Epidemiology of severe sepsis: 2008-2012

Stoller, Jeremy; Halpin, Laura E.; Weis, M.; Aplin, Brett; Qu, Weikai; Georgescu, Claudiu; Nazzal, Munier

doi:10.1016/j.jcrc.2015.09.034

Cited by 150 publications

(113 citation statements)

References 18 publications

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“…Two consecutive epidemiological surveys demonstrated an increasing incidence for severe sepsis [1, 2] from 2000 to 2012; it accounted for 500,000 annual emergency visits in USA in 2006 [3]. During the same period, attributable mortality rate declined from 40% in 2000 to 18% in 2012 [2]. …”

Section: Introductionmentioning

confidence: 99%

Recognition and treatment of severe sepsis in the emergency department: retrospective study in two French teaching hospitals

et al. 2017

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BackgroundSepsis management in the Emergency Department remains a daily challenge. The Surviving Sepsis Campaign (SSC) has released three-hour bundle. The implementation of these bundles in European Emergency Departments remains poorly described.The main objective was to assess the compliance with the Severe Sepsis Campaign 3-h bundle (blood culture, lactate dosage, first dose of antibiotics and 30 ml/kg fluid challenge). Secondary objectives were the analysis of the delay of severe sepsis recognition and description of the population.MethodsIn accordance with STROBE statement, we performed a retrospective study in two French University Hospital Emergency Departments from February to August 2015. Patients admitted during the study period were screened using the electronic files of the hospital databases. Patient’s files were reviewed and included in the study if they met severe sepsis criteria. Demographics, comorbities, treatments were recorded. Delays from admission to severe sepsis diagnosis, fluid loading onset and antibiotics administration were calculated.ResultsOne hundred thirty patients were included (76 men, mean age 71 ± 14 years). Blood culture, lactate dosage, antibiotics and 30 ml/kg fluid loading were performed within 3 hours in % [95% confidence interval] 100% [96–100%], 62% [54–70%], 49% [41–58%] and 19% [13–27%], respectively. 25 patients out of 130 (19% [13–27%]) fulfilled each criteria of the 3-h bundle. The mean fluid loading volume was 18 ± 11 ml/kg. Mean delay between presentation and severe sepsis diagnosis was 200 ± 263 min, from diagnosis to fluid challenge and first antibiotic dose, 10 ± 27 min and 20 ± 55 min, respectively.ConclusionCompliance with SSC 3-h bundle and delay between admission and sepsis recognition have to be improved. If confirmed by other studies, an improvement program might be deployed.

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Section: Introductionmentioning

confidence: 99%

Recognition and treatment of severe sepsis in the emergency department: retrospective study in two French teaching hospitals

et al. 2017

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“…E. Wang et al, 2012). It is anticipated that the rise in these chronic diseases will increase the global prevalence of sepsis (Ovbiagele et al, 2013;Stoller et al, 2016). Yet, therapeutic strategies to treat septic patients remain limited, as there are no FDA-approved drugs to treat sepsis, and the primary treatments are largely limited to anti-microbial drugs, supportive fluids, and vasopressors (Fink & Warren, 2014).…”

Section: Introductionmentioning

confidence: 99%

Loss of tissue non-specific alkaline phosphatase (TNAP) enzyme activity in cerebral microvessels is coupled to persistent neuroinflammation and behavioral deficits in late sepsis

