Conclusion
Muscle weakness following critical illness is a significant clinical problem. It is likely to contribute to the continuing morbidity and mortality of prolonged ICU stay. However, its pathophysiology remains poorly understood. Several major issues remain unresolved. These include the question of whether critical illness myopathy is a distinct illness or represents a continuum of skeletal MOF.
Also unresolved is the differentiation of a postulated specific, sepsis-related muscle failure from other causes of muscle dysfunction in the critically ill. In particular, differences between diffuse atrophy, the normal ageing process, and sepsis-induced injury need to be explored. Finally, the question of possible mitochondrial DNA damage in human sepsis should be addressed. Normal human ageing is characterized by gradual damage to mitochondrial DNA. Could the long-term adverse consequences of prolonged critical care be partially a result of an increase in this process — a sort of ‘ageing in the fast lane’?
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Keywords
- Mitochondrial Dysfunction
- Critical Illness
- Intensive Insulin Therapy
- Myosin Filament
- Critical Illness Polyneuropathy
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.
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Kothmann, E., Baudouin, S.V. (2006). Mitochondrial Dysfunction and Critical Illness Myopathy. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine. Yearbook of Intensive Care and Emergency Medicine, vol 2006. Springer, Berlin, Heidelberg. https://doi.org/10.1007/3-540-33396-7_8
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