BackgroundMost research on failure leading to revision total hip arthroplasty (THA) is reported from single centers. We searched PubMed between January 2000 and August 2010 to identify population- or community-based studies evaluating ten-year revision risks. We report ten-year revision risk using the Kaplan-Meier method, stratifying by age and fixation technique.ResultsThirteen papers met the inclusion criteria. Cemented prostheses had Kaplan-Meier estimates of revision-free implant survival of ten years ranging from 88% to 95%; uncemented prostheses had Kaplan-Meier estimates from 80% to 85%. Estimates ranged from 72% to 86% in patients less than 60 years old and from 90 to 96% in older patients.ConclusionData reported from national registries suggest revision risks of 5 to 20% ten years following primary THA. Revision risks are lower in older THA recipients. Uncemented implants may have higher ten-year rates of revision, regardless of age.

Objective To determine the positive predictive value of Medicare claims for identifying revision of total hip replacement (THR), a frequent marker of THR quality and outcome. Study Design and Setting We obtained Medicare Part A (Hospital) claims from seven states on patients that had primary THR from July 1995 through June 1996. We searched claims to determine whether these THR recipients had a subsequent revision THR through December 2006. We selected a sample of subjects with codes indicating both index primary and subsequent revision THR. We obtained medical records for both procedures to establish whether the revision occurred on the same side as index primary THR. Results Three hundred seventy-four subjects had codes indicating primary THR in 1995–96 and subsequent revision. Seventy-one percent (95% confidence interval: 66, 76) of the revisions were performed on the index joint and would be correctly attributed as revisions of the index THR, using Medicare Claims data. Conclusion Claims data on revision THR that do not contain information on the side that was operated on are ambiguous with respect to whether the revision was performed on the index or contralateral side. Claims-based analyses of revisions after an index THR should acknowledge and adjust for this source of potential misclassification.

IMPORTANCE A better pathophysiologic understanding of the neurodevelopmental abnormalities observed in neonates exposed in utero to Zika virus (ZIKV) is needed to develop treatments. The retina as an extension of the diencephalon accessible to in vivo microcopy with spectral-domain optical coherence tomography (SD-OCT) can provide an insight into the pathophysiology of congenital Zika syndrome (CZS).OBJECTIVE To quantify the microstructural changes of the retina in CZS and compare these changes with those of cobalamin C (cblC) deficiency, a disease with potential retinal maldevelopment. DESIGN, SETTING, AND PARTICIPANTSThis case series included 8 infants with CZS and 8 individuals with cblC deficiency. All patients underwent ophthalmologic evaluation at 2 university teaching hospitals and SD-OCT imaging in at least 1 eye. Patients with cblC deficiency were homozygous or compound heterozygotes for mutations in the methylmalonic aciduria and homocystinuria type C (MMACHC) gene. Data were collected from January 1 to March 17, 2016, for patients with CZS and from May 4, 2015, to April 23, 2016, for patients with cblC deficiency. MAIN OUTCOMES AND MEASURESThe SD-OCT cross-sections were segmented using automatic segmentation algorithms embedded in the SD-OCT systems. Each retinal layer thickness was measured at critical eccentricities using the position of the signal peaks and troughs on longitudinal reflectivity profiles.RESULTS Eight infants with CZS (5 girls and 3 boys; age range, 3-5 months) and 8 patients with cblC deficiency (3 girls and 5 boys; age range, 4 months to 15 years) were included in the analysis. All 8 patients with CZS had foveal abnormalities in the analyzed eyes (8 eyes), including discontinuities of the ellipsoid zone, thinning of the central retina with increased backscatter, and severe structural disorganization, with 3 eyes showing macular pseudocolobomas. Pericentral retina with normal lamination showed a thinned (<30% of normal thickness) ganglion cell layer (GCL) that colocalized in 7 of 8 eyes with a normal photoreceptor layer. The inner nuclear layer was normal or had borderline thinning. The central retinal degeneration was similar to that of cblC deficiency. CONCLUSIONS AND RELEVANCE CongenitalZika syndrome showed a central retinal degeneration with severe GCL loss, borderline inner nuclear layer thinning, and less prominent photoreceptor loss. The findings provide the first, to date, in vivo evidence in humans for possible retinal maldevelopment with a predilection for retinal GCL loss in CZS, consistent with a murine model of the disease and suggestive of in utero depletion of this neuronal population as a consequence of Zika virus infection.