Hyperglycemia and acquired weakness in critically ill patients: potential mechanisms
Open Access
- 1 January 2009
- journal article
- editorial
- Published by Springer Nature in Critical Care
- Vol. 13 (2) , 125
Abstract
Critical illness polyneuropathy/critical illness myopathy (CIP/CIM) is a major cause of mortality and long-term morbidity in critically ill patients, but the true incidence and prevalence of these syndromes are not known. Hermans and colleagues show that when intensive insulin therapy is used as part of routine clinical practice in the intensive care unit, the incidence of CIP/CIM as determined by electrophysiologic testing is reduced. Our understanding of the mechanisms responsible for inducing prolonged weakness in intensive care unit patients is limited, and the role of hyperglycemia in modulating these processes is unknown. Intensive insulin therapy currently remains the only effective therapeutic intervention that has been shown to reduce the incidence of CIP/CIM.Keywords
This publication has 15 references indexed in Scilit:
- Benefits of intensive insulin therapy on neuromuscular complications in routine daily critical care practice: a retrospective studyCritical Care, 2009
- Mechanism of induction of muscle protein loss by hyperglycaemiaExperimental Cell Research, 2009
- Contraction and Cation Contents of Skeletal Soleus and EDL Muscles in Age‐Matched Control and Diabetic RatsAnnals of the New York Academy of Sciences, 2006
- Intensive Insulin Therapy in the Medical ICUNew England Journal of Medicine, 2006
- Short‐term hyperglycemia produces oxidative damage and apoptosis in neuronsThe FASEB Journal, 2005
- Activation of caspase-3 is an initial step triggering accelerated muscle proteolysis in catabolic conditionsJournal of Clinical Investigation, 2004
- Intensive Insulin Therapy in Critically Ill PatientsNew England Journal of Medicine, 2001
- Normalizing mitochondrial superoxide production blocks three pathways of hyperglycaemic damageNature, 2000
- Effect of physical training on mitochondrial function in skeletal muscle of normal and diabetic ratsMetabolism, 1996
- Skeletal Muscle in Alloxan Diabetes: A Comparison of Isometric Contractions in Fast and Slow MuscleDiabetes, 1983