is no doubt that she is looking at a “sunset foot”. This is a careful note recording the history given and her findings on examination. She records a history of symptoms over 3 weeks, which goes back again to the third week in April. I find that this Note accurately records what the Claimant said to Nurse Finlayson. His account of the antibiotics prescribed in April is reasonably accurate, which suggests that he was able to give a reasonably reliable account that day. This is further confirmation of a significant downturn in the Claimant’s condition which must have occurred between the 21st April and 28th April. The Second Defendant’s diagnosis of athlete’s foot on 21st April, negligent as it was, is simply inexplicable if one assumes a presentation on that day of similar signs and symptoms to those noted here by Nurse Finlayson. The Claimant was clearly not asymptomatic before that downturn but his symptoms were milder, less disabling, and more intermittent than they later became. The accounts given by the Claimant to the A&E and SDTC on this day are not consistent with the symptoms beginning in February. O/E difficulty in walking in to CR L foot red, warm to the touch Blackened big toe with discolouration of toe nail Little toe small broken area and red Skin over foot dry ...Discussed and seen by Dr Rao, who referred patient to surgeons...”[32]The Claimant was then seen by a doctor, according to the note on the Care Continuum Progress sheet the SHO working under the direction of Mr Ahmed, a consultant surgeon, at 18.30 that day (12th May 2005):
“Painful black big toe Left – 3 weeks Initially noticed numbness of left leg + foot which gradually changed colour - Over last 3 months was getting pain in L leg on walking: claudication distance 100 yards - Very painful to stand on L foot now - Pain aggravates on lying flat : relieves on hanging foot down the bed - Can feel the foot and move toes.”
It was noted that the left femoral artery pulse was present but the left posterior tibial and the left dorsalis pedis were both absent, that capillary refill was more than 3 seconds, and the left foot was discoloured and cold with a gangrenous big toe. The doctor then carried out a clinical examination of the lower limbs using Doppler and recorded that the popliteal, PTA and dorsalis pedis pulses were all absent in the left leg. Initially noticed numbness of left leg + foot which gradually changed colour This Note was subject to criticism by Mr. Collin who felt that the record of claudication in the left leg was simply wrong. He said this because it is quite inconsistent with the earlier records which all record pain in the foot, but not the leg. This record refers to that symptom as being present for two months, i.e. back to mid-March. It is certainly true that this account is inconsistent with the earlier histories given, but the only real effort to record a proper history, examination and diagnosis prior to 12th May was that of Nurse Gazes on 6th April and by Dr. Thom on her x-ray request form on the same date and in the record of her opinion that there was ischaemia but not critical ischaemia. None of the GP records contains any real attempt to record a history from the Claimant. The history obtained by this doctor is not really consistent with any of the experts’ views as to how the pathology and therefore the signs and symptoms developed. This history suggests pain starting in the leg, three months earlier, and then, 3 weeks ago, blackening of the toe and “now” very painful to stand on the foot. It seems to me highly improbable that this apparently careful record of the history given by the Claimant is simply wrong in that it records things which he did not say and that it is more likely that the Claimant was in great pain at the time and, by this time, becoming rather tired of giving his history to different people. He had spoken on that day to the Podiatrist, the triage nurse and doctor at the A&E and to the triage nurse at the SDTC. The histories he gave were not consistent with each other and not consistent with the history given on 6th April either. However, I think it likely that this is a reliable note of the history provided, being taken by the first doctor with any special interest in the relevant condition whom the Claimant had seen. This suggests that there was a condition starting about three months earlier which involved the leg and foot in which the symptoms were less severe than they later became. About three weeks before this date, there had been a change in which the foot had become more painful and had changed colour. I do not think it likely that there had been gangrene as long before as 3 weeks, but rather that it was at that stage that the signs and symptoms became more severe than they had been. Three months before 12th May 2005 is, of course, February. I suspect that this note may be the origin of the witness statement which asserts that as the date when symptoms began. However, although I am satisfied that this is what the Claimant said to the SHO, I am not at all satisfied that this was accurate.

