Monday, 23 February 2009

MRSA, A Gross Professional Misconduct By a Health Professor and Corrupt No Win No Fee Solicitors

Post number 188

Professor Lord Robert Winston
H.M. Martial Law Government Prime Minister

At last, please note below a record of incomplete correspondence on Darren Pilley's MRSA case that you will find self explanatory. As to why Darren didn't finish school to save me the trouble to take up his case is something for the youth of today to bear in mind.

The records are incomplete because I do not have access to Solicitor Paul Faud's scare tactics used on Darren to sign off his rights. Apparently, Darren signed some form or other to clear the soilicitor of any wrong doing. I phoned Paul Fouad a few days ago and invited him to have a change of heart. He didn' want to know.

I thought you might find the case at hand of particular interest as a health professional. I will leave it to you to help me seek justice and fairly for Darren from the Window Dresser Alan Johnson.


Your deputy Mohammad

Mr D Pilley Taylor & Emmet Solicitors
12 …. 20 Arundale Gate
Sheffield S1 2PP
Surrey T 0114290 2200
F 0114 290 2295
DDI 0114 290 8208

27 February 2007

Dear Darren,


I enclose a copy of your medical expert report from professor Willett.

It is important that you read the report carefully as sometimes there may be errors of fact.

I am afraid that the report is largely unsupportive.

Basically your expert is saying that you sustained a serious fracture to your ankle and that infection in the wound was present almost immediately after the operation.

As someone who smoked 26 cigarettes a day, consumed 56 units of alcohol a week, and had an opiate addiction, you were at an increased risk of sustaining infection from the operation.

This should have been explained to you in detail prior to the operation and there is no clear evidence that it was.

However, Professor Willett believes that, despite this increased risk, you would still have had little option but to continue with the surgery. The doctors would have strongly advised you to proceed with surgery despite the increased risk factors.

The area that Professor Willett does question is the use of Augmentin antibiotics to treat the infection. He is unable to comment on the use of this antibiotic as it is outside his area of expertise. He is suggesting we obtain a microbiologist’s opinion as to whether this treatment was appropriate. I will now make enquiries of a suitable microbiologist as to whether he can prepare a Report on this point.

If there are any matters contained in the report with which you disagree or over which you require further explanation, kindly let me know.

I look forward to hearing from you.

Yours sincerely,

Paul Fuad
Taylor & Emmett


Keith M Willett FRCS
Professor of Orthopaedic Trauma Surgery, University of Oxford
Honrary Consultant Trauma & Orthopaedic Surgeon
T 01865 22210/743204
F 01865 222811
E-Mail: and
DX: 6540708 Headington 93 OX


Name: Darren Pilley
Date of Birth: 24/11/1970
Date of injury: 10/05/2003
Date of Medical Report: 14/02/2007
Instructing Party: Taylor & Emmett, Solicitors


I am a Professor of Orthopaedic Trauma Surgery in the University of Oxford and an Honorary Consultant Trauma and Orthopaedic Surgeon at the Jon Radcliffe Hospital, Oxford. I am a past president of the British Trauma society. A am Civilian Surgeon Advisor to the Royal Navy for Trauma and Orthopaedic Surgery.

In brief, I graduated in Medicine from Charing Cross Medical School (University of London) in 1981; became a fellow of the Royal College of Surgeons of England in 1985 and completed my specialist Higher Surgical Training in Orthopaedics and Trauma Surgery in 1991. I subsequently completed a Clinical Trauma Fellowship in Toronto, Canada. I was elected to the chair of Orthopaedic Trauma Surgery in 2004 after twelve years of NHS Consultant practise.

My clinical practice is exclusively with the immediate treatment, reconstructive surgery and rehabilitation of patients sustaining musculoskeletal injuries. I have a particular interest and have published research in the multiply-injured patients, acetabular, pelvic and limb fractures, fracture biomechanics, surgical training and services.

I act as a trauma surgery specialist advisor for the Department of Health, Audit Commission, for Health Authorities and for Surgical Training at the Royal Colleges of Surgeons o England. I was the Trauma and Orthopaedic speciality advisor to the Royal College of Surgeons for the Oxford Region from 1998-2000, a Royal College of Surgeons appointed member of the National Speciality Advisory Committee in Orthopaedics and Trauma until 2005 and currently on the Royal College of Surgeons of England Trauma Committee. I am chairman and a faculty member on national and international fracture treatment instructional courses and an Executive and Board member of the National Trauma Audit and Research Network.

This report was compiled with reference to:

• Medical, nursing and physiotherapy records and radiographs from the Ashford & St Peter’s Hospital NHS Trust.
• The claimant’s statement undated and unsigned.
• General Practitioner medical records.

This medical report was compiled with reference to medical records and radiographs only. I have not had the opportunity of interviewing or examining the claimant. This is my first report prepared on the claimant.


