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Pathophysiology of trauma — multiple organ failure

Pathophysiologie des traumatischen Multi-Organversagens

  • Main Topics: Surgery On Injuries To Visceral Organs — Part I
  • Published:
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Summary

Background: Multiple organ failure (MOF) is not a disease, but the result of a series of events that in some cases may lead to the death of patients in the intensive care unit.

Methods: This is a review of pathophysiologic alterations that may occur after trauma. In this respect emphasis will be placed on mechanisms and significance of trauma-related ischemia/reperfusion, activation of cellular/humoral systems, bacteria/endotoxin translocation, and related mediators that can cause or perpetuate the development of MOF.

Results: In general, the body’s response to trauma or stress is mediated by mediators derived by activation of humoral cascades, such as complement and coagulation systems and/or by a variety of cells, such as the monocytes/macrophages. Such a response, manifested as inflammation, should be beneficial to the host. From a certain threshold level of activation/inactivation, however, there might be an imbalance of the mediator system that could harm the host by leading to the development of MOF. Although the pathogenesis of MOF is most likely multifaceted, the cell’s oxygen status, adherence of neutrophils to the endothelium with subsequent transmigration, gut barrier failure leading to the translocation of bacteria/endotoxin, and an initially hyperinflammatory state followed by delayed immunosupression that predispose to infection have recently been considered as key events in this scenario.

Conclusions: The precise mechanisms, however, of the development of MOF have not been clearly understood. The relative importance of the cascades/mediators and their interrelationships remains to be defined.

Zusammenfassung

Grundlagen: Multiples Organversagen (MOV) ist keine Krankheit, sondern das Ergebnis einer Reihe von Ereignissen, die in manchen Intensivfällen zum Tode führen können.

Methodik: Die folgende Arbeit stellt einen Überblick über die möglichen pathophysiologischen Veränderungen nach einem Trauma dar. In diesem Zusammenhang werden die Mechanismen und Merkmale jener Vorgänge dargestellt, die während der Ischämie/Reperfusion, Aktivierung von humoralen/zellulären Kaskaden und Freisetzung von entsprechenden Mediatoren die Entwicklung des MOV verursachen und/oder perpetuieren.

Ergebnisse: Normalerweise wird die körperliche Antwort auf Trauma oder Streß durch Mediatoren bestimmt, welche sich durch die Aktivierung der humoralen Kaskaden, etwa der Komplement-und Gerinnungssystem, bzw. aus verschiedenen Zellen, z. B. Monozyten und Makrophagen, entwickeln. Diese Antwort, in Form einer Entzündung, sollte für den Organismus von Vorteil sein. Ab einer gewissen Schwelle der Aktivierung/Deaktivierung kann es jedoch zu einem Ungleichgewicht des Mediatorensystems kommen und folglich zur Entstehung des MOV. Obwohl die Pathogenese des MOV höchstwahrscheinlich vielseitig ist, werden in letzter Zeit als Schlüsselereignisse in diesem Szenario der Sauerstoffstatus der Zelle, die Anhaftung der Neutrophilen am Endothelium und ihre darauffolgende Transmigration, das Versagen der Viszeralschranken mit Translokation von Bakterien bzw. Endotoxinen, und ein anfangs hyperentzündlicher Zustand gefolgt von verspäteter Immunsuppression als Grundlage einer Prädisposition zur Infektion diskutiert.

Schlußfolgerungen: Die genauen Entstehungsmechanismen des MOV sind jedoch noch nicht geklärt. Die Aufklärung der vielfachen Wechselwirkungen mit ineinander übergreifenden Vorgängen bleibt noch offen.

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  1. Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, Donaueschingenstraße 13, A-1200, Vienna

    S. Bahrami M.D. & G. Schlag

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Bahrami, S., Schlag, G. Pathophysiology of trauma — multiple organ failure. Acta Chir Austriaca 30, 325–331 (1998). https://doi.org/10.1007/BF02620088

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