109 research outputs found

    FALÊNCIA HEPÁTICA AGUDA INDUZIDA POR PARACETAMOL: FISIOPATOLOGIA, DIAGNÓSTICO E MANEJO CLÍNICO

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    Introduction: Paracetamol, known as acetaminophen, is a non-steroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase-3 (COX-3). Its antipyretic and analgesic actions, combined with low cost and safety, make it widely used, even without a medical prescription. However, due to hepatic metabolism and its high hepatotoxic potential at elevated doses or in the presence of hepatic comorbidities, paracetamol is the leading cause of drug-induced acute liver injury worldwide. This study aims to discuss the pathophysiology, diagnosis, and clinical management of paracetamol-induced acute liver failure. Methodology: A search was conducted in the electronic databases PubMed, Scielo, and LILACS using the descriptors "Acetaminophen," "Overdose," "Treatment," and "Acetylcysteine." Fifteen relevant articles were selected after applying inclusion and exclusion criteria. Results and Discussion: Paracetamol is metabolized in the liver, producing inactive metabolites excreted in the urine. However, a small fraction is metabolized to N-acetyl-p-benzoquinone imine (NAPQI), a highly hepatotoxic compound that causes cell necrosis by covalently binding to hepatic proteins. NAPQI is neutralized by glutathione (GSH), forming an inert compound excreted in the urine. Symptoms of paracetamol intoxication range from mild (nausea, vomiting, abdominal discomfort) to severe (jaundice, hepatic encephalopathy, coagulopathy) and occur in four phases. Rapid identification of the condition, assessment of the ingested dose, and time since ingestion are crucial. Conclusion: Effective management requires rapid identification, accurate assessment of the ingested dose, monitoring of hepatic markers, and early administration of NAC. Timely interventions are essential to prevent fatal complications and ensure patient recovery.Introdução: O paracetamol, conhecido como acetaminofeno, é um medicamento anti-inflamatório não esteroidal (AINE) que inibe a ciclooxigenase-3 (COX-3. Sua ação antipirética e analgésica, combinada com baixo custo e segurança, torna-o amplamente utilizado, mesmo sem prescrição médica. No entanto, devido à metabolização hepática e seu alto potencial hepatotóxico em doses elevadas ou em presença de comorbidades hepáticas, o paracetamol é a principal causa de lesão hepática aguda induzida por drogas no mundo. Este estudo visa discutir a fisiopatologia, diagnóstico e manejo clínico da falência hepática aguda induzida por paracetamol. Metodologia: Realizou-se pesquisa nas bases de dados eletrônicas PubMed, Scielo e LILACS com os descritores “Acetaminophen”, “Overdose”, “Treatment” e “Acetylcysteine”. Foram selecionados 15 artigos relevantes após aplicação de critérios de inclusão e exclusão. Resultados e Discussão: O paracetamol é metabolizado no fígado, produzindo metabólitos inativos excretados pela urina. Porém, uma pequena fração é metabolizada e gera N-acetil-p-benzoquinona imina (NAPQI), um composto altamente hepatotóxico que causa necrose celular ao se ligar covalentemente às proteínas hepáticas. NAPQI é neutralizado pela glutationa (GSH), formando um composto inerte excretado pela urina. Os sintomas de intoxicação por paracetamol variam de leves (náuseas, vômitos, desconforto abdominal) a graves (icterícia, encefalopatia hepática, coagulopatia) e ocorrem em quatro fases. A rápida identificação da condição, avaliação da dose ingerida e o tempo desde a ingestão são cruciais. Conclusão: O manejo eficaz requer identificação rápida, avaliação precisa da dose ingerida, monitoramento de marcadores hepáticos, e administração precoce de NAC. Intervenções oportunas são essenciais para prevenir complicações fatais e garantir a recuperação do paciente

