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Pseudofracture: An Acute Peripheral Tissue Trauma Model
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Pathophysiology in patients with polytrauma.

H-C Pape1, E E Moore2, T McKinley3

  • 1Department of Trauma, University Hospital Zurich, University of Zurich, Raemistrasse 100, 8091 Zurich, Switzerland.

Injury
|May 16, 2022
PubMed
Summary
This summary is machine-generated.

Polytrauma pathophysiology involves complex immune responses and interactions between shock, coagulopathy, and injury. Understanding these pathways is crucial for effective patient management and surgical strategies.

Keywords:
Damage associated molecular patternsEndothelial permeabilityFour pathogenetic cyclesPolytrauma physiologySafe definitive surgerySecond hit phenomenonSoft tissue injury

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Area of Science:

  • Trauma Pathophysiology
  • Immunology
  • Surgical Management

Background:

  • Historically, hypoperfusion and endothelial permeability were primary focus in polytrauma.
  • Emerging evidence highlights the critical role of the innate immune response in modulating organ response.
  • The
  • genetic storm
  • theory implicates neutrophil activation post-injury.

Purpose of the Study:

  • To review the complex pathophysiology of polytrauma.
  • To explore the interplay of immune response, coagulation, and inflammation.
  • To discuss the role of staged surgeries in managing major fractures.

Main Methods:

  • Literature review of polytrauma pathophysiology.
  • Analysis of recent multi-center studies and theories.
  • Synthesis of interactions between pathogenetic cycles.

Main Results:

  • Innate immune response is as crucial as hypoperfusion in polytrauma.
  • Second hit phenomenon can be triggered by DAMPs and PAMPs.
  • Interactions between shock, coagulopathy, temperature loss, and soft tissue injuries significantly modify outcomes.

Conclusions:

  • Understanding the complex interplay of factors is key to managing polytrauma.
  • Staged surgeries offer a safer alternative for definitive treatment of major fractures.
  • The review provides a detailed summary of these critical pathogenetic mechanisms.