Sepsis: from bench to bedside

Detalhes bibliográficos
Autor(a) principal: Silva, Eliézer
Data de Publicação: 2008
Outros Autores: Passos, Rogério Da Hora, Ferri, Maurício Beller, Figueiredo, Luiz Francisco Poli de
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Clinics
Texto Completo: https://www.revistas.usp.br/clinics/article/view/17837
Resumo: Sepsis is a syndrome related to severe infections. It is defined as the systemic host response to microorganisms in previously sterile tissues and is characterized by end-organ dysfunction away from the primary site of infection. The normal host response to infection is complex and aims to identify and control pathogen invasion, as well as to start immediate tissue repair. Both the cellular and humoral immune systems are activated, giving rise to both anti-inflammatory and proinflammatory responses. The chain of events that leads to sepsis is derived from the exacerbation of these mechanisms, promoting massive liberation of mediators and the progression of multiple organ dysfunction. Despite increasing knowledge about the pathophysiological pathways and processes involved in sepsis, morbidity and mortality remain unacceptably high. A large number of immunomodulatory agents have been studied in experimental and clinical settings in an attempt to find an efficacious anti-inflammatory drug that reduces mortality. Even though preclinical results had been promising, the vast majority of these trials actually showed little success in reducing the overwhelmingly high mortality rate of septic shock patients as compared with that of other critically ill intensive care unit patients. Clinical management usually begins with prompt recognition, determination of the probable infection site, early administration of antibiotics, and resuscitation protocols based on "early-goal" directed therapy. In this review, we address the research efforts that have been targeting risk factor identification, including genetics, pathophysiological mechanisms and strategies to recognize and treat these patients as early as possible.
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spelling Sepsis: from bench to bedside SepsisShockInfectionOrgan DysfunctionOrgan Failure Sepsis is a syndrome related to severe infections. It is defined as the systemic host response to microorganisms in previously sterile tissues and is characterized by end-organ dysfunction away from the primary site of infection. The normal host response to infection is complex and aims to identify and control pathogen invasion, as well as to start immediate tissue repair. Both the cellular and humoral immune systems are activated, giving rise to both anti-inflammatory and proinflammatory responses. The chain of events that leads to sepsis is derived from the exacerbation of these mechanisms, promoting massive liberation of mediators and the progression of multiple organ dysfunction. Despite increasing knowledge about the pathophysiological pathways and processes involved in sepsis, morbidity and mortality remain unacceptably high. A large number of immunomodulatory agents have been studied in experimental and clinical settings in an attempt to find an efficacious anti-inflammatory drug that reduces mortality. Even though preclinical results had been promising, the vast majority of these trials actually showed little success in reducing the overwhelmingly high mortality rate of septic shock patients as compared with that of other critically ill intensive care unit patients. Clinical management usually begins with prompt recognition, determination of the probable infection site, early administration of antibiotics, and resuscitation protocols based on "early-goal" directed therapy. In this review, we address the research efforts that have been targeting risk factor identification, including genetics, pathophysiological mechanisms and strategies to recognize and treat these patients as early as possible. Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo2008-01-01info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://www.revistas.usp.br/clinics/article/view/1783710.1590/S1807-59322008000100019Clinics; Vol. 63 No. 1 (2008); 110-120 Clinics; v. 63 n. 1 (2008); 110-120 Clinics; Vol. 63 Núm. 1 (2008); 110-120 1980-53221807-5932reponame:Clinicsinstname:Universidade de São Paulo (USP)instacron:USPenghttps://www.revistas.usp.br/clinics/article/view/17837/19902Silva, EliézerPassos, Rogério Da HoraFerri, Maurício BellerFigueiredo, Luiz Francisco Poli deinfo:eu-repo/semantics/openAccess2012-05-22T18:37:11Zoai:revistas.usp.br:article/17837Revistahttps://www.revistas.usp.br/clinicsPUBhttps://www.revistas.usp.br/clinics/oai||clinics@hc.fm.usp.br1980-53221807-5932opendoar:2012-05-22T18:37:11Clinics - Universidade de São Paulo (USP)false
