Intensive Care Unit-acquired Weakness Patients Research Articles

Reliability, validity and usability of the K-force® grip dynamometer to evaluate handgrip-strength in patients with intensive care unit-acquired weakness.

Handgrip dynamometry is recognised as a method for evaluating volitional muscle strength in the intensive care, but conventional handgrip dynamometers cannot accurately measure grip strength in very weak patients. The aim of this study was to determine the reliability, validity and usability of the K-force® grip in patients with intensive care unit-acquired weakness. Evaluation of measurement properties of the K-force® grip. Two Intensive Care Units in The Netherlands. Patients diagnosed with intensive care unit-acquired weakness according to a Medical Research Council sum score <48. Intra- and inter-rater reliability of the K-force® grip were assessed using the intraclass correlation coefficient. Concurrent validity was examined using calibration weights. The usability was evaluated with the System Usability Scale. Intra-rater reliability showed an intraclass correlation coefficient of 0.987 for the dominant hand and 0.972 for the non-dominant hand. Inter-rater reliability showed coefficients of 0.944 for the dominant hand and 0.942 for the non-dominant hand. There was a perfect correlation (r = 1) between the K-force® grip and the calibration weights. The usability of the K-force® grip was rated excellent by 11 healthcare professionals with a System Usability Scale score of 86. The K-force® grip is a promising new tool for the evaluation of muscle strength in intensive care unit-acquired weakness patients who are too weak to use conventional hand dynamometers.

PEI/MMNs@LNA-542 nanoparticles alleviate ICU-acquired weakness through targeted autophagy inhibition and mitochondrial protection.

Intensive care unit-acquired weakness (ICU-AW) is prevalent in critical care, with limited treatment options. Certain microRNAs, like miR-542, are highly expressed in ICU-AW patients. This study investigates the regulatory role and mechanisms of miR-542 in ICU-AW and explores the clinical potential of miR-542 inhibitors. ICU-AW models were established in C57BL/6 mice through cecal ligation and puncture (CLP) and in mouse C2C12 myoblasts through TNF-α treatment. In vivo experiments demonstrated decreased muscle strength, muscle fiber atrophy, widened intercellular spaces, and increased miR-542-3p/5p expression in ICU-AW mice model. In vitro experiments indicated suppressed ATG5, ATG7 and LC3II/I, elevated MDA and ROS levels, decreased SOD levels, and reduced MMP in the model group. Similar to animal experiments, the expression of miR-542-3p/5p was upregulated. Gel electrophoresis explored the binding of polyethyleneimine/mesoporous silica nanoparticles (PEI/MMNs) to locked nucleic acid (LNA) miR-542 inhibitor (LNA-542). PEI/MMNs@LNA-542 with positive charge (3.03 ± 0.363 mV) and narrow size (206.94 ± 6.19 nm) were characterized. Immunofluorescence indicated significant internalization with no apparent cytotoxicity. Biological activity, examined through intraperitoneal injection, showed that PEI/MMNs@LNA-542 alleviated muscle strength decline, restored fiber damage, and recovered mitochondrial injury in mice. In conclusion, PEI/MMNs nanoparticles effectively delivered LNA-542, targeting ATG5 to inhibit autophagy and alleviate mitochondrial damage, thereby improving ICU-AW.

SPSB1-mediated inhibition of TGF-β receptor-II impairs myogenesis in inflammation.

