We undertook a prospective, randomised study in order to evaluate the efficacy of clamping the drains after intra-articular injection of saline with 1:500 000 adrenaline compared with post-operative blood salvage in reducing blood loss in 212 total knee arthroplasties. The mean post-operative drained blood volume after drain clamping was 352.1 ml compared to 662.3 ml after blood salvage (p < 0.0001). Allogenic blood transfusion was needed in one patient in the drain group and for three in the blood salvage group. Drain clamping with intra-articular injection of saline with adrenaline is more effective than post-operative autologous blood transfusion in reducing blood loss during total knee arthroplasty.

Revision arthroplasty after infection can often be complicated by both extensive bone loss and a relatively high rate of re-infection. Using allograft to address the bone loss in such patients is controversial because of the perceived risk of bacterial infection from the use of avascular graft material. We describe 12 two-stage revisions for infection in which segmental allografts were loaded with antibiotics using iontophoresis, a technique using an electrical potential to drive ionised antibiotics into cortical bone.

Iontophoresis produced high levels of antibiotic in the allograft, which eluted into the surrounding tissues. We postulate that this offers protection from infection in the high-risk peri-operative period. None of the 12 patients who had two-stage revision with iontophoresed allografts had further infection after a mean period of 47 months (14 to 78).

We examined the association between patient-related factors and the risk of initial, short- and long-term implant failure after primary total hip replacement. We used data from the Danish Hip Arthroplasty Registry between 1 January 1995 and 31 December 2002, which gave us a total of 36 984 patients. Separate analyses were carried out for three follow-up periods: 0 to 30 days, 31 days to six months (short term), and six months to 8.6 years after primary total hip replacement (long term). The outcome measure was defined as time to failure, which included re-operation with open surgery for any reason.

Male gender and a high Charlson co-morbidity index score were strongly predictive for failure, irrespective of the period of follow-up. Age and diagnosis at primary total hip replacement were identified as time-dependent predictive factors of failure. During the first 30 days after primary total hip replacement, an age of 80 years or more and hip replacement undertaken as a sequela of trauma, for avascular necrosis or paediatric conditions, were associated with an increased risk of failure. However, during six months to 8.6 years after surgery, being less than 60 years old was associated with an increased risk of failure, whereas none of the diagnoses for primary total hip replacement appeared to be independent predictors.

We examined the rates of infection and colonisation by methicillin-resistant Staphylococcus aureus (MRSA) between January 2003 and May 2004 in order to assess the impact of the introduction of an MRSA policy in October 2003, which required all admissions to be screened. Emergency admissions were treated prophylactically and elective beds ring-fenced. A total of 5594 admissions were cross-referenced with 22 810 microbiology results. The morbidity, mortality and cost of managing MRSA-carrying patients, with a proximal fracture of the femur were compared, in relation to age, gender, American Society of Anaesthesiologists grade and residential status, with a group of matched controls who were MRSA-negative.

In 2004, we screened 1795 of 1796 elective admissions and MRSA was found in 23 (1.3%). We also screened 1122 of 1447 trauma admissions and 43 (3.8%) were carrying MRSA. All ten ward transfers were screened and four (40%) were carriers (all p < 0.001). The incidence of MRSA in trauma patients increased by 2.6% per week of inpatient stay (r = 0.97, p < 0.001). MRSA developed in 2.9% of trauma and 0.2% of elective patients during that admission (p < 0.001). The implementation of the MRSA policy reduced the incidence of MRSA infection by 56% in trauma patients (1.57% in 2003 (17 of 1084) to 0.69% in 2004 (10 of 1447), p = 0.035). Infection with MRSA in elective patients was reduced by 70% (0.56% in 2003 (7 of 1257) to 0.17% in 2004 (3 of 1806), p = 0.06). The cost of preventing one MRSA infection was £3200.

Although colonisation by MRSA did not affect the mortality rate, infection by MRSA more than doubled it. Patients with proximal fractures of the femur infected with MRSA remained in hospital for 50 extra days, had 19 more days of vancomycin treatment and 26 more days of vacuum-assisted closure therapy than the matched controls. These additional costs equated to £13 972 per patient.

From this experience we have been able to describe the epidemiology of MRSA, assess the impact of infection-control measures on MRSA infection rates and determine the morbidity, mortality and economic cost of MRSA carriage on trauma and elective orthopaedic wards.

We studied prospectively the regional inflammatory response to a unilateral distal radial fracture in 114 patients at eight to nine weeks after injury and again at one year. Our aim was to identify patients at risk for a delayed recovery and particularly those likely to develop complex regional pain syndrome. In order to quantify clinically the inflammatory response, a regional inflammatory score was developed. In addition, blood samples were collected from the antecubital veins of both arms for comparative biochemical and blood-gas analysis.

The severity of the inflammatory response was related to the type of treatment (Kruskal-Wallis test, p = 0.002). A highly significantly-positive correlation was found between the regional inflammatory score and the length of time to full recovery (r² = 0.92, p = 0.01, linear regession). A regional inflammatory score of 5 points with a sensitivity of 100% but a specificity of only 16% also identified patients at risk of complex regional pain syndrome. None of the biochemical parameters studied correlated with regional inflammatory score or predicted the development of complex regional pain syndrome.

