Perioperative periprosthetic femur fracture associated with direct anterior total hip arthroplasty using metaphyseal fit and fill stem.

INTRODUCTION: This study aims to identify radiographic and clinical risk factors of perioperative periprosthetic femur fracture associated with the direct anterior approach (DAA) using a metaphyseal fit and fill stem. We hypothesize stem malalignment with this femoral implant places increased stress on the medial calcar region, which leads to an increased risk of periprosthetic fracture. METHODS: We compared patients with periprosthetic femur fractures following DAA total hip arthroplasty (THA) utilizing the Echo Bi-Metric Microplasty Stem (Zimmer Biomet, Warsaw, IN) to a cohort of patients who did not sustain a periprosthetic fracture from five orthopedic surgeons over four years. Postoperative radiographs were evaluated for stem alignment, neck cut level, Dorr classification, and the presence of radiographic pannus. Univariate and logistic regression analyses were performed. Demographic and categorical variables were also analyzed. RESULTS: Fourteen hips sustained femur fractures, including nine Vancouver B2 and five AG fractures. Valgus stem malalignment, proud stems, extended offset, and patients with enlarged radiographic pannus reached statistical significance for increased fracture risk. Low femoral neck cut showed a trend toward statistical significance. CONCLUSION: Patients undergoing DAA THA using a metaphyseal fit and fill stem may be at increased risk of perioperative periprosthetic fracture when the femoral stem sits proudly in valgus malalignment with extended offset and when an enlarged pannus is seen radiographically. This study identifies a specific pattern in the Vancouver B2 fracture cohort with regard to injury mechanism, time of injury, and fracture pattern, which may be attributed to coronal malalignment of the implant.

Septic gonococcal arthritis in a pediatric patient: Rare case report.

INTRODUCTION: Septic arthritis is an orthopedic emergency that requires rapid diagnosis and treatment due to the rapid destruction to cartilage. The responsible organism and etiology differs depending on patient age, especially in children. Gonococcal Arthritis in toddlers is a rare occurrence with few documented cases in the literature. An orthopedic surgeon is likely not to come across this either in training or through their careers. Consequently, its presentation and subsequent treatment algorithms leave several gray areas. PRESENTATION OF CASE: In this case report, we present a rare and not so straightforward presentation of a toddler with septic gonococcal arthritis along with a summary of treatment considerations described in the current literature and the course of treatment for this patient. Our patient is a toddler who originally presented to the emergency department with shoulder and knee pain for several days after an unwitnessed fall. He was subsequently discharged and presented again the next day with a knee effusion and elevated inflammatory markers. An MRI showed a large joint effusion without any underlying abscess or osteomyelitis to explain his elevated inflammatory markers. A knee aspiration was subsequently preformed which eventually grew out Neisseria Gonorrhea on hospital day 3 after the patient had been on antibiotics. He was taken back for an arthroscopic irrigation and debridement for definitive treatment. CLINICAL DISCUSSION/CONCLUSION: Disseminated gonococcal infection in toddlers is a rare occurrence without much information in the literature and should not be dismissed as a differential. We recommend a high index of suspicion with thorough work up. We also recommend surgical management of a septic joint due to DGI diagnosed via arthrocentesis (gross purulence, symptoms not improving on medical therapy, positive aspiration cultures, elevated synovial cell counts, and medically unstable patients) given the sequelae of medical management alone. The importance of interdisciplinary team collaboration that include pediatrician, infectious disease specialist, social worker, and government child safety associations is pivotal.

In Utero Particulate Matter Exposure Produces Heart Failure, Electrical Remodeling, and Epigenetic Changes at Adulthood.

BACKGROUND: Particulate matter (PM; PM2.5 [PM with diameters of <2.5 µm]) exposure during development is strongly associated with adverse cardiovascular outcomes at adulthood. In the present study, we tested the hypothesis that in utero PM2.5 exposure alone could alter cardiac structure and function at adulthood. METHODS AND RESULTS: Female FVB mice were exposed either to filtered air or PM2.5 at an average concentration of 73.61 µg/m3 for 6 h/day, 7 days/week throughout pregnancy. After birth, animals were analyzed at 12 weeks of age. Echocardiographic (n=9-10 mice/group) and pressure-volume loop analyses (n=5 mice/group) revealed reduced fractional shortening, increased left ventricular end-systolic and -diastolic diameters, reduced left ventricular posterior wall thickness, end-systolic elastance, contractile reserve (dP/dtmax/end-systolic volume), frequency-dependent acceleration of relaxation), and blunted contractile response to ß-adrenergic stimulation in PM2.5-exposed mice. Isolated cardiomyocyte (n=4-5 mice/group) function illustrated reduced peak shortening, ±dL/dT, and prolonged action potential duration at 90% repolarization. Histological left ventricular analyses (n=3 mice/group) showed increased collagen deposition in in utero PM2.5-exposed mice at adulthood. Cardiac interleukin (IL)-6, IL-1ß, collagen-1, matrix metalloproteinase (MMP) 9, and MMP13 gene expressions were increased at birth in in utero PM2.5-exposed mice (n=4 mice/group). In adult hearts (n=5 mice/group), gene expressions of sirtuin (Sirt) 1 and Sirt2 were decreased, DNA methyltransferase (Dnmt) 1, Dnmt3a, and Dnmt3b were increased, and protein expression (n=6 mice/group) of Ca2+-ATPase, phosphorylated phospholamban, and Na+/Ca2+ exchanger were decreased. CONCLUSIONS: In utero PM2.5 exposure triggers an acute inflammatory response, chronic matrix remodeling, and alterations in Ca2+ handling proteins, resulting in global adult cardiac dysfunction. These results also highlight the potential involvement of epigenetics in priming of adult cardiac disease.