Sepsis-induced intensive care unit-acquired weakness (ICUAW) features profound muscle atrophy and attenuated muscle regeneration related to malfunctioning satellite cells. Transforming growth factor beta (TGF-β) is involved in both processes. We uncovered an increased expression of the TGF-β receptor II (TβRII)-inhibitor SPRY domain-containing and SOCS-box protein 1 (SPSB1) in skeletal muscle of septic mice. We hypothesized that SPSB1-mediated inhibition of TβRII signalling impairs myogenic differentiation in response to inflammation. We performed gene expression analyses in skeletal muscle of cecal ligation and puncture- (CLP) and sham-operated mice, as well as vastus lateralis of critically ill and control patients. Pro-inflammatory cytokines and specific pathway inhibitors were used to quantitate Spsb1 expression in myocytes. Retroviral expression plasmids were used to investigate the effects of SPSB1 on TGF-β/TβRII signalling and myogenesis in primary and immortalized myoblasts and differentiated myotubes. For mechanistical analyses we used coimmunoprecipitation, ubiquitination, protein half-life, and protein synthesis assays. Differentiation and fusion indices were determined by immunocytochemistry, and differentiation factors were quantified by qRT-PCR and Western blot analyses. SPSB1 expression was increased in skeletal muscle of ICUAW patients and septic mice. Tumour necrosis factor (TNF), interleukin-1β (IL-1β), and IL-6 increased the Spsb1 expression in C2C12 myotubes. TNF- and IL-1β-induced Spsb1 expression was mediated by NF-κB, whereas IL-6 increased the Spsb1 expression via the glycoprotein 130/JAK2/STAT3 pathway. All cytokines reduced myogenic differentiation. SPSB1 avidly interacted with TβRII, resulting in TβRII ubiquitination and destabilization. SPSB1 impaired TβRII-Akt-Myogenin signalling and diminished protein synthesis in myocytes. Overexpression of SPSB1 decreased the expression of early (Myog, Mymk, Mymx) and late (Myh1, 3, 7) differentiation-markers. As a result, myoblast fusion and myogenic differentiation were impaired. These effects were mediated by the SPRY- and SOCS-box domains of SPSB1. Co-expression of SPSB1 with Akt or Myogenin reversed the inhibitory effects of SPSB1 on protein synthesis and myogenic differentiation. Downregulation of Spsb1 by AAV9-mediated shRNA attenuated muscle weight loss and atrophy gene expression in skeletal muscle of septic mice. Inflammatory cytokines via their respective signalling pathways cause an increase in SPSB1 expression in myocytes and attenuate myogenic differentiation. SPSB1-mediated inhibition of TβRII-Akt-Myogenin signalling and protein synthesis contributes to a disturbed myocyte homeostasis and myogenic differentiation that occurs during inflammation.

Effects of mechanical in-exsufflation in preventing postextubation acute respiratory failure in intensive care acquired weakness patients: a randomized controlled trial.

We hypothesized that the use of mechanical insufflation-exsufflation can reduce the incidence of acute respiratory failure within the 48-hour post-extubation period in intensive care unit-acquired weakness patients. This was a prospective randomized controlled open-label trial. Patients diagnosed with intensive care unit-acquired weakness were consecutively enrolled based on a Medical Research Council score ≤ 48/60. The patients randomly received two daily sessions; in the control group, conventional chest physiotherapy was performed, while in the intervention group, chest physiotherapy was associated with mechanical insufflation-exsufflation. The incidence of acute respiratory failure within 48 hours of extubation was evaluated. Similarly, the reintubation rate, intensive care unit length of stay, mortality at 28 days, and survival probability at 90 days were assessed. The study was stopped after futility results in the interim analysis. We included 122 consecutive patients (n = 61 per group). There was no significant difference in the incidence of acute respiratory failure between treatments (11.5% control group versus 16.4%, intervention group; p = 0.60), the need for reintubation (3.6% versus 10.7%; p = 0.27), mean length of stay (3 versus 4 days; p = 0.33), mortality at Day 28 (9.8% versus 15.0%; p = 0.42), or survival probability at Day 90 (21.3% versus 28.3%; p = 0.41). Mechanical insufflation-exsufflation combined with chest physiotherapy seems to have no impact in preventing postextubation acute respiratory failure in intensive care unit-acquired weakness patients. Similarly, mortality and survival probability were similar in both groups. Nevertheless, given the early termination of the trial, further clinical investigation is strongly recommended. NCT01931228.

