Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-17139
Sepsis, the systemic inflammatory response to an infection, is an increasingly common condition. It represents a major healthcare problem as affected patients have a high morbidity and mortality leading to high direct and indirect costs. This article describes the progression from a simple infection to septic shock and multi-organ failure, with a special emphasis on the body’s response at the cellular level.
Pathogen recognition by the host is followed by a cascade of pro- and anti-inflammatory mediators that attempt to defend the body and prevent further harm. Both pathogen virulence and host resistance regulate the severity of the inflammatory response. As a result of the inflammatory insult, mitochondria are damaged functionally and structurally. Since mitochondria are responsible for intracellular energy production, mitochondrial dysfunction places the cells at risk of developing energy failure and, consequently, cell death. However, sepsis is characterised by a lack of tissue necrosis and the ability of most – if not all – organs to recover completely. This underlines the assumption that organ dysfunction during sepsis is predominantly a functional problem which appears to relate to the creation of a new balance between energy generation and expenditure. Hence, organ dysfunction could be viewed as a protective mechanism for the patient and may represent a state analogous to hibernation, which can be reversed once the infection is overcome and inflammation has abated. More research is needed to develop better directed and timed therapeutic interventions that can reduce the high morbidity and mortality of this common condition.
|Item Type:||Journal Article, refereed, further contribution|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Clinic and Policlinic for Internal Medicine|
|DDC:||610 Medicine & health|
|Deposited On:||03 Mar 2009 11:27|
|Last Modified:||27 Nov 2013 18:18|
|Publisher:||EMH Swiss Medical Publishers|
|Additional Information:||Free full text article|
|Related URLs:||http://www.smw.ch/docs/archive200x/2008/43/smw-12319.html (Publisher)|
|Citations:||Web of Science®. Times Cited: 14|
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