Initially noticed numbness of left leg + foot which gradually changed colour

[33]He was seen by the Registrar at 19.00 who noted a gangrenous left big toe and “acute on chronic ischaemia”. He was given Heparin, to have an angiogram and he was admitted. It seems likely from the timed record on the Care Continuum Form that the SHO and the Registrar were working together at this time. That record shows the Claimant being seen by the SHO at or after 18:45. The Doppler (recorded by the SHO) is shown as being done at 19:00 and the Registrar is there recorded as seeing the Claimant at 19:15, rather than 19:00 as shown on the Registrar’s own note. These different times are probably the times when the notes were made during a fairly lengthy series of events which involved the SHO and the Registrar both seeing the Claimant. The fact that there were two doctors, one a Registrar, working together reduces the likelihood of any serious errors in the history being made. The Registrar does not record a history himself, and his diagnosis therefore relied upon that recorded by the SHO.[34]On 13th May 2005, Mr. Ahmed who was a consultant surgeon but not (I think) a consultant vascular surgeon, saw the Claimant. He recorded a history of symptoms over 5 weeks which included a claudication distance of 50 yards. On examination he noted “[History of] pain foot 1/12. Acute on chronic ischaemia Left foot. [History of] claudication at 50 metres.” His diagnosis is the same as that of the registrar, but he does not record any symptoms in the leg, as opposed to the foot. Some of the inconsistency must be due to inaccuracy by the Claimant in giving his account. However, his note is less precise than that of the SHO. Plainly the SHO, the Registrar and the Consultant all felt that this was “acute on chronic” ischaemia. They date the acute phase back three weeks or one month. Only the SHO has made a clear attempt to distinguish between the chronic and the acute symptoms.[35]On 13th May 2005 the Claimant underwent trans-femoral angiography [i.e. a radiological procedure to check the patency of the arteries] and thrombolysis [the breaking down of blood clots by pharmacological means: i.e. using “clot busting” drugs abbreviated as “tPA”]. It was reported in relation to the left leg:
“Left leg: Normal SFA [superficial femoral artery] to level of occlusion at or just above the adductor canal. Reasonable medial geniculate connects via collaterals to distal posterior tibial artery which passes into foot. A few segments of other calf arteries seen, but of poor calibre. Catheters passed to level of clot. 5mg tPA [tissue plasminogen activator] given over 90 minutes. Clot seen in proximal popliteal/distal SFA which did not clear. Wires passed readily into posterior tibial and peroneal but not anterior tibial. Immediately after wires removed clot re-accumulated. Foot cold and movement a little improved.

In discussion with Mr Andrews [surgeon] procedure abandoned and patient taken to theatre.”

In discussion with Mr Andrews [surgeon] procedure abandoned and patient taken to theatre.”[36]I have heard a great deal of expert evidence about this procedure, and its interpretation is central to the Claimant’s case. I shall record my findings after my review of the expert evidence. At this stage, however, it is helpful to interpolate the evidence of Dr. Ashleigh who showed me the angiograms and explained their significance. He concluded that this Note did not set out the findings on angiography entirely accurately. A segment of the PTA was seen to be patent, but this must have been occluded by blockages at both the distal and proximal end of the segment. It was fed by a collateral vessel and drained into a collateral vessel. It was not, therefore, the PTA which passed into the foot, but a collateral vessel. The thrombolysis achieved some temporary success in partially recanalising the popliteal artery, allowing the dye to pass down the PTA to the mid-calf level. The note records that the wires passed readily into the PTA and peroneal artery, but not into the ATA. It does not record how far they got. Mr. Collin thought that they might have got all the way to the ankle, but Dr. Ashleigh, supported by Professor McCollum, thought that this was unlikely. They both felt that if the wires had been passed as far as that this feat would have been recorded in the note. Whether this procedure was almost successful or a complete failure is an issue between the experts to which I shall return. What is known is that after 90 minutes Dr. Toye, the radiologist who was performing it, in discussion with Mr. Andrews the vascular surgeon decided to abandon it and to proceed to surgery. 90 minutes is an usually short time for thrombolysis although the dose of tPA was a high one. There is no note by either Dr. Toye or Mr. Andrews of the reason for the decision to abandon thrombolysis, unfortunately, but it is an obvious inference that they felt that it had not succeeded and was not likely to. I shall deal with other hypotheses when I come to the expert evidence.[37]Following the failure of thrombolysis to re-perfuse the left foot successfully, the Claimant was taken to theatre where a left popliteal artery embolectomy and fasciotomies were carried out. The operation note reads:
“Popliteal artery below knee, anterior tibial and tibio peroneal trunk isolated. Transvered arteriotomy at bifurcation. Very adherent/organised thrombus occluding vessel. Proximal embolectomy size 4 Fogarty clot removed good inflow. Distally unable to remove thrombus with the Fogarty but size 2/3 catheters passed to mid calf. Img TPA instilled in anterior tibial artery and tibio peroneal trunk. Also 1mg GTN given intra-arterially and Heparin flush, back flow plus....”
[38]A follow-up angiogram was taken on 1st June 2005 to assess the success of the embolectomy. It was reported as showing:
“complete occlusion of the left superficial femoral artery just above the adductor hiatus. Due to the occlusion there is no normal native vessel only collaterals. In the distal calf no circulation recorded into the foot.”
