Trauma and Emergency: Beyond Damage Control Surgery

Dear Colleagues,

Following major trauma, outcomes correlates with both appropriateness and timeliness of diagnosis and treatment but, first and foremost, with severity of injury.
In fact, a severe trauma almost instantaneously leads to a high level of cell death with the release of debris cell’s fragments. These DAMPs (damage-associated molecular patterns) sustain the following cascade and the pathophysiological consequences, structured in the mechanistic insight depicted in the so-called “Danger model”.
The “Danger model”, the paradigm described in 2002 by Matzinger, suggests that damage’s products and alarm signals from injured tissues are the main ones responsible for the activation of the immune system.
The extremely varying range of severity of sterile post-injury inflammation and its consequent inauspicious organ dysfunctions seems to correlate with the level of immune reaction, consistent with the degree of the initial tissue damage caused by the trauma.
mt-DNA is one of the most frequently investigated and probably one of the best described DAMPs, both a marker and instigator of sterile post-injury inflammation. It spreads after cell necrosis and by an active process when even intact functioning mitochondria can leak out of stressed cells responding to major trauma. Mitochondria and their products can turn into an enemy within the body, akin to a “Trojan horse”.
In addition to danger molecules, neutrophil-associated extracellular trap (NET) formation also plays an emerging role in sustaining inflammatory response.
First described by Brinkmann and colleagues, NETosis is a cell death pathway distinct from apoptosis and necrosis; it faces neutrophils, entering tissues and organs following an injury and forming neutrophil extracellular traps (NETs).
Although NETs play an important role in host defence by trapping pathogens, extensive formation of NETs with increased amounts of extracellular DNA may contribute to the spread of inflammation and tissue damage. Recent reports indicate that NETs may contribute to tissue damage and organ dysfunction.
A deep knowledge of these pathomechanisms might be extremely interesting in both predicting the outcome and defining the most therapeutically suitable approach after severe trauma.
We are extremely excited to explore all the new findings concerning this field in terms of pathophysiological knowledge, diagnostic and prognostic approaches, and therapeutic strategies.

Dr. Giuseppe Ietto
Dr. Gabriele Soldini
Dr. Francesco Amico
Dr. Caterina Franchi
Guest Editors

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