It is necessary to set out the facts in some detail.

Mr Cunningham was born on 31 August 1967. On 22 October 1985, when he was aged 18, Mr Cunningham was riding his motor bicycle over some rough ground when he hit an obstruction. The motor bicycle fell on top of him and landed on the front of his left leg just below the knee. It seems that the accident happened between 2.30 pm and 3.00 pm on 22 October.

Mr Cunningham was taken by ambulance to the North Manchester General Hospital. He was admitted to the Casualty Department at 3.20 pm. After a short interval he was seen by Dr Sukmvinder Bhandal, a Senior House Officer on duty in the Casualty Department that afternoon. Dr Bhandal had qualified as a Medical Practitioner in 1984 and had been in the Casualty Department since August 1985.

Dr Bhandal examined Mr Cunningham though there was an issue at the trial as to the extent of her examination. Mr Cunningham was then wheeled on a trolley to the x-ray Department nearby where x-rays were taken of his left leg. It is clear that Dr Bhandal suspected that the leg had been fractured but she was unable to see any sign of a fracture on the x-ray. She decided to take the x-ray to Mr Christopher Slack, who at that time was the Registrar in Accident and Emergency at the hospital. Mr Slack pointed out that the x-ray showed a crack in the tibial bone and told her: "This is a tibial plateau fracture". According to her evidence at the trial (40G) Dr Bhandal asked Mr Slack what should be done and he said: "Plaster of Paris cylinder." Dr Bhandal then returned to Mr Cunningham and gave instructions to a nurse that a cylinder plaster of Paris should be fitted. It seems that the plaster of Paris was then fitted by Mrs Gibson, a staff nurse. I shall return later to refer to the note which Dr Bhandal made in the medical records that afternoon.

The records show that at 3.45 pm Mr Cunningham received a dose of 50mg of pethidine. This pain killing drug was administered by Nurse Walsh, a student nurse, on the instructions of Dr Bhandal. The record of its administration was initialled by Mrs Gibson.

At some time during the next hour or so Dr Bhandal went off duty. The junior doctors in the department worked on a shift system. At 5.10 pm, as the medical records disclose, Mr Cunningham was given a further dose of 50mg of pethidine. This dose too was administered by Nurse Walsh and the record was initialled by Mrs Gibson, but the instructions for its administration were given by another unidentified doctor. Later that evening Mr Cunningham's mother and brother arrived at the hospital. He went home with them with instructions to attend the next day at the Fracture Clinic at Ancoats Hospital in Manchester.

I shall have to return later to refer to the evidence given by Mr Cunningham and his mother about his condition on the night of 22/23 October 1985.

On the following morning, Wednesday 23 October, Mr Cunningham went with his mother by ambulance to Ancoats Hospital. He was seen by Mr Slack, the Surgeon to whom Dr Bhandal had shown the x-rays the previous afternoon. I understand that the x-rays had been sent to Ancoats Hospital on 23 October so that they should be available for Mr Slack to consult if he wished. Mr Slack examined Mr Cunningham in the presence of his mother. There is a dispute as to the extent of the examination. The examination was made more difficult by the fact that the leg was encased in a plaster of Paris cylinder and both the plaster and the foot, apart from the toes, were covered with elastoplast. I shall have to refer later to the typed note in the records of the examination on 23 October.

After the examination Mr Cunningham was sent home with instructions to come back for a review on Thursday 31 October.

During the following days Mr Cunningham was in increasing pain. On 29 October he went to see his General Practitioner, Dr Morrison. Dr Morrison sent him back to Ancoats hospital with a covering note in these terms:

"This young man had a left leg plaster following a motorbike accident and the fracture of his tibia and fibula. His foot has been swollen since but is more swollen and painful now for the last 2 days. I would be grateful if you would examine him."

Mr Cunningham was admitted to the hospital as an emergency at 5.45 pm on 29 October. According to the medical records it was found on examination that the plaster of Paris was intact; the lower leg was protected with elastoplast all round which was preventing the plaster of Paris sliding down. The medical records following his admission contained the following entry:

"Urgent admission. Pain ++ since injury. Pain has gone from 'bad to worse'. Called a taxi today because of pain. Alone in his flat. O/E [on examination] foot is cold and blanched and swollen but I can feel dorsalis pedis pulse. ..... Capillary flow is slow to re appear after pressure. Flicker of active movement of toes ..... Anterior compartment is tense and tender with normal sensation of shin to ankle. Calf also tender but less tense. Post tib pulse not palpable.

..... Impression compartment syndrome compression rather than direct damage to vessels."

Decompression procedures were then instituted which involved a fibulectomy.

On the following day, 30 October, it was recorded that the forefoot including the toes was still cold and white with loss of sensation. Arteriograms were taken of the left leg. These arteriograms were examined by Dr Chadwick, the Senior Registrar in Radiology, who made the following record:

"..... no identifiable major arterial branches below the level of the knee. There may be a high popliteal bifurcation complicating the picture, but the appearances are of a popliteal artery block. Posterior tibial appears to fill from mid calf level."

