On 1^st April 2008 the Claimant underwent a total knee replacement (“TKR”) operation. He was discharged from hospital on 7^th April 2008. He was cared for by community nurses, and saw the operating surgeon, Mr. Manjure, for a review in outpatients on 24^th April 2008. A further review took place on 4^th June 2008, conducted by Mr. Manjure’s registrar Mr. Apsinghi. On 12^th June 2008 the Claimant was taken by ambulance to hospital and was admitted. He was suffering from an acute infection of staphylococcus aurea (“SA”) of the replacement knee joint. At this stage the infection was treated with antibiotics and by being washed out, but after a period of improvement, it was decided that it would be necessary to undertake revision surgery. This was carried out on 16^th October 2008.

The Claimant brings these proceedings to recover damages from the Defendant, alleging that Mr. Apsinghi was negligent when he saw the Claimant on 4^th June 2008. Originally there was a claim against the Claimant’s GP and also the practice (in respect of its practice nurse, Nurse Hughes, who treated the wound on 16^th May 2008), but those claims have been abandoned.

In short, the Claimant’s case is that Mr. Apsinghi did not properly examine his knee and advised no further treatment. It is alleged that he should have admitted the Claimant to hospital immediately in order to explore the wound and take samples for culture. If that had been done, then a course of anti-biotics and a surgical debridement would have removed the infection and saved the Claimant from the revision operation.

In the course of the treatment of the Claimant following the onset of the infection, it was discovered that a trocar sheath had been left inside the knee joint. It is not clear whether this happened in the course of the operation on 1^st April 2008 or during previous procedures. Originally, it was the Claimant’s case that the presence of the trochar had exacerbated the infection and also caused him pain. While the latter point is not abandoned, it is no longer the Claimant’s case that the trocar sheath had any influence on the infection.

This trial has been of the issues of liability, including causation, alone.

I heard from the Claimant and his wife and also from Mr. Manjure. There were unchallenged witness statements from Amit Sharma and Kalai Rajah. Mr. Apsinghi did not give oral evidence because he has returned to India and cannot be traced. His evidence was admitted under a hearsay notice and comprised a clinical letter written by him to the Claimant’s GP on 4^th June 2008 after he had seen the Claimant in outpatients that day. There is no reason for thinking that Mr. Apsinghi would have been able to add anything to the letter as it is unlikely that he would have had any independent recollection of the outpatients appointment.

The Claimant has suffered from serious knee problems for very many years. He had a TKR of the right knee in April 2004 following diagnosis of arthritic knees. His left knee remained troublesome and he underwent a medial opening wedge osteotomy on it in September 2006. This didn’t resolve the problem and led to the TKR in April 2008. Since then he has had a revision and there is no doubt that he has suffered a great deal and continues to do so. His wife has lived with all this throughout.

In cross-examination the Claimant was, initially, very slow in his answers and appeared to be unsure of many of the matters which he was questioned about. For example, he said that upon discharge from hospital on 7^th April 2008 his knee was oozing and he didn’t feel well and was feverish. This was in contrast to the hospital notes. He refused to acknowledge that the notes might be correct. He also said that he knew that there was something loose inside the knee (a reference to the trocar). His own expert, Mr. Baird, gave evidence that he would not have been aware of the trocar in the knee and that it would not have felt loose. In the end, the Claimant’s evidence was that his knee is still swollen and painful. Several times the Claimant’s account differed sharply from the contemporaneous medical notes. Once might be explicable but none of the medical attendants’ notes appears to be correct if the Claimant is to be believed.

Although his recollection was very poor, he was clear in his recollection of specific matters important to his case. For example, what he was wearing on 4^th June 2008 and whether Mr. Apsinghi asked him to take down his trousers so that the knee could be examined. My conclusion is that he is not trying to mislead the court, but is unable to give any clear and reliable evidence which relates particular matters to particular dates. His recollection of what his knee was like at various times has simply merged over the span of his lengthy suffering.

The same goes for his wife. She also came across as someone who had no wish or intention of giving misleading evidence but has lived with the Claimant’s suffering over a lengthy period. She ended her evidence in cross-examination by saying that she could not remember the detail of 2008 but just remembered that he was always in pain.

I am not satisfied that either the Claimant or his wife’s recollection and account of the events in 2008 is sufficiently reliable to override the written medical evidence and I therefore prefer what is written down.

Mr. Manjure’s evidence was not particularly controversial. Where he expresses an opinion I will defer to the experts in the case and ignore his view. The only matter in real issue was whether there were signs of infection in the knee when he saw the Claimant on 24^th April 2008 and this turns on what is written in his clinical letter of that date. I will deal with this later.

I will set out my views on the expert evidence separately.