I have been asked to give preliminary advice with a view to preparing at a later stage the report for the Court complying with Part 35 CPR. I have been given a background summary of the injury and treatment events and the progress of litigation. I have been asked the specific questions:

1. Please advise generally whether you feel that any element of Mr Pilley’s treatment fell below a reasonable standard and whether the duty of care to Mr Pilley was breached by the Trust.
2. Please indicate whether there were any opportunities to diagnose Mr Pilley’s infection at earlier stage and this was missed.
3. If an opportunity to diagnose the infection at an earlier stage was missed please outline the likely cause of treatment that would have been used and the likely outcome for Mr Pilley have avoided the need for a below the knee amputation.
4. Was a reasonable course of treatment followed once the infection was diagnosed?

For the benefit of the Counsel this report will be structured in clinically appropriate time periods for care. My explanatory notes and opinion will be identified in italics throughout this report.

This represents the period of the acute in-hospital stay following the claimant’s injury.

1.1 Claimant’s History: The history gleaned from the claimant’s statement indicates that he had an accident on 10 May 2003 when he fell down a flight of stairs at a friend’s house. He was fit and well and worked as a bus driver prior to that accident. It is recorded that his right leg went through the banister and he suffered a fracture to the right ankle. He was taken to St Peter’s Hospital in Chertsey and underwent surgery. He was in hospital for three to four weeks and had an aircast boot on the right leg. Infection was present almost immediately after the operation and despite attempts to remove the infection by antibiotic medication and further surgery the right leg deteriorated to a point where he had to undergo a below the knee amputation on 24 January 2005. It is the claimant’s view that the hospital was negligent in that the original surgery was performed incorrectly and that the infection developed in hospital. Certainly infection was diagnosed whilst he was still an in-patient.
1.2 Medical Records for the period 10 May to 12 May 2003: It was recorded that Mr Pilley was received at St Peter’s Hospital, Chertsey Accident and Emergency Department at 16:04 hours on 10 May 2003 by ambulance. It was recorded that he had fallen down the stairs under the influence of heroin injuring his right ankle. There was obvious deformity; the circulation was satisfactory but there were critical skin problems. The ankle was clinically dislocated with the skin tethered with severe pallor (no blood supply) over the medial malleolus (inner bony prominence of the ankle). An emergency closed manipulation (re-location) was performed under sedation, which was successful, and photographs were taken of the ankle. A below knee (back slab) was applied and post-reduction radiographs were undertaken. The claimant was then referred for further management to the orthopaedic team.
1.3 It is recorded the claimant was assessed by the orthopaedic surgeon and the history again recorded “Fell down the stairs under the influence of heroin and ETOH (alcohol). Right ankle fractured and obvious deformity occurred. One hour later came to A & E. Reduced by A & E doctors with morphine and medazolam sedation. In back slab currently stable. Digital pulses always present. Past medical history depression? Schizophrenia, heroin abuse, alcoholic on ? anti depressant medication. Previous ORIF (fixation) fractured left arm. Drowsy from medazolam. Comfortable in back slab.
1.4 Rdaiographs were considered to show a relocation tri-malleolar fracture of the right ankle.
1.5 The defined management plan was for thr claimant to be admitted and have intravenous access and blood screening undertaken. He was recommended for open reduction internal fixation of his fracture and consented. He was prescribed a course of chlodiazepoxide for anticipated alcohol withdrwal. Surgery was planned for, query the next morning.
1.6 Radiographs available to me, show a reduced tri-malleolar Weber C supra-syndesmotic fracturedislocation of the right ankle whaich has been reduced but remains displaced by 3-4mm at the main fracture sites.
1.7 A NHS consent form 1 was completed and signed by the claimant and the admitting SHO doctor (? Aziz).
1.8 It is recorded surgery was undertaken the following day (11 May 2003) by surgeons Kinmont and Khalleel and his assistant was Aziz. Surgery was recorded as open reduction internal fixation of the right ankle, medial and lateral sites. Fixation of the medial side was achieved with two partially threaded cancellous screws on the lateral side by a fibula one-third tubular plate and diastasis screw. The anaesthetic record indicates a general anaesthesia with supplementary spinal anaesthesia at L2/3. Anaesthetic agents given included local anaesthetic for the spinal injection, fentanyl, propofol and odencitrine for induction and seroflurane as a volatile agent. A tourniquet was applied for one hour and six minutes to the surgical leg. Chlorhexidine spirit was used as the skin antiseptic preparation. Wound closure was with clips and the post-operative instructions were for the claimant to be non-weight bearing, for the leg to be elevated and he was to be fitted with an aircast boot. There was to be a wound check at two weeks when the clips should be removed and he was to have an x-ray on arrival in the fracture clinic that day and a removal of the diastasis screw was planned for ten weeks.
1.9 Image intensifier recorded during surgery indicate that initial attempt at fixation with two diastasis screws was revised to a febular plate and single diastasis screw.
1.10 The claimant drug prescription chart records that there was intravenous administration of Augmentin 1.2gms (antibiotic dose) at 19:15 hours on 11 May 2003 at the induction of anaesthesia. Post-operatively three further doses were given at 6 am, noon, and 6 pm on 12 May 2003 (the day after surgery).
1.11 Post-operatively it was recorded that the claimant required regular oral analgesic medication and received the prescribed antibiotics. He was mobilised with a physiotherapist and discharged at 17:30 hours after his last dose of antibiotic on 12 May 2003. A two week appointment was made for a clinic review.
1.12 The final review by the physiotherapist prior to discharge indicated that his wound dressing had been reduced (made smaller). He was fitted with an aircast boot. He was taught non-weight bearing on crutches with which he coped well. He was considered safe and discharged.
1.13 Final radiographs (from the operating theatre) indicate that an anatomic reconstruction was achieved of the ankle joint mortice with appropriate stabilisation using standard implant techniques.
1.14 Comment on the Standard of Care of the Period 10 May to 12 May 2003: The claimant suffered high energy fracture dislocation of his right ankle. This was appropriately identified promptly in the Accident and Emergency Department and an emergency reduction under sedation was undertaken because of the skin damage over the inner side of the ankle. No radiograph was taken prior to reduction. This represents good emergency care of the claimant and I consider there to be no deficiencies in this element.
1.15 The claimant was then admitted under the orthopaedic team and assessed. He was appropriately recommended open reduction internal fixation to restore ankle congruence as a way to optimise long-term ankle function and reduced the risk of osteoarthritis. This was appropriate contemporary advice and the recommendation for treatment that would have been given by the vast majority of surgeons tp patients of this age with this fracture dislocation pattern.
1.16 The risk of infection in surgery of this type would be expected to be in the order of 1% to 5%. This would normally be included as part of the consenting process. In the claimant there are a few personal features that would represent a slightly increased risk including his alcohol consumption (56 units a week), smoking (twenty cigarettes a day) and opiate addiction (general indicator of poor nutritional and compliance). The traumatised skin over the inner (medial) aspect of the ankle was a specific risk for impaired wound healing. His relatively young age would count in his favour. These risk factors are insufficient to change the recommendation for surgery.
1.17 The NHS consent form 1 was completed by the claimant and introduced by Dr Aziz. It is designed to be completed by the health professional and to detail, in the sections of the form, the intended benefits and to indicate the serious or frequently occurring risks. It would be normal practice for infection to be listed on that form. These sections were left blank in the claimant’s case. I, therefore, do not have documentary evidence that infection was discussed with the claimant but in any event the risk was small and surgery would be strongly recommended; there being no other reliable treatment for this injury pattern at this stage.
1.18 Antibiotic cover was given for the surgery with the important pre-operative dose at induction of anaesthesia together with three (less important) doses post-operatively. This is consistent with the normal regime for hospital in 2003.
1.19 The use of Augmentin as the prophylaxis is an area to be discussed. The antibiotic policy for implant related surgery is established between the operating surgeons and the Infection Control Committee of the hospital. The selection of antibiotics is under the guidance of the advising microbiologist and should reflect the type of surgery, risk to the patient and the prevalence of types of bacteria in the hospital and Orthopaedic Unit. Whether Augmentin was the appropriate antibiotic should be reflected by the guidance of that committee in May 2003 for that institution. The selection of an appropriate antibiotic policy would also have to take into account avoiding the development of antibiotic resistance in the bacteria compliment present in the hospital. Reference to a microbiologist for an expert opinion on this point may be required.
1.20 For the care received by the claimant for the period 10 May to 12 May 2003 I cannot identify any elements of the surgical care that was deficient either by error or by omission. The antibiotic selection is outside my area of expertise but I would recognise that Augmentin was a standard therapy administered in many hospitals at that time.

