Adjunct therapy for sepsis: How early?

被引：7
作者：
Annane D. [1 ]
机构：
[1] General Intensive Care Unit, Raymond Poincaré Hospital (AP-HP), University of Versailles SQY, 92380 Garches
来源：
Current Infectious Disease Reports | 2010年 / 12卷 / 5期
关键词：
Activated protein C; Apoptosis; Coagulation; Hydrocortisone; Infection; Inflammation; Organ dysfunction; Shock;
D O I：
10.1007/s11908-010-0123-2
中图分类号：
学科分类号：
摘要：
Sepsis is a leading cause of death worldwide. The management of patients is primarily based on curing the infectious process with anti-infective drugs and/or surgical drainage. Simultaneously, treatment includes optimization of oxygen use by tissues via appropriate oxygen therapy and respiratory and hemodynamic management. At best, initiating appropriate anti-infective and symptomatic treatments should lead to patient improvement within a few hours. Activated protein C and hydrocortisone are the only two available adjunct therapies for sepsis. These treatments should optimally be started within 24 hours of the onset of shock. They should be initiated in those patients who did not adequately respond after 6 hours of optimal anti-infective and symptomatic treatments. © 2010 Springer Science+Business Media, LLC.
引用
收藏
页码：361 / 367
页数：6
相关论文
共 41 条
[1]  
Angus D.C., Linde-Zwirble W.T., Lidicker J., Et al., Epidemiology of severe sepsis in the United States: Analysis of incidence, outcome, and associated costs of care, Crit Care Med, 29, pp. 1303-1310, (2001)
[2]  
Annane D., Sebille V., Charpentier C., Et al., Effect of treatment with low doses of hydrocortisone and fludrocortisone on mortality in patients with septic shock, JAMA, 288, pp. 862-871, (2002)
[3]  
Bernard G.R., Vincent J.L., Laterre P.F., Et al., Efficacy and safety of recombinant human activated protein C for severe sepsis, N Engl J Med, 344, pp. 699-709, (2001)
[4]  
Riedemann T., Patchev A.V., Cho K., Almeida O.F., Corticosteroids: Way upstream, Mol Brain, 3, (2010)
[5]  
Annane D., Glucocorticoids in the treatment of severe sepsis and septic shock, Curr Opin Crit Care, 11, pp. 449-453, (2005)
[6]  
Muhlfelder T.W., Niemetz J., Kang S., Glucocorticoids inhibit the generation of leukocyte procoagulant (tissue factor) activity, Blood, 60, pp. 1169-1172, (1982)
[7]  
Van Giezen J.J., Jansen J.W., Inhibition of fibrinolytic activity in-vivo by dexamethasone is counterbalanced by an inhibition of platelet aggregation, Thromb Haemost, 68, pp. 69-73, (1992)
[8]  
Jorgensen K.A., Sorensen P., Freund L., Effect of glucocorticosteroids on some coagulation tests, Acta Haematol, 68, pp. 39-42, (1982)
[9]  
Patrassi G.M., Sartori M.T., Livi U., Et al., Impairment of fibrinolytic potential in long-term steroid treatment after heart transplantation, Transplantation, 64, pp. 1610-1614, (1997)
[10]  
Schmidt S., Rainer J., Ploner C., Et al., Glucocorticoid-induced apoptosis and glucocorticoid resistance: Molecular mechanisms and clinical relevance, Cell Death Differ, 11, SUPPL. 1, (2004)
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