Systemic and tissue neutrophil responses to experimental trauma

Abstract

Neutrophils are the most abundant type of circulatory white blood cells. Neutrophil activation can be triggered by stimuli such as bacterial invasion, obstruction of vessels, fractures or organ injuries. Upon severe trauma, or following myocardial infarction, a pathological neutrophil response can occur. This may form the basis for life threatening complications like organ failure. Furthermore, this may also lead to impaired wound or fracture healing in trauma cases. The current thesis demonstrates that prolonged surgery (> 60 minutes) for trauma is associated with aberrant neutrophil presence in blood. To be more precise, the total number of circulatory neutrophil drops significantly after 60 minutes of surgery. Moreover, the number of a specific subtype of neutrophils, which are normally virtually absent, rises during ongoing surgery. These findings could form a first pathophysiological background for the ‘Damage Control Surgery´-concept. In additional experiments it was shown that during these post-traumatic neutrophil alterations, the pulmonary as well as the bone marrows neutrophil populations also change markedly. Furthermore, in the case of isolated fractures, both blood and pulmonary neutrophil populations differ from healthy conditions for as long as two weeks. It was further shown that the applied treatment strategy for fracture fixation affects the viability of neutrophils in fracture hematoma. These novel insights may form the basis for novel treatment modalities and guidelines, resulting in improved outcome of trauma patients.