2.0 CARE FOR THE PERIOD 13 MAY TO 7 AUGUST 2003: This represents the period of out-patient follow up care following the initial fracture fixation.

2.1 Claimant’s History:
The claimant states that “Unfortunately I did not make a full recovery and I developed infections on my right leg which would not go away. The infections were present immediately after the operation and despite attempts to remove the infection by antibiotic medication and further surgery the right leg deteriorated.”
2.2 Medical Records for the Period 13 May to 7 August 2003: It is recorded that the claimant was assessed by his General Practitioner on 16 May 2003 recording the injuries to the ankle and foot and that he had an operation with fixation of multiple fractures he was certified unfit to work. The first recorded follow up attendance was recorded on 28 May 2003 at Chertsey Hospital. It is recorded that the wounds over the medial lateral side were healed. The staples were removed, dressings were applied and he was given an aircast boot and advice on gentle ankle mobilisation but he was to remain non-weight bearing. A further review was planned in three weeks to arrange removal of the diastasis screw.
2.3 It is recorded that the claimant attended the General Practitioner on 2 June 2003 for unrelated treatment. The next attendance was via the Accident and Emergency Department directly to the clinic on 4 June 2003 when it was recorded that the claimant had come early to the clinic as his ankle had become painful. It was noted that he “had been putting some weight on it!” Also the aircast boot had been rubbing on the medial side causing blistering and infection. A change of dressing was undertaken and as antibiotic (flucloxacilllin 250mgs q.d.s. orally) was prescribed. He was to remain strictly non-weight bearing and to take the boot off when not needed. He was to elevate the leg most of the time and be reviewed in two weeks.
2.4 At that subsequent review (?date June 2005) it was recorded to be five weeks from surgery. The lateral wound had healed well. There was a serous (clear-serum-like) discharge from the medial wound. Culture swabs were taken from the wound. It was re-dressed and he was to continue with the aircast boot and was prescribed a course of Ciprofloxacin antibiotic (covers a broad spectrum of bacteria including MRSA).
2.5 At a review on (?) 20 June 2003, six weeks from injury, it was recorded that the septic wound on the medial side was much better. Swabs had grown Staphylococcus Aureus (the commonest bacteria on skin and cause of wound infections: it was not MRSA) He was to continue with flucloxacillin and dressing. He was to be reviewed in one week.
2.6 At that review on 2 July 2003 it was recorded the medial wound was almost dry. He was seven weeks from surgery and he was able to (?) weight-bear while (?). Ankle plantarflexion was 30 degrees and there was no dorsi-flexion. He was referred to physiotherapy. A culture swab taken on 18 June 2003 was recorded as growing +++ Staphylococcus Aureus that was sensitive to erythromycin and flucloxacillin. It was resistant to plain penicillin. That result was accessed from a ward enquiry raised on 20 June 2003.
2.7 Comment on the Standard of Care Received by the Claimant for the period 13 May to 7 August 2003.
2.8 During this period the claimant was under out-patient care. The medial wound at the ankle was recognised to have become infected. He was initially given treatment with an empirical antibiotic (flucloxacillin). A culture swab, taken from the surface of the wound from the serous discharge, grew flucloxacillin sensitive bacteria: sensitive to the antibiotics that had been prescribed. The antibiotics were changed however, at the visit before the culture result was known, to Ciprofloxacinto which the bacteris was also sensitive. The treatment was changed back to the original flucloxacillin antibiotic one week later when the cultured organism and antibiotic sensitivities were known. That treatment resulted in the wound improving and being almost dry within a week.
2.9 Surgical site infection is a risk with any fracture implant surgery as indicated previously. The wound that failed to heal in the claimant and became infected was the one at the point where the skin was most severely compromised by the initial fracture dislocation; This was an important factor. It was also recorded that the claimant had been weight-bearing which would create a larger pressure load on the skin inside the aircast boot but that in my view would not be a major contribution to the infection although it would irritate the wound and compromise early healing.
2.10 Comparison of the radiographs dated 20 May 2003 and 25 June 2003 revealed a degree of osteopenia (demineralisation of the bone) consistent with the weight-bearing status. There were some non-specific bone changes at the medial malleolar fracture site that may have represented changes of infection. There was also a little loosening around the diastasis screw in the fibula; this is a normal appearance as a result of rotational forces due to ankle movement that month period.
2.11 The response to the infection was reasonable and appropriate. Initially empirical antibiotics were administered; a culture swab obtained after a delay of one week and that confirmed bacteria to which the antibiotics prescribed throughout the period were sensitive. This resulted in a documented improvement of the infection. The patient was to proceed with physiotherapy. This would be a practice adopted a substantial body of orthopaedic surgeons for this complication.
2.12 A more aggressive approach to potential implant related sepsis is adopted by some surgeon (including myself) and any potentially infected wound would be monitored without antibiotics and if infection progressed the wound would be opened, deep sample cultures taken and a more aggressive intravenous antibiotic course pursued. The policy adopted by the surgical team at that stage at St Peter’s Hospital was not, in my opinion, inappropriate. The Straphylococcus Aureus bacteriacultured was not a particularly resistant organism (it was not MRSA) but the presence of the implant screws in the medial malleolus, if involved in the infection (which was quite likely) would limit the chances of the infection being eradicated by oral antibiotic treatment. A good response, however, was documented.
2.13 I do not find that the care for the period 13 May 2003 to 24 July 2003 fell below a reasonable standard. I do not consider that the infection was treated inappropriated. It was diagnosed promptly and responded to and, although not as aggressive as pursued by some surgeons, the treatment undertaken was reasonable and common practice.