[39]The left foot remained ischaemic and non-viable and a left below knee amputation was carried out on 20th June 2005. He was subsequently provided with a prosthetic limb.[40]Findings of Fact In relation to the History i) I find that the reference to February 2005 in the Claimant’s witness statement is inaccurate. It is inconsistent with most of the contemporary clinical records. He began to suffer pain in his left foot in March, probably not very long before he presented to his GP complaining of pain in his left foot on 24th March 2005. Dr. Mongalee, who is not accused of negligence, failed to record any detailed history. If he made a diagnosis at all, he did not record one. I cannot therefore say when the pain began, but having regard to the Claimant’s occupation I do not think it likely that he struggled with pain at rest for a month or so without seeking some treatment. I think he probably did decide to see his doctor when he felt pain when using the clutch on his car, but I do not think that this took place in February. Although the SHO’s note of 12th May 2005 supports February as the start of symptoms, I do not think that the Claimant was giving an accurate history at that time. I prefer the probability that a man with an active job will not wait over a month before seeking treatment when he begins to suffer symptoms in his foot. One possibility is that he really was still suffering some minor symptoms in his foot which were the after effect of his road traffic accident. Then he began to suffer symptoms in the same foot from a different cause altogether although he did not appreciate this. It may well be that the localised pain on depressing the clutch experienced shortly before the 24th March was the start of the onset of symptoms truly attributable to the ischaemia. ii) I consider that the Claimant was probably suffering some pain at rest on 24th March 2005, as he said to Professor McCollum in July 2009. As I have already found, I do not think that by that date he had any clear idea when his various symptoms started, although I do think that his account of events in the third week of April is reasonably accurate because it is consistent with various contemporary records as I have tried to explain above. At the point when he consulted Dr. Mongalee, they both considered that he was fit to carry on working and he did so. At this point, on the balance of probability he was suffering significant pain, and including rest pain, but pain at a far lower level than he suffered later. The references to claudication in the notes by Anna Gazes on 6th April 2005 (paragraph 19 above), the SHO’s note of 12th May 2005 (paragraph 32 above), and the ward round note of Mr. Ahmed on 13th May 2005 (paragraph 34 above) all suggest that there was a time when the pain was experienced on exercise and that rest pain was less severe. The claudication in the leg if it occurred at all recorded by the SHO must have accompanied the occlusion of the crural arteries at their origin, that is proximally. This must have been at a point in the process after the arteries in the foot and distal calf vessels were occluded, and so rather later than the SHO’s Note would suggest. I find on the balance of probability that the pain he was suffering on 24th March 2005 was ischaemic in origin. No other cause for such pain has been identified and Mr. Collin’s observation in evidence that it may not have been ischaemic pain at all is not one I can accept. This seemed to me to ignore the findings of the 6th April and 12th May which clearly implicate ischaemia as the source of symptoms by late March 2005. iii) Relying on the history taken by the SHO on 12th May 2005, I think that there was some pain in the leg on exercise during the early phase of the development of the symptoms, but that the principal site of the pain was the foot. This probably began rather later than the foot pain, but was intermittent and not a major symptom which is why the Claimant did not mention it until 12th May. iv) On the 6th April there was a substantial deterioration in symptoms causing the Claimant, who is a stoical patient, to present at A&E at 02:51am. I think that he was probably unable to sleep because of the pain in his foot which implies that he was now experiencing quite severe pain at rest as well as claudication in the foot. He was concerned that he might have broken his foot. I find that Nurse Gazes and Dr. Thom carried out proper examinations of the Claimant and that their findings were properly arrived at and noted. I deal with Dr. Thom’s palpation of a pulse separately below. The Claimant was suffering ischaemia and, unless there was a pulse as Dr. Thom believed, this was limb threatening ischaemia involving at least occlusion of either two or three of the named calf arteries at some point above the ankle. Although the Claimant’s history was of symptoms back to September 2004, this cannot have been true. He had not presented as an emergency to A&E during that time, and something had obviously changed to cause him to do so then. This obviously confused the clinical picture appraised by Dr. Thom. v) In or about the third week in April (by which I mean the period between the consultations on 21st April and 28th April) an event occurred which involved the Claimant stubbing his toe on some material on the floor which caused a sharp deterioration in his symptoms. This finding relies on the comparison of the GP Notes for those two dates, the history given to Professor McCollum and the records on triage and when seen by the SHO on 12th May 2005. For about three weeks prior to admission on that date, things were very much worse than they had been. I think it unlikely that Dr. Hussain on 28th April and Dr. Gopal on 5th May would have both missed the gangrene, so I find that this became apparent between 5th May and 12th May. The event when he stubbed his toe did not cause any new emboli but did begin a process in which the foot (now very ischaemic) began to break down. It was in late April or early May that blockages were forming in the popliteal artery which had the effect of further reducing an already severely compromised supply to the lower limb. The Expert Evidence[41]I heard from expert witnesses in the following order:- i) Dr. Raymond Ashleigh, a consultant interventional vascular radiologist at the University Hospital of South Manchester NHS Foundation Trust who was called by the First Defendant. He was called first because he was the only radiologist to give evidence and he explained and interpreted the angiograms. It was convenient for Mr. Collin to hear this evidence before he gave his evidence. No other party relied on this category of expert evidence although the Claimant was given permission to do so