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Deficiency of the abductor mechanism is a well-recognised cause of pain and limping after total hip replacement (THR). This can be found incidentally at the time of surgery, or it may arise as a result of damage to the superior gluteal nerve intra-operatively, or after surgery owing to mechanical failure of the abductor muscle repair or its detachment from the greater trochanter. The incidence of abductor failure has been reported as high as 20% in some studies. The management of this condition remains a dilemma for the treating surgeon. We review the current state of knowledge concerning post-THR abductor deficiency, including the aetiology, diagnosis and management, and the outcomes of surgery for this condition.

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In the United Kingdom, national guidelines have stated that patients undergoing elective hip surgery are at increased risk for venous thromboembolic events (VTE) following surgery and have recommended thromboprophylaxis for 28-35 days (1, 2). Studies of direct thrombin inhibitors have hitherto concentrated on major bleeding. We prospectively assessed wound discharge in patients who underwent hip arthroplasty and who received oral dabigatran postoperatively between March 2010 and April 2010 (n=56). We compared these results to a retrospective matched group of patients who underwent similar operations six months earlier, at which time all patients were given subcutaneous dalteparin routinely postoperatively until discharge, and then discharged home on 150 mg aspirin daily for 6 weeks (n=67). Wound discharge after 5 days was significantly higher in the patients taking dabigatran (32% dabigatran n=18, 10% dalteparin n=17, p=0.003) and our rate of delayed discharges due to wound discharge significantly increased from 7% in the dalteparin group (n=5) to 27% for dabigatran (n=15, p=0.004). Patients who received dabigatran were more than five times as likely to return to theatre with a wound complication compared with those who received dalteparin (7% dabigatran n=4, vs. 1% dalteparin n=1), but this was not statistically significant (p=0.18). We now administer dalteparin until the wound is dry and then start dabigatran. Our study demonstrates the need for further clinical studies regarding wound discharge and direct thrombin inhibitors.

We have examined 26 retrieved, failed titanium-alloy femoral stems. The clinical details, radiological appearances and the histology of the surrounding soft tissues in each patient were also investigated. The stems were predominantly of the flanged design and had a characteristic pattern of wear. A review of the radiographs showed a series of changes, progressive with time. The first was lateral debonding with subsidence of the stem. This was followed by calcar resorption and fragmentation or fracture of the cement. Finally, osteolysis was seen, starting with a radiolucency at the cement-bone interface and progressing to endosteal cavitation. Three histological appearances were noted: granulomatous, necrobiotic and necrotic. We suggest that an unknown factor, possibly related to the design of the stem, caused it to move early. After this, micromovement at the cement-stem interface led to the generation of particulate debris and fracture of the cement. A soft-tissue reaction to the debris resulted in osteolysis and failure of fixation of the prostheses.