Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children

Castro, Roberta Esteves Vieira de; Medeiros, Daniela Nasu Monteiro; Prata‐Barbosa, Arnaldo; Magalhães‐Barbosa, Maria Clara de

doi:10.1097/pcc.0000000000002444

Cited by 162 publications

(271 citation statements)

References 4 publications

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“…2 Sepsis is confirmed to be accompanied with the presence of bacteria or a highly suspicious focus of infection. 3 Inflammation plays an important role during sepsis, and excessive inflammation can result in organ damage, chronic inflammation, fibrosis, and scarring.…”

Section: Introductionmentioning

confidence: 99%

Emodin alleviates sepsis‐mediated lung injury via inhibition and reduction of NF‐kB and HMGB1 pathways mediated by SIRT1

Liu

Wei

2021

The Kaohsiung J of Med Scie

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Inflammation plays an important role during sepsis, and excessive inflammation can result in organ damage, chronic inflammation, fibrosis, and scarring. The study aimed to investigate the specific mechanism of emodin by constructing in vivo and in vitro septic lung injury models via inhibition and reduction of NF-kB and high mobility group box 1 (HMGB1) pathways. A cecal ligation and puncture (CLP) model was built for adult male Sprague-Dawley rats. Concentrations of TNF-α, IL-1β, and IL-6 in bronchoalveolar lavage fluid were determined using commercially available ELISA kits. Hematoxylin and eosin staining was used for the right lung inferior lobes. Myeloperoxidase (MPO) activity of the lung tissue was detected by using the MPO kit. Murine alveolar epithelial cell line (MLE-12) cells were used for flow cytometry and Western blot to analyze the apoptosis rate and protein expression. Emodin significantly decreased CLP-induced cell apoptosis, upregulated expression of sirtuin 1 (SIRT1), and inhibited p-p65/p65 and HMGB1. In lipopolysaccharide (LPS) treated cell model, emodin treatment markedly decreased LPS-induced release of IL-1, IL-6, and tumor necrosis factor (TNF)-α, inhibited LPS-induced cell apoptosis and suppressed protein levels of P-P65/P65 and HMGB1. However, science of SIRT1 reversed the above effects by treatment of emodin. In summarize, this study found that emodin can alleviate sepsis-induced lung injury in vivo and in vitro through regulation of SIRT1.

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Section: Introductionmentioning

confidence: 99%

Emodin alleviates sepsis‐mediated lung injury via inhibition and reduction of NF‐kB and HMGB1 pathways mediated by SIRT1

Liu

Wei

2021

The Kaohsiung J of Med Scie

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“…We recruited 93 pediatric sepsis patients (0-18 ages) and 75 age-matched HS, who were from Guangzhou Women and Children's Medical Center, Guangzhou Medical University, China from November 2019 to August 2021 (Table 1). According to international guidelines 43 , pediatric sepsis is defined by its systemic inflammatory All the patients with sepsis were treated with antibiotics including cephalosporin, vancomycin and broad-spectrum penicillin after admission. Venous blood samples were drawn from septic patients when they were enrolled first day.…”

Section: Patient Recruitment and Isolation Of Human Plateletsmentioning

confidence: 99%

GSDMD-dependent platelet pyroptosis exacerbates NET formation and inflammation in severe sepsis

Tang

Chen

et al. 2022

Preprint

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Dysregulated inflammation is closely associated with increased mortality in sepsis. Platelets have emerged as key inflammatory cells implicated in the pathology of sepsis, including the development of thrombosis, thrombocytopenia, and neutrophil extracellular traps (NETs). Platelet’s contributions to rapid clinical deterioration and dysregulated inflammation in sepsis have not been defined. In our cohort, the incidence of thrombocytopenia, thrombocytopathy and excessive inflammatory cytokines released in patients with severe sepsis were significantly increased. Platelet proteomic analysis revealed significant up-regulation of Gasdermin D (GSDMD). Using platelet-specific Gsdmd deficient mice, we demonstrated a requirement for GSDMD in triggering platelet pyroptosis in cecal ligation and puncture (CLP)-induced sepsis. We further demonstrated that GSDMD-dependent platelet pyroptosis was induced by high levels of S100A8/A9 targeting platelet toll-like receptor 4 (TLR4). Pyroptotic platelet-derived oxidized mitochondrial DNA (ox-mtDNA) potentially promoted NET formation, which in turn contributed to platelet pyroptosis via the release of S100A8/A9, forming a positive feedback loop that led to excessive inflammatory cytokines release. Both pharmacological inhibition using Paquinimod and genetic ablation of the S100A8/A9-TLR4 signaling axis suppressed GSDMD-dependent platelet pyroptosis, thereby alleviating NET-mediated inflammation and improving survival in CLP-induced sepsis mice. Taken together, these findings provide new insights into the proinflammatory role of platelet pyroptosis in severe sepsis.

