critical illness myopathy
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Etiology
- prolonged (> 7 day) stay in ICU
- risk factors
Pathology
- along with critical illness polyneuropathy, contributes to critical illness weakness
Clinical manifestations
- inability to extubate
- flaccid predominantly proximal muscle weakness
- areflexia may be present
- not associated with cognitive impairment
Laboratory
- serum creatine kinase elevated
- plasma glucose may be elevated
Diagnostic procedures
- Medical Research Council muscle scale 1st step in evalutating critical illness weakness[1]
- electromyoagraphy (EMG)
- absent or dimininished sensory responses
- low-amplitude motor units
Differential diagnosis
- glucocorticoid myopathy
- preserved reflexes, normal serum creatine kinase, EMG only mildly abnormal
Management
- supportive
- wean off glucocorticoids[1]
- see critical illness weakness
More general terms
Additional terms
References
- ↑ 1.0 1.1 1.2 Medical Knowledge Self Assessment Program (MKSAP) 16, 17, 18. American College of Physicians, Philadelphia 2012, 2015, 2017
- ↑ Griffiths RD, Hall JB. Intensive care unit-acquired weakness. Crit Care Med. 2010 Mar;38(3):779-87. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20048676
- ↑ Hermans G, De Jonghe B, Bruyninckx F, Van den Berghe G Interventions for preventing critical illness polyneuropathy and critical illness myopathy. Cochrane Database Syst Rev. 2009 Jan 21;(1):CD006832 PMID: https://www.ncbi.nlm.nih.gov/pubmed/19160304
- ↑ Chawla J, Gruener G. Management of critical illness polyneuropathy and myopathy. Neurol Clin. 2010 Nov;28(4):961-77. PMID: https://www.ncbi.nlm.nih.gov/pubmed/20816273