if he wished. Dr. Ashleigh confirmed that his report of 12th December 2009 represented his true opinions and gave extensive and very helpful oral evidence explaining the anatomy and the processes with which this case is concerned. ii) Mr. Jack Collin, a consultant vascular surgeon at the John Radcliffe Hospital Oxford and Professorial Fellow at Trinity College Oxford. He prepared two documents which I have seen (I have not examined his condition and prognosis report) namely his report of 18th December 2009, and a document advising the Claimant’s solicitor on how to respond to some Part 18 requests dated the 20th January 2009. He also participated in the joint discussions between the three vascular surgeons and signed the joint statement which records their views on 7th July 2010. At the start of his evidence he said that he stood by his views expressed in the Report of December 2009 and the Joint Statement. They are different in some respects and he later explained that he meant that these documents accurately reflected his views at the time when he signed them. iii) Professor Charles McCollum who is Professor of Surgery at the University of Manchester and Honorary Consultant Surgeon at the South Manchester University Hospitals NHS Trust gave evidence on behalf of the First Defendant. He confirmed his report which is dated the 11th January 2009 and also confirmed the Joint Statement which he signed on 5th July 2010. iv) Mr. Stephen Brearley, Consultant General and Vascular Surgeon at Whipps Cross University Hospital and Honorary Senior Lecturer in the Joint Medical School of St Bartholomew’s and the Royal London Hospitals gave evidence on behalf of the Second Defendant. He confirmed his report of 18th January 2010 and his opinions in the Joint Statement. I have not seen a copy of that document signed by him, but he told me and I accept that he did sign it. His oral evidence was limited to the critical issues in the case as they had developed during the hearing of the rest of the evidence.[42]I also read the reports of the GP experts which were placed in the Bundle by agreement. In the event, I do not think that anything turns on them.[43]I wish to record my gratitude to all the expert witnesses for the help which they gave to the court in this difficult case. Although I will make criticisms of Mr. Collin’s evidence and to some extent of that of Professor McCollum, these are to be seen in the context of experts trying to piece together a coherent explanation for a confusing picture and not as evidence of any improper approach to their duties to the court.[44]The reports and the joint statement are all in evidence and I have read and had regard to all of that material. It seems to me that the best way to approach this evidence is to identify the areas of disagreement which are important and to make findings on those areas as I do so. I will then apply those findings to the factual findings I have made above and so decide the issue of causation.[45]The first general point which I wish to make is that I have had to deal with this case on the basis of assertion and counter-assertion. The assertions are supported by argument from principle or from experience. Each side has expressed their views firmly. Only one piece of research from the literature has been produced, which is an article by Mr. Brearley on the reliability of the detection of pulses on palpation. This paper is cited as Brearley S, Shearman CP, Simms MS Peripheral pulse palpation: an unreliable physical sign An Roy Coll Surg Eng 1992; 75: 169-171. I shall deal with that briefly when I address the pulse issue below. In the absence of literature supporting the opinions given in evidence, I have to judge them on the balance of probability doing the best I can. I have not decided the case either on any difference in the relative achievement or distinction of the experts, all of whom are very well qualified to give expert evidence and are distinguished practitioners. Neither have I rejected Mr. Collin’s evidence because he is outnumbered. That is a consequence of the Claimant’s choice to sue two defendants and the fact that the Claimant did not rely upon a radiologist. I have attempted to judge the issues by assessing the probability of the conclusions of the various experts being right. The absence of medical literature on these issues does not mean that medical science is unable to determine the cause of the Claimant’s injury, or that there were many causes of it. It is now, albeit rather late, effectively agreed that there was a process by which embolisation occurred in which small emboli were carried at least as far as the ankle and followed by further emboli which caused blockages proximally so that the three crural arteries became occluded and a major occlusion occurred at the SFA/popliteal artery which contained components which were of different ages, the component distal to the arteriotomy of the 13th May 2005 being older and more organised than that proximal part. The question is not what caused this problem but how and when it might have been reversed or arrested by the use of medical or surgical procedures with which the experts who gave evidence are, between them, thoroughly familiar.[46]I shall not attempt to decide every expert disagreement, only those which are necessary to enable me to decide the case. Mr. Collin’s Thesis[47]In his Report Mr. Collin approached the case on the basis that there was a single event which explained what happened, namely thrombo-embolic occlusion of the superficial femoral artery at the adductor canal. He said on page 11 of his Report In patients who suffer acute embolic occlusion of a normal superficial femoral artery, popliteal artery and origin of crural arteries thrombo-embolectomy is almost always successful in restoring blood flow to the limb and foot when the operation is performed within one week of the occlusion having occurred. If the restoration of the blood supply occurs before irreversible ischaemic changes have occurred within the foot then an amputation of the leg is prevented. .........By the time that the thrombus has been present within the artery for around 6 weeks it is usually not possible to remove the thrombus by attempted embolectomy. The medical records of the operation performed on 13th May 2005 confirm that it was possible to remove a substantial part of the blood clot that has occluded the superficial femoral, popliteal and crural arteries in the recent past. The fact that much of the thrombus could still be removed at operation on 13th May 2005 leads me to believe that if it had been possible to perform the operation around one week before 13th may 2005 then a thrombo-embolectomy would have been successful in restoring circulation to the left foot. The same facts lead me to conclude that it is likely that the thrombo-embolic occlusion occurred around the beginning of April 2005.