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Related Experiment Videos

Traumatic and septic shock alias post-trauma critical illness

R M Hardaway1

  • 1Texas Tech University Health Sciences Center, Department of Surgery, El Paso 79905, USA.

The British Journal of Surgery
|November 21, 1998
PubMed
Summary

A shock toxin, a thrombogenic aminophospholipid released during cell destruction, causes disseminated intravascular coagulation and organ failure in septic shock. Plasminogen activator can lyse microclots, restoring circulation.

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Disseminated intravascular coagulation in sepsis.

Seminars in thrombosis and hemostasis·2001
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A shock toxin that produces disseminated intravascular coagulation and multiple organ failure.

The American journal of the medical sciences·2001
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Traumatic shock alias posttrauma critical illness.

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A review of septic shock.

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Area of Science:

  • Cellular Biology
  • Pathophysiology
  • Medical Research

Background:

  • Increasing mortality rates in septic shock despite advances in medical care.
  • The fundamental causes of traumatic and septic shock remain incompletely understood.
  • Previous treatment strategies targeting endotoxin and host mediators have been largely unsuccessful.

Purpose of the Study:

  • To investigate the underlying cause of shock in trauma and sepsis.
  • To identify the specific agent responsible for shock pathophysiology.
  • To explore potential therapeutic interventions for shock-induced organ failure.

Main Methods:

  • Comprehensive literature review of traumatic and septic shock research from 1875 to the present.
  • Analysis of over 1000 articles detailing unsuccessful treatment attempts.

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  • Evaluation of historical and contemporary theories on shock causation.

    • Main Results:

    • Confirmation of the "shock toxin" concept, a thrombogenic aminophospholipid released from damaged cells.
    • Identification of this toxin as the cause of disseminated intravascular coagulation (DIC).
    • Demonstration that microvascular obstruction by microclots leads to multiple organ failure.

    Conclusions:

    • The identified shock toxin is a critical factor in the pathogenesis of trauma and septic shock.
    • Microclot formation due to the toxin obstructs organ microcirculation, leading to failure.
    • Plasminogen activator offers a potential therapeutic strategy to dissolve microclots and restore organ perfusion.