Objective: Intensive care unit-acquired weakness indicates increased morbidity and mortality. Nonexcitable muscle membrane after direct muscle stimulation develops early and predicts intensive care unit-acquired weakness in sedated, mechanically ventilated patients. A comparison of muscle histology at an early stage in intensive care unit-acquired weakness has not been done. We investigated whether nonexcitable muscle membrane indicates fast-twitch myofiber atrophy during the early course of critical illness.
Design: Prospective observational study.
Setting: Two intensive care units at Charité University Medicine, Berlin.
Patients: Patients at increased risk for development of intensive care unit-acquired weakness, indicated by Sepsis-related Organ Failure Assessment scores ≥8 on 3 of 5 consecutive days within their first week in the intensive care unit.
Measurements and Main Results: Electrophysiological compound muscle action potentials after direct muscle stimulation and muscle biopsies were obtained at median days 7 and 5, respectively. Patients with nonexcitable muscle membranes (n = 15) showed smaller median type II cross-sectional areas (p < .05), whereas type I muscle fibers did not compared with patients with preserved muscle membrane excitability (compound muscle action potentials after direct muscle stimulation ≥3.0 mV; n = 9). We also observed decreased mRNA transcription levels of myosin heavy chain isoform IIa and a lower densitometric ratio of fast-to-slow myosin heavy chain protein content.
Conclusion: We suggest that electrophysiological nonexcitable muscle membrane predicts preferential type II fiber atrophy in intensive care unit patients during early critical illness.
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From the Department of Anesthesiology and Operative Intensive Care Medicine (JB, SK, CO, AL-S, SW, CDS, SW-C), Campus Virchow-Klinikum & Campus Mitte, Charité University Medicine, Berlin, Germany; the Muscle Research Unit (JS, SS), Experimental and Clinical Research Center, a joint cooperation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Berlin, Germany; the Department of Traumatology and Reconstructive Surgery (CK), Campus-Virchow Klinikum, Charité University Medicine, Berlin, Germany; the Department of Neurosurgery with Pediatric Neurosurgery (KF), Campus-Virchow Klinikum, Charité University Medicine, Berlin, Germany; the Department of Endocrinology, Diabetes and Nutritional Medicine (JS), Campus Benjamin Franklin, Charité University Medicine, Berlin, Germany; and the Experimental and Clinical Research Center (JH, DL, JF), a joint cooperation between the Charité Medical Faculty and the Max-Delbrück Center for Molecular Medicine, Berlin, Germany and the Medical Department, Division of Cardiology, Campus Virchow-Klinikum, Charité University Medicine, Berlin, Germany.
Supported by clinical research group grant KFG 192 from the Deutsche Forschungsgemeinschaft (DFG).
Dr. Bierbrauer and Dr. Koch are equally contributing authors.
Dr. Spies received honoraria/speaking fees from Akzo, Fresenius, Braun, Baxter, Abbott, Essex, and GSK and received grants from Abott, Akzo, Aspect, Baxter, Braun, Deltex, Edwards, Fresenius, GSK, Köhler, Lilly, MSD, NovaLung, Orion, Pfizer, Pfrimmer, and Wyeth. Dr. Spranger, Dr. Spuler, and Dr. Weber-Carstens received a grant from the German Research Foundation. The Deutsche Forschungsgemeinschaft (DFG) supported the study through clinical research group grant KFG 192 and DFG FI 965/2-1 to Ms. Hamati, Ms. Lodka, and Dr. Fielitz. The remaining authors have not disclosed any potential conflicts of interest.
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