Human protein C zymogen concentrate in patients with severe sepsis and multiple organ failure after adult cardiac surgery

2009 ◽  
Vol 35 (11) ◽  
pp. 1959-1963 ◽  
Author(s):  
Martina Crivellari ◽  
Patrizia Della Valle ◽  
Giovanni Landoni ◽  
Federico Pappalardo ◽  
Chiara Gerli ◽  
...  
1999 ◽  
Vol 45 (4, Part 2 of 2) ◽  
pp. 41A-41A
Author(s):  
Yong Y Han ◽  
Leslie A Doughty ◽  
Danny Kofos ◽  
Joseph A Carcillo

2011 ◽  
Vol 21 (4) ◽  
pp. 236-246 ◽  
Author(s):  
L. S. Sitniakowsky ◽  
A. F. L. Later ◽  
L. M. G. van de Watering ◽  
M. Bogaerts ◽  
A. Brand ◽  
...  

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


Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 3606-3606 ◽  
Author(s):  
Paul Knoebl ◽  
Peter Schellongowski ◽  
Thomas Staudinger ◽  
Wolfgang R. Sperr ◽  
Christian Scheibenpflug

Abstract Purpura fulminans (PF) is rapidly progressing, life-threatening disorder, characterized by skin lesions with a typical morphology, disseminated intravascular coagulopathy, multiple organ failure, septic shock, most often, but not exclusively caused by infections (meningococci, pneumococci, and others). It is associated with a breakdown of the protein C system, an important regulator of blood coagulation, leading to consumption coagulopathy, intravascular fibrin deposition, downregulated fibrinolysis, disturbance of microcirculation and finally death from multiple organ failure. Mortality of severe sepsis with coagulopathy is as high as 80-100%, and persistent disabilities (i.e. amputations) are frequent in survivors. Several case series including more than 340 patients, suggest that substitution of protein C zymogen can impressively improve coagulopathy, reduce amputation rate and improve survival compared to historical controls in PF associated with sepsis in neonates, children and adults, encouraging some centers to incorporate it in their local guidelines for treatment of purpura fulminans. We report a series of 9 consecutive patients with purpura fulminans, treated with a plasma-derived protein C zymogen concentrate (Ceprotin®, Baxter, Vienna, Austria) for acute onset PF in 3 Vienna hospitals, in which the treatment guidelines included protein C replacement. Median age was 29 years (range 2 months to 73 years), 5 male, 4 female, 5 adult, 4 pediatric patients were treated, respectively. Six patients had meningococcal sepsis, 2 had overwhelming post-splenectomy infections, and 1 had heat-shock induced coagulopathy. All patients presented with typical skin lesions and acute critical illness and were admitted to intensive care units. Coagulopathy was present in 100%, severe vasopressor-dependent sepsis in 100%, acute renal failure in 89%, respiratory failure in 89%. Median SAPS II score in the adults was 78 (range 45-97), predicting a mortality of 78.3% (range 31-88.5%). All pediatric patients had a Glasgow Meningococcal Septicemia prognostic score >8, indicating a fatal outcome. Renal replacement therapy was necessary in 56%, mechanical ventilation in 89%. Initial protein C levels were markedly decreased in the 8 patients with infections. Standardized sepsis therapy was applied according to the surviving sepsis guidelines. Protein C was given as an initial bolus infusion (100 U/kg) followed by a continuous infusion with 10 U/kg/h, adjusted to obtain plasma protein C activity levels of 1.0 U/mL. In addition, platelet, red blood cell, fibrinogen and antithrombin concentrates were given as needed. In one patient (PF caused by heat shock) protein C infusion was stopped after 2 days, and he died after 10 days from refractory multiple organ failure. All other patients (with infection-induced PF) survived. Coagulopathy resolved within a few days, and all patients could successfully be weaned from intensive care therapy. Organ function was completely restored without residual dysfunction. One patient needed amputation of both forefeet and nose reconstruction, 6 patients had, in part extended, scar formation at the skin. Median follow up was 8 months (range 2-20). At that time all patients were fully active without apparent limitations. In conclusion, standardized, full-code sepsis therapy, together with protein C substitution, resulted in very high survival rate of patients with infection-induced PF (as compared to predicted mortality) and a low rate of disabilities in this otherwise deleterious disease. As Ceprotin® is approved only for congenital protein C deficiency, controlled clinical studies are urgently needed to gain more scientific evidence for this potentially life-saving, but still off-label therapy in patients with PF. Disclosures: Knoebl: Novo Nordisk: Consultancy, Honoraria; Baxter: Consultancy, Honoraria. Off Label Use: plasma derived protein C concentrate (Ceprotin(R)) for acquired protein C deficiency in purpura fulminans.


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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