Aims. Brace treatment is the cornerstone of managing developmental dysplasia of the hip (DDH), yet there is a lack of evidence-based treatment protocols, which results in wide variations in practice. To resolve this, we have developed a comprehensive nonoperative treatment protocol conforming to published consensus principles, with well-defined a priori criteria for inclusion and successful treatment. Methods. This was a single-centre, prospective, longitudinal cohort study of a consecutive series of infants with ultrasound-confirmed DDH who underwent a comprehensive nonoperative brace management protocol in a unified multidisciplinary clinic between January 2012 and December 2016 with five-year follow-up radiographs. The radiological outcomes were acetabular index-lateral edge (AI-L), acetabular index-sourcil (AI-S), centre-edge angle (CEA), acetabular depth ratio (ADR), International Hip Dysplasia Institute (IHDI) grade, and evidence of avascular necrosis (AVN). At five years, each hip was classified as normal (< 1 SD), borderline dysplastic (1 to 2 SDs), or dysplastic (> 2 SDs) based on validated radiological norm-referenced values. Results. Of 993 infants assessed clinically and sonographically, 21% (212 infants, 354 abnormal hips) had DDH and were included. Of these, 95% (202 infants, 335 hips) successfully completed bracing, and 5% (ten infants, 19 hips) failed bracing due to irreducible hip(s). The success rate of bracing for unilateral dislocations was 88% (45/51 infants) and for bilateral dislocations 83% (20/24 infants). The femoral nerve palsy rate was 1% (2/212 infants). At five-year follow-up (mean 63 months (SD 5.9; 49 to 83)) the prevalence of residual dysplasia after successful brace treatment was 1.6% (5/312 hips). All hips were IHDI grade I and none had AVN. Four children (4/186; 2%) subsequently underwent surgery for residual dysplasia. Conclusion. Our comprehensive protocol for nonoperative treatment of infant DDH has shown high rates of success and extremely low rates of residual dysplasia at a mean age of five years. Cite this article: Bone Joint J 2023;105-B(8):935–942

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Perthes’ disease is an uncommon hip disorder with limited data on the long-term outcomes in adulthood. We partnered with community-based foundations and utilized web-based survey methodology to develop the Adult Perthes Survey, which includes demographics, childhood and adult Perthes’ disease history, the University of California Los Angeles (UCLA) Activity Scale item, Short Form-36, the Hip disability and Osteoarthritis Outcome Score, and a body pain diagram. Here we investigate the following questions: 1) what is the feasibility of obtaining > 1,000 survey responses from adults who had Perthes’ disease using a web-based platform?; and 2) what are the baseline characteristics and demographic composition of our sample?

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The aim of this study was to inform the epidemiology and treatment of slipped capital femoral epiphysis (SCFE).

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To establish the survivorship, function, and metal ion levels in an unselected series of metal-on-metal hip resurfacing arthroplasties (HRAs) performed by a non-designer surgeon.

To evaluate the safety and efficacy of treating patients with Graf IIa developmental hip dysplasia. The management of the developmentally immature Graf Type IIa dysplastic hip is controversial. Some authors advocate early treatment with an abduction harness whilst others adopt watchful waiting. At our institution selective sonographic assessment for developmental dysplasia of the hip (DDH) was established in 1997 with prospective data collection. All infants diagnosed with Graf Type IIa hip(s) were treated with either a Pavlik harness or double nappies, with clinical and sonographic follow up until normalisation. Pelvic radiographs were routinely performed at 8 and 18 months follow up for assessment of residual dysplasia and/or complications of treatment. We evaluated the safety and efficacy of all treated patients between 2005 and 2013. Complete clinical and radiological follow up (mean 2.1 years, 0.7–6.5) was available for 103 of 118 infants. 69 were treated with a Pavlik harness and 49 with double nappies. The chosen treatment was successful in 110 hips with no documented complications, well developed ossific nuclei on follow up radiographs, and no further treatments undertaken. In the double nappy group 4 infants deteriorated sonographically so were changed to a Pavlik harness with subsequent normalisation and successful treatment. 3 patients required VDRO at age 18 months (17–20) and 1 patient required closed reduction and spica cast treatment at age 11 months. No further complications arose in this group. The 15 patients lost to follow up had successful initial treatment but failed to attend for radiographic review. Both Pavlik harness and double nappies are safe treatment modalities for Type IIa hip dysplasia. However, sonographic deterioration was observed in both groups with surgical intervention required in the minority, supporting the ongoing treatment of these immature hips

Purpose: We hypothesized that thrombophilia-hypofibrinolysis are risk factors for femoral head osteonecrosis. Separately, we hypothesized that when Enoxaparin is started at Ficat stages I or II in patients with idiopathic osteonecrosis and thrombophilia-hypofibrinolysis, progression of osteonecrosis can be stopped. Method: We compared measures of thrombophilia and hypofibrinolysis in 71 adults with idiopathic osteonecrosis, in 62 with corticosteroid-associated secondary osteonecrosis, and in gender-race matched healthy controls. In a prospective Enoxaparin treatment study, 16 patients (25 hips)with one or more thrombophilic-hypofibrinolytic disorders and Ficat Stages I–II idiopathic ON of the hip(s). Enoxaparin (60 mg/day) was given for the first 12 weeks of the study. Yearly X-rays were taken for 5–7 years follow-up (average 6 years). Maintenance of Ficat Stages I-II versus progression to Stages III–IV or total hip replacement was the study outcome. Results: Patients with idiopathic osteonecrosis were more likely than controls to have high (> 150%) levels of heritable thrombophilic Factor VIII (19/71 [27%] vs 3/66 [5%], p =.0004), and to have inherited high levels of hypofibrinolytic lipoprotein(a) (25/69 [36%] vs 12/67 [18%], p =.016). Patients with secondary osteonecrosis were more likely than controls to have high (> 150%) levels of Factor VIII (16/62 [26%] vs 5/60 [8%], p =.011), to be heterozygous for the Factor V Leiden mutation (6/61 [10%] vs 0/61 [0%], p =.028), and to have heritable thrombophilic resistance to activated protein C (8/51[16%] vs 2/59[3%], p =.042). After 3 months on Enoxaparin, based on intent to treat, 17 of 25 hips (68%) have remained Ficat Stages I–II at 6-year follow-up versus approximately 20% 2-year hip survival in untreated historical controls. This suggests that the original 12 week Enoxaparin thromboprophylaxis produced lasting benefit. Conclusion: Inherited thrombophilia-hypofibrinolysis are risk factors for both idiopathic and secondary osteonecrosis of the head of the femur. The importance of the diagnosis of thrombophilia-hypofibrinolysis lies in the potential to stop the progression of osteonecrosis when Enoxaparin is started at Ficat stages I–II. Enoxaparin seemingly prevents progression of idiopathic hip ON, causing a decrease in the incidence of total hip replacement at 6 years follow-up