Minocycline attenuates cardiac dysfunction in tumor-burdened mice.

Cardiovascular dysfunction as a result of tumor burden is becoming a recognized complication; however, the mechanisms remain unknown. A murine model of cancer cachexia has shown marked increases of matrix metalloproteinases (MMPs), known mediators of cardiac remodeling, in the left ventricle. The extent to which MMPs are involved in remodeling remains obscured. To this end a common antibiotic, minocycline, with MMP inhibitory properties was used to elucidate MMP involvement in tumor induced cardiovascular dysfunction. Tumor-bearing mice showed decreased cardiac function with reduced posterior wall thickness (PWTs) during systole, increased MMP and collagen expression consistent with fibrotic remodeling. Administration of minocycline preserved cardiac function in tumor bearing mice and decreased collagen RNA expression in the left ventricle. MMP protein levels were unaffected by minocycline administration, with the exception of MMP-9, indicating minocycline inhibition mechanisms are directly affecting MMP activity. Cancer induced cardiovascular dysfunction is an increasing concern; novel therapeutics are needed to prevent cardiac complications. Minocycline is a well-known antibiotic and recently has been shown to possess MMP inhibitory properties. Our findings presented here show that minocycline could represent a novel use for a long established drug in the prevention and treatment of cancer induced cardiovascular dysfunction.

In vitro particulate matter exposure causes direct and lung-mediated indirect effects on cardiomyocyte function.

Particulate matter (PM) exposure induces a pathological response from both the lungs and the cardiovascular system. PM is capable of both manifestation into the lung epithelium and entrance into the bloodstream. Therefore, PM has the capacity for both direct and lung-mediated indirect effects on the heart. In the present studies, we exposed isolated rat cardiomyocytes to ultrafine particulate matter (diesel exhaust particles, DEP) and examined their contractile function and calcium handling ability. In another set of experiments, lung epithelial cells (16HBE14o- or Calu-3) were cultured on permeable supports that allowed access to both the basal (serosal) and apical (mucosal) media; the basal media was used to culture cardiomyocytes to model the indirect, lung-mediated effects of PM on the heart. Both the direct and indirect treatments caused a reduction in contractility as evidenced by reduced percent sarcomere shortening and reduced calcium handling ability measured in field-stimulated cardiomyocytes. Treatment of cardiomyocytes with various anti-oxidants before culture with DEP was able to partially prevent the contractile dysfunction. The basal media from lung epithelial cells treated with PM contained several inflammatory cytokines, and we found that monocyte chemotactic protein-1 was a key trigger for cardiomyocyte dysfunction. These results indicate the presence of both direct and indirect effects of PM on cardiomyocyte function in vitro. Future work will focus on elucidating the mechanisms involved in these separate pathways using in vivo models of air pollution exposure.

In vitro effects of exercise on the heart.

Pathologic and physiologic factors acting on the heart can produce consistent pressure changes, volume overload, or increased cardiac output. These changes may then lead to cardiac remodeling, ultimately resulting in cardiac hypertrophy. Exercise can also induce hypertrophy, primarily physiologic in nature. To determine the mechanisms responsible for each type of remodeling, it is important to examine the heart at the functional unit, the cardiomyocyte. Tests of individual cardiomyocyte function in vitro provide a deeper understanding of the changes occurring within the heart during hypertrophy. Examination of cardiomyocyte function during exercise primarily follows one of two pathways: the addition of hypertrophic inducing agents in vitro to normal cardiomyocytes, or the use of trained animal models and isolating cells following the development of hypertrophy in vivo. Due to the short lifespan of adult cardiomyocytes, a proportionately scant amount of research exists involving the direct stimulation of cells in vitro to induce hypertrophy. These attempts provide the only current evidence, as it is difficult to gather extensive data demonstrating cell growth as a result of in vitro physical stimulation. Researchers have created ways to combine skeletal myocytes with cardiomyocytes to produce functional muscle cells used to repair pathologic heart tissue, but continue to struggle with the short lifespan of these cells. While there have been promising findings regarding the mechanisms that surround cardiac hypertrophy in vitro, the translation of in vitro findings to in vivo function is not consistent. Therefore, the focus of this review is to highlight recent studies that have investigated the effect of exercise on the heart, both in vitro and in vivo.