3.0 CARE for the PERIOD 8 AUGUST 2003 to 25 SEPTEMBER 2003
3.1 Medical Records for the Period from 8 August 2003 until 25 September 2003: It is recorded the claimant attended the Accident & Emergency Department of St Peter’s Hospital on 8 August 2003 with the history of a query abscess on an old scar. It is recorded that he had had fixation of an ankle in May 2003 and he developed a query abscess at the bottom of the scar which had burst three days ago. He was referred to Orthopaedic Surgery. A re-attendance is recorded in the Accident & Emergency Department the following day on 9 August 2003 when he re-presented with the same problem. It was recorded that he had been seen in the Accident & Emergency Department yesterday but DNW (did not wait). It was recorded that there was swelling over the lateral aspect of the ankle and it was painful. It had burst and discharged three days previously and the pain had eased. His temperature was 37.3 degrees (normal) and there was 1-2cm discharging abscess over the right lateral malleolus 2cm below the scar from the previous surgery. Wound swabs, blood tests and a radiograph were undertaken. He was referred to Orthopaedic Surgery. An ulcer/sinus without discharge was noted over the lower part of the right ankle lateral wound but without any erythema. There was minimal swelling and lower ankle movement was recorded as not affected. He was apyrexial (no fever). He was commenced on oral antibiotics, after the complications were discussed with the Orthopaedic Registrar on call and the claimant was to return to a Fracture Clinic.
3.2 At that Fracture Clinic review on 11 August 2003 he was seen by a Consultant (D.S.Elliott) who concluded there was infection around the diastasis screw which needed to be dealt with urgently and he was admitted directly for removal of the screw, curettage to the screw hole and antibiotics.
3.3 Surgery was undertaken the following day on 12 August 2003. TH screw was removed and the drill hole was curetted and lavaged. The wound was left open. A culture of bacteria from the operation revealed Staphylococcus Aereus that was sensitive to antibiotics (benzylpenicillin and flucloxacillin) to which the identified bacteria was sensitive for six days.; he was discharged on 18 August 2003 with a further one week course of oral penicillin and flucloxacillin.
3.4 T the clinic review on 26 August 2003 the wound looked clean. There was granulation at its base and he was to complete the oral antibiotic course (duration not specified).
3.5 By review on 24 September 2003 his wound had settled, the ankle movements were very good and he wished to return to work as a bus driver. He was signed back fit to work. He was advised if the plate did cause him problems then it could be removed in the future. He was discharged.
3.6 A radiograph on 9 August 2003 showed probable union of the fibula fracture. There was a radiographic lucency around the diastasis screw in both the fibula and distal tibia. The medial malleolar fracture appeared united but with some radial lucnecy around the screws (radial lucency can be explained by either mechanical loosening or infection).
3.7 Comment on the Standard of Care from 8 August to 25 September 2003: During this period the claimant developed infection on the opposite (lateral) side of the right ankle related to the diastasis screw. It did not clinically appear to affect the previous site of problem over the medial side or the more proximal fibula plate. The infection was identified promptly, responded to appropriately and it was the correct decision to proceed urgently for screw removal and cuterage of the screw drill hole to try and eradicate infection. The organism identified was a common Staphylococcus Aureus with a sensitivity to first line antibiotic penicillin therapy and this was administered. The administration of a week of intravenously followed by an oral course was appropriate. The length of the oral course is not clear within the medical records. This resulted in a clinical resolution of the infection.
3.8 This response, action and treatment were reasonable and appropriate. It was the equivalent to that that would be offered by many UK orthopaedic surgeons in this situation.
3.9 I would have concerns that it was a little premature to discharge the patient at the follow-up. There was a potential for residual sepsis to be present. The good clinical examination and resolution of the wound does, however, does not make that decision unreasonable, particularly as the claimant was given the option to return if there were any problems on an SOS basis.
3.10 In hindsight, further surveillance would have been more appropriate but I do not consider that it would have changed the next stages in the evolution of his infection.
3.11 Parallel blood tests were also undertaken (an indication of the inflammatory response of the body to infection) and these were normal or near normal. They did not support a significant osteomyelitis problem; CPR 14 (normal 0 to 6) on 11 August 2003. ESR 30 (normal 1 to 10), 11 August 2003, ESR 17 on 13 August 2003). These blood tests show relatively minor responses to local infection and would not support established osteomyelitis of concern.
3.13 Medical records for the period 26 September 2003 to 17 December 2003: It is recorded that the claimant re-attended the Accident & Emergency Department on 6 October 2003 with a further abscess over his right ankle. It had been present for four days. He was admitted to hospital. His case was discussed in a trauma meeting on the morning of 7 October 2003 and further surgery was recommended to drain the infection and remove the lateral plate. The surgery was undertaken on 8 October 2003. Granulation (reactive tissue to infection) was found along the sinus tract and up to the lower end of the plate implant. The sinus tract and cavity were curetted and the plate retained. The wound was left open and treated with an antiseptic pack. It was left to heal by secondary intention and intravenous antibiotics were commenced with a view to changing those depending on the cultured bacterial sensitivity. Again, Staphylococcus Aureus was cultured sensitive to flucloxacillin and metronidazole. The claimant was noted to show sensitivity to one of the dressings, so that was changed. The claimant remained an in-patient at the ACU (? Alcohol & Drug Dependency Unit).
