Advancing critical care recovery: The pivotal role of machine learning in early detection of intensive care unit-acquired weakness.

This editorial explores the significant challenge of intensive care unit-acquired weakness (ICU-AW), a prevalent condition affecting critically ill patients, characterized by profound muscle weakness and complicating patient recovery. Highlighting the paradox of modern medical advances, it emphasizes the urgent need for early identification and intervention to mitigate ICU-AW's impact. Innovatively, the study by Wang et al is showcased for employing a multilayer perceptron neural network model, achieving high accuracy in predicting ICU-AW risk. This advancement underscores the potential of neural network models in enhancing patient care but also calls for continued research to address limitations and improve model applicability. The editorial advocates for the development and validation of sophisticated predictive tools, aiming for personalized care strategies to reduce ICU-AW incidence and severity, ultimately improving patient outcomes in critical care settings.

Intensive care unit-acquired weakness - preventive, and therapeutic aspects; future directions and special focus on lung transplantation.

In this editorial, comments are made on an interesting article in the recent issue of the World Journal of Clinical Cases by Wang and Long. The authors describe the use of neural network model to identify risk factors for the development of intensive care unit (ICU)-acquired weakness. This condition has now become common with an increasing number of patients treated in ICUs and continues to be a source of morbidity and mortality. Despite identification of certain risk factors and corrective measures thereof, lacunae still exist in our understanding of this clinical entity. Numerous possible pathogenetic mechanisms at a molecular level have been described and these continue to be increasing. The amount of retrievable data for analysis from the ICU patients for study can be huge and enormous. Machine learning techniques to identify patterns in vast amounts of data are well known and may well provide pointers to bridge the knowledge gap in this condition. This editorial discusses the current knowledge of the condition including pathogenesis, diagnosis, risk factors, preventive measures, and therapy. Furthermore, it looks specifically at ICU acquired weakness in recipients of lung transplantation, because - unlike other solid organ transplants- muscular strength plays a vital role in the preservation and survival of the transplanted lung. Lungs differ from other solid organ transplants in that the proper function of the allograft is dependent on muscle function. Muscular weakness especially diaphragmatic weakness may lead to prolonged ventilation which has deleterious effects on the transplanted lung - ranging from ventilator associated pneumonia to bronchial anastomotic complications due to prolonged positive pressure on the anastomosis.

Neuromuscular problems of the critically Ill neonate and child.

Acute neuromuscular disorders occasionally occur in the Pediatric Neurologic Intensive Care Unit. Many of these are primary disorders of the motor unit that may present acutely or exacerbate during an intercurrent illness. Additionally, acute neuromuscular disorders may develop during an acute systemic illness requiring intensive care management that predispose the child to another set of acute motor unit disorders. This chapter discusses acute neuromuscular crises in the infant, toddler, and adolescent, as well as neuromuscular disorders resulting from critical illness.

Electrophysiological Screening to Assess Foot Drop Syndrome in Severe Acquired Brain Injury in Rehabilitative Settings.