For the purpose of this appeal it is not necessary to examine in detail Mr Cunningham's later treatment at Ancoats Hospital. Efforts were made to save the leg but these were unsuccessful. On 19 November 1985 Mr Cunningham's left foot was partially amputated. In April 1986 as a result of post-operative infection Mr Cunningham's left leg was amputated below the knee.

The injury to, and the subsequent amputation of, Mr Cunningham's left leg caused grave damage to the quality of his life. His career prospects were seriously affected; his social life was disrupted and he was no longer able to pursue the sports and other active interests which he had previously enjoyed; and, in the words of Dr Sidney Levine a consultant psychiatrist who examined him in June 1990, he came to suffer from a significant degree of persistent reactive depression.

On 18 February 1988 a writ was issued on behalf of Mr Cunningham claiming damages against the Health Authority. It was alleged that the nature and extent of his injury had not been correctly diagnosed and that his treatment had been defective and inadequate on, and in the days immediately following, 22 October 1985. On behalf of the Health Authority on the other hand these allegations of negligent diagnosis and treatment were denied.

On Monday 15 July 1991 the action came on for hearing before Henry J in Manchester. The judge heard evidence over the course of the next four days. On Tuesday 23 July 1991 the judge delivered his judgment dismissing Mr Cunningham's claim.

Mr Cunningham has now appealed.

It will be necessary to trace what happened at the trial in some detail. At the same time, as I have come to the conclusion that notwithstanding the passage of time justice requires that this matter should be retried, it is important that I should set out the facts in as neutral a manner as possible.

The Case for Mr Cunningham at the start of the Trial.

The popliteal artery descends into the lower leg just below the knee. The artery bifurcates and then bifurcates again. In the immediate area of the knee joint the artery is close to, being within about a centimetre of, the bone. It is therefore plain that any fracture or displacement of bones in the vicinity of the knee joint carries the risk of causing a lesion of the popliteal artery.

It is common ground that at the time of Mr Cunningham's readmission to hospital on 29 October 1985 the popliteal artery in his left leg had become severely blocked. From the medical evidence which we have seen it seems that this blockage could have come about in four possible ways, which can be described in simple terms as follows:

(a) The trauma could have damaged the muscle and the soft tissue of the upper leg. This damage would have led to swelling which would have exerted increasing pressure on the blood vessels including the popliteal artery. Eventually the constriction of the artery would cause a blockage. This process is known as a compartmental pressure syndrome.

(b) A compartmental pressure syndrome could have developed in a somewhat different manner than in (a) by reason of impaired venous return. The pressure would have built up because of the impairment of the venous return and eventually would have led as in (a) to the constriction and blockage of the popliteal artery. In neither (a) nor (b) would there have been any lesion of the popliteal artery itself.

(c) The trauma might have caused a minor or moderate lesion of the popliteal artery. The lesion would have been followed by the seepage of blood into the muscle with an increase in pressure and swelling. Here again the increasing pressure and swelling would have led to the constriction and eventual blockage of the popliteal artery.

(d) The trauma might have caused severe damage to the popliteal artery leading to an immediate and serious flow of blood into the surrounding muscle. As in (c), though more quickly, the increasing pressure and swelling would have led to the constriction and blocking of the popliteal artery.

At the outset of the trial the medical evidence to be called on behalf of Mr Cunningham supported (d), that is, the theory that there had been a severe lesion of the popliteal artery caused by the trauma itself. The medical evidence to be called on behalf of the Health Authority on the other hand supported (a), that is, the theory that the trauma had caused muscle and soft tissue damage which had led to increasing swelling and pressure and finally to the blocking of the artery through compartmental pressure syndrome.

Before the trial the solicitors acting for Mr Cunningham instructed a number of medical experts to consider the case and to advise. These experts included:

(1) Mr Neville Kay, a consultant orthopaedic surgeon, who prepared written reports dated 9 November 1987, 24 May 1988 and 4 May 1989.

(2) Professor Ronald Grainger, a consultant radiologist, who prepared written reports dated 3 June 1989 and 1 April 1990.

(3) Mr W MorrisJones, a consultant vascular and general surgeon who prepared a written report dated 13 July 1991.

The medical experts instructed on behalf of the Health Authority included:

(1) Professor J Stevens, a professor of orthopaedics, who prepared medical reports dated 18 May 1988 and 8 July 1991.

(2) Mr DE Markham, a consultant orthopaedic surgeon, who prepared a written report dated 1 February 1989.

(3) Mr T Glyn Thomas, a consultant orthopaedic surgeon, who prepared a written report dated 13 February 1989.

The first of these reports was that of Mr Neville Kay who examined Mr Cunningham on 7 November 1987. In his report dated 9 November Mr Kay recorded what he had been told by Mr Cunningham and what he had found on examination. In addition he referred to the medical records which he had seen and the x-rays. I should set out what Mr Kay said about the x-rays:

"I have been sent a series of sixteen miniaturised radiographic plates, but I can only clearly identify one as being the initial injury radiographic, namely that dated 22.10.85. This is an oblique view of the left leg showing a fracture of the upper end of the tibia, associated with a fracture of the fibula, and this appears to be associated with slight backward displacement of the fracture."