3.14 On 15 October 2003 it was recorded the wound was better and he was started on a two week course of antibiotics.
3.15 Dressing changes were recorded in the interval until a review formally by the orthopaedic surgeons on 11 November 2003. At that assessment it was recorded that he needed intravenous flucloxcillin antibiotics. He was to stop smoking and a vacuum dressing was applied to the wound. He was to be admitted from the orthopaedic clinic and blood tests taken for inflammatory markers (CRP, FBC and ESR). Intravenous antibiotics were administered (flucloxacillinand metronidazole) from 13 to 18 November 2003.
3.16 The claimant then appears to have been discharged from the ward. It appears that he was an in-patient under the Alcohol and Drug Dependency Unit concurrently during this period of his treatment. He was to continue dressing and be seen in two weeks in the clinic, having been discharged on an oral antibiotic course.
3.17 A review in the clinic on 4 December 2003 indicated that his wound was improving. He was advised to keep the foot elevated to reduce the swelling. Two weeks later (17 December 2003) it is recorded there was some water around the ankle with some aches and pains with movement and he was walking partially weight-bearing. The wound had improved and had settled down. An x-ray taken was considered to be satisfactory. The medial fracture was considered not to be united. The plate on the lateral side was considered satisfactory. A radiograph undertaken on 16 December 2003 (available to me) shows that the fibula fracture has united with a good callus response. There has been an increase in the mineral content of the medial malleolus although it remains patchy. The fractures all appear united. There were significant bone changes in the distal tibia in its lateral aspect at the site where the previous diastasis screw had been fixed with focal de-mineralisation consistent with bone reaction to the previous implant or infection.
3.18 The claimant was referred to physiotherapy because of ankle stiffness.
3.19 Comment on the Standard of Care for the period 26 September to 17 December 2003: During this period the claimant was admitted for recurrences of I infection related to the implants fixing his fracture. The fracture continued to progress to union. Treatment for the infection episodes involving admissions to hospital, surgical clearance of the infection site, intravenous antibiotics for one week followed by an oral course again is reasonable and appropriate. Concurrent blood tests did not suggest serious osteomyelitis although they were slightly elevated.
3.20 There were radiological changes over time to suggest a significant reaction in the bone to an underlying septic process. It is impossible to differentiate whether that is a scar response to the infection that has remained active. The presence of residual implants would prevent alternative imaging modalities such as MRI scanning that could have assisted.
3.21 During this period, it was apparent that the (occult) infection did persist probably predominantly in the distal tibia at the site of the previous diastasis screw placement.
3.22 IN retrospect a more radical approach may have had a greater chance of curing the infection but on a balance of probabilities in my opinion appropriate measures were undertaken and progression to more serious infection was inevitable, as it had already declared itself refractory to reasonable standard treatment. The amount of bone involved in infection by December 2003 in retrospect probably included a significant area in the distal tibia metaphysic adjacent to the ankle joint.
4.1 The claimant was assessed in the clinic on 5 February 2004. It is recorded that he continued to have a lot of pain in his right ankle, which was stiff and sore. It was clinically still warm. X-rays showed the fibula fracture had united but the Specialist Registrar who saw the claimant was concerned that there may be some diastasis (separation of the tibia and fibula) and it was recognised that the bone in the distal tibia looked abnormal. It was considered that he should have an examination under anaesthesia with removal of the medial screws and a MRI scan to see if there was any infection.
4.2 Medical records indicate the claimant was admitted as a day case on 16 February for implant removal. At that surgery the metal work was removed. The ankle was found to be stable on examination without any opening of the joint on stressing.
4.3 The Consultant Orthopaedic Surgeon reviewed following that surgery the claimant on 17 March 2004. It was recorded that he was getting some better sub-talar and ankle joint movement. Further physiotherapy was arranged. Concern was recognised that he may have chronic osteomyelitis in the distal tibia and that he had an un-reduced diastasis of the ankle joint that that probably contributed to the arthritic process. A MRI scan was arranged.
4.4 That MRI scan (available to me) was undertaken on 22 July 2004. That demonstrated an extensive high signal change in the distal tibia extending to the articular margin (of the ankle joint). There was patchy loss of the normal articular Cortex in the distal tibia. Posteriorly there was a breach in the cortex with a high signal change extending probably sub-periosteally (to the surface of the bone). Two high signal rings seen at the distal tibial shaft surrounded a circle of reduced signal suggested a possible dead bony fragment and that appeared to correspond with the site of one of the screw tracks; it was considered that this may be a small sequestrum (segment of dead bone). The conclusion was that the scan certainly suggested ongoing infection of the distal tibia; the possibility of an extension to the joint spaces was raised because of the reduced joint space and early high signal changes within the dome.
