The horror autotoxicus and multiple-organ failure
A. E. Baue
Department of Surgery, Saint Louis University Hospital, MO.
An injury or operation with tissue injury, ischemia, and sepsis provokes a
neuroendocrine, immune, and inflammatory response to promote survival and
heal the wound. If the injury is massive or complicated by infection, the
inflammatory response may become generalized and excessive, producing organ
and tissue damage and multiple-organ failure, a modern "horror
autotoxicus." Many inflammatory mediators have been identified. In isolated
organs, the use of blocking mediators to prevent combined
ischemia-reperfusion injury is feasible. With regional ischemia, activator
attenuation may be possible. It is unclear whether blockade or modulation
of all or part of an excessive inflammatory response will be possible,
helpful, and without hazard in patients with multisystem injuries or
sepsis. Feedback loops and control mechanisms of these systems will better
define such possibilities. Employment of growth factors and other
protective agents to stimulate wound healing, infection control, and host
resistance may be more helpful. Ultimately, prevention of multiple-organ
failure requires sound surgical judgment, techniques, and organ support.
Mediators or Markers of Injury, Inflammation, and Infection (Harbingers of Doom or Predictors of Disaster) and Biologic Puzzles or Ambiguities
Baue
Arch Surg 2007;142:89-93.
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Editorial III: Corticosteroids for septic shock--a standard of care?
Bloomfield and Noble
Br J Anaesth 2004;93:178-180.
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Presence of the M-type sPLA2 receptor on neutrophils and its role in elastase release and adhesion
Silliman et al.
Am. J. Physiol. Cell Physiol. 2002;283:C1102-C1113.
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S-Nitroso Human Serum Albumin Treatment Reduces Ischemia/Reperfusion Injury in Skeletal Muscle via Nitric Oxide Release
Hallstrom et al.
Circulation 2002;105:3032-3038.
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Incidence and Reversibility of Organ Failure in the Course of Sterile or Infected Necrotizing Pancreatitis
Le Mee et al.
Arch Surg 2001;136:1386-1390.
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Computer Simulation to Study Inflammatory Response
An and Lee
Simulation Gaming 2001;32:344-361.
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Is Interleukin 6 an Early Marker of Injury Severity Following Major Trauma in Humans?
Gebhard et al.
Arch Surg 2000;135:291-295.
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New Mechanisms by Which Secretory Phospholipase A2 Stimulates Neutrophils to Provoke the Release of Cytotoxic Agents
Zallen et al.
Arch Surg 1998;133:1229-1233.
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Limitations of Revascularization in Acute Ischemia-Reperfusion Syndromes
Perry
PERSPECT VASC SURG ENDOVASC THER 1996;9:63-66.