Classification, Incidence, and Outcomes of Sepsis and Multiple Organ Failure

Vincent, Jean‐Louis; Taccone, Fabio; Schmit, Xavier

doi:10.1159/000102071

Cited by 41 publications

(32 citation statements)

References 29 publications

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“…Indeed, the mortality associated with septic shock ranges from 40 to 70% [2,6,7]. The cornerstones of emergency management of sepsis are early goal-directed therapy, elimination of the septic focus, and broad-spectrum antibiotics [8][9][10].…”

Section: Introductionmentioning

confidence: 99%

Left ventricular end-diastolic area is a measure of cardiac preload in patients with early septic shock

Scheuren¹,

Wente

Hainer³

et al. 2009

European Journal of Anaesthesiology

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Section: Introductionmentioning

confidence: 99%

Left ventricular end-diastolic area is a measure of cardiac preload in patients with early septic shock

Scheuren¹,

Wente

Hainer³

et al. 2009

European Journal of Anaesthesiology

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“…However, if the infection is not contained, the pathogen, its toxins, and diverse mediators of the host are released to the circulation, producing a systemic inflammatory response syndrome that can cause severe sepsis or septic shock (8). Sepsis is usually treated in intensive care units (ICUs), and about 30% of the patients with severe sepsis die; this percentage rises to 50 to 70% if septic shock, the main cause of mortality in the ICU, develops (46).…”

mentioning

confidence: 99%

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

et al. 2011

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Severe sepsis is associated with early release of inflammatory mediators that contribute to the morbidity and mortality observed during the first stages of this syndrome. Although sepsis is a deadly, acute disease, high mortality rates have been observed in patients displaying evidence of sepsis-induced immune deactivation. Although the contribution of experimental models to the knowledge of pathophysiological and therapeutic aspects of human sepsis is undeniable, most of the current studies using animal models have focused on the acute, proinflammatory phase. We developed a murine model that reproduces the early acute phases but also the long-term consequences of human sepsis. We induced polymicrobial acute peritonitis (AP) by establishing a surgical connection between the cecum and the peritoneum, allowing the exit of intestinal bacteria. Using this model, we observed an acute phase with high mortality, leukopenia, increased interleukin-6 levels, bacteremia, and neutrophil activation. A peak of leukocytosis on day 9 or 10 revealed the persistence of the infection within the lung and liver, with inflammatory hepatic damage being shown by histological examination. Long-term (20 days) derangements in both innate and adaptive immune responses were found, as demonstrated by impaired systemic tumor necrosis factor alpha production in response to an inflammatory stimulus; a decreased primary humoral immune response and T cell proliferation, associated with an increased number of myeloid suppressor cells (Gr-1 ؉ CD11b ؉ ) in the spleen; and a low clearance capacity. This model provides a good approach to attempt novel therapeutic interventions directed to augmenting host immunity during late sepsis.Local inflammatory mechanisms triggered by an infection are usually enough to eradicate the pathogen. However, if the infection is not contained, the pathogen, its toxins, and diverse mediators of the host are released to the circulation, producing a systemic inflammatory response syndrome that can cause severe sepsis or septic shock (8). Sepsis is usually treated in intensive care units (ICUs), and about 30% of the patients with severe sepsis die; this percentage rises to 50 to 70% if septic shock, the main cause of mortality in the ICU, develops (46).As death by septic shock has been associated with an early excessive inflammatory response, most of the treatment strategies have been designed to block the inflammatory mediators involved in this phenomenon. This theory is based on animal models where the administration of large amounts of bacteria or lipopolysaccharide (LPS), a major component of the outer membrane of Gram-negative bacteria, generates a cytokine storm and where the blockade of these molecules increases the survival of animals (11). Nevertheless, clinical trials designed to neutralize inflammatory mediators have failed (45). The sepsis syndrome is not restricted to the activation of the inflammatory response, as compensatory anti-inflammatory mechanisms are also triggered, usually leading to immunosuppressio...

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“…One of the most active areas of research in intensive care in recent years involves the modulation of the septic response in order to reduce the persistently high mortality in this group of patients [55] . One avenue has been to investigate the potential benefit of CRRT in the sepsis syndrome [56,57] .…”

Section: Rrt For Sepsismentioning

confidence: 99%

Today’s Approach to the Critically Ill Patient with Acute Kidney Injury

Ricci

Ronco

2009

Blood Purif

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The present review describes recent evidence on all aspects relating to acute kidney injury (AKI): epidemiology, definition, diagnosis, medical and extracorporeal therapy. AKI is often underrecognized, but its outcome still remains unfavorable. In this light, definition, classification and diagnosis of AKI are fundamental today and may be reliably based on recently proposed RIFLE (risk, injury, failure, loss of function, end-stage kidney disease) classification. Pharmacological therapy of AKI is still scarcely effective, but renal replacement therapy has progressed to a more accurate and safe treatment and new interesting high-level trials and observational studies have been performed and are reviewed and commented. In the near future, however, only increased awareness of AKI incidence and early treatment or prevention of kidney injury progression will hopefully improve outcome of critically ill patients with renal failure.

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Classification, Incidence, and Outcomes of Sepsis and Multiple Organ Failure

Cited by 41 publications

References 29 publications

Left ventricular end-diastolic area is a measure of cardiac preload in patients with early septic shock

Left ventricular end-diastolic area is a measure of cardiac preload in patients with early septic shock

Model of Polymicrobial Peritonitis That Induces the Proinflammatory and Immunosuppressive Phases of Sepsis

Today’s Approach to the Critically Ill Patient with Acute Kidney Injury

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