BACKGROUND: Foot drop syndrome (FDS), characterized by severe weakness and atrophy of the dorsiflexion muscles of the feet, is commonly found in patients with severe acquired brain injury (ABI). If the syndrome is unilateral, the cause is often a peroneal neuropathy (PN), due to compression of the nervous trunk on the neck of the fibula at the knee level; less frequently, the cause is a previous or concomitant lumbar radiculopathy. Bilateral syndromes are caused by polyneuropathies and myopathies. Central causes, due to brain or spinal injury, mimic this syndrome but are usually accompanied by other symptoms, such as spasticity. Critical illness polyneuropathy (CIP) and myopathy (CIM), isolated or in combination (critical illness polyneuromyopathy, CIPNM), have been shown to constitute an important cause of FDS in patients with ABI. Assessing the causes of FDS in the intensive rehabilitation unit (IRU) has several limitations, which include the complexity of the electrophysiological tests, limited availability of neurophysiology consultants, and the severe disturbance in consciousness and lack of cooperation from patients. OBJECTIVES: We sought to propose a simplified electrophysiological screening that identifies FDS causes, particularly PN and CIPNM, to help clinicians to recognize the significant clinical predictors of poor outcomes in severe ABI at admission to IRU. METHODS: This prospective, single-center study included 20 severe ABI patients with FDS (11 females/9 males, mean age 55.10 + 16.26; CRS-R= 11.90 + 6.32; LCF: 3.30 + 1.30; DRS: 21.45 + 3.33), with prolonged rehabilitation treatment (≥2 months). We applied direct tibialis anterior muscle stimulation (DMS) associated with peroneal nerve motor conduction evaluation, across the fibular head (NCS), to identify CIP and/or CIM and to exclude demyelinating or compressive unilateral PN. RESULTS: At admission to IRU, simplified electrophysiological screening reported four unilateral PN, four CIP and six CIM with a CIPNM overall prevalence estimate of about 50%. After 2 months, the CIPNM group showed significantly poorer outcomes compared to other ABI patients without CIPNM, as demonstrated by the lower probability of achieving endotracheal-tube weaning (20% versus 90%) and lower CRS-R and DRS scores. Due to the subacute rehabilitation setting of our study, it was not possible to evaluate the motor results of recovery of the standing position, functional walking and balance, impaired by the presence of unilateral PN. CONCLUSIONS: The implementation of the proposed simplified electrophysiological screening may enable the early identification of unilateral PN or CIPNM in severe ABI patients, thereby contributing to better functional prognosis in rehabilitative settings.

Intensive Care Unit-Acquired Weakness after Liver Transplantation: Analysis of Seven Cases and a Literature Review.

Intensive Care Unit (ICU)-Acquired Weakness (ICU-AW) is a generalized muscle weakness that is clinically detected in critical patients and has no plausible etiology other than critical illness. ICU-AW is uncommon in patients undergoing orthotopic liver transplantation (OLT). Our report sheds light on the highest number of ICU-AW cases observed in a single center on OLT patients with early allograft dysfunction. Out of 282 patients who underwent OLT from January 2015 to June 2023, 7 (2.5%) developed generalized muscle weakness in the ICU and underwent neurophysiological investigations. The neurologic examination showed preserved extraocular, flaccid quadriplegia with the absence of deep tendon reflexes in all patients. Neurophysiological studies, including electromyography and nerve conduction studies, showed abnormalities with fibrillation potentials and the rapid recruitment of small polyphasic motor units in the examined muscles, as well as a reduced amplitude of the compound muscle action potential and sensory nerve action potential, with an absence of demyelinating features. Pre-transplant clinical status was critical in all patients. During ICU stay, early allograft dysfunction, acute kidney injury, prolonged mechanical ventilation, sepsis, hyperglycemia, and high blood transfusions were observed in all patients. Two patients were retransplanted. Five patients were alive at 90 days; two patients died. In non-cooperative OLT patients, neurophysiological investigations are essential for the diagnosis of ICU-AW. In this setting, the high number of red blood cell transfusions is a potential risk factor for ICU-AW.

Is It Polymyositis?

How to cite this article: Bansal T. Is It Polymyositis? Indian J Crit Care Med 2023;27(9):690-691.

[Intensive care unit-acquired weakness-Diagnostic value of neuromuscular ultrasound]. / Intensive Care Unit-Acquired Weakness ­ diagnostischer Stellenwert des neuromuskulären Ultraschalls.

