ArticleClinical neurophysiology practice2024
Diagnosis of "intensive care unit-acquired weakness" and "critical illness myopathy": Do the diagnostic criteria need to be revised?
Article in Clinical neurophysiology practice, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed.
- ICU-Acquired Weakness: Diagnostic Yield of a Clinical Diagnosis with Additional Quantification of Myosin Loss in Adult Critically Ill Patients.Journal of clinical medicine · 2026Article
- Analysis of the factors related to the knowledge, attitudes, and practices of nurses towards intensive care unit-acquired weakness: a cross-sectional survey.BMC nursing · 2026Article
- Review
- Neurophysiology and muscle histopathology in ICU-acquired muscle weakness: Lessons learned from COVID-19.Clinical neurophysiology practice · 2025Article
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3 authors.
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Abstract
Objectives: Intensive care unit acquired weakness (ICUAW) is a clinical diagnosis and an umbrella term for acquired weakness due to neuromuscular disorders such as critical illness myopathy (CIM) but also muscular inactivity/atrophy. Without a clear understanding of the distinct aetiology, it seems difficult to predict outcomes of ICUAW and to test and apply effective future treatments. The present study contrasts ICUAW with CIM and assesses the diagnostic and clinical relevance for affected patients. Methods: Data from a previous prospective cohort study investigating critically ill COVID-19 patients was analysed in a retrospective fashion. Patients were examined ten days after intubation with clinical assessment, nerve conduction studies, electromyography and muscle biopsy. Mortality was assessed during critical illness and at three months after hospital discharge. ICUAW and CIM were diagnosed according to the current diagnostic guidelines. Results: In this patient sample (n = 22), 92 % developed ICUAW, 55 % developed ICUAW and CIM, and 36 % had ICUAW but did not develop CIM. Overall, 27 % patients died during their stay in the intensive care unit. At three months after discharge, there were no further deaths, but in 14 % of patients the outcome was unknown. The diagnosis of CIM was more strongly associated with death during critical illness than ICUAW. No patient with ICUAW who did not fulfil the criteria for CIM died. Both clinical and electrophysiological criteria showed excellent sensitivity for CIM diagnosis, but only electrophysiological criteria had a high specificity. Determination of the myosin:actin ratio showed neither high sensitivity nor specificity for the diagnosis of CIM. Conclusions: The results of the present study support that ICUAW is a non-specific clinical diagnosis of low predictive power with regard to mortality. Further, diagnosing "ICUAW" seems also of little research value for both exploring the aetiology and pathophysiology of muscle weakness in critically ill patients and for evaluating potential treatment effects. Thus, more specific diagnoses such as CIM are more appropriate. Within the different diagnostic criteria for CIM, electrophysiological studies are the most sensitive and specific examinations compared to clinical and muscle tissue assessment. Significance: Avoiding an overarching diagnosis of "ICUAW" and instead focusing on specific diagnoses appears to have several relevant consequences: more precise diagnosis making, more accurate referral to aetiology and pathophysiology, improved outcome prediction, and development of more appropriate treatments.
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