The Claimant has suffered from a number of medical problems over the years but I will concentrate on those affecting his knees. In November 2000 he underwent bilateral knee arthroscopies, carried out by Mr. Scott, and was diagnosed with grade III/IV osteoarthritis of both knees. He received a bilateral washout and steroid injections. In February 2001 he was referred back to Mr. Scott because the considerable pain was affecting his ability to work.

On 30^th April 2004 the Claimant underwent a TKR of the right knee which appears to have been successful. In October of that year he was seen by a locum consultant, Mr. Eslami, and placed on a waiting list for left knee arthroscopy with a view to either subsequent proximal tibial osteotomy or a knee replacement.

On 19^th September 2006 a left medial opening wedge osteotomy was carried out on his left knee under Mr. Manjure. The Claimant was told to remain non-weight-bearing until review in 4 weeks. At a clinic on 22^nd November 2006 the Claimant complained of sudden onset of pain and swelling in his left knee. He was told that there would be a review the following year, which took place on 28^th April 2007 when he was advised that if the pain from his arthritis worsened he would require a TKR.

The TKR on the left knee took place under Mr. Manjure on 1^st April 2008. The notes state that the wound was closed with vicryl staples to the skin. A drain was removed on 2^nd April 2008 and the patient notes record that the wound was “clean and dry”. The Claimant said in his witness statement that by 6^th April 2008 the wound was “oozing a lot”, that he did not feel at all well and told the nurses that he was feverish. The notes record that he was complaining of feeling “hot and cold” and non-specific pains all over his body. Blood tests and other observations were normal. There is no record of “oozing”. The Claimant was discharged on 7^th April 2008 and the discharge notes record that the wound was redressed and was “clean and dry” and that he was “feeling better”. There was “mild pain in the left knee”. The Claimant said that the note was wrong when he was cross-examined, but as I have stated above, I find that he was mistaken in his recollection and that the medical notes are more likely to be correct.

On 9^th April 2008 the Claimant went to see his GP, Dr. Chafer. The GP notes state “sore but no sign of infection”. The Claimant says that he noticed “something loose in the joint” at this stage but for reasons already given, I reject this. The expert evidence is that it is highly unlikely. The Claimant now knows that a trochar was left in the joint following an earlier operation and it is perhaps unsurprising that he has got into his mind that it was floating about in the joint. There is no record of Dr. Chafer having been informed of this feeling.

The recovery was managed at the Claimant’s home by community nurses. The notes start on 8^th April 2008 when the nurse records that the knee is “slightly swollen” and that there is “some heat”. The Claimant tells her that the heat is better than when he was in hospital. On the 9^th the wound was redressed and the GP is noted as having visited and said that antibiotics were not needed. On 10^th April 2008 the knee is “slightly swollen and the wound dry and clean”. On 14^th April 2008 the nurse removed some of the clips and the remainder were removed on 26^th April 2008. Between 9^th and 16^th April 2008 there were daily visits by the nurse and no record of any oozing, swelling or anything else noteworthy.

On 16^th April 2008 the nurse records “some pain but wound clean and intact. 2 small leaking areas top and bottom”. On 17^th April 2008 the dressing was removed and one small area noted as still leaking to the top of the suture. At that stage the Claimant was discharged from the care of the nurses.

The Claimant does not accept the picture painted by these notes. He says that the nurses didn’t really do more than administer a daily injection. That is not borne out by the notes. He also says that on 17^th April 2008 the nurse recommended that he see his GP because of the state of his wound because it was not fully healed. There is no record of this in the note and, again, I reject the Claimant’s evidence about this. There is no record of a visit to Dr. Chafer between 17^th April 2008 and 29^th April 2008.

On 24^th April 2008 the Claimant attended a clinic when Mr. Manjure carried out a routine 28 day review. The Claimant’s evidence was that he told Mr. Manjure that the knee was sore and that there was something loose inside it. At the time of his witness statement it was thought that the trochur had something to do with the subsequent infection. There is no record in Mr. Manjure’s clinical letter (which were his notes) and I reject this evidence of the Claimant. Mr. Manjure’s letter is dated 29^th April 2008 but his evidence was that he dictated it as he went along at the clinic. Mr. Manjure records that the Claimant told him that he had increased pressure at night of the whole of his body. Mr. Manjure was unable to explain what this meant. He also records “there was no pain in the knee as such”. This can only have come from the Claimant and suggests strongly that if the kind of pain which the Claimant now says he was experiencing at the time was not present on 24^th April 2008. Mr. Manjure clearly removed the dressing and examined the knee wound carefully. He has no recollection of that clinic but his letter states that there is no sign of infection. This was either a reckless note made without examination or, as Mr. Manjure say, an examination is likely to have been carried out. I prefer the latter. The letter also records the results of blood samples which are consistent with there being no infection and no inflammation. There was a range of movements in the knee from 0 – 95 degrees which is also inconsistent with inflammation. Mr. Manjure concluded by listing a review in 6 weeks.

