From the Guidelines
Trauma causes a systemic inflammatory response syndrome (SIRS) through tissue necrosis, hemorrhage, and ischemia-reperfusion injury, which trigger a complex inflammatory cascade 1.
Pathophysiology of SIRS
The inflammatory response is initiated when damaged cells release damage-associated molecular patterns (DAMPs) into circulation, activating pattern recognition receptors on immune cells 1. This leads to the release of pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α), interleukin-1 (IL-1), and interleukin-6 (IL-6), which amplify the inflammatory response.
Key Factors Contributing to SIRS
Some key factors that contribute to the development of SIRS in trauma patients include:
- Tissue necrosis and hemorrhage
- Ischemia-reperfusion injury
- Release of reactive oxygen species
- Activation of the complement system
- Endothelial dysfunction
Clinical Implications
The overwhelming inflammatory response can lead to endothelial dysfunction, causing increased vascular permeability, tissue edema, and potentially organ dysfunction 1. If severe enough, this cascade can progress to multiple organ dysfunction syndrome.
Management
Management of trauma-induced SIRS focuses on controlling the initial injury, maintaining tissue perfusion, and providing supportive care while the inflammatory response resolves 1.
From the Research
Systemic Inflammatory Response Syndrome (SIRS) and Trauma
- Trauma can cause a systemic inflammatory response syndrome (SIRS) due to the activation of the immune system and the release of pro-inflammatory mediators 2.
- The initial pro-inflammatory response after trauma is followed by an anti-inflammatory response, which can result in immune suppression and a high risk of infection and sepsis 2.
- Extensive tissue injury can lead to the spillover of pro-inflammatory mediators into the peripheral bloodstream, further maintaining and augmenting the pro-inflammatory response 2.
Mechanisms of SIRS
- The host response to injury is usually appropriate in degree and self-limited, but in more severe injury, the host response may persist inappropriately, leading to SIRS and multiple organ dysfunction syndrome (MODS) 3.
- Inflammatory cells are recruited to the site of injury and elaborate cytokines, which promote repair locally but may be systemically released and trigger remote inflammation in severe injury 3.
- Cytokine biology is complex and poorly understood, and simple anticytokine strategies have failed to improve survival of critically ill patients 3.
Cytokines and SIRS
- Cytokines are inflammatory polypeptide molecules that play a crucial role in the systemic inflammatory response syndrome 4.
- Both pro- and anti-inflammatory cytokines are released following a variety of initiating stimuli, including endotoxin release, complement activation, and ischemia-reperfusion injury 4.
- Cytokine adsorption therapy provides a potential solution to improving outcomes following SIRS 4.
Definition and Aetiology of SIRS
- SIRS is the clinical expression of the action of complex intrinsic mediators of the acute phase reaction, and can be precipitated by events such as infection, trauma, pancreatitis, and surgery 5.
- SIRS can compromise the function of various organ systems, resulting in multiple organ dysfunction syndrome (MODS) 5.
- The concept of SIRS was developed to describe the complex pathophysiologic response to an insult, and to provide a set of clinical parameters to aid in the early identification of potential candidates for clinical trials to evaluate new treatments for sepsis 6.