[48]In the Joint Statement in answer to Question 13 the following answer is given:- JC considers that the anterior tibial and peroneal arteries were occluded before the critical occlusion of the popliteal artery. In his opinion, the popliteal artery occlusion occurred at the end of April or beginning of May 2005. SB and CM agreed that SM would not have had symptoms of severe ischaemia in his foot if there was inline flow in any artery supplying the foot. They agree that all the foot arteries would have had to be occluded for SM to develop rest pain. CM and SB were firm in their view that the named arteries supplying the foot were occluded by mid-March and that these occlusions would have extended into the distal calf arteries.[49]It will be appreciated that the answer of Mr. Collin here recorded is inconsistent with the Report, both as to the date when the popliteal artery occluded and as to the new opinion in the Joint Statement that the anterior tibial and peroneal arteries were occluded before the popliteal artery occluded.[50]In his oral evidence he explained that he had first dated the popliteal occlusion to 5 weeks before the operation because it had almost succeeded, but had not succeeded. This meant that the occlusion was at the outer end of the time frame within which surgery might be successful and that outer limit was six weeks. Having heard the evidence of Dr. Ashleigh he added a new piece of evidence which was that the thrombolysis by Dr. Toye was also almost successful which was a further indication of the recent nature of the occlusions. As I have indicated above, the evidence of Dr. Ashleigh suggests that the procedure was somewhat more successful than Dr. Toye’s note would suggest. However, he certainly did not himself describe it as “almost successful”. When it was put to Mr. Collin that he had changed his opinion he said that he had done so having considered the reports of Dr. Ashleigh, and Professor McCollum and Mr. Brearley. He felt that he had initially been in error in attempting to ascribe all the consequences to a single event.[51]An expert who is willing to change his mind in response to new material or to the opinions of others is not therefore rendered unreliable. Indeed, a refusal to react in this way to new evidence is more likely to lead to the rejection of the expert’s evidence if it shows inflexibility and a refusal to countenance any other opinion than his own. However, it is the fact that Mr. Collin’s Report did not to my mind adequately deal with what is known about the pathology in the calf and foot which means that I cannot accept his evidence that surgical or thrombolytic intervention one week before the 13th May 2005 would have revascularised the lower limb and returned it to a normal condition. For this reason, I find that Mr. Collin’s original view was untenable and the fact that he ever subscribed to it does undermine my confidence in his analysis of the case on other issues. On this issue I prefer the evidence of Dr. Ashleigh, Professor McCollum and Mr. Brearley. There were occlusions in the calf and foot below the popliteal occlusion and these were central to understanding the process and assessing its outcome. Any theory which fails to address these is a theory which does not take into account all the relevant evidence. Having espoused it, Mr. Collin has modified it but, as he said to me on a number of occasions, has not really changed his approach to the case. He continues to work back from the procedures of the 13th May 2005 and to assess the extent to which they had a chance of re-vascularising the limb on the basis of a false premise that there was a “single critical event.” Although he now accepts other events lower in the limb, he does not give them the importance they deserve. Therefore, his subsequent revisions of his opinion continue to be affected by his original error.[52]I have also been influenced by the document of the 20th January 2009 in which Mr. Collin advised the Claimant’s solicitors how to answer some Part 18 Requests. One of these questions asked whether it was the Claimant’s case that he was already suffering from critical ischaemia in the left limb by the time he was seen by the Second Defendant’s [sic] servants or agents on 6th April 2005. In answer, Mr. Collin listed 6 symptoms and said “The symptoms and signs present by 6th April 2005 were those of critical ischaemia of the left foot.” Of these signs, the first 3 depended on the accuracy of the Claimant’s witness statement which Mr. Collin now, and in his Report of December 2009, properly as I have found, invites me to disregard. There is no indication of that opinion in the January 2009 document. He did not list the finding of a pulse, which would have been an indication that the opinion given in January 2009 was wrong. He told me that he was unaware of this at that time although it is referred to in the Particulars of Claim. He now invites me to doubt whether there was critical, or “acute” or “limb threatening ischaemia” present on that day and gave me a list of reasons for doing so. He explained this by saying that the January 2009 document was simply a list of features which were supportive of acute critical ischaemia at 6th April 2005 and that he was simply trying to answer the question from the information present at the time. I did not wholly understand this explanation and it did not seem to me to answer the well made point that in January 2009 he was plainly accepting that the foot was critically ischaemic (and that Dr. Thom’s opinion to the contrary was therefore wrong), whereas now, in July 2010, he was saying the opposite. It is true that he is now aware of her report of palpating a pulse, but he should have been aware of that then. As I shall later explain, that finding is not reliable and not a sufficient reason for such a major change of opinion.[53]For these reasons I am unable to accept the evidence of Mr. Collin where it conflicts with that of Mr. Brearley and Professor McCollum. The Thesis of Professor McCollum and Mr. Brearley[54]Professor McCollum and Mr. Brearley both support a view set out in the Joint Statement in answer to question 11:- CM and SB are of the firm opinion that this was a progressive silting up of the arteries from the foot proximally into the calf and ultimately into the popliteal artery. JC is of the opinion that there was a stepwise deterioration due to emboli with the final deterioration due to occlusion of the popliteal artery.