The Claimant saw a GP on 29^th April 2008 because he was complaining that he could not cope with the pain. This is recorded in the notes and he was prescribed a stronger analgesic. The Claimant says that the wound was oozing, swollen and red but this is not recorded in the notes. He went back to the GP on 2^nd May 2008 and saw another doctor. There is no indication that he went because of his knee and the doctor diagnosed an infection called sarcosis barbae or beard rash. He was prescribed an antibiotic Flaxopen.

In his witness statement the Claimant says that his wound didn’t heal and he knew that it wasn’t the same as it had been after the first TKR in 2004. He was also sure that there was something loose in the joint. He says that he rang the GP surgery and made a specific appointment to see Dr. Chafer who he saw on 16^th May 2008. He told Dr. Chafer that his knee was really sore and oozing and that it looked a bit green “it was green and horrible”. Dr. Chafer told him that there might be some stitches which needed dealing with and referred him to the practice nurse, Nurse Hughes.

There is no record in the GP notes of any visit to Dr. Chafer on this day but there is a note that the Claimant saw Nurse Hughes. She made a record in the GP notes as follows: “Removal of suture of skin bottom of knee suture line still not completely healed keeps oozing and scabbing. o/e scab removed and suture discovered underneath. Removed and patient reassured should heal now”.

Whether the Claimant saw Dr. Chafer is not really relevant. It may be that he saw him very briefly and was then referred to Nurse Hughes or that he was sent directly to the nurse without seeing the doctor. At any rate, Nurse Hughes removed the suture. The experts agreed that what was most likely to have happened is that the suture was “trimmed”. It was protruding from the wound having not dissolved. This would cause irritation and, according to Mr. Cannon, prevent healing. The suture would have been part of a longer suture going into the wound. The nurse would have taken the exposed end, pulled it out and then cut it as near to the wound as possible. The remainder of the suture would then disappear into the wound and cease to have any irritating effect from exposure at the surface.

Nurse Hughes’ notes make no reference to the condition of the wound as being green or swollen or hot and stiff.

The Claimant says that after the visit on 16^th May 2008 the wound seemed to dry up a bit. He thought that things must be getting better but that the knee was still swollen and hot. As explained, while I accept that the knee would have been uncomfortable and painful, I am not able to accept the Claimant’s evidence that it was swollen or hot because I do not consider that he is a reliable historian.

On 4^th June 2008 the Claimant went to the clinic and saw Mr. Apsinghi. Mr. Majure was not able to deal with the review which was carried out by his registrar. Mr. Apsinghi’s clinical letter of that day is the only record of the consultation. He records that “On examination the wounds have healed well except for the distal part of the wound where he tells me that there was a stitch removed. There is no sign of infection. He has 0-95 degrees of movement”. Mr. Apsinghi advised the Claimant to report to Mr. Majure’s secretary if the wound didn’t heal and that he should be reviewed in 3 months.

In his witness statement the Claimant says that he told Mr. Apsinghi that his knee still hurt, was sore to the touch and was very swollen “it was just like a balloon and was a pinkish red in colour. It was very hot”. He says that Mr. Apsinghi did nothing much else apart from listen. In cross-examination he said that he remembered the appointment precisely because nothing happened. When it was pointed out to him that the letter records “on examination” he said that he couldn’t remember if he had been examined. His evidence was particularly unclear in this passage of cross-examination. Eventually he said that Mr. Apsinghi had stopped him from speaking – this in answer to a question whether he was really saying that he didn’t mention the swelling, heat and redness to the registrar. Nor was there any reference to this in his witness statement. Again, the Claimant is not reliable in his evidence about this. In re-examination he said that he recalled what he was wearing and that he had not been asked to remove his trousers. After 6 years that is not credible.

I have not heard from Mr. Apsinghi and therefore it is possible that he might have been able to shed some light on what happened. It is improbable though because he would have seen a large number of patients that day and since. I am left with interpreting the letter.

In my judgment Mr. Apsinghi must have examined the knee and taken the dressing off to do so. There is a distinction in the letter between what he was told and what he saw on examination. He saw that the wound was well healed except for the distal part. He also records that there was no sign of infection. This means that he saw no inflammation, no redness and felt no heat. Nor can there have been any significant pain mentioned. The degree of movement recorded is not consistent with inflammation and infection.

The Claimant went home and in his witness statement he says that the wound did not get better and that it was still extremely painful. By 11^th June 2008 it had got worse. On 12^th June 2008 he was in so much pain that he called an ambulance and was taken to the A & E department of Luton and Dunstable. Once more the Claimant does not accept that the hospital notes record accurately what he had told the various members of the medical staff who saw him. I prefer the contemporaneous written records to the Claimant’s account of the development of his knee leading to his attendance at A & E. It is necessary the set out what is recorded.

