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Organ failure in the ICU: cellular alterations
James N Fullerton1, Mervyn Singer
1Division of Medicine, Centre for Clinical Pharmacology, Rayne Institute, London, United Kingdom.
Seminars in Respiratory and Critical Care Medicine
|October 13, 2011
Summary
Multiple organ failure involves cellular dysfunction without significant cell death, suggesting a metabolic shutdown due to impaired mitochondrial energy production. Recovery of mitochondrial function precedes patient recovery in sepsis.
Area of Science:
- Physiology
- Biochemistry
- Cellular Biology
Background:
- Multiple organ failure (MOF) is characterized by physiological and biochemical abnormalities.
- MOF involves cellular perturbations but lacks significant cell death.
- Oxygen is available but its utilization is impaired in MOF.
Purpose of the Study:
- To review the paradigm of metabolic shutdown in MOF.
- To discuss the role of mitochondrial dysfunction in MOF.
- To explore the recovery of mitochondrial function in sepsis.
Main Methods:
- Review of temporal changes in oxygen utilization during sepsis.
- Examination of evidence for mitochondrial derangements.
- Analysis of mitochondrial function recovery preceding clinical recovery.
Main Results:
- Cellular abnormalities in MOF are reconciled with limited cell death and impaired oxygen utilization.
- Metabolic shutdown triggered by decreased mitochondrial energy production is a valid paradigm for MOF.
- Recovery of mitochondrial function precedes clinical improvement in septic patients.
Conclusions:
- Metabolic shutdown is a key mechanism in multiple organ failure.
- Mitochondrial dysfunction plays a critical role in the pathophysiology of sepsis-induced MOF.
- Restoration of mitochondrial energy production is essential for patient recovery.
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