6 research outputs found

    Accidents and errors in the operating theatre : incidence and mechanisms

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    RESUMO - Os blocos operatĂłrios tĂȘm uma prevalĂȘncia alta de erros e acidentes. Estes vĂŁo desde as interrupçÔes do fluxo cirĂșrgico, a acidentes minor e eventos catastrĂłficos. O autor revĂȘ as ĂĄreas de actividade do bloco operatĂłrio em que os erros acontecem com mais frequĂȘncia e identifica os mecanismos e a origem mais comuns — factores humanos e de equipa, factores organizacionais, a complexidade das tarefas, as influĂȘncias do ambiente e o puro acaso. Os erros tĂ­picos e os padrĂ”es de erros sĂŁo revisitados tal como os mecanismos de ocorrĂȘncia: cirurgia errada, no doente errado, no ĂłrgĂŁo errado e no lado errado, corpos estranhos deixados, infecção cirĂșrgica e trombose venosa — embolia pulmonar. As relaçÔes mal estabelecidas entre o volume cirĂșrgico e a performance sĂŁo discutidas, bem como, as suas complicaçÔes. A segurança dos doentes no bloco operatĂłrio Ă© um tema actual que recebeu recentemente grande atenção da OMS que o tomou mesmo como prioridade.ABSTRACT - Operation theatres are the health care spots where error and accident prevalence is higher. Those adverse events span from surgical flow interruptions to minor accidents to catastrophic events. The author reviews the activity areas where errors most likely occur and identifies their major determinants and mechanisms — human factors, system factors, team factors, task complexity, ambiance and pure chance. Typical errors and error patterns are revisited, as well as their occurring mechanisms — wrong patient, wrong surgery, wrong organ, wrong side surgeries, unwanted foreign bodies left, surgical infection and deep venous thrombosis plus pulmonary embolism. The unsettled relations between surgical performance and volume load is discussed also. Patient safety in the operating theatre is a most actual topic that recently deserved WHO attention and even became that organization’s priority.info:eu-repo/semantics/publishedVersio

    2 nd Brazilian Consensus on Chagas Disease, 2015

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    Abstract Chagas disease is a neglected chronic condition with a high burden of morbidity and mortality. It has considerable psychological, social, and economic impacts. The disease represents a significant public health issue in Brazil, with different regional patterns. This document presents the evidence that resulted in the Brazilian Consensus on Chagas Disease. The objective was to review and standardize strategies for diagnosis, treatment, prevention, and control of Chagas disease in the country, based on the available scientific evidence. The consensus is based on the articulation and strategic contribution of renowned Brazilian experts with knowledge and experience on various aspects of the disease. It is the result of a close collaboration between the Brazilian Society of Tropical Medicine and the Ministry of Health. It is hoped that this document will strengthen the development of integrated actions against Chagas disease in the country, focusing on epidemiology, management, comprehensive care (including families and communities), communication, information, education, and research

    a pilot study in cardiac surgery

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    Funding This work was supported by Fraunhofer AICOS and Vodafone Portugal and funded by the National Foundation of Science and Technology under the projects DSAIPA/AI/0094/2020 and Lisboa-05-3559-FSE-3.BACKGROUND: The existing digital healthcare solutions demand a service development approach that assesses needs, experience, and outcomes, to develop high-value digital healthcare services. The objective of this study was to develop a digital transformation of the patients' follow-up service after cardiac surgery, based on a remote patient monitoring service that would respond to the real context challenges. METHODS: The study followed the Design Science Research methodology framework and incorporated concepts from the Lean startup method to start designing a minimal viable product (MVP) from the available resources. The service was implemented in a pilot study with 29 patients in 4 iterative develop-test-learn cycles, with the engagement of developers, researchers, clinical teams, and patients. RESULTS: Patients reported outcomes daily for 30 days after surgery through Internet-of-Things (IoT) devices and a mobile app. The service's evaluation considered experience, feasibility, and effectiveness. It generated high satisfaction and high adherence among users, fewer readmissions, with an average of 7 ± 4.5 clinical actions per patient, primarily due to abnormal systolic blood pressure or wound-related issues. CONCLUSIONS: We propose a 6-step methodology to design and validate a high-value digital health care service based on collaborative learning, real-time development, iterative testing, and value assessment.publishersversionpublishe

    HGF Stimulation of Rac1 Signaling Enhances Pharmacological Correction of the Most Prevalent Cystic Fibrosis Mutant F508del-CFTR

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    Cystic fibrosis (CF), a major life-limiting genetic disease leading to severe respiratory symptoms, is caused by mutations in CF transmembrane conductance regulator (CFTR), a chloride (Cl(-)) channel expressed at the apical membrane of epithelial cells. Absence of functional CFTR from the surface of respiratory cells reduces mucociliary clearance, promoting airways obstruction, chronic infection, and ultimately lung failure. The most frequent mutation, F508del, causes the channel to misfold, triggering its premature degradation and preventing it from reaching the cell surface. Recently, novel small-molecule correctors rescuing plasma membrane localization of F508del-CFTR underwent clinical trials but with limited success. Plausibly, this may be due to the mutant intrinsic plasma membrane (PM) instability. Herein, we show that restoration of F508del-CFTR PM localization by correctors can be dramatically improved through a novel pathway involving stimulation of signaling by the endogenous small GTPase Rac1 via hepatocyte growth factor (HGF). We first show that CFTR anchors to apical actin cytoskeleton (via Ezrin) upon activation of Rac1 signaling through PIP5K and Arp2/3. We then found that such anchoring retains pharmacologically rescued F508del-CFTR at the cell surface, boosting functional restoration by correctors up to 30% of wild-type channel levels in human airway epithelial cells. Our findings reveal that surface anchoring and retention is a major target pathway for CF pharmacotherapy, namely, to achieve maximal restoration of F508del-CFTR in patients in combination with correctors. Moreover, this approach may also translate to other disorders caused by trafficking-deficient surface proteins
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