The triage nurse notes records the Claimant telling her: “the knee is now swollen and hot scar has been discharging”. The houseman notes a history which must have been related to him by the Claimant: “Scar never totally healed – 2 oozing points. Getting better and mobilising well”. “Last 24 hours increased pain and swelling in joint and reduced mobility. Stiffness”. Another doctor notes that the symptoms “started yesterday (afternoon)”.

What the notes record is that the wound was getting better but on the afternoon of the 11^th everything blew up and led to the need to his admission. This is a wholly inconsistent account from that given by the Claimant. I find that while the wound had not completely healed, it was getting better until the Claimant suffered the acute symptoms of a deep infection of the knee joint. These became apparent on 11^th June 2008.

The Claimant’s case on liability is that Mr. Apsinghi’s review on 4^th June 2008 was entirely cursory and that, contrary to his note, the knee was swollen, red and hot. I have rejected that factual case for the reasons set out above. The amended particulars of claim set out 5 allegations of breach of duty in relation to the 4^th June 2008:

In his final submission, Mr. Trusted narrowed his case. He said that the Claimant should have been admitted on 4^th June 2008 (the expert evidence was that this would probably have happened on 5^th June 2008 once a decision had been taken to admit him) so that a surgical investigation could be carried out. This would have led to a debridement of the wound and joint and treatment with intravenous antibiotics. Therefore, Mr. Trusted submitted, there were 2 issues for the court:

The Defendant’s case is that there was no infection on 4^th June 2008 and no evidence which would have led a reasonably competent surgical registrar to conclude that it was necessary to admit the Claimant for the kind of invasive procedures advocated by the Claimant. Nor was it a breach of duty not to do more than to keep the Claimant under review. Although Mr. Barnes, counsel for the Defendant, did not concede that Mr. Apsinghi was negligent to suggest a review in 3 months, Mr. Cannon, the Defendant’s orthopaedic expert, was clear that there should have been a review in a week to 10 days. Even if it was negligent not to advise such a review, it is common ground that there was no causative effect because by then it was too late to avoid the subsequent consequences.

There was no dispute about the test to be applied which is the well know dictum of McNair J in Bolan v Friern Hospital Management Committee [1957] 1 WLR 583:

“I would myself prefer to put it this way, that a [medical practitioner] is not guilty of negligence if he has acted in accordance with a practice accepted as proper by a responsible body of medical men skilled in that particular art … Putting it the other way round, a man is not negligent, if he is acting in accordance with such a practice, merely because there is a body of opinion who would take a contrary view”.

Each side called 2 experts, an orthopaedic surgeon and a microbiologist each. While the microbiologists’ reports were described as relating to causation, their evidence was relevant to the issue of liability. This is because in this type of case, the orthopaedic surgeons would, if it was indicated, discuss the position with a microbiologist before making any treatment decision. It is therefore important to know what a microbiologist would have advised if consulted on or shortly after 4^th June 2008. They also gave relevant evidence about the development of the infection and the source of the infection which subsequently led to the need for revisionary surgery.

All the experts were at the top of their field and highly experienced. Each had also experience in the medico/legal area. Mr. Baird, the Claimant’s orthopaedic expert, had been a senior consultant at the Chelsea and Westminster Hospital and Mr. Cannon, the Defendant’s expert, is a consultant at the Royal and National Orthopaedic Hospital Stanmore. The Claimant’s microbiology expert was Dr. Louise Teare. She has been Director of Infection Prevention and Control in Mid-Essex Hospitals NHS Trust since 2006. Professor French was the Defendant’s microbiology expert and he was a consultant at Guys and Thomas’s Hospital NHS Trust and Head of Infection Control at Moorfields Eye Hospital. He is now retired from NHS practice.

Mr. Baird’s opinion in his original report is set out at paragraph 46. He noted that the distal part of the wound had not healed and that Mr. Apsinghi had been told that a stitch had been removed by the nurse. Normally, he would expect a wound such as this to have healed within 9 weeks of the operation. Mr. Apsinghi should not have advised that the wound should be reviewed in 3 months but should have analysed why it was not healing. He would expect that any retained stitch would be likely to be colonised with SA and this risk should have been know to Mr. Apsinghi as a competent orthopaedic surgeon. There was therefore a significant risk that the bacteria would reach the joint and exploratory surgery was necessary.

Mr. Baird’s view was maintained in the joint statement although he said that if no frank pus had been found during the exploration of the wound, phrophylactic antibiotics would have be given

The experts were agreed on the signs and symptoms of infection. Dr. Teare referred to the classical symptoms of wound infection: Rubor (redness), Tumor (swelling), Kalor (heat) and Dollor (pain). Any 2 of these or a discharging wound or a wound swab with puss cells and/or aseptically taken aspirant which grows micro-organisms, satisfies the definition. It was also accepted that, following an operation, you can get redness, pain and swelling. What you are looking for is significant changes to the pattern.