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“…The initiation of outpatient management requires the availability of monitoring and serial re-evaluation in the event of change in patient status. [101][102][103] If these conditions cannot be met, then use of or transition to an in-patient setting is recommended.…”

Section: Treatmentmentioning

confidence: 99%

Multisystem Inflammatory Syndrome in Children Associated with COVID-19 Infection: A Comprehensive Review

Meza-Contreras

Galdos-Bejar

Escalante-Kanashiro

2022

J Pediatr Intensive Care

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The Multisystem Inflammatory Syndrome in Children (MIS-C) is a postinfectious syndrome associated with coronavirus disease 2019 (COVID-19) disease in children. The aim of this study is to conduct a thorough review to assist health care professionals in diagnosis and management of this complication of COVID-19 disease in children. A thorough systematic review was conducted through an on-line search based on MIS-C with the primary focus on epidemiology, clinical characteristics, diagnosis, pathophysiology, management, and long-term follow-up. This syndrome is characterized by an exaggerated and uncontrolled release of proinflammatory cytokines involving dysfunction of both innate and adaptive immunity. In this review, a summary of observational studies and case reports was conducted, in which we found that MIS-C generates multiple-organ failure frequently presenting with hemodynamic instability further characterized by Kawasaki-like symptoms (such as persistent high fever, polymorphic rash, and bilateral conjunctivitis) and predominance of gastrointestinal and cardiovascular signs and symptoms. Keys to effective management involve early diagnosis, timely treatment and re-evaluation following hospital discharge. Diagnosis is marked by significant elevation of inflammatory biomarkers, laboratory evidence of COVID-19 infection or history of recent exposure, and absence of any other plausible explanation for the associated signs, symptoms, and presentation. Management includes hemodynamic stabilization, empiric antibiotic therapy (de-escalation if cultures and polymerase chain reaction studies indicate no bacterial co-infection), immunomodulatory therapy (methylprednisolone, intravenous immunoglobulin, anakinra, tocilizumab, siltuximab, Janus kinase inhibitors, tumor necrosis factor-α inhibitors), antivirals (remdesivir), and anticoagulation (acetylsalicylic acid, unfractionated or low-molecular-weight heparin or new oral anticoagulants). In addition, we identified poor prognostic risk factors to include concurrent comorbidities, blood-component consumption and marrow suppression (lymphopenia, thrombocytopenia), depletion of homeostatic components (hypoalbuminemia), and marked evidence of a hyperinflammatory response to include elevated values of ferritin, C-reactive protein, and D-dimer. MIS-C constitutes a postinfectious syndrome characterized by a marked cytokine storm, characterized by fever, bilateral conjunctivitis, and multiple organ dysfunction. Promoting future research and long-term follow-up will be essential for the development of guidelines and recommendations leading to effective identification and management of MIS-C.

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Surviving Sepsis Campaign International Guidelines for the Management of Septic Shock and Sepsis-Associated Organ Dysfunction in Children

Cited by 162 publications

References 4 publications

Emodin alleviates sepsis‐mediated lung injury via inhibition and reduction of NF‐kB and HMGB1 pathways mediated by SIRT1

Emodin alleviates sepsis‐mediated lung injury via inhibition and reduction of NF‐kB and HMGB1 pathways mediated by SIRT1

GSDMD-dependent platelet pyroptosis exacerbates NET formation and inflammation in severe sepsis

Multisystem Inflammatory Syndrome in Children Associated with COVID-19 Infection: A Comprehensive Review

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