Our study suggests that patients with a distal radial fracture and a regional inflammatory score of 5 points or more at eight to nine weeks after injury should be considered for specific anti-inflammatory treatment.

In order to identify the risk factors and the incidence of post-operative spinal epidural haematoma, we analysed the records of 14 932 patients undergoing spinal surgery between 1984 and 2002. Of these, 32 (0.2%) required re-operation within one week of the initial procedure and had an International Classification of Diseases (ICD)-9 code for haematoma complicating a procedure (998.12). As controls, we selected those who had undergone a procedure of equal complexity by the same surgeon but who had not developed this complication. Risks identified before operation were older than 60 years of age, the use of pre-operative non-steroidal anti-inflammatories and Rh-positive blood type. Those during the procedure were involvement of more than five operative levels, a haemoglobin < 10 g/dL, and blood loss > 1 L, and after operation an international normalised ratio > 2.0 within the first 48 hours. All these were identified as significant (p < 0.03). Well-controlled anticoagulation and the use of drains were not associated with an increased risk of post-operative spinal epidural haematoma.

We have managed 21 patients with a fracture of the tibia complicated by bone and soft-tissue loss as a result of an open fracture in 10, or following debridement of an infected nonunion in 11, by resection of all the devitalised tissues, acute limb shortening to close the defect, application of an external fixator and metaphyseal osteotomy for re-lengthening. The mean bone loss was 4.7 cm (3 to 11). The mean age of the patients was 28.8 years (12 to 54) and the mean follow-up was 34.8 months (24 to 75).

All the fractures united with a well-aligned limb. The mean duration of treatment for the ten grade-III A+B open fractures (according to the Gustilo-Anderson classification) was 5.7 months (4.5 to 8) and for the nonunions, 7.6 months (5.5 to 12.5). Complications included one refracture, one transient palsy of the peroneal nerve and one equinus contracture of 10°.

We studied 51 patients with osteo-articular tuberculosis who were divided into two groups. Group I comprised 31 newly-diagnosed patients who were given first-line antituberculous treatment consisting of isoniazid, rifampicin, ethambutol and pyrazinamide. Group II (non-responders) consisted of 20 patients with a history of clinical non-responsiveness to supervised uninterrupted antituberculous treatment for a minimum of three months or a recurrence of a previous lesion which on clinical observation had healed. No patient in either group was HIV-positive. Group II were treated with an immunomodulation regime of intradermal BCG, oral levamisole and intramuscular diphtheria and tetanus vaccines as an adjunct for eight weeks in addition to antituberculous treatment. We gave antituberculous treatment for a total of 12 to 18 months in both groups and they were followed up for a mean of 30.2 months (24 to 49). A series of 20 healthy blood donors served as a control group.

Twenty-nine (93.6%) of the 31 patients in group I and 14 of the 20 (70%) in group II had a clinicoradiological healing response to treatment by five months.

The CD4 cell count in both groups was depressed at the time of enrolment, with a greater degree of depression in the group-II patients (686 cells/mm³ (sd 261) and 545 cells/mm³ (sd 137), respectively; p < 0.05). After treatment for three months both groups showed significant elevation of the CD4 cell count, reaching a level comparable with the control group. However, the mean CD4 cell count of group II (945 cells/mm³ (sd 343)) still remained lower than that of group I (1071 cells/mm³ (sd 290)), but the difference was not significant. Our study has shown encouraging results after immunomodulation and antituberculous treatment in non-responsive patients. The pattern of change in the CD4 cell count in response to treatment may be a reliable clinical indicator.

A nationwide study of Perthes’ disease in Norway was undertaken over a five-year period from January 1996. There were 425 patients registered, which represents a mean annual incidence of 9.2 per 100 000 in subjects under 15 years of age, and an occurrence rate of 1:714 for the country as a whole. There were marked regional variations. The lowest incidence was found in the northern region (5.4 per 100 000 per year) and the highest in the central and western regions (10.8 and 11.3 per 100 000 per year, respectively). There was a trend towards a higher incidence in urban (9.5 per 100 000 per year) compared with rural areas (8.9 per 100 000 per year). The mean age at onset was 5.8 years (1.3 to 15.2) and the male:female ratio was 3.3:1.

We compared 402 patients with a matched control group of non-affected children (n = 1 025 952) from the Norwegian Medical Birth Registry and analysed maternal data (age at delivery, parity, duration of pregnancy), birth length and weight, birth presentation, head circumference, ponderal index and the presence of congenital anomalies. Children with Perthes’ disease were significantly shorter at birth and had an increased frequency of congenital anomalies.

Applying Sartwell’s log-normal model of incubation periods to the distribution of age at onset of Perthes’ disease showed a good fit to the log-normal curve. Our findings point toward a single cause, either genetic or environmental, acting prenatally in the aetiology of Perthes’ disease.