I am satisfied that Mr. Apsinghi’s statement that there were no signs of infection, should be interpreted as evidence that there were no signs of infection within the well known definition. There were not 2 of the 4 indicators, nor a discharging wound with puss cells that were visible. He did not take any swab and therefore no cultures were taken.

Mr. Baird (and Dr. Teare) were concerned that this wound had not healed completely by 4^th June 2008. Mr. Baird’s view is that Mr. Apsinghi should have questioned why it had not healed, concluded that this may have been because of the suture and therefore there was a significant risk of the joint becoming infected.

Mr. Cannon’s opinion was that the reason the wound had not completely healed was because of a vicryl suture reaction which was treated correctly by Nurse Hughes on 16^th May 2008. He said in his report that the wound seemed to be healing when reviewed on 4^th June 2008. A reaction to sutures on the surface is not uncommon and managed by removal of the scab and underlying suture. Both experts agreed that the presentation to Nurse Hughes was typical of a vicryl suture reaction. There was no evidence of any deep infection until 48 hours before the Claimant’s admission on 12^th June 2008.

At this stage it is necessary to deal with an issue which became a significant part of the cross-examination of the microbiologist experts, namely the distinction between infection and colonisation by bacteria. It is also helpful to look at how the evidence in relation to this issue developed.

Mr. Baird said in his report (paragraph 47) that there was likely to have been some colonisation with SA on 4^th June 2008. A competent orthopaedic surgeon should have realised that there was a significant risk of the bacteria reaching the joint and causing a serious infection. Mr. Cannon acknowledged in his report that there was a potential pathway from the open dermis of an unhealed wound to the joint, through which an infection could spread and that the most likely explanation for the infection on 12^th June 2008 was self-inoculation into an unhealed wound on or around that date.

In her original report, Dr. Teare said that the Claimant was infected with SA by 2^nd May 2008. This was the sarcosis barbae on his face and is not a reference to the knee wound or joint. The Claimant was an SA carrier on the surface of his body for this and other reasons. The only reference to “colonisation” is with regard to the facial hair and that the surgical records indicate that there was no pre-operative washing. She then says that it was inevitable that the wound site would have been contaminated with SA by 16^th May 2008 which would have become established there. Finally, she says “If infection had been suspected as a possibility …. On 4^th June 2008, [the Claimant] could have been admitted and surgically explored”.

Professor French started by stating that a diagnosis of peri-prosthetic infection is difficult and requires a high index of clinical suspicion. This is common ground. He thought that SA had entered the joint during the week before the acute symptoms on 12^th June 2008 (ie 3^rd to 8^th June 2008). He did not think that there would have been clinical signs of infection on either 16^th May or 4^th June 2008. He agreed that as a result of the sarcosis barbae, the claimant was colonised with SA and susceptible to SA skin infections which may have been the source of the joint infection. As there were no symptoms, it was reasonable for Mr. Apsinghi not to take a wound swab, which would in any case have been misleading because of the microbial colonization from the surrounding skin. A wound swab would not have indicated a deep infection and antibiotics would not have been mandated if the swab was positive.

In their joint report, the orthopaedic experts agreed that the presentation to Nurse Hughes on 16^th May 2008 was typical of a vicryl suture reaction and that there was no deep infection of the knee prior to 48 hours before 12^th June 2008. They also agreed that it was unlikely that if the Claimant had presented on 4^th June 2008 with a small area of unhealed wound it was unlikely that the unhealed wound would lead directly to the knee joint. Mr. Cannon thought that the small open wound created a minimal risk of infection to the joint which would be managed by keeping it under review, whereas Mr. Baird agreed that there was a small risk of infection, but said that the consequences of a deep infection was sufficiently serious to justify the remedial action he proposes.

The microbiologists joint report records that they agreed that the Claimant was probably a long term SA carrier and that this meant that while SA would be present on the body, it would not cause an infection in the absence of a skin break. They also agreed that it was possible for previously colonised SA to invade the body without an obvious skin break via haematogenous (blood) transmission. They were then asked in the joint meeting agenda, at what point they considered that SA would have (a) colonised and (b) infected the joint. Their joint answer to (a) was that the wound could have become colonised at any time or not colonised at all. As to (b), they agreed that there was no doubt that he had a deep infection but that they were not certain that he ever had a superficial surgical site infection. They then agreed that the joint was, on balance, infected on about 6^th June 2008 and not before.

Finally, the microbiologists agreed that they were doubtful that the infection to the joint had spread from the superficial would infection because of the absence of pus and any inflammatory process. They therefore agreed that on balance, the likely route for infection was haematogenous. Dr. Teare gave oral evidence in which she suggested that in agreeing this she had not intended to agree that the haematogenous route would be totally independent of the wound. This is in my judgment unsustainable. Professor French’s view which he explained in his oral evidence, was that the most likely route of infection of the joint was the sarcosis barbae and by haematogenous means – not via the wound. This is contrary to the view of the orthopaedic surgeons. It is difficult to read the joint statement in any way other than that Dr. Teare agreed that the infection did not come through the wound.

