Pathophysiology of polytrauma.

By M. Keel, O. Trentz. Injury, 2005

870 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

A genomic storm in critically injured humans (2011, background): “Current dogma argues that exaggerated inflammation contributes to adverse outcome (Giannoudis, 2003; Keel and Trentz, 2005; Xu et al., 2009; Zhang et al., 2010), and complicated outcomes are commonly associated with second hits or multiple inflammatory events induced by clinical episodes of…”
Fracture healing under healthy and inflammatory conditions (2012, background): “possibly as a result of the complex post-traumatic systemic inflammatory response, characterized by rapid proinflammatory cytokine and chemokine release, complement activation, and overactivation of PMNs”
The role of complement in inflammatory diseases from behind the scenes into the spotlight. (2007, background): “Severe inflammation, developing as a consequence of reperfusion of large areas of ischemic tissue, may even lead to systemic inflammatory response syndrome or multiple organ dysfunction syndrome, which accounts for up to 30 to 40% of intensive care unit mortality.(44) The complement system seems to ”
Complement and coagulation: strangers or partners in crime? (2007, background): “By contrast, trauma that causes injury to the vasculature and subsequentbleeding,whichwouldusuallyactivatebloodcoagulation, is also associated with a risk of infection and the activation of an inflammatory reaction [ 3 ].”