Elsevier

Journal of Critical Care

Volume 62, April 2021, Pages 65-71
Journal of Critical Care

Early neuromuscular electrical stimulation reduces the loss of muscle mass in critically ill patients – A within subject randomized controlled trial

https://doi.org/10.1016/j.jcrc.2020.11.018Get rights and content

Highlights

  • Neuromuscular electrical stimulation diminishes the loss of muscle mass but not of muscle strength in critically ill patients.

  • Less reduction of muscle mass with NMES was observed in patients who are prone to lose muscle mass.

  • Obtaining a good muscle contraction was not compulsory for attenuating the loss of muscle mass.

Abstract

Purpose

To investigate the effect of Neuromuscular Electrical Stimulation (NMES) on muscle thickness, strength and morphological and molecular markers of the quadriceps.

Materials and methods

Adult critically ill patients with an expected prolonged stay received unilateral quadriceps NMES sessions for 7 consecutive days. Before and after the intervention period, quadriceps thickness was measured with ultrasound. After the intervention period, strength was assessed in cooperative patients and muscle biopsies were taken. Multivariable regression was performed to identify factors affecting muscle thickness loss.

Results

Muscle thickness decreased less in the stimulated leg (−6 ± 16% versus −12 ± 15%, p = 0.014, n = 47). Strength was comparable. Opioid administration, minimal muscle contraction and more muscle thickness loss in the non-stimulated muscle were independently associated with better muscle thickness preservation. Stimulated muscles showed a shift towards larger myofibers and higher MyHC-I gene expression. NMES did not affect gene expression of other myofibrillary proteins, MuRF-1 or atrogin-1. Signs of myofiber necrosis and inflammation were comparable for both muscles.

Conclusions

NMES attenuated the loss of muscle mass, but not of strength, in critically ill patients. Preservation of muscle mass was more likely in patients receiving opioids, patients with a minimal muscle contraction during NMES and patients more prone to lose muscle mass.

Introduction

Critically ill patients admitted to the intensive care unit (ICU) often suffer from a dramatic loss of muscle mass and strength, known as intensive care unit-acquired weakness (ICUAW) [1]. On average, patients lose about 11% of their muscle mass in the first week after ICU admission and this loss is more pronounced in patients with multiple organ failure [2,3]. It appears attractive to counteract this muscle mass loss before the patient is even able to cooperate [4]. Therefore, the effects of neuromuscular electrical stimulation (NMES) have been investigated in acutely critically ill patients [[5], [6], [7], [8], [9], [10], [11], [12], [13]]. Both Gerovasili [5] and Meesen [10] concluded that muscle mass was better preserved in groups receiving NMES as compared to control groups. However, other studies [[7], [8], [9],11] could not confirm these results. These studies are difficult to compare, mostly due to methodological heterogeneity in the assessment of muscle mass. Various outcome measures were used, including circumference measures, CT-scan and ultrasound. Other studies focused on the effect of NMES on muscle strength [6,9,11,13,14]. Routsi et al. [6] and Rodriguez et al. [9] showed that NMES resulted in a significantly better preserved muscle strength. Fischer et al. [11] showed that muscle strength was higher in the NMES group at ICU discharge, but not at hospital discharge. Kho et al. [13] and Grunow et al. [14] did not find any difference in strength between the NMES and sham treated group. A few studies investigated the effect of NMES in muscle biopsies. Dirks et al. showed that muscle fibre cross-sectional area (CSA) did not decrease in the stimulated muscles, compared to ~20% decrease in fibre CSA in the unstimulated muscles [15]. Wollersheim et al. confirmed this preservation of fibre CSA and showed a higher gene expression for myosin heavy chains in the NMES treated muscles [16]. Weber-Carstens et al. showed attenuation of atrophy in type II fibres only [17]. In addition, Strasser et al. observed signs of more synthesis and less degradation of proteins in the muscles treated with NMES [18]. None of the aforementioned studies investigated the effects of NMES on muscle thickness, muscle strength and morphological and molecular markers of muscle atrophy simultaneously.

The primary aim of this study was to investigate the effect of 7 days of unilateral NMES on quadriceps muscle thickness. The combined thickness of the rectus femoris and intermedius were used for this analysis. Secondary outcomes were muscle strength and morphological and molecular markers of muscle atrophy. In addition, factors associated with changes in muscle thickness were explored.

Section snippets

Study design

The effect of unilateral NMES in critically ill patients was assessed in a randomized controlled design. Patients were included between day 2 and day 4 after their admission to the ICU. The attending intensivist judged whether the patient was expected to stay at least 7 more days in the ICU before the patient was considered for inclusion in the study.

Randomisation

Opaque sealed envelopes were used to randomize which quadriceps muscle was selected for stimulation. Five envelopes contained a paper with

Patient characteristics and quality of NMES

Between May 2014 and September 2016, 1710 critically ill patients were screened. The consolidated standards of reporting trials (CONSORT) flow chart is depicted in Fig. 1. Fifty patients were included in the study. Three patients did not complete the study period as consent was withdrawn. Patient characteristics are shown in Table 1. The online supplement shows the patient characteristics of the subgroups (Table S1 shows the data for the patients that performed a strength test and the data for

Discussion

This study showed that NMES can attenuate muscle mass loss in critically ill patients. No differences in strength were observed. A shift towards larger myofibers and significantly higher gene expression for MyHC-I in the stimulated muscle was observed, while no differences in signs of muscle fibre necrosis or inflammation were observed in both muscles. Preservation of muscle mass was more likely in patients who received opioids, who had a poorer muscle contraction during NMES, or who were more

Limitations of the study

Our study has some limitations to address. First, our patients were not blinded for the intervention as the control muscle did not receive any sham stimulation. However, most patients were not cooperative during the intervention period. In addition, as our primary outcome is an effort-independent measure of muscle thickness performed by a blinded investigator, this is not considered to induce bias. Second, no long-term consequences or functional outcomes were investigated. Our focus was on the

Conclusions

Muscle mass was better preserved in the muscle treated with NMES as compared to the control muscle, coinciding with a shift towards larger type 1 and type 2 myofibers in the stimulated muscle as compared with the non-stimulated muscle. Muscle strength was not different between the stimulated and control muscle. Patients receiving opioids and those who exhibited more pronounced loss of muscle mass in the non-stimulated muscle benefitted most of NMES, while a good muscle contraction in all

Author contributions

Conceptualization: Gosselink, Hermans, Vanhorebeek

Data curation: Segers, Vanhorebeek

Formal analysis: Segers, Hermans, Vanhorebeek, Langer

Investigation: Segers, Charususin, Clerckx, Frickx, Demeyere, Wei, Casaer, Derde, Derese, Pauwels

Methodology: Segers, Gosselink, Hermans, Vanhorebeek, Van den Berghe

Supervision: Gosselink, Hermans, Vanhorebeek

Validation: Segers, Gosselink, Hermans, Vanhorebeek, Langer

Writing - original draft: Segers, Gosselink, Hermans, Vanhorebeek

Writing - review & editing:

Declaration of Competing Interest

None of the authors have declared any conflict of interest related to the subject of this study. The authors acknowledge DJO Global (Herentals, Belgium) for providing the neuromuscular stimulation equipment used in this study.

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