Mr Kay continued:

"Regrettably, the fracture is through a site where it is well recognised that the popliteal artery divides and becomes fixed. This is a common site of injury to the artery, for at this stage the artery is vulnerable not only to surgical hazard during high tibial osteotomies, but also traumatic hazard as a result of the fracture.

I think the balance of probabilities is, therefore, that the artery was actually damaged at the time of the injury."

Later in the report Mr Kay referred to an arteriogram which he had seen, though I am not clear what document was before him. Mr Kay made this comment:

"The fact that the arteriogram showed a popliteal artery block would support the diagnosis that the damage was done at the time of the accident, namely that the fracture itself caused the damage to the artery as distinct from the plaster being put on too tight or too soon, which is what the patient believes."

In May 1988 the medical records including, it seems, the original x-rays and arteriograms were examined by Professor Stevens on behalf of the Health Authority. In his report dated 18 May 1988 Professor Stevens set out the history as disclosed in the documents and concluded in his report as follows:

"I firmly believe that in this instance there was a slow building up of oedema plus haematoma to compress the popliteal vessels and cause this syndrome. I simply cannot believe that anyone developing a compartment compression syndrome would have been discharged when he attended as an out patient as this man did."

In the following February further reports on the case were prepared on behalf of the Health Authority by Mr Markham and Mr Glyn Thomas. In his report dated 1 February 1989 Mr Markham recorded that he had carefully studied the papers and the case notes and he quoted a number of extracts from them. In the latter part of his report he expressed his opinion:

"There can be no doubt that Mr. Cunningham insidiously developed a compartment syndrome in his left leg following soft tissue injuries to the limb when his motor cycle fell across the leg. I do not consider that the fracture was significant in the development of this compartment syndrome. It is not uncommon for this condition to develop in an insidious way.

The surgeon who saw him in the fracture clinic on the day after the injury was very experienced and I am quite sure would have noticed discolouration, insensitivity and swelling of the toes had they been present. I am, therefore, confident knowing the surgeon concerned and having read his note that there was no evidence of peripheral vascular deficit on that day."

Mr Glyn Thomas' report dated 13 February 1989 was to the same effect. He concluded his report in these terms:

"The main point at issue is the interview on 23.10.85. In my view Mr. Slack's management on that date shows a satisfactory standard of care of the condition as it presented to him then. It is likely, in my view, that the compartment compression syndrome developed after that interview, as can so often happen."

It seems probable, though at present it is far from certain, that both Mr Markham and Mr Glyn Thomas had access to the original x-rays at the time when they wrote their reports. However that may be, it is quite clear that Professor Stevens saw the original x-ray plates because he made copies of them for his own use and indeed brought these copies to the court on the first day of the trial.

In April 1989 the solicitors then acting for Mr Cunningham sent to Mr Kay copies of the three reports which had been obtained on behalf of the Health Authority. Having read these reports and considered the two earlier reports which he had made Mr Kay restated his opinion in his letter to the solicitors dated 4 May 1989. He set out the ways in which a compartmental pressure syndrome can develop and expressed the view that the most likely sequence of events was that there had been direct arterial damage. A little later Mr Kay continued:

"In essence, therefore, I think the views of a radiologist on this arteriogram are going to be crucial and indeed helpful. Either the artery was damaged at the time of the accident by direct trauma from a fracture as I believe, or alternatively simply squeezed and closed by pressure developing within the compartments of the leg."

It was in these circumstances that Professor Grainger was instructed. It seems that Professor Grainger produced his first report in two parts. The earlier section was dated 3 June 1989 in which Professor Grainger referred to the papers which he had examined at that stage. The more important part of his report, however, was the second section which was dated 8 September 1989 and was prepared after he had been sent some miniature films. It will be necessary to make a number of references to this part of the report.

Professor Grainger began this section of his report as follows:

"The radiology involved in this case will play a very important part in consideration of possible negligence. Sixteen miniature films measuring 100mm square were sent to me. [Two of these films were x-rays and fourteen were arteriograms] I requested that the original radiographs should be located and referred to me as the miniature films were obviously copies of large films. On 5 September 1989 Mr.Lipworth [Mr. Cunningham's solicitor] telephoned me reporting that the hospital has advised him that the original films were copied on to miniature films and the original films were then destroyed as there is no filing space in the hospital to accommodate."

A little later in the report Professor Grainger commented on the miniature x-ray films:

"22.10.85. Two films frontal and lateral of the upper two-thirds of the calf and including the knee joint are available. There is a fracture involving the tibial plateau and the tibia immediately below it. There is minimal backward shift of the upper tibial fragments perhaps by one or two millimetres. There is a fracture of the neck of the fibula. In addition there is a very large soft tissue swelling. This swelling measures about twice the diameter of the upper tibia in its cross section dimension and in its vertical extension covers from the knee joint down to the junction of the upper third and lower two-thirds of the tibial shaft. This swelling is of considerable radio density suggesting that it may be due to bleeding. The skin is not swollen or oedematous. Swelling is very well contained and is predominantly behind the upper third of the calf with only a little swelling extending on either side of the tibia and fibula in the frontal view. The skin and subcutaneous tissues are not oedematous. The swelling is producing a marked local displacement of the tissues at the posterior aspect of the upper part of the calf and this should be obvious clinically. The appearances are very suggestive of a localised severe swelling arising from the tissues deep to the skin and closely related to the posterior aspect of the tibia. In view of the history of the fall from the motorbike with the bicycle falling on the left leg, the most likely cause for this very large swelling is an acute heamorrhage from damage to a major blood vessel in the upper calf."