Establishment and validation of a risk prediction model for intensive care unit-acquired weakness

To explore the risk factors of intensive care unit-acquired weakness (ICU-AW), and to establishment and verify its risk prediction model. A modeling group of 231 patients who met the inclusion criteria and were admitted to the intensive care unit (ICU) of the First Hospital of Jiaxing from July 2019 to June 2020 was collected by convenience sampling method. According to whether they developed ICU-AW, they were divided into ICU-AW group (55 cases) and non ICU-AW group (176 cases). The clinical data were collected concerning patients' individual information, disease-related factors, treatment-related factors and laboratory indicators, and the differences of the above indexes between two groups were compared. Logistic regression was used to analyze the ICU-AW risk factors and a risk prediction model was constructed. Calculate the area under ROC curve (AUC) to test the prediction effect of the model. At the same time, 60 patients who admitted to ICU from July to October 2020 and met the standards were collected to verify the model. Compared with non ICU-AW group, there were more males in ICU-AW group [61.8% (34/55) vs. 44.3% (78/176), P < 0.05], with higher levels of systemic inflammatory response syndrome (SIRS), sepsis, immobilization and the use of neuromuscular blockers [SIRS: 30.9% (17/55) vs. 3.4% (6/176), sepsis: 12.7% (7/55) vs. 2.3% (4/176), immobilization: 72.7% (40/55) vs. 39.2% (69/176), the use of neuromuscular blockers: 50.9% (28/55) vs. 14.2% (25/176), all P < 0.05], and acute physiology and chronic health evaluation II (APACHE II) score, blood lactic acid level and duration of mechanical ventilation, length of hospital stay were all increased [APACHE II score: 18 (15, 24) vs. 12 (8, 17), blood lactic acid (mmol/L): 2 (1, 2) vs. 1 (1, 2), duration of mechanical ventilation (days): 7 (4, 12) vs. 2 (2, 5), length of hospital stay (days): 10 (6, 16) vs. 5 (3, 9), all P < 0.05]. SIRS, APACHE II score, duration of mechanical ventilation and blood lactic acid were included to construct a risk prediction model [odds ratio (OR) values were 4.835, 1.083, 1.210, 1.790, P values were 0.018, 0.013, 0.015, 0.013]. The model equation was P = exp [-5.207+(1.576×SIRS)+(0.079×APACHE II)+(0.191×duration of mechanical ventilation)+(0.582×blood lactic acid)]. Internal verification: Calibration diagram showed the calibration curve above the ideal curve, AUC = 0.888, 95% confidence interval (95%CI) was 0.839-0.938; when the cut-off value was 0.166, the sensitivity was 89.1%, the specificity was 75.6%, and the maximum index was 0.649. External verification: Calibration diagram showed that the calibration curve was above the ideal curve, and the plotted AUC = 0.853, 95%CI was 0.753-0.953. When the cut-off value of the corresponding predictive risk value was 0.367, the sensitivity was 68.8%, the specificity was 86.4%, and the maximum approximate index was 0.552. The risk prediction model of ICU-AW constructed in this study has good consistency and prediction efficiency, which can provide reference for medical personnel to identify high-risk groups of ICU-AW patients in the early stage and provide targeted interventions in advance.