[55]I accept the evidence of Dr. Ashleigh which was given impartially and which was uninfluenced by the disagreement between eminent vascular surgeons. He was not involved in the joint discussions with them and did not find himself taking any polarised position. His analysis makes it quite clear that there were occlusions in the calf arteries of different ages. Even when some recanalisation of the popliteal artery was achieved by thrombolysis, the dye did not enter the anterior tibial or peroneal arteries and only travelled to the mid-calf level in the posterior tibial artery. The findings also showed a patent segment of the posterior tibial artery with occlusions at each end. These must be of different ages. Because the thrombolysis had some effect on the recent blockage at the popliteal artery it follows that all blockages in the posterior tibial artery were older than the popliteal blockage. All of this suggests that the oldest blockages in the calf were in the anterior tibial and peroneal arteries, with some blockages of different ages to the posterior tibial artery which may have been more recent. More recent still was the occlusion at the popliteal artery, although even that was shown at operation to have components of different ages. It seems highly likely that these blockages were caused by small emboli travelling from the defect in the abdominal aorta and that they had been preceded by earlier, smaller emboli which had occluded some of the vessels in the foot without wholly removing the blood supply to any part of the foot. This is likely given the random way in which emboli of different sizes will have been thrown off by the lesion in the aorta.[56]Therefore, I accept the opinion of Professor McCollum and Mr. Brearley that the blockages began in the foot and calf, but I also consider that the theory of “silting up” as I originally understood it is not made out. This is partly for the reason given by Mr. Collin, namely that such occlusions in the foot would have caused tissue death long before the first sign of gangrene became apparent shortly before the 12th May 2005. Even at that date a supply to the foot by collateral vessels was being maintained, even though there was now an occlusion at the popliteal artery. Otherwise the whole foot would have died, especially if the foot had been symptomatic for this reason since mid-February as they both contend. Further, I accept the point made by Mr. Woolf that the theory has undergone some change in the presentation. Professor McCollum said that he never intended to suggest that the whole foot was “silted up”, up to and including the final distribution vessels into the toes. The answer to Question 13 of the Joint Statement is set out at paragraph 49 above. The passage setting out the opinion of Mr. Brearley and Professor McCollum was put to Professor McCollum and he suggested that it was not well phrased and that what they had actually meant was that all the arteries supplying the foot would have had to be occluded for SM to develop rest pain. However, it is clear from the last sentence of that answer that the occlusions were in the foot arteries and extending “into the distal calf arteries”. There are other references to the silting up theory in the Report and it is never clearly stated that this did not involve occlusion of the supply to the toes. Further, I noted that Professor McCollum dealt with Mr. Collin’s point about tissue death by stressing emphatically that as a young man the Claimant would develop collateral circulation “within days” of the occlusion which would delay tissue death until further occlusions occurred later in the process. I contrasted this with his evidence that the popliteal occlusion had occurred more than two weeks before the operation and probably as much as four weeks before the operation. He relied upon the presence of a developed collateral supply at the site of the occlusion which he said would take time to develop: he thought it might take 2, 3, or 4 weeks. When asked about this he said that when he described development of collaterals “within days” he had meant that they would start to develop within days. I did not find this a satisfactory explanation of his evidence and this contrast somewhat reduced my confidence in his account. Finally, both Professor McCollum and Mr. Brearley relied heavily on this history given by the Claimant which I have found to be inaccurate. In particular, I have given credence to a record by the SHO that the Claimant did complain that he had suffered pain in the leg in the early phase of the development of his condition. I have also found that the development of the symptoms was not in fact as insidious as he described in his witness statement, but started shortly before the 24th March, became suddenly worse in the early hours of 6th April and again between 21st and 28th April. The experts cannot be blamed for relying on the history given, but the fact that they did so undermines their conclusions when it turns out that they were misled by an inaccurate witness statement.[57]Therefore, the development of symptoms was not a single event as first postulated by Mr. Collin, but neither was it “silting up” in the sense of complete occlusion to all the vessels of the foot starting at the toes and moving gradually up the foot and then the leg. This was what I understood the Defendants’ case to be at the start of the trial, and this is how I read the Reports. It has now been explained that this is not what was meant. I find that there was a series of occlusions in the calf and foot before the occlusion of the popliteal artery which caused the anterior tibial artery and the peroneal artery to be occluded and then the posterior tibial artery to be occluded. This was followed by the occlusion of the popliteal artery which occurred in late April or early May 2005. This explains why the foot remained vital as long as it did.[58]In these circumstances it is not necessary to address Mr. Collin’s evidence about the procedures of the 13th May at any length. On my finding as to the condition of the left lower limb on that day and the duration of the blockages in the calf and foot those procedures had a very limited chance of success on any view. However, I wish to record my finding that I do not accept that either procedure was almost successful. Both achieved some limited success followed by almost immediate re-clotting. Mr. Collin said that they might well have succeeded if i) The thrombolysis had been continued for a whole day as is normal practice; and ii) The thrombo-embolectomy had included a cannulation of the posterior tibial artery which was the one which had a patent segment and which had been opacified to the mid-calf on the angiogram.