Sepsis: from bench to bedside

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

Sepsis: From Bench to Bedside

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

Distúrbios de condução cardíaca e taquicardia ventricular como complicação da granulomatose com poliangiíte em uma paciente. Relato de caso e revisão da literatura

RESUMO A granulomatose com poliangiíte é um raro distúrbio inflamatório sistêmico que se caracteriza por vasculite de pequenas artérias, arteríolas e capilares, associada a lesões granulomatosas necrotizantes. Este artigo relata o caso de uma paciente com diagnóstico prévio de granulomatose com poliangiíte, admitida à unidade de terapia intensiva com quadro de crises convulsivas e instabilidade hemodinâmica em razão de bloqueio atrioventricular completo. Estas manifestações se associaram a múltiplos episódios de taquicardia ventricular sustentada; não havia alterações estruturais cardíacas, nem se detectaram distúrbios hidroeletrolíticos. Na unidade de terapia intensiva, a paciente foi submetida à implantação de marca-passo provisório, imunossupressão com uso de corticosteroides e terapia imunobiológica, resultando em melhora hemodinâmica completa. Distúrbios graves da condução cardíaca em pacientes com granulomatose com poliangiíte são raros, mas associam-se à grande morbidade. O reconhecimento precoce e o uso de intervenções específicas são capazes de prevenir a ocorrência de desfechos desfavoráveis, especialmente na unidade de terapia intensiva

A clinical score to predict mortality in septic acute kidney injury patients requiring continuous renal replacement therapy: the HELENICC score

Abstract Background This study aimed to identify predictors of early (7-day) mortality in patients with septic acute kidney injury (AKI) who required continuous renal replacement therapy (CRRT). Methods Prospective cohort of 186 septic AKI patients undergoing CRRT at a tertiary hospital, from October 2005 to November 2010. Results After multivariate adjustment, five variables were associated to early mortality: norepinephrine utilization, liver failure, medical condition, lactate level, and pre-dialysis creatinine level. These variables were combined in a score, which demonstrated good discrimination, with a C-statistic of 0.82 (95% CI = 0.76–0.88), and good calibration (χ 2 = 4.3; p = 0.83). SAPS 3, APACHE II and SOFA scores demonstrated poor performance in this population. Conclusions The HEpatic failure, LactatE, NorepInephrine, medical Condition, and Creatinine (HELENICC) score outperformed tested generic models. Future studies should further validate this score in different cohorts