The failure and subsequent withdrawal of the ASR device in both its resurfacing and THR form has been well documented. The National Joint Registry report of 2010 quoted figures of 12–13% failure at five years. Adverse reaction to metal debris (ARMD) is a poorly understood condition and patients developing severe metal reactions may go unrecognised for sometime. In 2004 a single surgeons prospective study of the ASR bearing surface was undertaken. We present the ARMD failure rates of the ASR resurfacing and ASR THR systems. The diagnosis of ARMD was made by the senior author and was based on clinical history, examination, ultrasound findings, metal ion analysis of blood and joint fluid, operative findings and histopathological analysis of tissues retrieved at revision. Mean follow up was 52 months (24–81) and 70 patients were beyond 6 years of the procedure at the time of writing. Kaplan Meier survival analysis was carried out firstly with joints designated “failure” if the patient had undergone revision surgery or if the patient had been listed. A second survival analysis was carried out with a failure defined as a serum cobalt > 7µg/L. Full explant analysis was carried out for retrieved prostheses.Background
Patients and Methods
Adverse reaction to metal debris (ARMD) is an increasingly recognised complication of metal-on-metal hip arthroplasty. A previous study described poor results following revision and recommended early intervention1. We determined the outcome of revision for ARMD and present the largest case series to date. Between 2005 and 2010, 98 patients (101 hips) underwent revision for ARMD. The diagnosis of ARMD was based on clinical history, examination, appearance at revision and histology. Patients were reviewed at 3, 6 and 12 months and annually thereafter. Patient satisfaction, Harris hip scores (HHS) and metal ions were analysed.Introduction
Methods
Stable ankle fractures can be successfully treated non-operatively with a below knee plaster cast. In some European centres it is standard practice to administer thromboprophylaxis, in the form of low molecular weight heparin, to these patients in order to reduce the risk of deep venous thrombosis (DVT). The aim of our study was to assess the incidence of DVT in such patients in the absence of any thromboprophylaxis. We designed a prospective study, which was approved by the local ethics committee. We included 100 consecutive patients with ankle fractures treated in a below knee plaster cast. At the time of plaster removal (6 weeks), patients were examined for signs of DVT. A colour doppler duplex ultrasound scan was then performed by one of the two experienced musculoskeletal ultrasound technicians. We found that 5 patients developed a DVT. Two of these were above knee, involving the superficial femoral vein and popliteal vein respectively. The other three were below knee. None of the patients had any clinical symptoms or signs of DVT. None of the patients developed pulmonary embolism. Of these five patients, four had some predisposing factors for DVT. The annual incidence of DVT in the normal population is about 0.1%. This can increase to about 4.5% by the age of 75. DVT following hip and knee replacement can occur in 40-80% of cases. Routine thromboprophylaxis may be justified in these patients. However, with a low incidence of 5% following ankle fractures treated in a cast, we believe that routine thromboprophylaxis is not justified.