Professor Grainger next considered the arteriogram films:

"30.10.85. A series of fourteen miniature arteriogram films is available. There is no date on the films but presumably they were taken on 30.10.85. They are taken of the left leg and include frontal projections from the lower portions of the shaft of the femur down to the ankle. Unfortunately only frontal (anteroposterior) projection films have been taken and as they are under-exposed (at least as seen on the miniature films) the detail of the anatomy in the region of the knee joint is not adequately seen. It can be seen that the upper part of the popliteal artery is patent and normal but about six inches (15 cm) of the popliteal artery behind the knee joint and behind the upper end of the tibia is completely invisible and cannot be assessed. In the calf the only substantial patent major artery is the peroneal artery and there has obviously been an occlusion of the popliteal artery behind the left knee joint with lack of filling of its two main branches. However because of the inadequate visibility of the popliteal artery, it is impossible to answer Mr. Kay's question as to whether the popliteal artery is occluded by compression from outside (as by a compartment compression syndrome) or whether it is occluded because of primary damage or laceration or thrombosis of the artery."

A little later in the report Professor Grainger set out his detailed comments in eight numbered paragraphs. I should refer to paras 2 and 7 of these comments:

"2. It may be argued that the original radiographs did not show soft tissue swelling as obviously as does the miniature film. This is possible as the miniaturisation process alters the contrast of the films but I am very confident that the original films would have shown very good evidence of this large localised swelling behind the upper portion of the tibia.

It is very unfortunate that the arteriogram of 30.10.85 does not show the popliteal artery in the region of its blockage. This information would have been obtained by taking a lateral film during arteriography with the leg turned laterally so the projection of the popliteal artery would have been obtained free from obscuration of the tibia. This however apparently was unfortunately not undertaken.

..................

7. I have not seen the radiologist's report of the films 22.10.85. It would be interesting to know whether the films were reported on by a radiologist and what his report was. I believe that this very substantial and localised soft tissue swelling should have been reported on those films but the treatment decided upon at the Accident Emergency Department would probably have been decided on before the radiographic report was available."

At the end of his report Professor Grainger expressed his conclusion:

"I firmly believe that the popliteal artery or vein was damaged by the fall of the motor cycle on the leg at the time of the initial injury. These lacerated vessels caused a very substantial haematoma which was evident within the first few hours and is clearly seen on the radiographs of 22.10.85 and should have been noted and recognised by the clinician treating the injury. The swelling of the left leg is so localised and occurred so quickly that the distinct possibility of severe vascular damage should have been considered at that time and if there was any clinical doubt a complete leg plaster should not have been applied."

Professor Grainger made a further written report dated 1 April 1990 in which he attempted to deal with some questions which had been raised by Mr Cunningham's solicitors. It is clear, however, from this report that Professor Grainger was still working on the miniature films and he remained confident that it was likely that the popliteal artery was damaged at or immediately after the accident. He wrote:

"There is no doubt in my mind that the film 22.10.85 indicates the very strong likelihood that the left popliteal artery was severely damaged at or immediately after the accident and that the artery bled immediately causing a very large haematoma (that is escape of blood) and that this haematoma and damage to the popliteal artery was the cause of the subsequent ischaemia of the left foot and leg. I would have thought from the radiograph 22.10.85 that the swelling behind the knee was so great and well localised that it could well have been detected clinically. That particular radiograph is absolutely vital to the case. I believe that it is much less likely that a compression syndrome due to post injury swelling in the compartments of the calf could be the cause of a subsequent ischaemia of the left leg and foot."

So matters stood when the case came on for hearing before Henry J on 15 July 1991.

The Trial.

I have not seen any transcript of the opening speech by counsel for Mr Cunningham. It seems fair to assume, however, that counsel would have anticipated that there would be a sharp conflict of evidence about Mr Cunningham's condition in October 1985, and in particular his condition on 22 and 23 October, and that the evidence of the radiologist would be of great importance.

Mr Cunningham and his mother gave evidence on the first day of the trial. Mr Cunningham said that on the night of 22/23 October he could not sleep and that his toes were stone cold. This evidence was supported by Mrs Cunningham, and both witnesses referred to the fact that she had tried to warm his toes first with a hot water bottle and then with a hairdryer. They also referred to the colour of the toes when Mr Cunningham was examined by Mr Slack on 23 October. Mr Cunningham said that he could not move his toes and that they were a yellow colour. Mrs Cunningham said they were white and tinged with purple.

Dr Bhandal and Mrs Gibson also gave evidence on the first day. Not surprisingly Dr Bhandal had to rely in a large measure on the note which she had made on 22 October and on what she described as her routine. We have seen a copy of her note in which she made a record of her examination and on which the entries of the administration of two doses of pethidine were made. She said in her evidence that she "would have felt" the pulses behind the ankle and on the dorsum of the foot. It is to be observed, however, that no note of the presence of these pulses was made in the hospital records.