Intensive care unit-acquired weakness (ICUAW) is one of the most common neuromuscular complications in intensive care medicine. The clinical diagnosis and assessment of the severity using established diagnostic methods (e.g., clinical examination using the Medical Research Council Sum Score or electrophysiological examination) can be difficult or even impossible, especially in sedated, ventilated and delirious patients. Neuromuscular ultrasound (NMUS) has increasingly been investigated in ICUAW as an easy to use noninvasive and mostly patient compliance-independent diagnostic alternative. It has been shown that NMUS appears to be a promising tool to detect ICUAW, to assess the severity of muscular weakness and to monitor the clinical progression. Further studies are needed to standardize the methodology, to evaluate the training effort and to optimize outcome predication. The formulation of an interdisciplinary neurological and anesthesiological training curriculum is warranted to establish NMUS as a complementary diagnostic method of ICUAW in daily clinical practice.

COVID-19-Induced Myopathy and Diaphragmatic Weakness: A Case Report.

Coronavirus disease 2019 (COVID-19) is a respiratory illness caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus that can induce myopathy, which can evolve into potentially life-threatening muscle weakness, including diaphragmatic paralysis. We present a case report of a 57-year-old female treated in the medical ICU for acute respiratory distress syndrome (ARDS) triggered by active COVID-19 infection, who subsequently developed worsening respiratory weakness from underlying COVID-19 myopathy manifesting as respiratory muscle weakness. Our patient's muscle biopsy highlights the development of muscle atrophy without evidence of inflammatory myopathy, making the presence of pre-existing autoimmune myopathy unlikely. While literature cites different biochemical etiologies for the development of myopathy, the exact mechanism behind this phenomenon is not yet defined.

Neuromuscular Ultrasound in Intensive Care Unit-Acquired Weakness: Current State and Future Directions.

Intensive care unit-acquired weakness (ICUAW) is one of the most common causes of muscle atrophy and functional disability in critically ill intensive care patients. Clinical examination, manual muscle strength testing and monitoring are frequently hampered by sedation, delirium and cognitive impairment. Many different attempts have been made to evaluate alternative compliance-independent methods, such as muscle biopsies, nerve conduction studies, electromyography and serum biomarkers. However, they are invasive, time-consuming and often require special expertise to perform, making them vastly impractical for daily intensive care medicine. Ultrasound is a broadly accepted, non-invasive, bedside-accessible diagnostic tool and well established in various clinical applications. Hereby, neuromuscular ultrasound (NMUS), in particular, has been proven to be of significant diagnostic value in many different neuromuscular diseases. In ICUAW, NMUS has been shown to detect and monitor alterations of muscles and nerves, and might help to predict patient outcome. This narrative review is focused on the recent scientific literature investigating NMUS in ICUAW and highlights the current state and future opportunities of this promising diagnostic tool.

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

BACKGROUND: 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-ß) is involved in both processes. We uncovered an increased expression of the TGF-ß receptor II (TßRII)-inhibitor SPRY domain-containing and SOCS-box protein 1 (SPSB1) in skeletal muscle of septic mice. We hypothesized that SPSB1-mediated inhibition of TßRII signalling impairs myogenic differentiation in response to inflammation. METHODS: 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-ß/TßRII 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. RESULTS: SPSB1 expression was increased in skeletal muscle of ICUAW patients and septic mice. Tumour necrosis factor (TNF), interleukin-1ß (IL-1ß), and IL-6 increased the Spsb1 expression in C2C12 myotubes. TNF- and IL-1ß-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 TßRII, resulting in TßRII ubiquitination and destabilization. SPSB1 impaired TßRII-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. CONCLUSIONS: Inflammatory cytokines via their respective signalling pathways cause an increase in SPSB1 expression in myocytes and attenuate myogenic differentiation. SPSB1-mediated inhibition of TßRII-Akt-Myogenin signalling and protein synthesis contributes to a disturbed myocyte homeostasis and myogenic differentiation that occurs during inflammation.

Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.