Nwafor¹,

Chakraborty

Brichacek

et al. 2019

Preprint

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Word Count: 7312Conflicts of Interest: The authors declare no conflicts of interest with the content of this article. Highlights• Alkaline phosphatase activity in brain microvessels is diminished in sepsis.• Loss of alkaline phosphatase activity is coupled to the loss of barrier integrity.• Brain infiltration of myeloid and T-lymphoid cells persists in late sepsis.• Septic mice exhibit a novel anti-nociceptive phenotype.• Cortical astrogliosis and microgliosis persist in late sepsis. AbstractSepsis is characterized as a host response to systemic inflammation and infection that may lead to multi-organ dysfunction and eventual death. While acute brain dysfunction is common among all sepsis patients, chronic neurological impairment is prevalent among sepsis survivors. The brain microvasculature has recently emerged as a major determinant of sepsis-associated brain dysfunction, yet the mechanisms that underlie its associated neuroimmune perturbations and behavioral deficits are not well understood.A growing body of data suggests that the loss of tissue nonspecific alkaline phosphatase (TNAP) enzyme activity in cerebral microvessels may be associated with changes in endothelial cell barrier integrity. The objective of this study was to determine the important mechanisms linking alterations in cerebrovascular TNAP enzyme activity to underlying neurological impairment in late sepsis. We hypothesized that the disruption of TNAP enzymatic activity in cerebral microvessels would be coupled to the sustained loss of brain microvascular integrity, elevated neuroinflammatory responses, and behavioral deficits. Male mice were subjected to cecal ligation and puncture (CLP), a model of experimental sepsis, and assessed up to seven days post-sepsis. All mice were observed daily for sickness behavior and underwent behavioral testing. Our results showed a significant decrease in brain microvascular TNAP enzyme activity in the somatosensory cortex and spinal cord of septic mice but not in the CA1 and CA3 hippocampal regions.Analyses of whole brain myeloid and T-lymphoid cell populations also revealed a persistent elevation of infiltrating leukocytes, which included both neutrophil and monocyte myeloid derived suppressor cells (MDSCs). Regional analyses of the somatosensory cortex, hippocampus, and spinal cord revealed significant astrogliosis and microgliosis in the cortex and spinal cord of septic mice that was accompanied by significant microgliosis in the CA1 and CA3 hippocampal regions. Assessment of behavioral deficits revealed no changes in learning and memory or evoked locomotion.However, the hot plate test uncovered a novel anti-nociceptive phenotype in our septic mice, and we speculate that this phenotype may be a consequence of sustained GFAP astrogliosis and loss of TNAP activity in the somatosensory cortex of septic mice. Taken together, these results demonstrate that the loss of TNAP enzyme activity in cerebral microvessels during late sepsis is coupled to sustained neuroimmune dysfunction which may underlie, in part, th...

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“…Approximately 750,000 patients are infected with sepsis each year and over 225,000 of these patients die from the condition in the United States (2). However, the prevalence of sepsis has increased by 5% annually (3,4). To date, anti-infective therapeutic agents and supportive care have been considered effective therapeutic strategies against sepsis.…”

Section: Introductionmentioning

confidence: 99%

Effects of imipenem combined with low‑dose cyclophosphamide on the intestinal barrier in septic rats

Guo

Zhang

et al. 2018

Exp Ther Med

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Anti-infection therapy combined with immunotherapy is one of the important research approaches for treating sepsis. However, the combination of anti-infection and immunotherapy therapeutic agents may have an adverse effect on intestinal barrier function. In the present study, it was hypothesized that imipenem combined with low-dose cyclophosphamide (CTX) could improve the sepsis survival rate compared with imipenem treatment alone. In addition, the alterations in the intestinal barrier were investigated and the possible mechanisms of altering intestinal barrier function in septic rats treated with imipenem combined with low-dose CTX or imipenem alone were explored. To investigate the effect of imipenem combined with low-dose CTX on the intestinal barrier, the markers of histopathology, intestinal permeability, intestinal epithelial apoptosis, cytokines interleukin (IL)-6, IL-10 and tumor necrosis factor (TNF)-α, and tight junction proteins zonula occludens (ZO)-1, occludin and claudin-2, were quantitatively and qualitatively evaluated. The results indicated that imipenem combined with low-dose CTX significantly improved the survival rate of rats compared with imipenem alone (P<0.05). However, no significantly difference between the treatment with imipenem combined with low-dose CTX and imipenem treatment alone was indicated with regard to histopathology, intestinal permeability, intestinal epithelial apoptosis and the expression of claudin-2, ZO-1 and TNF-α. However, imipenem combined with low-dose CTX significantly reduced IL-6 and IL-10 expression and significantly increased occludin expression compared with imipenem alone (P<0.05). It was concluded that imipenem combined with low-dose CTX could improve the survival rate of rats with sepsis compared with rats treated with imipenem alone. The present findings suggest that imipenem combined with low-dose CTX may cause damage to the intestinal barrier function and the mechanism may be associated with a reduction in IL-10 expression.

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Epidemiology of severe sepsis: 2008-2012

Cited by 150 publications

References 18 publications

Recognition and treatment of severe sepsis in the emergency department: retrospective study in two French teaching hospitals

Recognition and treatment of severe sepsis in the emergency department: retrospective study in two French teaching hospitals

Loss of tissue non-specific alkaline phosphatase (TNAP) enzyme activity in cerebral microvessels is coupled to persistent neuroinflammation and behavioral deficits in late sepsis

Effects of imipenem combined with low‑dose cyclophosphamide on the intestinal barrier in septic rats

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