4.5 At the clinic review on 18 August 2004 for the san result it is recorded that his ankle was not too bad. He could stand and walk fully weight-bearing without much pain. There was aching most of the time and stiffness after long sitting and first thing in the morning.
4.6 Following a Consultant review (15 September 2004) the claimant was for a planned admission on 1 December 2004 for an exploration under general anaesthesia to try and remove the sequestrum and to try to clear the distal tibia of infection.
4.7 It is recorded the claimant was admitted for surgery and underwent sequestrectomy and open debridement of an osteomyelitis abscess of the distal right tibia on 27 September 2004. Two Consultant Surgeons undertook the surgery. A nectrotic bone abscess was identified in the distal tibia and connected to the hole laterally from the previously infected diastasis screw. There was sequestrum around the site of the proximal diastasis that was curetted and cavity irrigated. Intravenous antibiotics were given at the end of the procedure and Gnetamicin antibiotic beads laid inside the bone cavity. Those antibiotic beads were planned to be removed in six weeks. The claimant was subsequently re-admitted and underwent that surgery on 8 November 2004. No further infection was identified at the time. Further tissue was sent for culture. The culture sample sent at the time of bead removal showed no growth and clinically the ankle was quite quiet. The plan was to review him with a possible MRI scan. No further antibiotics were administered.
4.8 The claimant re presented on 22 December 2004 with further infection. He was admitted for further drainage and started on intravenous antibiotics. There was a warm red area over the front of his distal tibia. Surgery was undertaken on 24 December 2004 when a further bone abscess was drained. An extension of the bone window revealed a further cystic area of infection. The claimant was discharged on a further course of flucloxacillin to which previous bacteria had been sensitive. Culture samples subsequently grew +/-coagulase negative Staphylococcus (probably contaminant of doubtful significance.)
4.9 A review by his treating Consultant on 12 January 2005 recorded that the claimant was requesting a below the knee amputation for his chronic osteomyelitis of the right tibia. The leg was still discharging. The surgeon recognised that this had been on the cards to amputate his leg for some time and that he was acceding to the claimant’s wishes to undertake that promptly. He was appropriately referred for pre-amputation advice limb fitting clinic in Roehampton.
4.10 Comment on the Standard of Care for the Period 18 December 2003 to 12 January 2005: During this period it was recognised that the claimant had a chronic osteomyelitis in his distal tibia that had occurred as a result of the infection from the screw. All the metalwork was appropriately removed and he subsequently underwent a MRI scan to define the osteomyelitis process and extent. He was then appropriately offered and underwent exploratory surgery to try and clear the abscess. Again cultures confirmed that it was a Staphylococcus Aureus bacteria and a small piece of local dead bone possibly harbouring the infection was also removed. Despite that surgery the infection recurred. Radiographs already showed involvement of the ankle joint with destruction of the articular cartilage and post-septic arthritis.
4.11 Attempts at surgical clearance of infection were unsuccessful and the claimant was left with a chronically infected and disabling problem relating to his right ankle.
4.12 Given his limited mobility amputation was a reasonable option to consider and undertake at that time.
4.13 The staged surgical attempts to clear infection undertaken by the surgeons were appropriate and followed the normal sequence of events and, indeed, were done, in my opinion, promptly and at appropriate times as defined by the progression of disease.
4.14 Deep infection in bone occurs insidiously and may initially appear as a superficial problem that will often respond to local treatment. Intermittent recurrences are as indication of a more significant problem either related to the implant or bone. The appropriate sequence of events in contemporary practice starts with local surgical treatment supported by antibiotics, if that is unsuccessful and infection persists this is usually suppressed with antibiotics until fracture healing as occurred so that fracture stability is maintained implants can be removed safely. If infection persists beyond this time it is usually deep in the bone, established and difficult to cure. Eradication involves identification of the deep infection and attempts as surgical clearance with antibiotic support. These steps were followed in the treatment of the claimant at reasonable time periods but without success, the infection being refractory to treatment.
4.15 The organism causing the infection is a standard skin organism and was almost certainly introduced as a contaminant from the patient’s skin at the time of surgery. This is a recognised event in all surgical procedures but in most cases the antiseptic precautions and antibiotic cover in conjunction with the patients immune system overcome the innoculum (number of bacteria). Implant fracture surgery complicated by infection affects a very small number of patients (1-5%). Below knee amputation as a final end point for a chronic myelitis of the distal tibia is an extremely unusual outcome following ankle fracture surgery but it is a recognised complication. I do not consider on the balance of probabilities this was avoidable had treatment been undertaken in any other manner. Appropriate steps, decisions and treatments were pursued.


