We wished to estimate the incidence of surgical-site infection (SSI) after total hip replacement (THR) and hemiarthroplasty and its strength of association with major risk factors. The SSI surveillance service prospectively gathered clinical, operative and infection data on inpatients from 102 hospitals in England during a four-year period.

The overall incidence of SSI was 2.23% for 16 291 THRs, 4.97% for 5769 hemiarthroplasty procedures, 3.68% for 2550 revision THRs and 7.6% for 198 revision hemiarthroplasties. Staphylococcus aureus was identified in 50% of SSIs; 59% of these isolates were methicillin-resistant (MRSA). In the single variable analysis of THRs, age, female gender, American Society of Anesthesiologists (ASA) score, body mass index, trauma, duration of operation and pre-operative stay were significantly associated with the risk of SSI (p < 0.05). For hemiarthroplasty, the ASA score and age were significant factors. In revision THRs male gender, ASA score, trauma, wound class, duration of operation and pre-operative stay were significant risk factors. The median time to detection of SSI was eight days for superficial incisional, 11 days for deep incisional and 11 days for joint/bone infections. For each procedure the mean length of stay doubled for patients with SSI. The multivariate analysis identified age group, trauma, duration of operation and ASA score as significant, independent risk factors for SSI. There was significant interhospital variation in the rates of SSI. MRSA was the most common pathogen to cause SSI in hip arthroplasty, especially in patients undergoing hemiarthroplasty, but coagulase-negative Staph. aureus may be more important in deep infections involving the joint.

The aim of this study was to establish a classification system for the acromioclavicular joint using cadaveric dissection and radiological analyses of both reformatted computed tomographic scans and conventional radiographs centred on the joint. This classification should be useful for planning arthroscopic procedures or introducing a needle and in prospective studies of biomechanical stresses across the joint which may be associated with the development of joint pathology.

We have demonstrated three main three-dimensional morphological groups namely flat, oblique and curved, on both cadaveric examination and radiological assessment. These groups were recognised in both the coronal and axial planes and were independent of age.

Between 1987 and 2006 we performed a modified Thompson’s quadricepsplasty on 40 fracture-related stiff knees and followed the patients for a mean of 7.9 years (2 to 11.1). The factors affecting the final gain of movement were investigated. A total of 15 knees required lengthening of the rectus femoris. The mean flexion gain was 70.2° (42.3° to 112.5°). According to Judet’s criteria, the results were excellent in 30 knees, good in seven, and fair in three. The range of movement which was achieved intra-operatively was related to the gain of knee flexion on univariate analysis. Five patients had complications: deep infection in one, recurrent patellar dislocation in one, and rupture of the extensor mechanism in three. This modified technique gives satisfactory results. Achieving maximum knee flexion intra-operatively seems to be the most important factor in enhancing the outcome in patients with stiffness of the knee following fracture.

We have developed an animal model to examine the formation of heterotopic ossification using standardised muscular damage and implantation of a beta-tricalcium phosphate block into a hip capsulotomy wound in Wistar rats. The aim was to investigate how cells originating from drilled femoral canals and damaged muscles influence the formation of heterotopic bone. The femoral canal was either drilled or left untouched and a tricalcium phosphate block, immersed either in saline or a rhBMP-2 solution, was implanted. These implants were removed at three and 21 days after the operation and examined histologically, histomorphometrically and immunohistochemically.

Bone formation was seen in all implants in rhBMP-2-immersed, whereas in those immersed in saline the process was minimal, irrespective of drilling of the femoral canals. Bone mineralisation was somewhat greater in the absence of drilling with a mean mineralised volume to mean total volume of 18.2% (sd 4.5) versus 12.7% (sd 2.9, p < 0.019), respectively.

Our findings suggest that osteoinductive signalling is an early event in the formation of ectopic bone. If applicable to man the results indicate that careful tissue handling is more important than the prevention of the dissemination of bone cells in order to avoid heterotopic ossification.

We examined the usefulness of neutrophil CD64 expression in detecting local musculoskeletal infection and the impact of antibiotics on its expression. Of 141 patients suspected of musculoskeletal infection, 46 were confirmed by microbiological culture to be infected and 95 had infection excluded. The median CD64 count of patients with localised infection was 2230 molecules per cell (interquartile range (IQR) 918 to 4592) and that of the patients without infection was 937 molecules per cell (IQR 648 to 1309) (p < 0.001). The level of CD64 correlated with the CRP level in patients with infection, but not in those without infection (r = 0.59, p < 0.01). Receiver operator characteristic curve analysis revealed that CD64 was a good predictor of local infection. When the patients were subdivided into two groups based on the administration of antibiotics at the time of CD64 sampling, the sensitivity for detecting infection was better in those who had not received antibiotics.

These results suggest that measurement of CD64 expression is a useful marker for local musculoskeletal infection.

We have conducted a case-control study over a period of ten years comparing both deep infection with methicillin-resistant staphylococcus aureus (MRSA) and colonised cases with a control group.