Following the joint meeting, Dr. Teare met counsel in conference and in her oral evidence she said that during this meeting she became aware that the joint report “could be mis-interpreted”. A further document was therefore served by the Claimant setting out her comments and qualifications in relation to the replies previously set out in the joint statement. In summary, she set out a view of how the joint became infected which is not set out in her report. Her view now is that the wound became colonised with SA and that this was the source of the subsequent joint infection. She then described how, in her opinion, that “colonising bacteria at the site of the wound had reached a critical mass and were able to move from the colonising to the infecting mode”. These would then spread in the blood to the joint. This was what she had meant when she had agreed with Professor French’s view that the most likely source was haematogenous. She went on to say that there was probably contiguous spread as well. This flatly contradicts her view in the joint statement. Nor was she able to refer to any documentary support for the proposition that bacteria change from colonisation mode to infective mode.

Professor French’s evidence was more impressive about this, even if one ignores the significant change in Dr. Teare’s position. Generally, his answers in cross-examination were much more straightforward and he was nothing like as defensive as Dr. Teare, being much more ready to agree with Mr. Trusted’s question even if it developed the argument against his opinions. He didn’t recognise that bacteria have different forms or modes. He did not agree that the body reacts to a chance in the organism. It was a balance between the organism and the host, primarily in the host, although he also said that the experts didn’t know exactly how. The organism SA is virulent from the word go.

In cross-examination Dr. Teare was very very reluctant to agree with any of the propositions put to her by Mr. Barnes. Instead of answering questions clearly and directly, she frequently launched off into a detailed explanation for and justification of her theory about the change from colonisation to infective mode – even if the question was not directed at this issue. She tried to elide the concept of colonisation with infection, suggesting that when the transformation was in progress, the host’s defensive mechanisms (ie white blood cells) would respond. She would not at first accept the simple concept that colonisation was when the bacteria were present causing no damage to the host. Eventually she did accept this proposition “in general terms”. She argued rather than answered questions and, as a result, came across much more as an advocate for the Claimant than an expert witness. This was very apparent from the way in which she would answer a question by trying to repeat the whole case.

This issue is relevant because it affects how one judges the conclusions which a reasonably competent surgeon should have reached if he had been in Mr. Apsingi’s shoes and the steps would should then have been taken. Mr. Baird and Dr. Teare’s approach was to suggest that there was an aggressive organism inside the wound which was causing a reaction in the host which needed urgent and invasive surgical treatment.

I prefer the evidence of Professor French on this point. I was not convinced by Dr. Teare’s theory that the bacteria changed from one mode into an infective mode. Furthermore, once it was agreed that the wound was not infected on 4^th June 2008 then it was difficult, if not impossible, to support an argument that there should have been surgical exploration, debridement and treatment with aggressive antibiotics. As the case has developed, and following the respective joint meetings, each of the Claimant’s experts has introduced important new evidence which supports an argument that a surgeon should have suspected an aggressive colony of SA bacteria at the base of the suture, threatening the joint, and in the process of changing into an “infective mode”. This would, it is said, explain the presence of a small bit of pus at the base of the suture and give a reason for the treatment. I have no reason to doubt that the experts are genuinely trying to find a medical explanation for the ultimate infection, but they are doing so wearing advocacy hats and not looking at the case as objectively as Professor French and Mr. Cannon.

Mr. Cannon was asked in cross-examination why a wound would take more than 9 weeks to heal if it was not infected. He said that there might be a number of reasons. The fact that there had been a previous operation on this site and therefore a poor blood supply, Fibrosis round the wound and the presence of the vicryl stitch protrusion. It was put to him that this was not referred to in his report but I do not accept that there is anything in this point. His reasons appear logical and were not seriously challenged. Mr. Baird on the other hand, did suggest that he had considered any other reason for the failure of the wound to heal. What an orthopaedic surgeon is required to do is to consider the balance of risk in a given situation. In order to do that he must consider the causes of the wound not healing and the likelihood of one of them being the presence of bacteria. He did not do that in his report. Furthermore, he said that the presence of bacteria colonised on the vicryl suture would be a reason for the wound not healing. He was able to produce no learning to support this view and it was not supported by Mr. Cannon. Professor French thought that there might have been SA colonised at the bottom of the stitch but that they were not causing any infection.