[59]Professor McCollum said that he detected during the trial that the catheter had in fact punctured the posterior tibial artery and that this meant that tPA could not be infused any further. This would explain why it was abandoned. Mr. Brearley agreed that there was a puncture but felt that Dr. Toye had been unaware of this because it is not noted as it should have been. Therefore he felt that the procedure was abandoned because it had failed and that Dr. Toye had never really thought it would succeed. This seems more plausible to me either than Professor McCollum’s explanation or Mr. Collin’s suggestion that it was abandoned too early when it still had a chance of success.[60]The surgeons agreed that it would have been better to ensure that the posterior tibial artery was cannulated when the thrombo-embolectomy was performed. This would have required a lower arteriotomy and was clearly not done. However, thrombo-embolectomy is described by Mr. Brearley as follows in an important passage of his report at paragraph 30, which is a passage which I accept as being correct:- The blockages in Mr. Marcus’s case involved small arteries in his calf and very small arteries in his foot. The foot arteries are too small for embolectomy to be feasible and even if the calf arteries can be cleared, they will inevitably re-thrombose if flow in them is prevented by blockages downstream.[61]Therefore, I find that the attempts to rescue the limb on 13th May 2005 were doomed to fail and were not almost successful. This removes the basis of Mr. Collin’s conclusion. I therefore find that they would have been no more successful, on the balance of probabilities, had they been attempted 1 week earlier. The question to which I now turn is when they became hopeless. The Principal Issue[62]In reality the case revolves around one issue. It is whether Professor McCollum and Mr. Brearley are right in saying that there would be no symptoms from occlusions of two out of the three crural arteries, and that symptoms would only be experienced once all three were blocked and the supply to the foot was being maintained by collaterals only. Mr. Collin said that he felt that symptoms could occur when two out of three of the crural arteries were occluded. Surprisingly, perhaps, I was not referred to any medical literature on the point and must resolve according to the strength of the arguments. I prefer the evidence of Mr. Brearley and Professor McCollum on this issue because:- i) I accept the evidence of Professor McCollum that the foot does not require a large supply of blood because there is relatively little musculature there. He told me that a normal crural artery is 2-3mm in diameter and can deliver 1 pint per minute, whereas the foot needs 400 mls per minute. If one assumes that one such vessel is patent and takes into account what he described as the “immense capacity of a young man to develop collaterals to supply the foot”, then it seems to me to be logical to conclude that a single patent crural artery can deliver an essentially normal supply of blood to the foot. ii) I accept Mr. Brearley’s evidence that when patients present with symptoms in one leg, it is normal practice to examine both legs radiologically and that this sometimes reveals that two of three crural arteries are blocked in the asymptomatic limb. iii) Mr. Brearley demonstrated the point by occluding one of the two arteries which supply his own left hand. He said that his hand did not change colour or become painful but that a normal supply was maintained. He told me that a similar process would operate in the foot. iv) Mr. Collin felt that the occlusion of two vessels would cause pain at rest in the foot. This was because of the sudden onset of the occlusions which means that as a young man he would not have time to develop collaterals while the blockages were developing as older people do. The blockage would occur and there would be no collaterals to make good the lost supply of blood. This seems highly theoretical and I do not think that it was supported by any evidence. I accept the evidence of Professor McCollum on this issue. The collaterals would develop “within days” and would restore the circulation to near normal levels.[63]I have found that there was quite severe rest pain as at 6th April and that there was rest pain related to the compromised blood supply to the limb on 24th March. I have accepted that this involved occlusion of all three vessels at the earlier of those dates. For embolectomy or thrombolysis to be likely to succeed the procedures must be attempted within 3 weeks at the very outside (the evidence is 2-3 weeks after the blockage they are more likely to fail than to succeed). As it happens, the relevant date for the Second Defendants is 14th April 2005, which is exactly three weeks after the 24th March. The relevant date for the First Defendant is 20th April 2005. However, I have found that the limb became symptomatic shortly before the 24th March and not on the 24th March. I find therefore that as at these dates the procedures would have been more likely to fail than to succeed. This is by the application of the agreed evidence on causation to which I refer at paragraph 6(i) above. This conclusion is reinforced by the presence of the blockages in the foot which would have the effect described by Mr. Brearley in the passage of his report quoted above. The palpation of the pulse on 6th April 2005[64]If this was a genuine finding, then obviously my preference for the evidence of Professor McCollum and Mr. Brearley that all three vessels must be occluded before the limb becomes symptomatic must be wrong. A pulse at the ankle as found by Dr. Thom would mean that the posterior tibial artery was patent at that date.[65]I have not found this an easy issue. There are arguments both ways, but in the end I have decided that Dr. Thom probably did not feel a pulse at the ankle and misled herself when she thought that she did. This is not a negligent error and is a mistake which many doctors will make. According to Mr. Brearley’s paper, which is the only published study on the subject of which I am aware, there is a false positive rate of 14% among doctors who are not vascular surgeons.[66]This evidence conflicts with the certainty with which Professor McCollum gave his evidence that such a sign is worthless. In 86% of cases it appears that the doctor making the finding will be right. I would have been more convinced by this if he had set it out in his Report. At the date when that Report was written the First Defendants, by whom he was instructed, were relying on that pulse as one of the facts in support of their pleaded case that Dr. Thom was not negligent. I asked him about this and he told me that he had communicated this view to the solicitors for the First Defendant in a letter which he thought was written in about April 2010. He also told me that he had not been supportive of Dr. Thom’s position. Of course, I accept his evidence on these two matters, but the fact that the material has not been disclosed and that his opinion on this issue did not emerge until the Joint Statement means that I cannot evaluate it by reference to its development and see how it was first expressed. I therefore have only a very dismissive opinion expressed orally which is at variance with the only published research on the point.