Risk factors associated with deep infection were vascular diseases, chronic obstructive pulmonary disease, admission to a high-dependency or an intensive-care unit and open wounds. Those for colonisation were institutional care, vascular diseases and dementia. Older age was a risk factor for any MRSA infection. The length of hospital stay was dramatically increased by deep infection.

These risk factors are useful in identifying higher-risk patients who may be more susceptible to MRSA infection. A strategy of early identification and isolation may help to control its spread in trauma units.

Surgical dislocation of the hip in the treatment of acetabular fractures allows the femoral head to be safely displaced from the acetabulum. This permits full intra-articular acetabular and femoral inspection for the evaluation and potential treatment of cartilage lesions of the labrum and femoral head, reduction of the fracture under direct vision and avoidance of intra-articular penetration with hardware. We report 60 patients with selected types of acetabular fracture who were treated using this approach. Six were lost to follow-up and the remaining 54 were available for clinical and radiological review at a mean follow-up of 4.4 years (2 to 9).

Substantial damage to the intra-articular cartilage was found in the anteromedial portion of the femoral head and the posterosuperior aspect of the acetabulum. Labral lesions were predominantly seen in the posterior acetabular area. Anatomical reduction was achieved in 50 hips (93%) which was considerably higher than that seen in previous reports. There were no cases of avascular necrosis. Four patients subsequently required total hip replacement. Good or excellent results were achieved in 44 hips (81.5%). The cumulative eight-year survivorship was 89.0% (95% confidence interval 84.5 to 94.1). Significant predictors of poor outcome were involvement of the acetabular dome and lesions of the femoral cartilage greater than grade 2. The functional mid-term results were better than those of previous reports.

Surgical dislocation of the hip allows accurate reduction and a predictable mid-term outcome in the management of these difficult injuries without the risk of the development of avascular necrosis.

Highly active anti-retroviral therapy has transformed HIV into a chronic disease with a long-term asymptomatic phase. As a result, emphasis is shifting to other effects of the virus, aside from immunosuppression and mortality. We have reviewed the current evidence for an association between HIV infection and poor fracture healing.

The increased prevalence of osteoporosis and fragility fractures in HIV patients is well recognised. The suggestion that this may be purely as a result of highly active anti-retroviral therapy has been largely rejected. Apart from directly impeding cellular function in bone remodelling, HIV infection is known to cause derangement in the levels of those cytokines involved in fracture healing (particularly tumour necrosis factor-α) and appears to impair the blood supply of bone.

Many other factors complicate this issue, including a reduced body mass index, suboptimal nutrition, the effects of anti-retroviral drugs and the avoidance of operative intervention because of high rates of wound infection. However, there are sound molecular and biochemical hypotheses for a direct relationship between HIV infection and impaired fracture healing, and the rewards for further knowledge in this area are extensive in terms of optimised fracture management, reduced patient morbidity and educated resource allocation. Further investigation in this area is overdue.

Technological advances and shorter rescue times have allowed early and effective resuscitation after trauma and brought attention to the host response to injury. Trauma patients are at risk of progressive organ dysfunction from what appears to be an uncontrolled immune response. The availability of improved techniques of molecular diagnosis has allowed investigation of the role of genetic variations in the inflammatory response to post-traumatic complications and particularly to sepsis.

This review examines the current evidence for the genetic predisposition to adverse outcome after trauma. While there is evidence supporting the involvement of different polymorphic variants of genes in determining the post-traumatic course and the development of complications, larger-scale studies are needed to improve the understanding of how genetic variability influences the responses to post-traumatic complications and pharmacotherapy.

We report the incidence and location of deep-vein thrombosis in 312 patients who had sustained high-energy, skeletal trauma. They were investigated using magnetic resonance venography and Duplex ultrasound.

Despite thromboprophylaxis, 36 (11.5%) developed venous thromboembolic disease with an incidence of 10% in those with non-pelvic trauma and 12.2% in the group with pelvic trauma. Of patients who developed deep-vein thrombosis, 13 of 27 in the pelvic group (48%) and only one of nine in the non-pelvic group (11%) had a definite pelvic deep-vein thrombosis. When compared with magnetic resonance venography, ultrasound had a false-negative rate of 77% in diagnosing pelvic deep-vein thrombosis. Its value in the pelvis was limited, although it was more accurate than magnetic resonance venography in diagnosing clots in the lower limbs. Additional screening may be needed to detect pelvic deep-vein thrombosis in patients with pelvic or acetabular fractures.

The stress response to trauma is the summation of the physiological response to the injury (the ‘first hit’) and by the response to any on-going physiological disturbance or subsequent trauma surgery (the ‘second hit’).

Our animal model was developed in order to allow the study of each of these components of the stress response to major trauma. High-energy, comminuted fracture of the long bones and severe soft-tissue injuries in this model resulted in a significant tropotropic (depressor) cardiovascular response, transcardiac embolism of medullary contents and activation of the coagulation system. Subsequent stabilisation of the fractures using intramedullary nails did not significantly exacerbate any of these responses.