Though the exact sequence of events is no longer clear it seems probable that it was not until about the mid day adjournment on the first day of the trial that Mr Cunningham's advisers heard for the first time that any full size copies of the x-rays were still in existence. Dr Bhadwan gave evidence that afternoon. In the course of her cross examination she was asked about the x-rays. It was suggested to her that she had seen the miniatures but she replied that she had not seen anything. At this stage counsel for the Health Authority intervened to say that some copy x-rays had arrived that morning. He continued:

"These are copies. We believe the originals were destroyed. There is the large scale copy and a condensed copy."

At the outset of the hearing on Tuesday, 16 July counsel for the Health Authority addressed the court again on the question of the x-rays. He said:

"Your lordship will have been aware we have only had the copy x-rays available, and all those in court believe the originals have been destroyed. They have not been destroyed, they were found this morning in the place where they have always been for a very long time, namely in the records of the hospital under the name of Mr. Cunningham. There are not many originals which are put there in the sense they look different from the copies which we have had so far."

Counsel then confirmed that the x-ray photographs were full size ones and were taken on 22 October. He continued:

" ... And there are a significantly larger number of angiograms than anybody believed was in existence from the number of copies, and they all deal with the question raised by Professor Grainger in his report that he says angiograms were not taken of the relevant angle, and he cannot find out exactly what happened. They were taken, and they are here, and Professor Grainger will be looking at them this morning.

There are other consequences of this, and I do not think, on the background, I ought to say more than they could well affect the view one takes of our alternative diagnosis."

A discussion then followed between counsel and the judge as to what action should be taken. Counsel for the Health Authority was concerned whether or not the original x-rays would justify the views which had been expressed by the three orthopaedic surgeons who were to be called on behalf of the defence.

The attitude of counsel for Mr Cunningham at that stage was to ask for a short adjournment of about half an hour to enable his experts to look at the new x-rays. The court then adjourned for thirty minutes (E53C).

When the court resumed counsel for Mr Cunningham addressed the judge:

"My experts have had the opportunity to consider the original films. They are in a position to proceed today, but they do feel that it does cast new light on the case, and I say this, obviously, from the plaintiff's point of view. They believe at this stage it materially strengthens the plaintiff's case."

Counsel for the Health Authority on the other hand wanted a further adjournment. He told the judge (E54A):

"The position I face is that there is evidence there are x-rays which to the untutored eye that is the new x-rays but it is not entirely untutored because I have been given the help of the radiologist, who indicates that the diagnosis of the compartment pressure syndrome is likely to be inappropriate."

In the end the judge decided to proceed and Professor Grainger was called to give evidence.

In his evidence in chief Professor Grainger

(a) Drew attention to the critical position in relation to the popliteal artery of the fracture line shown on the original x-ray (E57E) and stated

(b) That the miniature x-ray showed a remarkable enhancement of the original x-ray (E59B).

(c) That the miniature x-ray showed a white area which indicated extensive bleeding deep in the muscle in the leg (E59G)

(d) That the original angiogram taken on 30 October 1985 showed a retrograde thrombosis (E61D).

At the conclusion of his evidence in chief Professor Grainger repeated the conclusion which he had expressed in his report dated 11 September 1989 that "the popliteal artery or vein was damaged by the fall of the motor cycle on the leg at the time of the initial injury". At that stage counsel for the Health Authority reserved his cross examination.

Mr Kay gave evidence on Tuesday afternoon. He expressed the view that the site of the fracture signalled danger and that if there had been swelling present the case was "mandatory for admission" (E65C).

On Wednesday 17 July Professor Grainger was cross examined by counsel for the Health Authority. It was in the course of his cross examination that the suggestion was first made that there might have been some damage to the popliteal artery at the outset and that had been followed by bleeding into the calf muscle which eventually led to the subsequent pressure on the artery. Professor Grainger (E80E) accepted that this was a possibility.

In re-examination Professor Grainger referred again to the area of whiteness shown in particular on the miniature copy of the x-ray. He pointed out (E82D) that his report had been based on the miniature copy.

The next relevant witness was Mr Slack. He accepted that he had no recollection of Mr Cunningham's case (E88A). He explained, however, what his usual practice was and then made reference to the note which, I understand, he dictated on 23 October 1985. It was in these terms:

"This boy injured his leg coming off a motor bike yesterday. Xray showed an undisplaced fracture of the upper tibia. He is at the moment comfortable in a plaster cylinder. He can just about move his toes although as yet cannot do a straight leg raise. He should mobilise about the house with crutches. Should practise straight leg raising and practise moving his toes.

Review on Thursday morning. Xray through plaster on arrival."

It seems clear from the note and from Mr Slack's evidence about the note that he treated the case as a routine case which did not give any particular cause for concern. He said that at that time there was no particular pressure of work at the clinic and there was no administrative reason for him to hurry. He explained (E102B) that the first thing he would have looked for in his examination on 23 October was "circulatory problems".

The judge then heard the evidence of Professor Stevens who was called on behalf of the Health Authority. In addition, on Thursday 18 July, he heard the evidence of Mr Glyn Thomas and the further evidence including the cross examination of Mr Kay.