Mitochondria are key structures providing most of the energy needed to maintain homeostasis. They are the main source of adenosine triphosphate (ATP), participate in glucose, lipid and amino acid metabolism, store calcium and are integral components in various intracellular signaling cascades. However, due to their crucial role in cellular integrity, mitochondrial damage and dysregulation in the context of critical illness can severely impair organ function, leading to energetic crisis and organ failure. Skeletal muscle tissue is rich in mitochondria and, therefore, particularly vulnerable to mitochondrial dysfunction. Intensive care unit-acquired weakness (ICUAW) and critical illness myopathy (CIM) are phenomena of generalized weakness and atrophying skeletal muscle wasting, including preferential myosin breakdown in critical illness, which has also been linked to mitochondrial failure. Hence, imbalanced mitochondrial dynamics, dysregulation of the respiratory chain complexes, alterations in gene expression, disturbed signal transduction as well as impaired nutrient utilization have been proposed as underlying mechanisms. This narrative review aims to highlight the current known molecular mechanisms immanent in mitochondrial dysfunction of patients suffering from ICUAW and CIM, as well as to discuss possible implications for muscle phenotype, function and therapeutic approaches.

Quantitative muscle MRI displays clinically relevant myostructural abnormalities in long-term ICU-survivors: a case-control study.

BACKGROUND: Long-term data on ICU-survivors reveal persisting sequalae and a reduced quality-of-life even after years. Major complaints are neuromuscular dysfunction due to Intensive care unit acquired weakness (ICUAW). Quantitative MRI (qMRI) protocols can quantify muscle alterations in contrast to standard qualitative MRI-protocols. METHODS: Using qMRI, the aim of this study was to analyse persisting myostructural abnormalities in former ICU patients compared to controls and relate them to clinical assessments. The study was conducted as a cohort/case-control study. Nine former ICU-patients and matched controls were recruited (7 males; 54.8y ± 16.9; controls: 54.3y ± 11.1). MRI scans were performed on a 3T-MRI including a mDTI, T2 mapping and a mDixonquant sequence. Water T2 times, fat-fraction and mean values of the eigenvalue (λ1), mean diffusivity (MD), radial diffusivity (RD) and fractional anisotropy (FA) were obtained for six thigh and seven calf muscles bilaterally. Clinical assessment included strength testing, electrophysiologic studies and a questionnaire on quality-of-life (QoL). Study groups were compared using a multivariate general linear model. qMRI parameters were correlated to clinical assessments and QoL questionnaire using Pearson´s correlation. RESULTS: qMRI parameters were significantly higher in the patients for fat-fraction (p < 0.001), water T2 time (p < 0.001), FA (p = 0.047), MD (p < 0.001) and RD (p < 0.001). Thighs and calves showed a different pattern with significantly higher water T2 times only in the calves. Correlation analysis showed a significant negative correlation of muscle strength (MRC sum score) with FA and T2-time. The results were related to impairment seen in QoL-questionnaires, clinical testing and electrophysiologic studies. CONCLUSION: qMRI parameters show chronic next to active muscle degeneration in ICU survivors even years after ICU therapy with ongoing clinical relevance. Therefore, qMRI opens new doors to characterize and monitor muscle changes of patients with ICUAW. Further, better understanding on the underlying mechanisms of the persisting complaints could contribute the development of personalized rehabilitation programs.

Statin-Induced Anti-3-Hydroxy-3-Methylglutaryl-Coenzyme A Reductase (Anti-HMGCR) Myopathy.

Statins are known to pharmacologically target 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR). Several subtypes of anti-HMGCR autoimmune myopathies have been reported as a result of statin use. Although these types vary widely, a severe and rare form of statin-induced myopathy is immune-mediated necrotizing myopathy (IMNM), resulting in severe muscle injury that does not respond to statin cessation and is associated with poor outcomes. Diagnosis is confirmed through biopsy confirming the necrosis of biopsy fibers, in addition to elevated anti-HMGCR serum levels. Management lacks proper guidelines, however, immunosuppressive therapy has been proposed as a possible intervention. The aim of this report is to increase providers' knowledge of the presentation and possible treatment of statin-induced immune-mediated necrotizing myopathy.