    AMILOIDOSE CARDÍACA: SUPERANDO A LACUNA ENTRE O RECONHECIMENTO E O MANEJO EFETIVO

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    Introduction: Cardiac amyloidosis (CA) is a rare condition caused by the accumulation of amyloid proteins in the heart, resulting in impaired cardiac function. CA is often underdiagnosed due to its nonspecific clinical presentation and lack of awareness about the disease. This article aims to understand the pathophysiology, diagnosis, and management of CA. Methodology: A systematic review was conducted using databases such as Scielo and PubMed, with the descriptors "Amyloidosis" AND "Cardiovascular System," yielding 3306 studies, of which 23 were selected for better addressing the chosen topic and being published in English or Portuguese. Inclusion and exclusion criteria were applied to ensure the quality of the selected studies. Results: CA can be caused by different types of amyloidosis, with light-chain amyloidosis (AL) and transthyretin amyloidosis (ATTR) being the most common. Symptoms are nonspecific and include dyspnea, fatigue, and edema, often leading to diagnostic errors. Diagnosis involves a combination of methods, including imaging tests and tissue biopsy. Treatment aims to slow disease progression and alleviate symptoms, tailored according to the type and stage of CA. Conclusion: CA represents a diagnostic and therapeutic challenge due to its varied clinical presentation and complexity. Awareness of the signs and symptoms of the disease is crucial for early diagnosis and better patient management. Continuous development of clinical and therapeutic approaches is necessary to optimize outcomes for patients affected by this debilitating condition.Introdução: A amiloidose cardíaca (AC) é uma condição rara causada pelo acúmulo de proteínas amiloides no coração, resultando em comprometimento da função cardíaca. A AC é frequentemente subdiagnosticada devido à sua clínica inespecífica e à falta de conscientização sobre a doença. Este artigo visa compreender a fisiopatologia, diagnóstico e manejo da AC. Metodologia: Realizou-se uma revisão sistemática utilizando bases de dados como Scielo e Pubmed, utilizando os descritores “Amyloidosis” AND “Cardiovascular System”, obtendo-se 3306 estudos, dos quais 23 foram selecionados por abordarem melhor o tema escolhido e serem publicados em inglês ou português. Os critérios de inclusão e exclusão foram aplicados para garantir a qualidade dos estudos selecionados. Resultados: A AC pode ser causada por diferentes tipos de amiloidose, sendo a amiloidose de cadeia leve (AL) e a amiloidose associada à transtirretina (ATTR) as mais comuns. Os sintomas são inespecíficos e incluem dispneia, fadiga e edema, levando frequentemente a erros diagnósticos. O diagnóstico envolve uma combinação de métodos, incluindo exames de imagem e biópsia tecidual. O tratamento visa retardar a progressão da doença e aliviar os sintomas, sendo personalizado de acordo com o tipo e estágio da AC. Conclusão: A AC representa um desafio diagnóstico e terapêutico devido à sua apresentação clínica variada e complexidade. A conscientização sobre os sinais e sintomas da doença é crucial para um diagnóstico precoce e um melhor manejo dos pacientes. O desenvolvimento contínuo de abordagens clínicas e terapêuticas é necessário para otimizar os resultados para os pacientes afetados por essa condição debilitante

    Prevalence, associated factors and outcomes of pressure injuries in adult intensive care unit patients: the DecubICUs study

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    Funder: European Society of Intensive Care Medicine; doi: http://dx.doi.org/10.13039/501100013347Funder: Flemish Society for Critical Care NursesAbstract: Purpose: Intensive care unit (ICU) patients are particularly susceptible to developing pressure injuries. Epidemiologic data is however unavailable. We aimed to provide an international picture of the extent of pressure injuries and factors associated with ICU-acquired pressure injuries in adult ICU patients. Methods: International 1-day point-prevalence study; follow-up for outcome assessment until hospital discharge (maximum 12 weeks). Factors associated with ICU-acquired pressure injury and hospital mortality were assessed by generalised linear mixed-effects regression analysis. Results: Data from 13,254 patients in 1117 ICUs (90 countries) revealed 6747 pressure injuries; 3997 (59.2%) were ICU-acquired. Overall prevalence was 26.6% (95% confidence interval [CI] 25.9–27.3). ICU-acquired prevalence was 16.2% (95% CI 15.6–16.8). Sacrum (37%) and heels (19.5%) were most affected. Factors independently associated with ICU-acquired pressure injuries were older age, male sex, being underweight, emergency surgery, higher Simplified Acute Physiology Score II, Braden score 3 days, comorbidities (chronic obstructive pulmonary disease, immunodeficiency), organ support (renal replacement, mechanical ventilation on ICU admission), and being in a low or lower-middle income-economy. Gradually increasing associations with mortality were identified for increasing severity of pressure injury: stage I (odds ratio [OR] 1.5; 95% CI 1.2–1.8), stage II (OR 1.6; 95% CI 1.4–1.9), and stage III or worse (OR 2.8; 95% CI 2.3–3.3). Conclusion: Pressure injuries are common in adult ICU patients. ICU-acquired pressure injuries are associated with mainly intrinsic factors and mortality. Optimal care standards, increased awareness, appropriate resource allocation, and further research into optimal prevention are pivotal to tackle this important patient safety threat