dc.title.none.fl_str_mv Sepsis: from bench to bedside
title Sepsis: from bench to bedside
spellingShingle Sepsis: from bench to bedside
Silva, Eliézer
Sepsis
Shock
Infection
Organ Dysfunction
Organ Failure
title_short Sepsis: from bench to bedside
title_full Sepsis: from bench to bedside
title_fullStr Sepsis: from bench to bedside
title_full_unstemmed Sepsis: from bench to bedside
title_sort Sepsis: from bench to bedside
author Silva, Eliézer
author_facet Silva, Eliézer
Passos, Rogério Da Hora
Ferri, Maurício Beller
Figueiredo, Luiz Francisco Poli de
author_role author
author2 Passos, Rogério Da Hora
Ferri, Maurício Beller
Figueiredo, Luiz Francisco Poli de
author2_role author
author
author
dc.contributor.author.fl_str_mv Silva, Eliézer
Passos, Rogério Da Hora
Ferri, Maurício Beller
Figueiredo, Luiz Francisco Poli de
dc.subject.por.fl_str_mv Sepsis
Shock
Infection
Organ Dysfunction
Organ Failure
topic Sepsis
Shock
Infection
Organ Dysfunction
Organ Failure
description Sepsis is a syndrome related to severe infections. It is defined as the systemic host response to microorganisms in previously sterile tissues and is characterized by end-organ dysfunction away from the primary site of infection. The normal host response to infection is complex and aims to identify and control pathogen invasion, as well as to start immediate tissue repair. Both the cellular and humoral immune systems are activated, giving rise to both anti-inflammatory and proinflammatory responses. The chain of events that leads to sepsis is derived from the exacerbation of these mechanisms, promoting massive liberation of mediators and the progression of multiple organ dysfunction. Despite increasing knowledge about the pathophysiological pathways and processes involved in sepsis, morbidity and mortality remain unacceptably high. A large number of immunomodulatory agents have been studied in experimental and clinical settings in an attempt to find an efficacious anti-inflammatory drug that reduces mortality. Even though preclinical results had been promising, the vast majority of these trials actually showed little success in reducing the overwhelmingly high mortality rate of septic shock patients as compared with that of other critically ill intensive care unit patients. Clinical management usually begins with prompt recognition, determination of the probable infection site, early administration of antibiotics, and resuscitation protocols based on "early-goal" directed therapy. In this review, we address the research efforts that have been targeting risk factor identification, including genetics, pathophysiological mechanisms and strategies to recognize and treat these patients as early as possible.
publishDate 2008
dc.date.none.fl_str_mv 2008-01-01
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
format article
status_str publishedVersion
dc.identifier.uri.fl_str_mv https://www.revistas.usp.br/clinics/article/view/17837
10.1590/S1807-59322008000100019
url https://www.revistas.usp.br/clinics/article/view/17837
identifier_str_mv 10.1590/S1807-59322008000100019
dc.language.iso.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv https://www.revistas.usp.br/clinics/article/view/17837/19902
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv application/pdf
dc.publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
publisher.none.fl_str_mv Hospital das Clínicas, Faculdade de Medicina, Universidade de São Paulo
dc.source.none.fl_str_mv Clinics; Vol. 63 No. 1 (2008); 110-120
Clinics; v. 63 n. 1 (2008); 110-120
Clinics; Vol. 63 Núm. 1 (2008); 110-120
1980-5322
1807-5932
reponame:Clinics
instname:Universidade de São Paulo (USP)
instacron:USP
instname_str Universidade de São Paulo (USP)
instacron_str USP
institution USP
reponame_str Clinics
collection Clinics
repository.name.fl_str_mv Clinics - Universidade de São Paulo (USP)
repository.mail.fl_str_mv ||clinics@hc.fm.usp.br
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