Sepsis induces interleukin 6, gp130/JAK2/STAT3, and muscle wasting

BackgroundSepsis and inflammation can cause intensive care unit‐acquired weakness (ICUAW). Increased interleukin‐6 (IL‐6) plasma levels are a risk factor for ICUAW. IL‐6 signalling involves the glycoprotein 130 (gp130) receptor and the JAK/STAT‐pathway, but its role in sepsis‐induced muscle wasting is uncertain. In a clinical observational study, we found that the IL‐6 target gene, SOCS3, was increased in skeletal muscle of ICUAW patients indicative for JAK/STAT‐pathway activation. We tested the hypothesis that the IL‐6/gp130‐pathway mediates ICUAW muscle atrophy.MethodsWe sequenced RNA (RNAseq) from tibialis anterior (TA) muscle of cecal ligation and puncture‐operated (CLP) and sham‐operated wildtype (WT) mice. The effects of the IL‐6/gp130/JAK2/STAT3‐pathway were investigated by analysing the atrophy phenotype, gene expression, and protein contents of C2C12 myotubes. Mice lacking Il6st, encoding gp130, in myocytes (cKO) and WT controls, as well as mice treated with the JAK2 inhibitor AG490 or vehicle were exposed to CLP or sham surgery for 24 or 96 h.ResultsAnalyses of differentially expressed genes in RNAseq (≥2‐log2‐fold change, P < 0.01) revealed an activation of IL‐6‐signalling and JAK/STAT‐signalling pathways in muscle of septic mice, which occurred after 24 h and lasted at least for 96 h during sepsis. IL‐6 treatment of C2C12 myotubes induced STAT3 phosphorylation (three‐fold, P < 0.01) and Socs3 mRNA expression (3.1‐fold, P < 0.01) and caused myotube atrophy. Knockdown of Il6st diminished IL‐6‐induced STAT3 phosphorylation (−30.0%; P < 0.01), Socs3 mRNA expression, and myotube atrophy. JAK2 (− 29.0%; P < 0.01) or STAT3 inhibition (−38.7%; P < 0.05) decreased IL‐6‐induced Socs3 mRNA expression. Treatment with either inhibitor attenuated myotube atrophy in response to IL‐6. CLP‐operated septic mice showed an increased STAT3 phosphorylation and Socs3 mRNA expression in TA muscle, which was reduced in septic Il6st‐cKO mice by 67.8% (P < 0.05) and 85.6% (P < 0.001), respectively. CLP caused a loss of TA muscle weight, which was attenuated in Il6st‐cKO mice (WT: −22.3%, P < 0.001, cKO: −13.5%, P < 0.001; WT vs. cKO P < 0.001). While loss of Il6st resulted in a reduction of MuRF1 protein contents, Atrogin‐1 remained unchanged between septic WT and cKO mice. mRNA expression of Trim63/MuRF1 and Fbxo32/Atrogin‐1 were unaltered between CLP‐treated WT and cKO mice. AG490 treatment reduced STAT3 phosphorylation (−22.2%, P < 0.05) and attenuated TA muscle atrophy in septic mice (29.6% relative reduction of muscle weight loss, P < 0.05). The reduction in muscle atrophy was accompanied by a reduction in Fbxo32/Atrogin‐1‐mRNA (−81.3%, P < 0.05) and Trim63/MuRF1‐mRNA expression (−77.6%, P < 0.05) and protein content.ConclusionsIL‐6 via the gp130/JAK2/STAT3‐pathway mediates sepsis‐induced muscle atrophy possibly contributing to ICUAW.

