Sepsis and Severe Physical Injury
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Tumour necrosis factor (TNF)- and interleukin (IL)-1-activated endothelial cells produce nitric oxide, free radicals and other mediators that are potent vascular dilators. This may contribute to therapy-resistant hemodynamic shock conditions, for example in severe infections and after extensive physical injuries. Activation of smooth muscle cells and the accumulation of a number of inflammatory mediators, including cytokines, depolarises nociceptors in nerve endings causing pain.
The activated endothelial cells also produce procoagulant factors, which may contribute to clot formation. If substantial amounts of cytokines are produced and/or released in the circulation, seen during bacterial sepsis, disseminated, intravascular coagulation (DIC) may result (see figure below). A life-threatening condition develops if DIC affects the blood flow to vital organs.
DIC - Gangrene in patient with meningococcal sepsis
