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Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids
Author(s) -
Barohn Richard J.,
Jackson Carlayne E.,
Rogers Susan J.,
Ridings Larry W.,
McVey April L.
Publication year - 1994
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/mus.880170613
Subject(s) - medicine , muscle weakness , weakness , anesthesia , muscle biopsy , discontinuation , paralysis , neuromuscular junction , compound muscle action potential , neuromuscular blocking agents , rhabdomyolysis , surgery , biopsy , electrophysiology , neuroscience , biology
The long‐term use of nondepolarizing neuromuscular blocking agents (ND‐NMBA) has recently been implicated as a cause of prolonged muscle weakness, although the site of the lesion and the predisposing factors have been unclear. We report 3 patients (age 37–52 years) with acute respiratory insufficiency who developed prolonged weakness following the discontinuation of ND‐NMBAs. Two patients also received intravenous corticosteroids. Renal function was normal but hepatic function was impaired in all patients, and all had acidosis. Electrophysiologic studies revealed low amplitude compound motor action potentials, normal sensory studies, and fibrillations. Repetitive stimulation at 2 Hz showed a decremental response in 2 patients. The serum vecuronium level measured in 1 patient 14 days after the drug had been discontinued was 172 ng/mL. A muscle biopsy in this patient showed loss of thick, myosin filaments. The weakness in these patients is due to pathology at both the neuromuscular junction (most likely due to ND‐NMBA) and muscle (most likely due to corticosteroids). Hepatic dysfunction and acidosis are contributing risk factors. © 1994 John Wiley & Sons, Inc.