Intensive Care Unit-Acquired Weakness in Patients With Acute Kidney Injury: A Contemporary Review.

Acute kidney injury (AKI) and intensive care unit-acquired weakness (ICU-AW) are 2 frequent complications of critical illness that, until recently, have been considered unrelated processes. The adverse impact of AKI on ICU mortality is clear, but its relationship with muscle weakness-a major source of ICU morbidity-has not been fully elucidated. Furthermore, improving ICU survival rates have refocused the field of intensive care toward improving long-term functional outcomes of ICU survivors. We begin our review with the epidemiology of AKI in the ICU and of ICU-AW, highlighting emerging data suggesting that AKI and AKI treated with kidney replacement therapy (AKI-KRT) may independently contribute to the development of ICU-AW. We then delve into human and animal data exploring the pathophysiologic mechanisms linking AKI and acute KRT to muscle wasting, including altered amino acid and protein metabolism, inflammatory signaling, and deleterious removal of micronutrients by KRT. We next discuss the currently available interventions that may mitigate the risk of ICU-AW in patients with AKI and AKI-KRT. We conclude that additional studies are needed to better characterize the epidemiologic and pathophysiologic relationship between AKI, AKI-KRT, and ICU-AW and to prospectively test interventions to improve the long-term functional status and quality of life of AKI survivors.

Early detection of ICU-acquired weakness in septic shock patients ventilated longer than 72 h.

PURPOSE: ICU-acquired weakness, comprising Critical Illness Polyneuropathy (CIP) and Myopathy (CIM) is associated with immobilization and prolonged mechanical ventilation. This study aims to assess feasibility of early detection of CIP and CIM by peroneal nerve test (PENT) and sensory sural nerve action potential (SNAP) screening in patients with septic shock and invasively ventilated for more than 72 h. METHODS: We performed repetitive PENT screening from 72 h after intubation until detecting a pathological response. We tested SNAPs in pathological PENT to differentiate CIP from CIM. We performed muscle strength examination in awake patients and recorded time from intubation to first in-bed and out-of-bed mobilization. RESULTS: Eighteen patients were screened with PENT and 88.9% had abnormal responses. Mean time between intubation and first screening was 94.38 (± 22.41) hours. Seven patients (38.9%) had CIP, two (11.1%) had CIM, one (5.6%) had CIP and CIM, six (33.3%) had a pathological response on PENT associated with ICU-acquired weakness (but no SNAP could be performed to differentiate between CIP and CIM) and two patients had (11.1%) had no peripheral deficit. In patients where it could be performed, muscle strength testing concorded with electrophysiological findings. Twelve patients (66.7%) had out-of-bed mobilization 10.8 (± 7.4) days after admission. CONCLUSION: CIP and CIM are frequent in septic shock patients and can be detected before becoming symptomatic with simple bedside tools. Early detection of CIP and CIM opens new possibilities for their timely management through preventive measures such as passive and active mobilization.

A prospective clinical study on the mechanisms underlying critical illness myopathy-A time-course approach.