Professor Stevens stated that he thought that Mr Cunningham had had a perfectly normal foot when seen by Dr Bhandal and a perfectly normal foot when seen by Mr Slack on the following day (E119G). In addition he said that his explanation for the area of intense white on the miniature x-ray was that it had something to do with the process of miniaturisation (E120D), and that he would reject the possibility that there had been some damage to the popliteal artery at the time of the injury.

Mr Glyn Thomas was even more critical of the value of the miniature x-rays (E134B). He said:

"I think that as an orthopaedic surgeon I certainly would not base any clinical decision on the appearance of those miniature x-rays, which, after all, are copies, if not copies of copies of the original."

Subsequently he added "they are very inferior quality photographs".

A little later Mr Glyn Thomas dealt with the possibility that there had been some damage to the popliteal artery at the time of the original trauma. He said (E138C):

"I would not entirely agree with Professor Stevens about the way in which [the compartment compression] developed. I think it has to be speculative, anyway, but I think that a likely mechanism of the development of this syndrome was that there was some damage to the popliteal artery, that this reduced the blood supply to the muscles of the calf to the extent that they began to suffer from lack of oxygen, accumulated the products of muscular activity, swelled and, later, because they were swollen, became bulkier than the fascial envelope in which they were provided and set up a classic compartment compression syndrome.

It may also have done some direct damage to the muscles themselves at the time of the injury causing them to swell, but my contention is that this was a progressive change, and that it will have occurred in the days following the injury, and that evidence of that would not have been present necessarily on 22nd and 23rd, but will have been only too apparent by 29th."

There then followed this exchange:

"Q. Do I understand that to mean that the starting point of the damage or the injury which occurs is damage to the popliteal artery?

A. I think that could have been a very significant factor, though direct damage to this muscle could also have played a part.

Q. That is, damage to the popliteal artery at or about the time of the original trauma?

A. Yes."

Both Professor Stevens and Mr Glyn Thomas were at one, however, in stating unambiguously that in their view no signs of damage to the popliteal artery could have been detected clinically on 22 or 23 October 1985. In stating this conclusion they laid particular stress on the fact that Mr Slack had used the word "comfortable" in his note. If the popliteal artery had been damaged and the circulation to the lower leg and foot had been seriously interfered with Mr Cunningham would have suffered ischaemic pain. Such pain was very severe and could not have been overlooked by Mr Slack on 23 October.

The Judgment.

The judge gave judgment on Tuesday 23 July 1991. At page 3 of the judgment the judge referred to the arteriogram which was taken on Mr Cunningham's re admission to hospital. The judge continued (J3G):

"The arteriogram shows that that artery was occluded somewhere behind the knee joint, but because of the direction of the shot one cannot tell from the arteriogram precisely where that occlusion was. The block that can be seen there could have been caused in either of two ways. The plaintiff's case is that that block was caused through primary damage to or laceration of the artery at the time of the accident and the mechanism that could cause this has been explained by the plaintiff's experts and is essentially accepted by the defendant. Alternatively and this is the defendant's case that that block could have been caused by a compartment pressure syndrome, that is to say, the slow and insidious build up of oedema and haematoma within the fascia or sheets of fibrous tissues investing the muscle. That is what the defendant's expert say that happened and the issue effectively resolves as to whether the plaintiff was adequately examined first in casualty on 22 October, and secondly in the fracture clinic on 23 October."

At page 10 of his judgment the judge considered the question of pain. He said (J10B):

"The case for the plaintiff is that arterial damage was present and there to be seen. We have here the plaintiff's complaints of pain and what he says as to swelling and the hardness of the limb. So far as the swelling is concerned there is no issue between the parties but that there would have been some swelling there. There was, therefore, pain and swelling, but the confusing factor is that there would have been to a greater or lesser degree pain and swelling even with a fracture that did not affect the artery. When one looks to the evidence as to the quality of the pain, the experts agree that the nature of the pain that we are here considering, if there had been arterial damage, there would have been ischaemic pain. This would have been pain of a quite different order to fracture pain on the evidence and one would have expected the contemporary note to say pain plus or something of that nature. The note, as I have said, shows that there is no specific reference to pain, and Dr. Bhandal says in relation to that that as there is no specific reference to it, so she did not think that there was pain over and above what one would normally expect with a fracture. This account that she gives is supported, as I have said, by the doses of pethidine 250 milligram doses which, as I have said, was in accordance with clinic practice for moderate pain, and that shows that in Dr. Bhandal's eyes at any rate, the pain was ordinary, nor did Sister Gibson see anything extraordinary about it."

The judge then turned to consider the evidence of the x-rays. He said (J11A):

"The next piece of evidence to be looked at for evidence of arterial damage is the x-ray. ... Professor Grainger, the radiologist called on behalf of the plaintiff's final position, was that that swelling could well have been detected clinically. In reaching that position he retreated from a more exposed position. Earlier he had said that it was manifest from the x-ray alone that there was very considerable swelling and not just ordinary swelling. The reason why he retreated after the cross examination from this position was that the size of the swelling depended on how much muscle the individual had and there was no picture of the patient's other limb; so there was nothing to compare the ordinary state of the leg with the swollen state, and additionally the x-ray was not taken straight on; so his final position was just that the swelling could well have been detected clinically, and Yes, Dr. Bhandal said that she did detect it."

