Iatrogenic nerve injury in primary and revision reverse total shoulder arthroplasty

INTRODUCTION Iatrogenic nerve injury in orthopedic surgery can impair functional outcomes. During the last years, a steady increase in the number of performed reverse total shoulder arthroplasties has been reported and complications associated with this procedure are continuously described. Neurological complications, however, remain underreported. The aims of this study were to calculate the incidence of iatrogenic nerve injury after primary and revision reverse total shoulder arthroplasty in a large patient cohort, as well as identify associated patient-and surgery-related risk factors. MATERIALS AND METHODS A retrospective review of our institution's internal Reverse Total Shoulder Arthroplasty (RTSA) database from September 2005 to December 2019 was undertaken and 34 patients with iatrogenic nerve injuries were identified, resulting in a neurological complication rate of 2.6%. Group comparisons between patients with nerve injuries (n = 34) and the remaining cohort without nerve injuries (n = 1275) were performed to identify patient- and surgery-related risk factors. RESULTS Of the 34 cases with iatrogenic nerve injury, damage to terminal nerve branches occurred in 21 patients, whereas a brachial plexus lesion was diagnosed in the other 13. Nerve revision surgery was necessary in four patients. At final follow-up 13 patients (45%) had residual motor deficits and 17 (59%) had residual sensory deficits. Higher numbers of previous surgeries of the affected shoulder correlated with subsequent nerve injury (p = 0.035). Operative time was significantly longer in patients, who developed a neurologic deficit, showing a correlation between duration of surgery and occurrence of nerve injury (p = 0.013). Patients with neurologic complications were significantly younger than patients without nerve damage (median 68 vs. 72 years, p = 0.017). CONCLUSIONS In specialists' hands reverse total shoulder arthroplasty is a rather safe procedure regarding the risk of neurologic injury. However, multiple previous surgeries of the affected shoulder increase the risk of neurological complications. Cases with post-operative neurologic compromise are rare and usually recover well, with few patients suffering long-term functional deficits from iatrogenic nerve injury. LEVEL OF EVIDENCE Level III, retrospective cohort study

Oral flucloxacillin for treating osteomyelitis

Flucloxacillin (FLU) administered by the oral route is widely used for treating various infections, but there are no published retrospective or prospective trials of its efficacy, or its advantages or disadvantages compared to parenteral treatment or other antibiotics for treating osteomyelitis. Based on published in vitro data and expert opinions, other non-β-lactam oral antibiotics that have better bone penetration are generally preferred over oral FLU. We reviewed the literature for studies of oral FLU as therapy of osteomyelitis (OM), stratified by acute versus chronic and pediatric versus adult cases. In striking contrast to the prevailing opinions and the few descriptive data available, we found that treatment of OM with oral FLU does not appear to be associated with more clinical failures compared to other oral antibiotic agents. Because of its narrow antibiotic spectrum, infrequent severe adverse effects, and low cost, oral FLU is widely used in clinical practice. We therefore call for investigators to conduct prospective trials investigating the effectiveness and potential advantages of oral FLU for treating OM

p38 MAPK Inhibition Improves Heart Function in Pressure-Loaded Right Ventricular Hypertrophy

Although p38 mitogen-activated protein kinase (MAPK) is known to have a role in ischemic heart disease and many other diseases, its contribution to the pathobiology of right ventricular (RV) hypertrophy and failure is unclear. Therefore, we sought to investigate the role of p38 MAPK in the pathophysiology of pressure overload-induced RV hypertrophy and failure. The effects of the p38 MAPK inhibitor PH797804 were investigated in mice with RV hypertrophy/failure caused by exposure to hypoxia or pulmonary artery banding. In addition, the effects of p38 MAPK inhibition or depletion (by small interfering RNA) were studied in isolated mouse RV fibroblasts. Echocardiography, invasive hemodynamic measurements, immunohistochemistry, collagen assays, immunofluorescence staining, and Western blotting were performed. Expression of phosphorylated p38 MAPK was markedly increased in mouse and human hypertrophied/failed RVs. In mice, PH797804 improved RV function and inhibited cardiac fibrosis compared with placebo. In isolated RV fibroblasts, p38 MAPK inhibition reduced transforming growth factor (TGF)-b-induced collagen production as well as stress fiber formation. Moreover, p38 MAPK inhibition/depletion suppressed TGF-b-induced SMAD2/3 phosphorylation and myocardin-related transcription factor A (MRTF-A) nuclear translocation, and prevented TGF-b-induced cardiac fibroblast transdifferentiation. Moreover, p38 MAPK inhibition in mice exposed to pulmonary artery banding led to diminished nuclear levels of MRTF-A and phosphorylated SMAD3 in RV fibroblasts. Together, our data indicate that p38 MAPK inhibition significantly improves RV function and inhibits RV fibrosis. Inhibition of p38 MAPK in RV cardiac fibroblasts, resulting in coordinated attenuation of MRTF-A cytoplasmic-nuclear translocation and SMAD3 deactivation, indicates that p38 MAPK signaling contributes to distinct disease-causing mechanisms