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Acute corticosteroid myopathy in intensive care patients
Author(s) -
Hanson Philippe,
Dive Alain,
Brucher JeanMarie,
Bisteau Michel,
Dangoisse Michel,
Deltombe Thierry
Publication year - 1997
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/(sici)1097-4598(199711)20:11<1371::aid-mus4>3.0.co;2-7
Subject(s) - medicine , myopathy , propofol , anesthesia , muscle biopsy , electromyography , intensive care unit , mechanical ventilation , neuromuscular blocking agents , biopsy , physical medicine and rehabilitation
Several recent studies have attributed the occurrence of acute myopathy in intensive care unit patients to the combination of corticosteroids and neuromuscular junction blocking agents (NMBAs) used for mechanical ventilation. We present 4 patients who developed acute myopathy after administration of high doses of glucocorticoids during sedation with propofol without any NMBAs. All patients had elevated creatine kinase levels. Electrophysiological studies indicated normal motor and sensory nerve conduction velocities but reduced motor nerve response amplitudes. Needle electromyography identified abnormal spontaneous activity; motor unit potentials were polyphasic of low amplitude and short duration, characteristic of a myopathic process. Muscle biopsy demonstrated a prominent acute necrotizing myopathy in all 4 patients with a loss of thick filaments. Our observations support glucocorticoids rather than NMBAs as the main offending drug in acute corticosteroid myopathy. The predisposing factor should be the hypersensitivity of paralyzed muscles to corticosteroids regardless of the drug inducing paralysis: NMBAs or propofol. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 1371–1380, 1997