In court, for the first time, he mentioned that if the wound had been explored surgically, a small bit of pus would probably have been found at the bottom of the suture because even if there wasn’t an infection, the colonisation of the wound by SA would lead to pus without an infection. Mr. Cannon did not agree with this when he addressed the point in his oral evidence – not having been given an opportunity to do so at the joint meeting because Mr. Baird had not raised it then. The importance of the point from Mr. Baird’s point of view was that the presence of pus would justify an intervention with aggressive antibiotics. In the joint statement he had said that treatment with antibiotics was dependent upon finding frank pus at the time of exploration. All the experts agreed in their oral evidence that treatment with antibiotics would not be appropriate unless there was a clinical reason to and that this would not be the case if there was no infection. This was because there were potential side effects and the risk of antibiotic resistance, both to the patient himself and more generally to the public at large.

Mr. Cannon gave a striking answer when he was questioned about this. He said that he couldn’t say because he never explored the wound unless there was evidence of an infection. Therefore the possibility of pus at the base of a suture without infection was not something he had experience of. Professor French said that if there was no infection in the joint and none in the superficial wound he would not expect pus to be found on an exploration of the wound.

I reject Mr. Baird’s evidence that it was probable that frank pus would have been found at the base of the suture if an exploration of the wound had been carried out. It would have been the case if the wound had been infected but the evidence is that neither the wound nor the joint were infected on 4^th June 2008 or at the time the exploration would have taken place. It follows that, subject to the points I make below, even if there had been an exploration, antibiotics would not have been mandated.

Mr. Cannon’s was criticised in relation to his evidence about stitch abscesses. It was also said that he gave evidence of the presence of pus on the surface of the wound. In his original report Mr. Cannon had said that the standard management of a stitch abscess did not involve antibiotics . At the joint meeting the experts were asked if “stitch abscess” was the proper terminology. The experts for Nurse Hughes and the Claimant said that this was not a stitch abscess and Mr. Cannon said that this expression was loose terminology, which would by definition be a swollen area in the wound with pus. In cross-examination he was asked about this and said that it was a reference to the presentation on 16^th May 2008. This was challenged and the report is not clear whether he meant that date or 4^th June 2008. I accept his evidence that the expression is a loose or slang for a stitch reaction of some sort. At the start of his cross-examination he was very clear that a scab would form containing white cells and fluid but not pus. He became defensive as a result of his original use of loose terminology and ultimately said that there would be pus on the dermis because there would be if there was a suture infection. In re-examination he was clear that he would not have expected to see any pus. I am quite satisfied that the never believed that there was an infection or that there was actual pus visible, this was a suture reaction.

Having decided that Mr. Apsinghi did carry out an examination of the would, with the dressing taken off, and concluded that there was no evidence of infection, the issues which in my judgment arise are as follows:

I have found that the state of the wound on 4^th June 2008 was as is set out in Mr. Apsinghi’s letter. There was no sign of infection, the wounds had healed well except for the distal part where a stitch had been removed. There was 0 – 95 degrees of movement. There would have been a scab but no obvious signs of pus. The wound was healing and there was an explanation for the small opening, which was the suture reaction which had been treated.

Mr. Trusted submits that SA bacteria were colonising this wound and that the suture was a nidus for infection of the joint. This, he says, is consistent with the orthopaedic experts’ view that there was a higher risk of infection. I accept that these experts agree that there were a number of factors increasing the risk of infection, which included the following:

The experts also agreed that the risk of infection of a knee joint after a TKR led to a high degree of suspicion. He submits that Mr. Apsinghi should have taken a swab of the wound and discussed the case with a microbiologist even if there was no sign of pus.

Mr. Baird was the only expert who said that a swab should have been taken on 4^th June 2008. He accepted that the results might be misleading because a positive result might lead down the wrong alley and that there were risks. It was put to him that if there were no clinical signs there was no need for a swab. He answered that this depended on the situation. If there had been a recent TKR and the wound had not healed for a few weeks he would be concerned that it was a portal of entry for bugs. He’d want to know what they were and would be worried about MRSA. Dr. Teare said that if there was no significant sign of infection then there was no indication for taking a swab and that doing so would be unhelpful. Later she backtracked when she was referred to Mr. Baird’s view and wasn’t prepared to say that it was wrong, but I am satisfied that her first answer is right and that there was no indication for a swab in this case.

Both the Claimant’s experts agreed that where there was no sign of infection you don’t treat with antibiotics. This would not therefore have been a suitable treatment on 4^th June 2008.

This leaves the Claimant’s main contention, which is that there should have been an admission followed by surgical exploration leading to identification of an infection, debridement and antibiotic treatment. Mr. Baird accepted that if there had been no evidence of infection (such as pus) during the exploratory examination of the wound, he would have closed it up and would not have administered antibiotics or carried out any further procedures at that stage. This is consistent with his agreement to item 7(iii) in the joint statement.

It has not been proved to the standard required that there would have been pus at the base of the suture or any other evidence of infection in the wound if the exploratory surgery had been carried out. If a swab had been taken then this would not have assisted for the reasons set out above. The exploratory operation would not therefore have led to debridement and treatment with antibiotics. This leads to the question whether exploratory surgery and debridement should have been carried out anyway.

