Steffen Weber-Carstens and Joachim Spranger

Summary

Critical illness myopathy (CIM) is a major complication in critically ill intensive care unit (ICU) patients. The pathogenesis is basically unclear, although the clinical impact is considerable with prolonged duration of ICU care and increased morbidity and mortality in these patients. Preliminary electrophysiological data from our group indicate that CIM develops early within the first 5 days of critical illness. Indeed, early diagnosis could facilitate preventative or therapeutic strategies. The mechanisms are likely to involve cellular alterations in carbohydrate and lipid metabolism including mitochondrial dysfunction. We aim to clarify the interplay between CIM, systemic inflammatory response syndrome (SIRS), and defective metabolism by investigating molecular markers of tissue-specific and whole-body inflammation, insulin sensitivity, and metabolic dysfunction in tissue biopsies, microdialysis samples, and plasma from SIRS patients. We will thereby prospectively investigate the relationship between CIM and SIRS and will identify markers for CIM in SIRS patients. We also speculate that impaired insulin sensitivity is likely to contribute to CIM and assume that improved insulin sensitivity may lower the incidence of CIM. If this hypothesis is supported by our prospective observational data, we will perform a pilot trial, to test whether isovolumetric electrical muscle stimulation (EMS) that improves insulin sensitivity, can be applied to critical ill patients and whether this treatment is associated with a beneficial outcome.