(iii) An update on the systemic response to trauma

Clinical care of the injured is evolving rapidly. Understanding of the cellular and humoral interactions which link shock, coagulopathy and inflammation has expanded rapidly and provided the framework for clinical developments. Tissue hypoxia and hypoperfusion drives protein-C mediated acute coagulopathy and endothelial cell and leukocyte dysfunction. When severe, tissue damage occurs and is manifest as Adult Respiratory Distress Syndrome (ARDS)/Multisystem Organ Failure (MOF) or sepsis from relative immune-compromise.

Extensive surgery can constitute a ‘second hit’ to physiological reserves, hence Damage Control Surgery (DCS) aims to control life-threatening bleeding and the lethal triad, and Damage Control Orthopaedics (DCO) utilizes temporary external fixation for the initial management of major fractures to confer the benefits of early stabilization, without the risks of major surgery.

Damage Control Resuscitation (DCR) describes a seamless strategy, with surgery as a lynch pin. Haemostasis and restoration of tissue perfusion and oxygenation are enshrined as surgical goals. Supporting fluid strategies restrict initial volumes during resuscitation, then switch to haemostatic resuscitation with high ratios of blood to blood products. Rapid control of bleeding and coagulopathy appear to moderate the systemic inflammatory response, with much improved survival and swifter progress to definitive reconstruction. At present, manipulation of the systemic inflammatory response to injury is only possible by the indirect means offered by DCR.