Is worsening multiple organ failure the cause of death in patients with severe sepsis?*

2011 ◽  
Vol 39 (5) ◽  
pp. 1050-1055 ◽  
Author(s):  
Jean-Louis Vincent ◽  
David R. Nelson ◽  
Mark D. Williams
1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 41A-41A
Author(s):  
Yong Y Han ◽  
Leslie A Doughty ◽  
Danny Kofos ◽  
Joseph A Carcillo

Medicine ◽  
2016 ◽  
Vol 95 (35) ◽  
pp. e4651 ◽  
Author(s):  
Michaela-Diana Fitrolaki ◽  
Helen Dimitriou ◽  
Maria Venihaki ◽  
Marianna Katrinaki ◽  
Stavroula Ilia ◽  
...  

2018 ◽  
Vol 8 (3) ◽  
pp. 31-35
Author(s):  
Lich Pham Van ◽  
Chuong Tran Xuan ◽  
Thuy Nguyen Le Lam

Background: Severe sepsis is a sepsis leading to organ dysfunction. It has rapid progression, multiple organ damage and high mortality. Patients and Methods: Prospective study was performed on 78 patients diagnosed clinically severe sepsis, hospitalized and treated at the ICU of the Dak Lak General Hospital, from April, 2016 to June, 2017. Results: The mean age was 56.55 ± 18.40 years. The rate of positive blood cultures was 57.7%, the majority of bacteria isolated were Staphylococcus aureus, E. coli and Klebsiella pneumonia. 62.8% of patients recovered from the disease, 37.2% died. Mortality rates associated with respiratory, skin- mucosal and gastrointestinal sources were 46.7%, 42.9% and 36.4%, respectively. The high mortality rate related to factors such as primary sources of infection, age (0.0325), respiratory failure (p < 0.001), multiple organ failure (p=0.0015), APACHE II score (mean: 22.83 ± 8.15 (p < 0.0001). Conclusions: The common bacteria causing severe sepsis were Staphylococcus aureus, E. coli and Klebsiella pneumonia. Factors related to mortality were age, male, respiratory failure, multiple organ failure, APACHE II score. Key words: severe sepsis, treatment, Dak Lak General hospital


2009 ◽  
Vol 35 (11) ◽  
pp. 1959-1963 ◽  
Author(s):  
Martina Crivellari ◽  
Patrizia Della Valle ◽  
Giovanni Landoni ◽  
Federico Pappalardo ◽  
Chiara Gerli ◽  
...  

2012 ◽  
Vol 33 (2) ◽  
pp. 206-211 ◽  
Author(s):  
Outi Kallinen ◽  
Kreu Maisniemi ◽  
Tom Böhling ◽  
Erkki Tukiainen ◽  
Virve Koljonen

1996 ◽  
Vol 22 (S1) ◽  
pp. S43-S43
Author(s):  
S A Nasraway ◽  
R Balk ◽  
C Sessler ◽  

Blood ◽  
2010 ◽  
Vol 116 (6) ◽  
pp. 1002-1010 ◽  
Author(s):  
Robert Silasi-Mansat ◽  
Hua Zhu ◽  
Narcis I. Popescu ◽  
Glenn Peer ◽  
Georgia Sfyroera ◽  
...  

AbstractSevere sepsis leads to massive activation of coagulation and complement cascades that could contribute to multiple organ failure and death. To investigate the role of the complement and its crosstalk with the hemostatic system in the pathophysiology and therapeutics of sepsis, we have used a potent inhibitor (compstatin) administered early or late after Escherichia coli challenge in a baboon model of sepsis-induced multiple organ failure. Compstatin infusion inhibited sepsis-induced blood and tissue biomarkers of complement activation, reduced leucopenia and thrombocytopenia, and lowered the accumulation of macrophages and platelets in organs. Compstatin decreased the coagulopathic response by down-regulating tissue factor and PAI-1, diminished global blood coagulation markers (fibrinogen, fibrin-degradation products, APTT), and preserved the endothelial anticoagulant properties. Compstatin treatment also improved cardiac function and the biochemical markers of kidney and liver damage. Histologic analysis of vital organs collected from animals euthanized after 24 hours showed decreased microvascular thrombosis, improved vascular barrier function, and less leukocyte infiltration and cell death, all consistent with attenuated organ injury. We conclude that complement-coagulation interplay contributes to the progression of severe sepsis and blocking the harmful effects of complement activation products, especially during the organ failure stage of severe sepsis is a potentially important therapeutic strategy.


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