We retrospectively examined the prevalence and natural history of asymptomatic lumbar canal stenosis in patients treated surgically for cervical compressive myelopathy in order to assess the influence of latent lumbar canal stenosis on the recovery after surgery. Of 214 patients who had undergone cervical laminoplasty for cervical myelopathy, we identified 69 (32%) with myelographically documented lumbar canal stenosis. Of these, 28 (13%) patients with symptomatic lumbar canal stenosis underwent simultaneous cervical and lumbar decompression. Of the remaining 41 (19%) patients with asymptomatic lumbar canal stenosis who underwent only cervical surgery, 39 were followed up for ≥ 1 year (mean 4.9 years (1 to 12)) and were included in the analysis (study group). Patients without myelographic evidence of lumbar canal stenosis, who had been followed up for ≥ 1 year after the cervical surgery, served as controls (135 patients; mean follow-up period 6.5 years (1 to 17)). Among the 39 patients with asymptomatic lumbar canal stenosis, seven had lumbar-related leg symptoms after the cervical surgery.

Kaplan–Meier analysis showed that 89.6% (95% confidence interval (CI) 75.3 to 96.0) and 76.7% (95% CI 53.7 to 90.3) of the patients with asymptomatic lumbar canal stenosis were free from leg symptoms for three and five years, respectively. There were no significant differences between the study and control groups in the recovery rate measured by the Japanese Orthopaedic Association score or improvement in the Nurick score at one year after surgery or at the final follow-up.

These results suggest that latent lumbar canal stenosis does not influence recovery following surgery for cervical myelopathy; moreover, prophylactic lumbar decompression does not appear to be warranted as a routine procedure for coexistent asymptomatic lumbar canal stenosis in patients with cervical myelopathy, when planning cervical surgery.

Injury to the sciatic nerve is one of the more serious complications of acetabular fracture and traumatic dislocation of the hip, both in the short and long term. We have reviewed prospectively patients, treated in our unit, for acetabular fractures who had concomitant injury to the sciatic nerve, with the aim of predicting the functional outcome after these injuries.

Of 136 patients who underwent stabilisation of acetabular fractures, there were 27 (19.9%) with neurological injury. At initial presentation, 13 patients had a complete foot-drop, ten had weakness of the foot and four had burning pain and altered sensation over the dorsum of the foot. Serial electromyography (EMG) studies were performed and the degree of functional recovery was monitored using the grading system of the Medical Research Council. In nine patients with a foot-drop, there was evidence of a proximal acetabular (sciatic) and a distal knee (neck of fibula) nerve lesion, the double-crush syndrome.

At the final follow-up, clinical examination and EMG studies showed full recovery in five of the ten patients with initial muscle weakness, and complete resolution in all four patients with sensory symptoms (burning pain and hyperaesthesia). There was improvement of functional capacity (motor and sensory) in two patients who presented initially with complete foot-drop. In the remaining 11 with foot-drop at presentation, including all nine with the double-crush lesion, there was no improvement in function at a mean follow-up of 4.3 years.

High energy fractures of the pelvis are a challenging problem both in the immediate post-injury phase and later when definitive fixation is undertaken. No single management algorithm can be applied because of associated injuries and the wide variety of trauma systems that have evolved around the world.

Initial management is aimed at saving life and this is most likely to be achieved with an approach that seeks to identify and treat life-threatening injuries in order of priority. Early mortality after a pelvic fracture is most commonly due to major haemorrhage or catastrophic brain injury. In this article we review the role of pelvic binders, angiographic embolisation, pelvic packing, early internal fixation and blood transfusion with regard to controlling haemorrhage.

Definitive fixation seeks to prevent deformity and reduce complications. We believe this should be undertaken by specialist surgeons in a hospital resourced, equipped and staffed to manage the whole spectrum of major trauma. We describe the most common modes of internal fixation by injury type and review the factors that influence delayed mortality, adverse functional outcome, sexual dysfunction and venous thromboembolism.

Injury to the perforating branch of the peroneal artery has not been reported previously as a cause of acute compartment syndrome following soft-tissue injury to the ankle. We describe the case of a 23-year-old male who sustained such an injury resulting in an acute compartment syndrome. In a review of the literature, we could find only five previous cases, all of which gave rise to a false aneurysm which was detected after the acute event.

Between 1998 and 2002, 37 neuropathies in 32 patients with a displaced supracondylar fracture of the humerus who were referred to a nerve injury unit were identified. There were 19 boys and 13 girls with a mean age of 7.9 years (3.6 to 11.3). A retrospective review of these injuries was performed. The ulnar nerve was injured in 19, the median nerve in ten and the radial nerve in eight cases. Fourteen neuropathies were noted at the initial presentation and 23 were diagnosed after treatment of the fracture. After referral, exploration of the nerve was planned for 13 patients. Surgery was later cancelled in three because of clinical recovery. Six patients underwent neurolysis alone. Excision of neuroma and nerve grafting were performed in four. At follow-up, 26 patients had an excellent, five a good and one a fair outcome.