Systemic inflammation after trauma

Abstract

Trauma is still one of the main reasons for death among the population worldwide. Mortality occurring early after injury is due to "first hits", including severe organ injury, hypoxia, hypovolaemia or head trauma. Massive injury leads to activation of the immune system and the early inflammatory immune response after trauma has been defined as systemic inflammatory response syndrome (SIRS). "Second hits" such as infections, ischaemia/reperfusion or operations can further augment the pro-inflammatory immune response and have been correlated with the high morbidity and mortality in the latter times after trauma. SIRS can lead to tissue destruction in organs not originally affected by the initial trauma with subsequent development of multi-organ dysfunction (MOD). The initial pro-inflammatory response is followed by an anti-inflammatory response and can result in immune suppression with high risk of infection and sepsis. Trauma causes activation of nearly all components of the immune system. It activates the neuroendocrine system and local tissue destruction and accumulation of toxic byproducts of metabolic respiration leads to release of mediators. Extensive tissue injury may result in spillover of these mediators into the peripheral bloodstream to further maintain and augment the pro-inflammatory response. Hormones like ACTH, corticosteroids and catecholamines as well as cytokines, chemokines and alarmins play important roles in the initiation and persistence of the pro-inflammatory response after severe injury. The purpose of this review is therefore to describe the immunological events after trauma and to introduce important mediators and pathways of the inflammatory immune response.