Nor, in my judgment, was there any indication to take any blood samples. It is probable that they would not have shown anything to indicate further treatment since there was no infection at that stage.

Finally, I deal with the Claimant’s main argument, that he should have been admitted and the wound explored surgically.

Mr. Baird agreed that there were risks with a surgical investigation, although he sought to downplay them. The procedure would involve taking the patient back into theatre and, probably, a general anaesthetic – although Mr. Baird suggested as an afterthought a spinal block. There are risks associated with this. The surgeon would be opening tissue which was healing or had healed and cutting into healthy tissue. Mr. Baird suggested that the operation would proceed according to what the surgeon found and once he was satisfied that there was no infection the wound would be closed. He said that you would only debride damaged tissue (ie tissue which had been damaged by an infection). I am satisfied that the surgical intervention also increased the risk of infection getting deep into the wound (Mr. Baird said this was minimal but it was still a risk).

Mr. Cannon accepted that there was a serious risk of deep infection said that the surgeon has to balance the risks of surgery with the risks of deep infection. His evidence was that there was no urgency to take this patient back to surgery on 4^th June 2008. There were risks, with an open wound and for the other reasons set out above, of bacteria getting into the joint and developing into an infection. If that happened then the results could be very serious, but his view was that the situation should be treated more conservatively by keeping it under review. He thought that no competent surgeon would have left it for 3 months, he would have reviewed the patient in a week to 10 days. The orthopaedic experts agreed in their joint report that the risks of a joint infection with an open wound were minimal (Cannon) or small (Baird). The difference between them was that Mr. Baird judged that the consequences of infection would be so severe that it justified surgical intervention however small the risk.

In my judgment this claim is brought with a significant element of hindsight. Both the Claimant’s experts have approached the matter in the knowledge that if there had been a surgical debridement and then treatment with aggressive antibiotics the infection would have been prevented and the need for revision avoided. Mr. Cannon agrees with this. With hindsight, this would have happened if Mr. Apsinghi had advised this course on 4^th June 2008, although the final decision would have been Mr. Manjure’s. That is not the issue in this case, which is whether Mr. Apsinghi fell below the relevant standard of care. In my judgment he did not. I am not satisfied that no reasonably competent orthopaedic surgeon would have dealt with the case in the way in which Mr. Apsinghi did. It was not negligent to take the more conservative approach. There were risks attached to surgical intervention and no clinical signs which indicated a need to take such steps.

The only matter upon which I find that Mr. Apsinghi did fall below the relevant standard is the time that he set for review. This should not have been 3 months but no more than 10 days. It is common ground that this breach caused no loss because that would have been too late to save the subsequent consequences.

Breach of duty in relation to the trochar sheath is accepted.

The only issue for me to determine is the route of the infection. Professor French’s opinion was that the infection was haemotogenous and had not entered the joint from the wound. He did not say this in his original report but said that, on reflection, this was the most probable route because there was no evidence of infection in the wound. Mr. Trusted described this as absurd. It is however what Dr. Teare agreed in the original joint statement and, as the statement makes quite clear, they considered 3 possible routes for both colonisation and infection: at the time of surgery, extension from a superficial infection and haematogenous spread. They stated expressly that they agreed that support for the haematogenous spread came from the sarcosis barbae infection although scratching was referred to. It would not be consistent with this that the joint statement contemplated any bacteria from the beard rash getting into the wound by manual transfer. It must have been into the blood at the point of infection. The suggestion is not absurd, it was agreed by the experts as being the most probable.

Dr. Teare sought to resile from this but I am unconvinced by her explanation but in any case it is extremely difficult to take it seriously in the light of her agreement in the joint statement.

Professor French was criticised for not mentioning this route of infection in his original report. This would undoubtedly have strengthened the defence but I do not agree with Mr. Trusted that it undermines his opinion. This issue was not originally a significant one but it was discussed fully at the joint meeting and led to the experts agreeing. Dr. Teare’s position is much more undermined by the fact that she makes no mention of her theory either at the meeting or in the joint statement.

I therefore find that the most probable route of infection is haematogenous and not via the open wound.

Finally, there is the issue of damages as a result of the trochar being left in the wound. Since the wound had to be opened in any event in order to treat it once the infection had taken hold, the Claimant has not suffered any loss as a result of the need to remove the trochar sheath. It was removed during these procedures. Nor has he suffered any pain or distress as a result of its presence in the joint. While he believes that there was something loose inside the joint, his own expert says that this was unlikely. Mr. Trusted urges me to remit this matter for a further assessment of damages. I see no point. It is quite clear that the Claimant has suffered no loss and there is no point in prolonging these proceedings further.

I therefore dismiss the claim.