Newsletter

[ Vol. 12 No. 1 ] (January - April 2011 )
Update on the pathophysiology of sepsis

Konstantin Mayer
University of Giessen Lung Center (UGLC), Department of Internal Medicine, Pulmonary and Critical Care Medicine, Klinikstr, Giessen, Germany

Sepsis is the leading cause of death in non-coronary intensive care units. Mortality rates ranging between 30 to 60% with the number of patients increasing by up to 1.5% annually, faster than the anticipated growth of the population in the United States. In septic shock a massive hyper-inflammatory reaction is crated by the host in the initial phase of the disease. In parallel, an anti-inflammatory reaction is also initiated, that has been termed “compensatory anti-inflammatory response syndrome” (CARS). A multitude of mediators and cells are involved in the disease with the key pro-inflammatory cytokines responsible for the cytokine storm at the beginning of sepsis. High mobility group B-1 and the toll-like receptors have been identified as further key players. Exaggerated apoptosis of lymphocytes is a key feature in the CARS phase and may lead to secondary immune-suppression and infection. Next to inflammatory reaction, sepsis has an impact on the neuro-endocrine reactions of the body and the metabolic response. We are still lacking a fast and accurate method for the determination of the immune status of a septic patient. Therefore, the optimal use, timing, and dose of immune-modulating drugs in septic patients are an ongoing matter of debate.

From   
PENSA 2009
“Energizing Nutrition Support Practice for Life”
June 5-7 2009, Shangri-La Hotel, Kuala Lumpur, Malaysia 
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