Risk factors and diagnostic methods of intensive care unit-acquired weakness

To explore the risk factors of intensive care unit-acquired weakness (ICU-AW) and the characteristics of Medical Research Council (MRC) score and electromyogram. A case control study was conducted. Patients with mechanical ventilation ≥ 7 days and MRC score admitted to department of respiratory and critical care medicine of China-Japan Friendship Hospital from September 2018 to January 2020 were enrolled, and they were divided into ICU-AW group (MRC score < 48) and non-ICU-AW group (MRC score ≥ 48) according to MRC score. The general situation, past medical history, related risk factors, MRC score, respiratory support mode, laboratory examination results, electromyogram examination results, ICU-AW related treatment, outcome and length of ICU stay were collected, and the differences between the two groups were compared. The risk factors of ICU-AW were analyzed by binary multivariate Logistic regression, and the characteristics of MRC score and electromyogram were analyzed. A total of 60 patients were enrolled in the analysis, including 17 patients in ICU-AW group and 43 patients in non-ICU-AW group. Univariate analysis showed that there were significant differences in acute physiology and chronic health evaluation II (APACHE II) score, sequential organ failure assessment (SOFA) score, brain natriuretic peptide (BNP), blood urea nitrogen (BUN) on the first day of ICU admission and the ratio of invasive mechanical ventilation between ICU-AW group and non-ICU-AW group [APACHE II score: 21 (18, 25) vs. 18 (15, 22), SOFA score: 7 (5, 12) vs. 5 (3, 8), BNP (ng/L): 364.3 (210.1, 551.2) vs. 160.1 (66.8, 357.8), BUN (mmol/L): 9.9 (6.2, 17.0) vs. 6.0 (4.8, 9.8), invasive mechanical ventilation ratio: 88.2% vs. 46.5%, all P < 0.05]. Binary multivariate Logistic regression analysis showed no independent risk factor for ICU-AW. The average MRC score of 17 ICU-AW patients was 33±11. The limb weakness was symmetrical, and the proximal limb weakness was the main manifestation. Electromyography examination showed that the results of nerve conduction examination in ICU-AW patients mainly revealed that the amplitude of compound muscle action potential (CMAP) and sensory nerve action potentials (SNAP) were decreased, and the conduction velocity was slowed down; needle electromyography showed increased area of motor unit potential (MUP), prolonged time limit and a large number of spontaneous potentials. Prognosis evaluation showed that compared with non-ICU-AW group, patients in ICU-AW group underwent more tracheotomy (70.6% vs. 11.6%), longer length of ICU stay (days: 57±52 vs. 16±8), and more rehabilitation treatment (58.8% vs. 14.0%), and the differences were statistically significant (all P < 0.01). The occurrence of ICU-AW may be related to high APACHE II score and SOFA score, high levels of BNP and BUN on the first day of ICU admission and the proportion of invasive mechanical ventilation, but the above factors are not independent risk factors for ICU-AW. The MRC score of ICU-AW patients was characterized by symmetrical limb weakness, mainly proximal limb weakness; in electromyography examination, the nerve conduction examination results mainly showed that CMAP and SNAP amplitude were decreased, and conduction velocity was slowed down; needle electromyography examination showed increased MUP area, prolonged duration and a large number of spontaneous potentials.

Current practice and obstacle factors of intensive care unit-acquired weakness assessment

To investigate the current status of intensive care unit-acquired weakness (ICU-AW) assessment, analyze the assessment barriers, and to provide reference to improve ICU-AW assessment. A convenient sampling cross-sectional survey was conducted. First, an interview outline which based on related domestic and international literatures and combining with the research purpose of this study were designed. Thirteen medical personnel (8 ICU nurses, 3 ICU doctors, 1 respiratory therapist and 1 physiotherapist) who worked in the intensive care unit (ICU) of the First Hospital of Lanzhou University were enrolled with convenience sampling method to interview. Second, the topics were comprehensively analyzed and extracted, and then a questionnaire was constructed, and the reliability and validity was assessed. Finally, the questionnaire survey including the general situation of ICU medical staffs, the current practices of ICU-AW and influencing factors was implemented in China. The retest reliability was 0.92 and expert validity was 0.96 of the questionnaire. There were 3 563 respondents in 31 provinces, municipalities and autonomous regions which eliminated 357 unqualified questionnaires, including 173 respondents from neonatal or pediatric ICU, 89 respondents whose working time was less than 6 months, and 95 invalid respondents, and then there were finally 3 206 valid questionnaires and the response rate were 90.0%. Those 3 206 respondents included 616 doctors (19.2%), 2 371 nurses (74.0%), 129 respiratory therapists (4.0%), 51 physiotherapist (1.6%) and 39 dietitians (1.2%). The mean age was (30.7±6.3) years old. Most of them had bachelor's degree (65.9%), master and above was 14.1%. Associate senior physician and above was 8.0%; ICU working time was (5.94±4.50) years. In clinical practice, only 26.5% of the ICU medical staffs confirmed that they had treated or taken care for ICU-AW patients; 52.9% of medical staffs evaluated ICU-AW only based on clinical experience, and only 12.3% used ICU-AW assessment tools. The majority of respondents believed that ICU-AW knowledge training should be performed (81.8%), ICU-AW assessment should be as important as other complications (pressure sore, infected ventilator associated pneumonia, etc., 75.1%), and ICU-AW assessment should be part of daily treatment and care activities (61.2%). However, only 10.2% of respondents had received ICU-AW related knowledge training, and 42.7% respondents believed that their ICU-AW related knowledge could not meet clinical needs. Only 18.7% respondents would actively assess whether patients suffered from ICU-AW or not, and 42.3% respondents thought that ICU-AW should be assessed every day, and the assessment tools were also inconsistent. There were 44.0% respondents considered the Medical Research Council Muscle score (MRC-score) scale was the optimal tool for diagnosing ICU-AW, the following were neuro-electrophysiological examination (17.2%) and manual muscle strength (MMT, 11.1%). The main cause of the ICU-AW assessment barriers was the lack of ICU-AW related knowledge (88.1%), and the following were lack of ICU-AW assessment guidelines (76.5%), patients' cognitive impairment or limited understanding ability (84.6%), unable to cooperate with the assessment due to critical illness (83.0%), and inadequate attention to ICU-AW assessment by the department (77.5%). The current status of ICU-AW assessment were unsatisfying in China, and the main barriers were lack of skills and knowledge.

