nisms and the different causes of acute weakness in patients in an intensive care unit (ICU). Interestingly severe systemic illness in and of itself was found to cause AQM. 2 The following case report underlines another important point, the possible recurrence of AQM in patients who need to be retreated in an ICU.
This 48-year-old woman was intubated because of acute asthmatic attack. Between days 1 and 4, the patient received pancuronium bromide (total amount, 120 mg), methylprednisolone (125 mg every 6 h), theophylline, erythromycine, and omeprazolum intravenously. The initial specimen of arterial blood showed respiratory acidosis. On day 3, we observed a peak of creatine kinase (CK) (2500 U/L). A flaccid tetraparesis with absent stretch reflexes was noticed at day 6. Extubation was possible at day 10. The weakness improved slowly over 3 months. A small aneurysm of the middle cerebral artery was discovered by cerebral magnetic resonance imaging, and a surgical clipping was performed 3 months later. Despite 12 mg of vecuronium and 250 mg of methylprednisolone given intravenously, no weakness or changes of stretch reflexes were observed. Two years later, the patient was reintubated because of respiratory failure. Between days 1 and 5, the patient received methylprednisolone (125 mg every 6 h), theophylline, erythromycine, ceftriaxone, and a single dose of vecuronium (6 mg) intravenously. The specimen of arterial blood showed again respiratory acidosis. On day 6, we observed a peak of CK (4100 U/L). A generalized weakness with absent stretch reflexes was noticed at day 10. At this time, a muscle biopsy revealed diffuse atrophic fibers and rare necrotic fibers. By immunocytochemistry, 90% of the atrophic fibers reacted for fast myosin and a 30% for slow myosin. The presence of developmental and neonatal myosins in 50% of atrophic fibers was consistent with regeneration. This biopsy demonstrates the selective loss of myosin filaments. The patient could be weaned from the respirator at day 46 and could leave the hospital after 80 days, with an almost complete recovery.
The evidence of calpain-mediated proteolysis found in AQM with myosin deficiency greatly improves our understanding of the illness. However, the reports of AQM patients not exposed to corticosteroids or neuromuscular blocking agents, 2 and our case of recurrent AQM further complicate the problem of the triggering events. It is suggested that systemic metabolic failure with respiratory acidosis seems to play a role.