The judge then referred to the fact that Professor Grainger had suggested that the swelling reflected a massive bleed caused by direct damage to the artery. A little later, however, (J12E) the judge stated that he shared Mr Glyn Thomas' unease as to the evidential value of the miniaturised x-rays

At page 12 G the judge turned to consider what Mr Cunningham's condition would have been at the time of his examination by Dr Bhandal on 22 October had there been "bleeding from direct vessel damage leading to a very large and very localised haematoma." The judge listed four matters:

(a) Agonising pain;

(b) Swelling which was unusual in size;

(c) The pulses distal to the fracture site would either not be present or be severely reduced;

(d) Immobility of the toes with perhaps a tendency to turn blue.

At pages 14 to 17 the judge examined the evidence of Mr Slack. It is clear that although the judge was troubled by certain aspects of Dr Bhandal's evidence he concluded (J13G) that he was inclined to accept her evidence because of the positive view he formed of her. As to Mr Slack the judge expressed the view that he did not consider that the contemporary note made by Mr Slack was either self serving or defensive. He concluded that in the circumstances it was inevitable, as it seemed to him, that Mr Slack did examine Mr Cunningham's toes on 23 October. He continued (J17G):

"He examined those toes to test for circulation; that would involve getting the patient to move the toes; it would be touching the toes for their temperature, squeezing for the capillary action and observing their colour. I do not believe that he would have done one of those tests, that is to say, ask the plaintiff to move his toes, without also having done the others, and in those circumstances it would need very powerful evidence indeed to persuade me either that he did not do the tests or that he missed what all agreed would, on the plaintiff's thesis, have been plain. If Mr. Slack was negligent he would have to have been very negligent indeed; he would have had literally to have failed to inspect at all. His evidence as to the inspection he carried out and finding nothing unusual or alarming about the plaintiff's condition is consistent with his note and the inferences to be drawn from it and is consistent with Dr. Bhandal's evidence."

At page 19 of his judgment the judge expressed his conclusion. He said (J19B):

"In the various evidence of the pattern of pain which, as I say, each side relied on in support of their case, it seems to me that that pattern of pain is essentially neutral in the question I have to decide. In those circumstances I am left with the evidence of Mr. Slack and Dr. Bhandal as to the tests they did and the results they got from those tests as against Professor Grainger's interpretation of the contrast in the miniatures as supported by certain aspects of the plaintiff's account of the symptoms that he suffered [at] the time. In those circumstances it seems to me that I must prefer the evidence of Dr. Bhandal and Mr. Slack as to the tests they did, the results they obtained and the observations they had made for reasons which I have endeavoured to set out in this judgment."

The Appeal.

The appeal was conducted by Mr Cunningham in person. He seeks a new trial. By his amended notice of appeal and in the course of his submissions he advanced a number of arguments which can be conveniently set out as follows:

(1) That the judge erred in his interpretation of the evidence of Professor Grainger.

(2) That the judge failed to give sufficient weight to certain features of the evidence.

(3) That the judge unreasonably concluded that Mr Cunningham's own evidence was unreliable.

(4) That the judge, when considering the evidence of Mr Slack regarding the examination on 23 October 1985 and his note in relation thereto, failed to consider the evidence of Mrs Cunningham.

(5) That he was entitled to a new trial by reason of the matters set out in further statements by Professor Grainger and Mr Kay and in a statement by Mr MorrisJones, a consultant vascular surgeon.

It will be convenient to consider the fifth ground first which can be looked at in conjunction with the application to adduce further evidence.

I can turn at once therefore to the question whether the Court of Appeal is entitled to have regard to this further medical evidence.

The general powers of the Court of Appeal are set out in RSC Ord 59 r 10. Rule 10(2) is concerned with the reception of further evidence. It provides:

"The Court of Appeal shall have power to receive further evidence on questions of fact, either by oral examination in court, by affidavit, or by deposition taken before an examiner, but, in the case of an appeal from a judgment after trial or hearing of any cause or matter on the merits, no further evidence (other than evidence as to matters which have occurred after the date of the trial or hearing) shall be admitted except on special grounds."

The words "special grounds" in Ord 59 r 10(2) have now to be considered in the light of the conditions relating to the reception of further evidence laid down in Ladd v Marshall [1954] 3 All ER 745, [1954] 1 WLR 1489 and as approved in Skone v Skone [1971] 2 All ER 528, [1971] 1 WLR 812 by the House of Lords. It is sufficient to refer to a short passage in the judgment of Denning LJ In Ladd v Marshall supra where he said at 1491:

"When a litigant has obtained a judgment in a court of justice ... he is by law entitled not to be deprived of that judgment without very solid grounds ... If it is sought to deprive him of his judgment by further evidence, three conditions must be satisfied before it can be received: first, it must be shown that the evidence could not have been obtained with reasonable diligence for use at the trial; secondly, the evidence must be such that, if given, it would probably have an important influence on the result of the case, though it need not be decisive; thirdly, the evidence must be such as is presumably to be believed, or, in other words, it must be apparently credible though it need not be incontrovertible."