BACKGROUND: Critical illness myopathy (CIM) is a consequence of modern critical care resulting in general muscle wasting and paralyses of all limb and trunk muscles, resulting in prolonged weaning from the ventilator, intensive care unit (ICU) treatment and rehabilitation. CIM is associated with severe morbidity/mortality and significant negative socioeconomic consequences, which has become increasingly evident during the current COVID-19 pandemic, but underlying mechanisms remain elusive. METHODS: Ten neuro-ICU patients exposed to long-term controlled mechanical ventilation were followed with repeated muscle biopsies, electrophysiology and plasma collection three times per week for up to 12 days. Single muscle fibre contractile recordings were conducted on the first and final biopsy, and a multiomics approach was taken to analyse gene and protein expression in muscle and plasma at all collection time points. RESULTS: (i) A progressive preferential myosin loss, the hallmark of CIM, was observed in all neuro-ICU patients during the observation period (myosin:actin ratio decreased from 2.0 in the first to 0.9 in the final biopsy, P < 0.001). The myosin loss was coupled to a general transcriptional downregulation of myofibrillar proteins (P < 0.05; absolute fold change >2) and activation of protein degradation pathways (false discovery rate [FDR] <0.1), resulting in significant muscle fibre atrophy and loss in force generation capacity, which declined >65% during the 12 day observation period (muscle fibre cross-sectional area [CSA] and maximum single muscle fibre force normalized to CSA [specific force] declined 30% [P < 0.007] and 50% [P < 0.0001], respectively). (ii) Membrane excitability was not affected as indicated by the maintained compound muscle action potential amplitude upon supramaximal stimulation of upper and lower extremity motor nerves. (iii) Analyses of plasma revealed early activation of inflammatory and proinflammatory pathways (FDR < 0.1), as well as a redistribution of zinc ions from plasma. CONCLUSIONS: The mechanical ventilation-induced lung injury with release of cytokines/chemokines and the complete mechanical silencing uniquely observed in immobilized ICU patients affecting skeletal muscle gene/protein expression are forwarded as the dominant factors triggering CIM.

A Global Survey on Diagnostic, Therapeutic and Preventive Strategies in Intensive Care Unit-Acquired Weakness.

Background and Objectives: Intensive care unit-acquired weakness (ICU-AW) is one of the most frequent neuromuscular complications in critically ill patients. We conducted a global survey to evaluate the current practices of diagnostics, treatment and prevention in patients with ICU-AW. Materials and Methods: A pre-survey was created with international experts. After revision, the final survey was endorsed by the European Society of Intensive Care Medicine (ESICM) using the online platform SurveyMonkey®. In 27 items, we addressed strategies of diagnostics, therapy and prevention. An invitation link was sent by email to all ESICM members. Furthermore, the survey was available on the ESICM homepage. Results: A total of 154 healthcare professionals from 39 countries participated in the survey. An ICU-AW screening protocol was used by 20% (28/140) of participants. Forty-four percent (62/141) of all participants reported performing routine screening for ICU-AW, using clinical examination as the method of choice (124/141, 87.9%). Almost 63% (84/134) of the participants reported using current treatment strategies for patients with ICU-AW. The use of treatment and prevention strategies differed between intensivists and non-intensivists regarding the reduction in sedatives (80.0% vs. 52.6%, p = 0.002), neuromuscular blocking agents (76.4% vs. 50%, p = 0.004), corticosteroids (69.1% vs. 37.2%, p < 0.001) and glycemic control regimes (50.9% vs. 23.1%, p = 0.002). Mobilization and physical activity are the most frequently reported treatment strategies for ICU-AW (111/134, 82.9%). The availability of physiotherapists (92/134, 68.7%) and the lack of knowledge about ICU-AW within the medical team (83/134, 61.9%) were the main obstacles to the implementation of the strategies. The necessity to develop guidelines for the screening, diagnosing, treatment and prevention of ICU-AW was recognized by 95% (127/133) of participants. Conclusions: A great heterogeneity regarding diagnostics, treatment and prevention of ICU-AW was reported internationally. Comprehensive guidelines with evidence-based recommendations for ICU-AW management are needed.

Screening Power of Short Tau Inversion Recovery Muscle Magnetic Resonance Imaging in Critical Illness Myoneuropathy and Guillain-Barre Syndrome in the Intensive Care Unit.

