Nationwide Trends of Severe Sepsis in the 21st Century (2000–2007)

Kumar, Gagan; Kumar, Nilay; Taneja, Amit; Kaleekal, Thomas; Tarima, Sergey; McGinley, Emily L.; Jiménez, Edgar; Mohan, Anand; Khan, Rumi Ahmed; Whittle, Jeff; Jacobs, Elizabeth R.; Nanchal, Rahul

doi:10.1378/chest.11-0352

Cited by 557 publications

(433 citation statements)

References 29 publications

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“…Severe sepsis was defined using the ICD‐9‐CM codes for severe sepsis or septic shock, septicemia, bacteremia, or fungemia with at least 1 organ dysfunction (Tables 1 and 2). 18, 19, 20, 21 This definition of severe sepsis is consistent with the 2001 American College of Chest Physicians/Society of Critical Care Medicine consensus criteria for severe sepsis: consequent organ dysfunction, hypoperfusion, or hypotension 22. Using previously validated algorithms for microbiological cultures, septic patients were classified into “culture‐positive” and “culture‐negative” sepsis 21.…”

Section: Methodsmentioning

confidence: 95%

Tako‐Tsubo Cardiomyopathy in Severe Sepsis: Nationwide Trends, Predictors, and Outcomes

Vallabhajosyula

Deshmukh

Kashani

et al. 2018

JAHA

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BackgroundThere are limited data on the presentation of Takotsubo cardiomyopathy (TTC) in severe sepsis.Methods and ResultsThis was a retrospective cohort study using the National Inpatient Sample database (2007–2013) of all adults with severe sepsis. TTC was identified in patients with severe sepsis using previously validated administrative codes. The primary outcome was in‐hospital mortality, and secondary outcomes included resource utilization and discharge disposition. Regression analysis was performed for the entire cohort and a propensity‐matched sample. An exploratory analysis was performed for predictors of TTC incidence and mortality in TTC. During this 7‐year period, in 7.1‐million hospitalizations for severe sepsis, TTC was diagnosed in 10 746 (0.15%) admissions. TTC was noted more commonly in whites, females, and among 65‐ to 79‐year‐old individuals. TTC was independently associated with lower in‐hospital mortality in severe sepsis (odds ratio, 0.58; 95% confidence interval, 0.51–0.65). This association was more prominent in females (odds ratio, 0.51; 95% confidence interval, 0.44–0.59]) compared with males (odds ratio, 0.69; 95% confidence interval, 0.55–0.85]). Presentation in later years of the study period, middle‐age, female sex, and white race were independent predictors for the diagnosis of TTC. Age ≥80 years, black race, greater comorbidity, and multiorgan dysfunction were independently associated with higher in‐hospital mortality among TTC admissions.Conclusions TTC is observed with increasing frequency in severe sepsis and was associated with a significantly lower in‐hospital mortality compared with patients without TTC. Presentation in later years of the study period, middle age, female sex, and white race were independent predictors for the diagnosis of TTC in severe sepsis.

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Section: Methodsmentioning

confidence: 95%

Tako‐Tsubo Cardiomyopathy in Severe Sepsis: Nationwide Trends, Predictors, and Outcomes

Vallabhajosyula

Deshmukh

Kashani

et al. 2018

JAHA

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“…Sepsis is a systemic inflammatory response syndrome that results from infection of invading microorganisms and is associated with substantial clinical mortality in the United States (27%), with no effective therapy to improve patient survival (Angus et al, 2001;Cohen, 2002;Kumar et al, 2011).…”

Section: Brief Definitive Reportmentioning

confidence: 99%

Phospholipase D2 drives mortality in sepsis by inhibiting neutrophil extracellular trap formation and down-regulating CXCR2

Lee¹,

Kim²,

Kook³

et al. 2015

J Cell Biol

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We determined the function of phospholipase D2 (PLD2) in host defense in highly lethal mouse models of sepsis using PLD2 / mice and a PLD2-specific inhibitor. PLD2 deficiency not only increases survival but also decreases vital organ damage during experimental sepsis. Production of several inflammatory cytokines (TNF, IL-1, IL-17, and IL-23) and the chemokine CXCL1, as well as cellular apoptosis in immune tissues, kidney, and liver, are markedly decreased in PLD2 / mice. Bactericidal activity is significantly increased in PLD2 / mice, which is mediated by increased neutrophil extracellular trap formation and citrullination of histone 3 through peptidylarginine deiminase activation. Recruitment of neutrophils to the lung is markedly increased in PLD2 / mice. Furthermore, LPS-induced induction of G protein-coupled receptor kinase 2 (GRK2) and down-regulation of CXCR2 are markedly attenuated in PLD2 / mice. A CXCR2-selective antagonist abolishes the protection conferred by PLD2 deficiency during experimental sepsis, suggesting that enhanced CXCR2 expression, likely driven by GRK2 down-regulation in neutrophils, promotes survival in PLD2 / mice. Furthermore, adoptively transferred PLD2 / neutrophils significantly protect WT recipients against sepsis-induced death compared with transferred WT neutrophils. We suggest that PLD2 in neutrophils is essential for the pathogenesis of experimental sepsis and that pharmaceutical agents that target PLD2 may prove beneficial for septic patients.

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“…Severe sepsis and septic shock is the final common pathway and one of the leading causes of global childhood mortality (1,2). Poor clinical outcomes are related to many factors including patient factors such as malnutrition, lack of readily available resources to appropriately triage, diagnose and treat sepsis, and suboptimal adherence to specific sepsis management guidelines (3)(4)(5)(6)(7)(8)(9).…”

Section: Introductionmentioning

confidence: 99%