Morgenthaler, Timothy I.

BACKGROUNDAlthough effective methods for venous thromboembolism prophylaxis (VTE‐P) have been known for decades, reliable implementation has been challenging.OBJECTIVEDevelop reliable VTE‐P systems for adult and for pediatric patients to reduce preventable venous thromboembolism (VTE).DESIGNWe used a discovery and diffusion system to first develop an effective system in 1 hospital location, and then spread the principle best practices across the entire 22‐hospital system.SETTINGTwenty‐two Mayo Clinic hospitals (adults and children).PATIENTSAdult and pediatric patients.INTERVENTION(1) Ensure that a VTE‐P is declared at admission by providing a mandatory VTE‐P “tollgate” that requires the provider to assess the risk for VTE and provide an appropriate order for VTE‐P. (2) Use clinical decision support to provide ongoing surveillance and alerts to providers when there is a lapse in the VTE‐P plan.MEASUREMENTSIn adults, VTE compliance as measured by the Centers for Medicare and Medicaid Services Core Measures VTE‐1 and VTE‐2, preventable VTE as measured by VTE‐6, and in pediatric patients, appropriate VTE measures as determined by chart audit.RESULTSVTE‐1 and VTE‐2 have approached 97% to 100% and preventable VTE has declined to 0% for the last 3 quarters. Similarly, the pediatric VTE‐P screening tool was evaluated and piloted with >92% compliance in risk documentation, appropriate VTE‐P >64%, and 0 VTE events during the study period.CONCLUSIONAn integrated system‐wide approach can lead to measurable improvements in VTE‐P process and outcome measures. Journal of Hospital Medicine 2016;11:S15–S21. © 2016 Society of Hospital Medicine

Objectives/HypothesisMultiple system atrophy (MSA) is a degenerative neurologic disorder that can affect vocal fold mobility. Our aim was to further elucidate the impact of vocal fold motion impairment (VFMI) in MSA.Study DesignRetrospective case series.MethodsWe undertook a retrospective review of all MSA patients reporting voice or respiratory symptoms from 1975 to 2010 at Mayo Clinic Rochester who also received otolaryngologic examination.ResultsThirty‐eight MSA patients demonstrated VFMI. Median duration of vocal or respiratory symptoms prior to diagnosis of MSA was 12.0 months (range, 1–60 months). Stridor was present in 25 (68%) of patients. There was bilateral VFMI in 32 (82.4%) of the patients and isolated VFMI of the left true vocal fold (TVF) in six (17.6%) of the patients. No patients had isolated right VFMI. There was isolated unilateral or bilateral paresis in 21 (55.3%) of the patients and unilateral or bilateral complete paralysis in 15 (39.5%) of the patients. One patient presented with left TVF paralysis and right TVF paresis, whereas one other patient had findings of right TVF paralysis and left TVF paresis comprising the remaining 5.2% of patients with VFMI. The median survival after diagnosis of VFMI was 51.6 months. Unilateral or bilateral TVF paralysis was statistically associated with a decreased overall survival (P = .0384). The presence of stridor was not associated with adverse prognosis.ConclusionsThe increasing severity of VFMI negatively impacts overall survival in patients with MSA. Therefore, otolaryngologic examination is warranted at the time of MSA diagnosis.Level of Evidence4. Laryngoscope, 124:730–735, 2014

Abstract Pneumocystis carinii is an opportunistic organism that causes severe lung injury in immunocompromised hosts. Macrophage responses to P. carinii are poorly defined. Arachidonic acid (AA) and its metabolites are potent mediators of inflammation and have been implicated in host response to microorganisms. We therefore examined the production of eicosanoids from rat and rabbit alveolar macrophages stimulated with purified P. carinii. [14C]AA-labeled rabbit macrophages released 8.50 ± 1.33% of the incorporated [14C]AA after 90 min in response to P. carinii (P = 0.0001 compared with unstimulated controls). In contrast, a similar number of rat alveolar macrophages exhibited a smaller but significant response to P. carinii, releasing 3.84 ± 1.54% of their [14C]AA after 90 min (P = 0.001 compared with control). We further determined that P. carinii stimulated substantial production of prostaglandin E2 and concurrently a small amount of leukotriene B4 release from alveolar macrophages. To further investigate whether serum opsonization of P. carinii enhances these alterations in AA metabolism, we assessed the effect of P. carinii immune serum on P. carinii-induced AA release. P. carinii opsonized with this antiserum caused significantly greater AA release from rat alveolar macrophages than either unopsonized P. carinii or organisms opsonized with nonimmune serum. Previous studies suggest that P. carinii interacts with macrophage β-glucan and mannose receptors. However, incubation of macrophages with P. carinii in the presence of either soluble β-glucan or α-mannan failed to alter the release of AA from macrophages in response to P. carinii. Macrophage release of eicosanoids represents a potentially important host inflammatory response to P. carinii infection.