I understand that my duty is to the Court, both in preparing reports and in giving oral evidence. I have complied and will continue to comply with this duty.

I confirm that insofar ad the facts stated in my report are within my own knowledge, I have made clear which they are and I believe them to be true, and that the opinions I have expressed represent my true and complete professional opinion.

Signed K.M. Willett FRCS
Professor of Orthopaedic Trauma Surgery,
Honorary Consultant Trauma and Orthopaedic Surgeon

Now, my reply to the Professor's report for Darren:

Your Ref: PF/JWO/75938-1-8

Mr Paul Fouad
Messrs Taylor & Emmet Solicitors
20 Arundel Gate
Sheffield S1 2PP

16 April 2007

Dear Paul,


Thank you for your letter of 27 February 2007 and the accompanying report by Professor Keith M Willett of 14 February. I regret the delay in replying due to my unhappiness with the report and I had to consult friends for advice.

Please insure that this reply reaches Dr Masterson, your appointed Microbiologist (whom you authorised on 4 April) before he compiles his report for you. My views and any additional data I provide may have a bearing on his findings.

Firstly, I agree with your comments that Professor Willett’s report may contain errors of fact, and the report is largely unsupportive. Therefore, any comments related to blaming me for the loss of my leg is irrelevant and cannot be taken seriously in a court of law.