Testosterone improves muscle function of the extensor digitorum longus in rats with sepsis

Among patients with intensive care unit-acquired weakness (ICUAW), skeletal muscle strength often decreases significantly. The present study aimed to explore the effects of testosterone propotionate on skeletal muscle using rat model of sepsis. Male SD rats were randomly divided into experimental group, model control group, sham operation group and blank control group. Rats in experimental group were given testosterone propionate two times a week, 10 mg/kg for 3 weeks. Maximal contraction force, fatigue index and cross-sectional area of the extensor digitorum longus (EDL) were measured. Myosin, IGF-1, p-AKT and p-mTOR levels in EDL were detected by Western blot. Histological changes of the testis and prostate were detected by hematoxylin and eosin staining. We found that maximal contraction force and fatigue index of EDL in experimental group were significantly higher than in model control group. Cross-sectional area of fast MHC muscle fiber of EDL in group was significantly higher than in model control group. The levels of myosin, IGF-1, p-AKT and p-mTOR of EDL in experimental group were significantly higher than in model control group. In addition, no testicle atrophy and prostate hyperplasia were detected in experimental group. In conclusion, these results suggest that testosterone propionate can significantly improve skeletal muscle strength, endurance and volume of septic rats, and the mechanism may be related to the activation of IGF-1/AKT pathway. Moreover, testosterone propionate with short duration does not cause testicular atrophy and prostate hyperplasia in septic rats. Therefore, testosterone propionate is a potential treatment for muscle malfunction in ICUAW patients.

Serum amyloid A1 mediates myotube atrophy via Toll-like receptors.