[67]Mr. Brearley did set out his opinion on this issue at paragraph 29 of his Report and cited his own paper in support. I did not find his oral evidence about the capabilities of medical students at Oxford University very helpful, because his own research shows that students are much less good than experienced doctors at detecting this sign reliably. However, on balance I have concluded that he is right and that I should accord this sign recorded by Dr. Thom very little weight. Taking into account the overall clinical picture which includes my finding that all three vessels must be occluded to cause symptoms and that on that day, the 6th April, the limb was very symptomatic it seems to me that it is unlikely that there was a pulse and the probable explanation of that clinical record is that Dr. Thom was in error. The Claimant did not call Dr. Thom but relied on her statement as hearsay. I do not know therefore what she would have said under cross-examination which reduces the weight which I can attach to her evidence. Ultimately therefore I accept the evidence of Professor McCollum and Mr. Brearley that all three vessels were occluded on that day, and that they had been since a date prior to 24th March. Earlier provision of anti-coagulant medication[68]Professor McCollum and Mr. Collin both agreed that there was a window when anticoagulation could have stabilised the position allowing development of collaterals and saving the limb. Mr. Collin thought that this would occur if the therapy was provided at any time before what he called “the critical event”, and it would have prevented that critical event. Professor McCollum thought that the window was from mid-March to 6th April 2005. The reason he takes the 6th April 2005 as the end-point of his window of opportunity is because of the clinical findings on that day which he considers were signs of acute or limb threatening ischaemia. I accept this. He considers that the foot described in the notes on that day was beyond saving by anti-coagulant medication. Mr. Brearley agrees. I have found that the symptoms were not as long established as these experts believed, but it is not the duration of the symptoms which is important on this issue but the degree to which blockages were affecting the limb at that time. The anti coagulant medication could not dissolve blockages but only prevent further blockages occurring.[69]In answering this issue, it seems to me that I should scrutinise Mr. Collin’s reasoning. He continues to rely on a “critical event” which reflects his early approach to the case. I think that he continues to underplay the significance of the blockages in the calf and foot. He suggests that the anti coagulation would have left the Claimant with minor symptoms only, which ignores the fact that the symptoms on 6th April were not minor. I have found that they became worse later, but it is clear that the Claimant was suffering severe pain on 6th April or he would not have gone to the A&E at 02:51am. Mr. Collin’s thesis depends upon the leg being salvageable as long as there was no occlusion to the popliteal artery. On the balance of probability I accept the evidence that as at the 6th April it was already too late for anti-coagulation to save the lower limb of the Claimant. Reasons for refusing to accept Professor McCollum’s evidence that the Claimant might not have been admitted on 20th April and that the date for causation is even later than that[70]In view of my findings this is not a decisive issue, but I wish to record that I reject Professor McCollum’s evidence on it because it is inconsistent with what happened when the Claimant was finally presented to surgeons on the 12th May 2005. He was immediately admitted. I know that there was gangrene present by that stage, which was not there on 20th April 2005, but this is part of a process which needed to be urgently arrested before tissue death occurred. It seems entirely inconsistent with the gloomy prognosis for the limb as at 6th April 2005 to suggest that vascular surgeons might properly have delayed admission and treatment for some days after the 20th April 2005. Result[71]I have therefore with considerable regret accepted that anti-coagulants could not have saved the leg unless given before 6th April 2005 and that thrombolysis and embolectomy would probably have failed if tried at any time on or after 14th April 2005. Therefore the only damages which I can award to the Claimant are general damages for pain and suffering for 28 days against the Second Defendant and 22 days against the First Defendant. This pain was not relieved as it should have been by appropriate analgesia. The analgesia negligently prescribed by the Second Defendant in this period will, on the evidence, have had little effect. No award can achieve anything substantial for this Claimant and the exercise has an academic feel to it at the end of this difficult and very costly litigation. Nevertheless, doing the best I can to reflect the very severe nature of the pain which he avoidably suffered, I award him £2,000 by way of general damages against the Second Defendant and assess the sum payable in respect of the period when the First and Second Defendant are jointly and severally liable to him as £1,500. This means that the Claimant will receive the total sum of £2,000. My provisional view is that this will mean that as between the Defendants the First Defendants will pay £750 and the Second Defendants £1250. I will hear further submissions and rule if this is in dispute.[72]I wish to express my sadness at this outcome which will deprive the Claimant of a large sum of money which would make a real difference to his life. I have thought very carefully indeed about the ways in which it might be open to me to find for him, but have concluded that this is a clear case where, on the balance of probabilities, the Defendants could not have achieved the saving of his leg even if they had been as careful as they should have been. In these circumstances it is agreed that I do not need to consider the decision of the Court of Appeal in Bailey v. The Ministry of Defence and Another [2009] 1 WLR 1052. This case is within Hotson v. East Berkshire Area Health Authority [1987] AC 750.

Cited in 1 later judgment