In the present case we are concerned with the first and second conditions laid down in Ladd v Marshall. No one suggests that if the further evidence were admitted it would not be "apparently credible".

I should refer first to the further evidence of Professor Grainger which is to be found in a letter from him dated 25 January 1993 and a new report dated 28 January 1993. The new report, which Professor Grainger would wish to put forward in substitution for the previous report dated 11 September 1989, is in the following terms:

"This new report is based on an examination of the original full-sized radiographs. The report of 11.9.89 was based on examination of miniature copy films which are now known to be very poor copies leading to misinterpretation.

A. Two radiographs of the left leg of 22.10.85.

There is a comminuted fracture through the upper end of the left tibia extending into the articular surface of the tibial condyles. The upper tibia is completely traversed by the fracture and the upper fragment is displaced about two-three mm.

There is ill defined soft tissue swelling behind and medial to the knee joint and upper tibia. There is no marked increase in radio-density within this swelling as is seen on the miniature copies.

B. Femoral and Tibial Arteriogram of 30.10.85.

These films are of perfectly adequate diagnostic quality and are not of the poor quality which I described after an examination of the miniature copies.

There is complete occlusion of the left popliteal artery at the level of the lower femoral epiphyseal plate (which has now undergone normal union). There are a few arteries, probably all superficial arising at the obstruction and providing a fair but inadequate run off. There are no deep muscular arteries demonstrated below the knee. At the ankle level there is a patent artery on the medial aspect of the ankle, probably the posterior tibial.

I believe the cause of the obstruction of the popliteal artery is direct damage to the artery at the instant of the injury. There may be a few centimetres of retrograde thrombosis of the popliteal artery until the collateral arteries are reached. This is a common occurrence. I do not think this occlusion of the popliteal artery is likely to be due to compartment syndrome. If that were the correct diagnosis, I would expect that some arteries to the muscles of the leg would be patent in one or more of the three osseous fascial compartments of the leg. The complete occlusion of the popliteal artery proximal to the knee joint is very unlikely to be secondary to compartment syndrome resulting from muscle swelling of the calf muscles which in some cases causes compression and occlusion of the capillaries with retrograde thrombosis."

In addition to this new report by Professor Grainger and his explanatory letter we have also seen a letter from Mr Kay dated 2 March 1993 and a letter from Mr MorrisJones dated 2 July 1993. The letter from Mr Kay, however, does not add anything fresh to the radiological evidence. As to the evidence of Mr MorrisJones it is to be observed that at the trial counsel for Mr Cunningham apparently decided not to call a vascular surgeon as a witness, who would, as I understand it, have been Mr MorrisJones: see E86E

In my judgment therefore the application to adduce further evidence must be confined to the evidence of Professor Grainger.

Counsel for the Health Authority strongly opposed the admission of any further evidence. It was submitted that neither the first nor the second of the Ladd v Marshall conditions were satisfied. This submission was developed as follows:

(a) Though it was unfortunate that the original x-rays and angiograms had not been found until the beginning of the trial no harm had been done. Counsel for Mr Cunningham had been offered but had declined an adjournment. Professor Grainger had had an opportunity before he gave evidence to examine the originals and to compare them with the miniaturised copies.

(b) The new report of Professor Grainger dated 28 January 1993 amounted in effect to an attempt by him to correct and supplement the evidence which he had given at the trial. This evidence could have been given in July 1991 or at any rate would have been available had Mr Cunningham's advisers taken advantage of the offer of an adjournment.

(c) It was clear from Professor Grainger's letter dated 25 January 1993 that as the result of further tests which had been carried out in conjunction with photographic experts he now regarded the evidential value of the miniaturised copies as worthless. This new information did not help Mr Cunningham but on the contrary undermined some of the evidence given on his behalf at the trial. Indeed it confirmed the doubts which MrGlyn Thomas had voiced about the miniatures and to which the judge had made reference in his judgment.

(d) It could not be shown that the further evidence would have an important influence on the result of the case. The radiological evidence was merely a factor to be taken into account and it would still have to be set against the evidence of the two doctors who saw Mr Cunningham at the time.

(e) Although the late appearance of the original x-rays and angiograms had introduced an element of surprise Mr Cunningham's advisers had not asked for an investigation to be made as to why the discovery had been made so late. They had elected to go ahead after a short pause on Tuesday 16 July 1991. It was now much too late to seek a new trial.

These are formidable arguments. In the end, however, I have come to the conclusion that the further evidence contained in Professor Grainger's letter and his new report should be admitted.

The facts of the case are unusual. Professor Grainger made his first report in June 1989. It is clear from the second part of that report that he made attempts to obtain the original documents but he was told that the documents had been destroyed. In preparing his evidence for the trial therefore Professor Grainger focussed his attention on documents which, it is now said, are seriously misleading. It seems clear that at the trial that Professor Grainger still regarded the miniaturised copies as in certain respects "enhancements" of the originals. He now says, as I understand it, that far from being "enhancements" of the originals the miniaturised copies give a distorted picture.

The whole emphasis of Professor Grainger's evidence has changed. Instead o