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.

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.

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.

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.
OBJECTIVE: 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 (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.

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 (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.
Die Intensive Care Unit-Acquired Weakness (ICUAW) stellt eine der häufigsten neuromuskulären Komplikationen in der Intensivmedizin dar. Besonders bei analgosedierten, beatmeten oder deliranten Patienten können die klinische Diagnosestellung und Schweregradbeurteilung anhand etablierter diagnostischer Methoden (z. B. der klinischen Untersuchung mithilfe des Medical Research Council Sum Score oder elektrophysiologischen Untersuchungen) schwierig bis unmöglich werden. Der neuromuskuläre Ultraschall (NMUS) ist als eine einfach anwendbare, nichtinvasive und weitgehend von der Patienten-Compliance unabhängige Untersuchungsmöglichkeit zunehmend häufiger bei ICUAW untersucht worden. Hierbei konnte gezeigt werden, dass NMUS dazu geeignet zu sein scheint, eine ICUAW zu detektieren, den Schweregrad der muskulären Schwäche einzuschätzen und den klinischen Verlauf zu monitoren. Weiterführende Studien zur Vereinheitlichung der Untersuchungsmethodik, zur Evaluation des Trainingsaufwandes und zur Outcome-Prädikation sind notwendig. Die Formulierung eines interdisziplinären (neurologisch-anästhesiologischen) Weiterbildungscurriculums könnte die Grundlage der Etablierung des NMUS als komplementäres Verfahren zur Diagnostik der ICUAW in der klinischen Praxis bilden.

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.

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.

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.