Secondly, has Professor Willett not realised that his report is merely a weak attempt to conceal the fact that my infection may very well have been MRSA? Please read the following mathematical derivation (a bit similar to solving simultaneous equations). If so, the consequences to his professionalism, grasp of justice and fair play can and will be seriously questioned in the courts. His reputation as a respected Professor may be at stake:

Extensive reference is made in the report to terms ‘infection’ and ‘antibiotics’, the latter extensively used unsuccessfully in eradicating the infection right from the start. We all agree that the infection was contracted almost immediately after the first operation subsequent to my breaking my ankle. Professor Willett repeatedly assures readers that the infection was not MRSA. However, he confirms that the bacteria is a strain of Staphylococcus Aereus. Using Dr Willett’s report, we seem to have Something Something Staphylococcus Aereus or SSSA. At the same time, Dr Willett uses the term ‘Sensitive’ instead of ‘Resistant’. He says that the Staphylococcus in question is Sensitive to 6 antibiotics, namely, Augmentin, Ciprofoxacillin, Erythromicin, Penicilin, Metronidazole, and Gentamicin beads. The latter used unsuccessfully in the bone cavity as a last resort but failed and the only option left was to amputate. I never requested that my leg be amputated, and this part of the report is certainly devoid of facts. I blame St Peters for supplying Professor Willett with false information.

To continue Dr Willett’s own logic on questioning the infection as MRSA or not, one can safely substitute the term ‘Sensitive’ with ‘Resistant’ in his analysis. In other words, the bacteria was not Sensitive to the 6 antibiotics but was Resistant to them or the infection would have been eradicated and my leg saved. In fact, The Oxford Thesaurus defines Sensitive as responsive, attuned, etc. The bacteria was not responsive to any of the antibiotics mentioned. To be absolutely on safe ground in this logical debate, the term Resistant is better suited to use instead of Sensitive. Therefore, we now have Something Resistant Staphylococcus Aereus or SRSA. At this point, Professor Willett (although not a Microbiologist, but conversant on the subject according to his report and impressive CV) should have questioned the hospital infection control team (a fairly strong team of 2 doctors and 3 nurses during the period in question) as to why did they not test the bacteria for resistance to Methicilin antibiotic to ascertain whether the Staphylococcus was MRSA? If not MRSA, then Methicilin would have certainly killed it off and my leg would have been saved.

Common sense dictates that the hospital infection team must have tried Methicilin on my bacteria to kill it off and eradicate the infection. Did they not? Isn’t Methicilin the first port of call? or has any reference to trials with Methicilin been cleverly omitted from the records to conceal the fact that my infection was indeed MRSA. Needless to say, the substitution of the first S in the abbreviation SRSA above with M gives the reader MRSA. Simple logic and it does not require extensive expertise to challenge Professor Willett’s claim that my infection was not MRSA.

If the above derivation is unclear, then please give Mohammad a call on 1784 ........, and he would happily explain all.

I reiterate that the derivation above by Mohammad is arrived at solely from analysing the data given in Professor Willett’s own report. There was no need for us to offer our own medical and Microbiological expertise on the case at hand. In layman’s terms, this has been a case of giving professor Willett enough rope to hang himself. And he has, wouldn’t you agree, Paul? As mentioned on the phone, precious public funds have been wasted on Professor Willett’s report. We all know too well that surgery was unavoidable – the loss of one limb was weighed up against my life which would have been lost if the infection spread to my vital organs. A child will understand this. Let us hope, Mr Masterson’s findings are accurate and relevant to my case.

Please allow me to say this about Professor Willett’s report: The more I read the report, the more disbelief and utter shock is experienced by me, my parent and others. How can it be possible in the 21st century that a noted academic takes an innocent member of the public for a ride in broad daylight, merely for personal gains and siding with the mighty NHS, while totally disregarding my welfare and my future security. I will have to live in utter poverty for the rest of my life if the likes of Professor Willett have their way for personal gains. The press and the media will have a field day if I am forced to approach them to seek justice. I will, if the need arises.

Another factor that reduces the impact of Professor Willett’s report in the eyes of unbiased readers such as court officials is his exonerating The NHS Trust concerned, of all probabilities of hospital acquired infections ever having a history in St Peter’s Hospital. My own press cuttings covering infection related articles in the local press on St Peter’s hospital were entirely ignored by Professor Willett. Furthermore, while he blames me for my alcohol/drug abuse, Schizophrenia (I have never suffered this illness in my life or else my elderly parents, the family GP and others will have been all aware and records of treatment would have existed), he seems ignorant of the fact that 5,000 people die in UK hospitals yearly as a result of hospital acquired infections.

I conclude by saying that it seems highly likely that my infection was MRSA, but facts have been cleverly concealed by the use of the English language as a tool. I would be very interested to read Dr Masterson’s comments on the subject. In fact, I would like his specific ruling in/out of the two strands of the genome, +++ Staphylococcus Aereus and +/- Coagulase Negative Staphylococcus, both mentioned in Professor Willet’s report, for their resistance to Methicilin.

You may use this e-mail address in future if you find it more convenient, and in order to conclude this case at a speedier rate.

Yours sincerely,

Darren Pilley

CC Mr & Mrs Alan Pilley (mum and dad) Have I ever suffered from Schizophrenia?
Walton On Thames


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