New Approaches to Critical Illness Polyneuromyopathy: High-Resolution Neuromuscular Ultrasound Characteristics and Cytok
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ORIGINAL WORK
New Approaches to Critical Illness Polyneuromyopathy: High‑Resolution Neuromuscular Ultrasound Characteristics and Cytokine Profiling Anna Lena Fisse1* , Caroline May2, Jeremias Motte1, Xiomara Pedreiturria1, Thomas G. K. Breuer3, Christiane Schneider‑Gold1, Katrin Marcus2, Ralf Gold1, Min‑Suk Yoon4† and Kalliopi Pitarokoili1† © 2020 The Author(s)
Abstract Background: Diagnosis of intensive care unit acquired weakness (ICUAW) is challenging. Pathogenesis of underly‑ ing critical illness polyneuromyopathy (CIPNM) remains incompletely understood. This exploratory study investigated whether longitudinal neuromuscular ultrasound examinations and cytokine analyses in correlation to classical clinical and electrophysiological assessment contribute to the understanding of CIPNM. Methods: Intensive care unit patients were examined every 7 days until discharge from hospital. Clinical status, nerve conduction studies, electromyography as well as ultrasound of peripheral nerves and tibial anterior muscle were performed. Cytokine levels were analyzed by a bead-based multiplex assay system. Results: Of 248 screened patients, 35 patients were included at median of 6 days (IQR: 8) after admission to intensive care unit. Axonal damage was the main feature of CIPNM. At the peak of CIPNM (7 days after inclusion), nerve ultra‑ sound showed cross-sectional area increase of tibial nerve as a sign of inflammatory edema as well as hypoechoic nerves as a possible sign of inflammation. Cytokine analyses showed signs of monocyte and macrophage activation at this stage. Fourteen days after inclusion, cytokines indicated systemic immune response as well as profiles associ‑ ated to neovascularization and regeneration. Conclusions: Exploratory neuromuscular ultrasound and cytokine analyses showed signs of inflammation like mac‑ rophage and monocyte activation at the peak of CIPNM followed by a systemic immune response parallel to axonal damage. This underlines the role of both axonal damage and inflammation in pathogenesis of CIPNM. Keywords: Intensive care unit acquired weakness, Critical illness polyneuropathy, Critical illness myopathy, Critical illness polyneuromyopathy, Nerve ultrasound, Cytokines
*Correspondence: [email protected] † Min-Suk Yoon and Kalliopi Pitarokoili have contributed equally to this work. 1 Department of Neurology, St. Josef‑Hospital, Ruhr-University Bochum, Gudrunstrasse 56, 44791 Bochum, Germany Full list of author information is available at the end of the article
Introduction Intensive care unit acquired weakness (ICUAW) is a frequent problem in intensive care medicine and occurs in up to 67% of patients who are mechanically ventilated for more than 10 days [1]. The defining clinical symptom of ICUAW is a generalized symmetric muscle weakness, leading to a flaccid tetraparesis [2]. This results in prolonged ventilator dependency, prolonged hospitalization
and rehabilitation [3] as well as to worse clinical outcome [4]. Causes of ICUAW are critical illness polyneuropathy and critical illne
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