Pathophysiology: remote organ injury

Research output: Chapter in Book/Report/Conference proceedingChapterAcademic

Abstract

Trauma results in tissue damage. Thereby, the extracellular matrix is disrupted and cells break apart spilling their contents. DAMPs are endogenously released molecules derived from cells or cellular compartments such as the nucleus, mitochondria, or the cytosol. They activate the immune system and are pro-inflammatory in nature. They play an important pathogenetic role in the development of multiple organ dysfunction syndrome after injury. Polymorphonuclear granulocytes are the first immune cells activated. They produce proteinases, radical oxygen species and can phagocytose debris and bacteria. They are activated due to ischemia-reperfusion subsequent to trauma and resuscitation or by the DAMPs. They extravasate in the organs and this may lead to organ damage. Other immune cells such as monocytes and lymphocytes play also a role in the pathogenesis of multiple organ dysfunction syndrome. NK-cells, for instance, seem to be important in producing cytokines. Cytokines such as IL-6 and IL-10 are important in the immune response and activate several other systems. Their presence is associated with posttraumatic multiple organ dysfunction syndrome. In conclusion, the pathogenesis of multiple organ dysfunction syndrome after a traumatic insult is orchestrated by different systems. These are mutually activating and perpetuating each other. This knowledge is important to understand the posttraumatic pathology and develop treatment strategies. © Springer Nature Switzerland AG 2011, 2016, 2022, corrected publication 2022.
Original languageEnglish
Title of host publicationTextbook of Polytrauma Management
Subtitle of host publicationA multidisciplinary approach
EditorsHans-Christoph Pape, Joseph Borrelli, Ernest E. Moore, Roman Pfeifer, Philip F. Stahel
PublisherSpringer Nature
Chapter12
Pages127-134
Number of pages8
Edition3
ISBN (Electronic)9783030959067
ISBN (Print)9783030959050, 9783030959081
DOIs
Publication statusPublished - 2022

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