Acute myopathy with selective degeneration of myosin filaments following status asthmaticus treated with methylprednisolone and vecuronium

Waclawik, Andrzej J.; Sufit, Robert; Beinlich, Brad R.; Schutta, Henry S.

doi:10.1016/0960-8966(92)90022-x

Cited by 54 publications

(29 citation statements)

References 15 publications

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“…However, the characteristic feature is the loss of myosin-thick filaments. 22,29,32,35,110,111,115 Suspicion for myosin loss is raised when there is reduced or patchy reactivity on myosin adenosine triphosphatase-reacted sections. It may be present primarily in atrophic fibers, 129 making it less noticeable.…”

Section: Critical Illness Myopathymentioning

confidence: 99%

“…Earlier uncontrolled studies in asthmatics associated CIM with the use of these drugs. [10][11][12][13][14][15][16][17][18][19][20]71,[110][111][112][113][114][115] There may be a dose relationship with NMJ blockers, 21 but a dose relationship with corticosteroids is uncertain. There have been pathologically confirmed cases of CIM with myosin loss in which neither corticosteroids nor NMJ blockers were administered.…”

Section: Lacomismentioning

confidence: 99%

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Neuromuscular Disorders in Critically Ill Patients: Review and Update

Lacomis

2011

Journal of Clinical Neuromuscular Disease

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Neuromuscular disorders that are diagnosed in the intensive care unit (ICU) usually cause substantial limb weakness and contribute to ventilatory dysfunction. Although some lead to ICU admission, ICU-acquired disorders, mainly critical illness myopathy (CIM) and critical illness polyneuropathy (CIP), are more frequent and are associated with considerable morbidity. Approximately 25% to 45% of patients admitted to the ICU develop CIM, CIP, or both. Their clinical features often overlap; therefore, nerve conduction studies and electromyography are particularly helpful diagnostically, and more sophisticated electrodiagnostic studies and histopathologic evaluation are required in some circumstances. A number of prospective studies have identified risk factors for CIP and CIM, but their limitations often include the inability to separate CIM from CIP. Animal models reveal evidence of a channelopathy in both CIM and CIP, and human studies also identified axonal degeneration in CIP and myosin loss in CIM. Outcomes are variable. They tend to be better with CIM, and some patients have longstanding disabilities. Future studies of well-characterized patients with CIP and CIM should refine our understanding of risk factors, outcomes, and pathogenic mechanisms, leading to better interventions.

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Section: Critical Illness Myopathymentioning

confidence: 99%

Section: Lacomismentioning

confidence: 99%

Neuromuscular Disorders in Critically Ill Patients: Review and Update

Lacomis

2011

Journal of Clinical Neuromuscular Disease

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“…12 While myosin loss is consistently reported in this myopathy, prominent N lines have not been previously highlighted. A review of the literature reveals the presence of N lines, although usually not commented on, in other cases of acute quadriplegic myopathy, 1,4,9,17 as well as in other myopathies with myosin loss, namely congenital muscular dystrophy, 16 dermatomyositis, 3 and a myopathy associated with thrombotic thrombocytopenic purpura. 2 Hence, myosin loss, the common denominator in these myopathies, may play a role in the emergence of N lines.…”

mentioning

confidence: 96%

N lines in a myopathy with myosin loss

1998

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“…Several cases have demonstrated a loss of thick myofilating.2,6,8,1 1, 13,20,21,23,24,28 ments on muscle biopsy.8, 28 In only one previous case has an abnormal decremental response with standard repetitive stimulation (RS) been reported. 28 In addition, there has not been an attempt to correlate the clinical, electrophysiologic, pharmacologic, and histologic findings.…”

mentioning

confidence: 98%

Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids

Barohn¹,

Jackson²,

Rogers³

et al. 1994

Muscle and Nerve

112

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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.

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Acute myopathy with selective degeneration of myosin filaments following status asthmaticus treated with methylprednisolone and vecuronium

Cited by 54 publications

References 15 publications

Neuromuscular Disorders in Critically Ill Patients: Review and Update

Neuromuscular Disorders in Critically Ill Patients: Review and Update

N lines in a myopathy with myosin loss

Prolonged paralysis due to nondepolarizing neuromuscular blocking agents and corticosteroids

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