BackgroundCritically ill patients frequently develop muscle atrophy and weakness in the intensive‐care‐unit setting [intensive care unit‐acquired weakness (ICUAW)]. Sepsis, systemic inflammation, and acute‐phase response are major risk factors. We reported earlier that the acute‐phase protein serum amyloid A1 (SAA1) is increased and accumulates in muscle of ICUAW patients, but its relevance was unknown. Our objectives were to identify SAA1 receptors and their downstream signalling pathways in myocytes and skeletal muscle and to investigate the role of SAA1 in inflammation‐induced muscle atrophy.MethodsWe performed cell‐based in vitro and animal in vivo experiments. The atrophic effect of SAA1 on differentiated C2C12 myotubes was investigated by analysing gene expression, protein content, and the atrophy phenotype. We used the cecal ligation and puncture model to induce polymicrobial sepsis in wild type mice, which were treated with the IкB kinase inhibitor Bristol‐Myers Squibb (BMS)‐345541 or vehicle. Morphological and molecular analyses were used to investigate the phenotype of inflammation‐induced muscle atrophy and the effects of BMS‐345541 treatment.ResultsThe SAA1 receptors Tlr2, Tlr4, Cd36, P2rx7, Vimp, and Scarb1 were all expressed in myocytes and skeletal muscle. Treatment of differentiated C2C12 myotubes with recombinant SAA1 caused myotube atrophy and increased interleukin 6 (Il6) gene expression. These effects were mediated by Toll‐like receptors (TLR) 2 and 4. SAA1 increased the phosphorylation and activity of the transcription factor nuclear factor ‘kappa‐light‐chain‐enhancer' of activated B‐cells (NF‐κB) p65 via TLR2 and TLR4 leading to an increased binding of NF‐κB to NF‐κB response elements in the promoter region of its target genes resulting in an increased expression of NF‐κB target genes. In polymicrobial sepsis, skeletal muscle mass, tissue morphology, gene expression, and protein content were associated with the atrophy response. Inhibition of NF‐κB signalling by BMS‐345541 increased survival (28.6% vs. 91.7%, P < 0.01). BMS‐345541 diminished inflammation‐induced atrophy as shown by a reduced weight loss of the gastrocnemius/plantaris (vehicle: −21.2% and BMS‐345541: −10.4%; P < 0.05), tibialis anterior (vehicle: −22.7% and BMS‐345541: −17.1%; P < 0.05) and soleus (vehicle: −21.1% and BMS‐345541: −11.3%; P < 0.05) in septic mice. Analysis of the fiber type specific myocyte cross‐sectional area showed that BMS‐345541 reduced inflammation‐induced atrophy of slow/type I and fast/type II myofibers compared with vehicle‐treated septic mice. BMS‐345541 reversed the inflammation‐induced atrophy program as indicated by a reduced expression of the atrogenes Trim63/MuRF1, Fbxo32/Atrogin1, and Fbxo30/MuSA1.ConclusionsSAA1 activates the TLR2/TLR4//NF‐κB p65 signalling pathway to cause myocyte atrophy. Systemic inhibition of the NF‐κB pathway reduced muscle atrophy and increased survival of septic mice. The SAA1/TLR2/TLR4//NF‐κB p65 atrophy pathway could have utility in combatting ICUAW.

Effects of CoughAssist therapy on sputum excretion efficacy among patients with intensive care unit-acquired weakness

Objective To explore effects of CoughAssist on sputum excretion efficacy among patients with intensive care unit-acquired weakness (ICU-AW) . Methods From January 2016 to December 2017, we selected 84 ICU-AW patients with mechanical ventilation of ICU in Hu'nan Provincial People's Hospital by convenience sampling. All of the patients were divided into control group and observation group with the random number table, 42 cases in each group. Two groups all received routine treatment and nursing. On this basis, observation group carried out CoughAssist therapy. We compared the sputum excretion effects, results of sputum smear/sputum culture, arterial blood gas indexes, respiratory mechanics indexes, the incidence of ventilator-associated pneumonia (VAP) , time of mechanical ventilation, hospital days in ICU and the score of Medical Research Council (MRC) of patients between two groups. Results There were no statistical difference in the volume of sputum excretion of patients in two groups before dividing groups (P>0.05) . One to three days after treatment, the volume of sputum excretion and number of effective sputum excretion patients in observation group were more than those in control group; the positive rate of sputum culture of patients in observation group was lower than that in control group; the differences were all statistical (P 0.05) . Conclusions The application of CoughAssist in ICU-AW patients with mechanical ventilation can improve the sputum excretion effects as well as respiratory function and shorten the time of mechanical ventilation and hospital days in ICU, and improve the clinical effects. Key words: Respiration, artificial; Intensive care unit-acquired weakness; CoughAssist; Sputum excretion