Introduction: Critical illness myoneuropathy (CIMN) or intensive care unit (ICU)-acquired weakness (AW) is a common cause of weakness in ICU patients. Guillain-Barre syndrome (GBS) is also a common cause of acute neurological weakness in the ICU. It is diagnosed by clinical features, nerve conduction studies (NCS), and muscle/nerve biopsies. Methods: The short tau inversion recovery (STIR) muscle magnetic resonance (MR) images of seven patients with suspected CIMN and seven GBS patients over a 5-year period from February 2015 till May 2020 were analyzed. Results: All seven patients with CIMN showed diffuse muscle edema, predominating in the lower limbs. Only one patient with GBS showed abnormal magnetic resonance imaging (MRI) changes (14%) and MRI was normal in 86%. The sensitivity of MRI to detect CIMN was 100%, whereas the specificity was 85.7%. Thus, the positive predictive value (PPV) of MRI in this situation was 87.5% and the negative predictive value (NPV) was 100%. Conclusion: Muscle STIR imaging may help to differentiate between CIMN and GBS. How to cite this article: Maramattom BV. Screening Power of Short Tau Inversion Recovery Muscle Magnetic Resonance Imaging in Critical Illness Myoneuropathy and Guillain-Barre Syndrome in the Intensive Care Unit. Indian J Crit Care Med 2022;26(2):204-209.

A Rare Case of COVID-19-Induced Chronic Demyelinating Polyneuropathy.

Chronic autoimmune demyelinating polyneuropathy (CIDP) is a rare autoimmune disorder in which the body's immune system attacks the myelin sheaths. Myelin sheaths are the fatty insulation covering and protecting the nerves, and damage to these can lead to neurological symptoms like numbness, tingling, and weakness. CIDP is a chronic disease in the Guillain-Barré syndrome spectrum. Numerous case reports of autoimmune diseases linked to coronavirus disease 2019 (COVID-19) have been seen since the onset of COVID-19 pandemic. We present one such challenging case of COVID-19-induced CIDP.

Therapeutic Potential of Electromyostimulation (EMS) in Critically Ill Patients-A Systematic Review.

Ample evidence exists that intensive care unit (ICU) treatment and invasive ventilation induce a transient or permanent decline in muscle mass and function. The functional deficit is often called ICU-acquired weakness with critical illness polyneuropathy (CIP) and/or myopathy (CIM) being the major underlying causes. Histopathological studies in ICU patients indicate loss of myosin filaments, muscle fiber necrosis, atrophy of both muscle fiber types as well as axonal degeneration. Besides medical prevention of risk factors such as sepsis, hyperglycemia and pneumonia, treatment is limited to early passive and active mobilization and one third of CIP/CIM patients discharged from ICU never regain their pre-hospitalization constitution. Electromyostimulation [EMS, also termed neuromuscular electrical stimulation (NMES)] is known to improve strength and function of healthy and already atrophied muscle, and may increase muscle blood flow and induce angiogenesis as well as beneficial systemic vascular adaptations. This systematic review aimed to investigate evidence from randomized controlled trails (RCTs) on the efficacy of EMS to improve the condition of critically ill patients treated on ICU. A systematic search of the literature was conducted using PubMed (Medline), CENTRAL (including Embase and CINAHL), and Google Scholar. Out of 1,917 identified records, 26 articles (1,312 patients) fulfilled the eligibility criteria of investigating at least one functional measure including muscle function, functional independence, or weaning outcomes using a RCT design in critically ill ICU patients. A qualitative approach was used, and results were structured by 1) stimulated muscles/muscle area (quadriceps muscle only; two to four leg muscle groups; legs and arms; chest and abdomen) and 2) treatment duration (≤10 days, >10 days). Stimulation parameters (impulse frequency, pulse width, intensity, duty cycle) were also collected and the net EMS treatment time was calculated. A high grade of heterogeneity between studies was detected with major cofactors being the analyzed patient group and selected outcome variable. The overall efficacy of EMS was inconclusive and neither treatment duration, stimulation site or net EMS treatment time had clear effects on study outcomes. Based on our findings, we provide practical recommendations and suggestions for future studies investigating the therapeutic efficacy of EMS in critically ill patients. Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/], identifier [CRD42021262287].