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Acute corticosteroid myopathy in intensive care patients
P Hanson1, A Dive, J M Brucher
1Department of Physical Medicine, Mont-Godinne University Hospital UCL, Yvoir, Belgium.
Muscle & Nerve
|October 28, 1997
Summary
High-dose glucocorticoids, not neuromuscular blockers, may cause acute myopathy in ICU patients. Muscle damage was observed even without neuromuscular junction blocking agents, suggesting steroid hypersensitivity in paralyzed muscles.
Area of Science:
- Intensive Care Medicine
- Neurology
- Pathology
Background:
- Acute myopathy in intensive care unit (ICU) patients is often linked to corticosteroids and neuromuscular junction blocking agents (NMBAs).
- Recent studies suggest a potential association between these agents and critical illness myopathy.
Purpose of the Study:
- To investigate the role of glucocorticoids versus NMBAs in the development of acute myopathy.
- To identify the primary causative agent in corticosteroid-induced myopathy.
Main Methods:
- Case series of 4 ICU patients who developed acute myopathy.
- Analysis of clinical data, creatine kinase levels, electrophysiological studies (nerve conduction, electromyography), and muscle biopsy results.
- Comparison of outcomes in patients receiving high-dose glucocorticoids with propofol sedation versus those receiving NMBAs.
Main Results:
- All 4 patients exhibited elevated creatine kinase levels and characteristic myopathic changes on electromyography.
- Muscle biopsies revealed acute necrotizing myopathy with loss of thick filaments.
- Electrophysiological studies showed reduced motor nerve response amplitudes but normal nerve conduction velocities.
Conclusions:
- Glucocorticoids, rather than NMBAs, are likely the primary cause of acute corticosteroid myopathy.
- Muscle hypersensitivity to corticosteroids, irrespective of the paralyzing agent (NMBAs or propofol), may be a key predisposing factor.