    Search for heavy neutral leptons in final states with electrons, muons, and hadronically decaying tau leptons in proton-proton collisions at s\sqrt{s} =13 TeV

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    International audienceA search for heavy neutral leptons (HNLs) of Majorana or Dirac type using proton-proton collision data at s\sqrt{s} =13 TeV is presented. The data were collected by the CMS experiment at the CERN LHC and correspond to an integrated luminosity of 138 fb1^{-1}. Events with three charged leptons (electrons, muons, and hadronically decaying tau leptons) are selected, corresponding to HNL production in association with a charged lepton and decay of the HNL to two charged leptons and a standard model (SM) neutrino. The search is performed for HNL masses between 10 GeV and 1.5 TeV. No evidence for an HNL signal is observed in data. Upper limits at 95% confidence level are found for the squared coupling strength of the HNL to SM neutrinos, considering exclusive coupling of the HNL to a single SM neutrino generation, for both Majorana and Dirac HNLs. The limits exceed previously achieved experimental constraints for a wide range of HNL masses, and the limits on tau neutrino coupling scenarios with HNL masses above the W boson mass are presented for the first time

    Search for heavy neutral leptons in final states with electrons, muons, and hadronically decaying tau leptons in proton-proton collisions at s\sqrt{s} =13 TeV

    No full text
    A search for heavy neutral leptons (HNLs) of Majorana or Dirac type using proton-proton collision data at s\sqrt{s} =13 TeV is presented. The data were collected by the CMS experiment at the CERN LHC and correspond to an integrated luminosity of 138 fb1^{-1}. Events with three charged leptons (electrons, muons, and hadronically decaying tau leptons) are selected, corresponding to HNL production in association with a charged lepton and decay of the HNL to two charged leptons and a standard model (SM) neutrino. The search is performed for HNL masses between 10 GeV and 1.5 TeV. No evidence for an HNL signal is observed in data. Upper limits at 95% confidence level are found for the squared coupling strength of the HNL to SM neutrinos, considering exclusive coupling of the HNL to a single SM neutrino generation, for both Majorana and Dirac HNLs. The limits exceed previously achieved experimental constraints for a wide range of HNL masses, and the limits on tau neutrino coupling scenarios with HNL masses above the W boson mass are presented for the first time

    Search for heavy neutral leptons in final states with electrons, muons, and hadronically decaying tau leptons in proton-proton collisions at s\sqrt{s} =13 TeV

    No full text
    International audienceA search for heavy neutral leptons (HNLs) of Majorana or Dirac type using proton-proton collision data at s\sqrt{s} =13 TeV is presented. The data were collected by the CMS experiment at the CERN LHC and correspond to an integrated luminosity of 138 fb1^{-1}. Events with three charged leptons (electrons, muons, and hadronically decaying tau leptons) are selected, corresponding to HNL production in association with a charged lepton and decay of the HNL to two charged leptons and a standard model (SM) neutrino. The search is performed for HNL masses between 10 GeV and 1.5 TeV. No evidence for an HNL signal is observed in data. Upper limits at 95% confidence level are found for the squared coupling strength of the HNL to SM neutrinos, considering exclusive coupling of the HNL to a single SM neutrino generation, for both Majorana and Dirac HNLs. The limits exceed previously achieved experimental constraints for a wide range of HNL masses, and the limits on tau neutrino coupling scenarios with HNL masses above the W boson mass are presented for the first time
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