Weakness In Intensive Care Unit Research Articles

Effectiveness of an Educational Program on Nurses' Knowledge Toward Early Prediction of Acquired Weakness in The Intensive Care Unit.

Abstract:
 Objectives: The present study aims to evaluate effectiveness of educational program the nurses' knowledge towards early prediction of acquired weakness in the intensive care unit.
 Methodology: A pre-experimental study design (comparison of two groups), which was achieved through the pre and post-test method for the study sample through the application of an educational program in the intensive care unit of Al-Zahra Teaching Hospital in Kut city, Wasit Governorate. The study was conducted for the period from 28th April 2022 to 15th August 2022 by selecting a purposive (non-probability) sample for this study. The study sample size was (52) nurses, divided into two groups, each one containing (26) nurse as a control group and a study group. The study group was shown the educational program while the control group was not exposed to the educational program.
 Results: The results of the study show a clear positive effect on the nurses' knowledge toward the early predictive acquired weakness in the intensive care unit. The study indicated that their high significant differences between the control group and study group, between the pre and post for the study group after presenting them with the educational program.
 Recommendations: The study recommended to design and construct an educational program for the nursing staff, whereby through the program emphasizing the directed and familiarize with how to deal with acquired weakness in intensive care unit and who reduce complications that result from long stay in ICU.
 Keys of words: effectiveness educational programs, nurses' knowledge, acquired weakness, intensive care unit

The Role of Technological Rehabilitation in Patients with Intensive Care Unit Weakness: A Randomized Controlled Pilot Study

Intensive-Care-Unit-Acquired Weakness (ICU-AW) is the most common neuromuscular impairment in critically ill patients and can have a significant impact on long-term disability. Early rehabilitation has been suggested to facilitate the natural recovery process. This is a pilot, randomized, single-blind study that aimed to evaluate the effectiveness of intensive combined technological rehabilitation treatment including focal muscle vibration and non-immersive virtual reality for patients with severe acquired brain injury (sABI) and ICU-AW. Twenty-four patients were randomized into the conventional group, which performed only conventional rehabilitation, and the experimental group, which also performed technological treatment. At baseline and after 3 weeks of treatment, assessments of motor function, autonomy, disability and quality of life were conducted. At the end of the intervention, both groups showed significant improvements. However, patients in the experimental group achieved greater improvements in disability (p = 0.001) and quality of life (p = 0.001). The results show that intensive structured rehabilitation is effective in improving the motor function, disability and quality of life of patients with severe acquired brain injury and acquired weakness. The combination of non-immersive virtual reality training and focal muscle vibration can result in a significant improvement in overall disability and quality of life compared with conventional treatment alone.

Safety and efficacy of electrical stimulation for lower-extremity muscle weakness in intensive care unit 2019 Novel Coronavirus patients: A phase I double-blinded randomized controlled trial.

Intensive care unit (ICU) prolonged immobilization may lead to lower-extremity muscle deconditioning among critically ill patients, particularly more accentuated in those with 2019 Novel Coronavirus (COVID-19) infection. Electrical stimulation (E-Stim) is known to improve musculoskeletal outcomes. This phase I double-blinded randomized controlled trial examined the safety and efficacy of lower-extremity E-Stim to prevent muscle deconditioning. Critically ill COVID-19 patients admitted to the ICU were randomly assigned to control (CG) or intervention (IG) groups. Both groups received daily E-Stim (1 h) for up to 14 days on both gastrocnemius muscles (GNMs). The device was functional in the IG and non-functional in the CG. Primary outcomes included ankle strength (Ankles) measured by an ankle-dynamometer, and GNM endurance (GNMe) in response to E-Stim assessed with surface electromyography (sEMG). Outcomes were measured at baseline, 3 and 9 days. Thirty-two (IG = 16, CG = 16) lower extremities in 16 patients were independently assessed. The mean time between ICU admission and E-Stim therapy delivery was 1.8 ± 1.9 days (p = 0.29). At 3 days, the IG showed an improvement compared to the CG with medium effect sizes for Ankles (p = 0.06, Cohen's d = 0.77) and GNMe (p = 0.06, d = 0.69). At 9 days, the IG GNMe was significantly higher than the CG (p = 0.04, d = 0.97) with a 6.3% improvement from baseline (p = 0.029). E-Stim did not alter vital signs (i.e., heart/respiratory rate, blood saturation of oxygen), showed no adverse events (i.e., pain, skin damage, discomfort), nor interfere with ICU standard of care procedures (i.e., mechanical ventilation, prone rotation). This study supports the safety and efficacy of early E-Stim therapy to potentially prevent deterioration of lower-extremity muscle conditions in critically ill COVID-19 patients recently admitted to the ICU. If confirmed in a larger sample, E-Stim may be used as a practical adjunctive therapy. [https://clinicaltrials.gov/], identifier [NCT04685213].

Generalized Weakness in Intensive Care Unit: Review Article

Background: Muscle weakness is common in the surgical intensive care unit (ICU). Low muscle mass at ICU admission is a significant predictor of adverse outcomes. The consequences of ICU-acquired muscle weakness depend on the underlying mechanism. Severe perioperative acquired weakness that is associated with adverse outcomes (prolonged mechanical ventilation, increases in ICU length of stay, and mortality) occurs with persistent (time frame: days) activation of protein degradation pathways, decreases in the drive to the skeletal muscle, and impaired muscular homeostasis. Methods: In this article, we review the current state-of-the-art of the basic pathophysiology of nerve and muscle weakness after critical illness and explore the current literature on ICUAW with a special emphasis on the most important mechanisms of weakness. In addition to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and etiology. Results: ICU-AW can be caused by a critical illness polyneuropathy, acritical illness myopathy, or muscle disuse atrophy, alone or in combination. Its diagnosis requires both clinical assessment of muscle strength and complete electrophysiological evaluation of peripheral nerves and muscle Conclusion: ICU-AW can be prevented by early treatment of the underlying disease, goal-directed therapy, restrictive use of immobilizing medications, optimal nutrition, activating ventilatory modes, early rehabilitation, and preventive drug therapy.

Narrative review of muscle weakness and wasting in pediatric critical illness

: Muscle weakness and wasting is increasingly recognized as a problem in children admitted to the pediatric intensive care unit (PICU). Muscle weakness and wasting could potentially affect a child’s function and development, imposing a burden on the child and their families. We aimed to summarize the literature on muscle weakness and wasting in critically ill children, discuss methods to measure muscle changes as well as areas for future research. Intensive care unit weakness in children has been reported through numerous case reports and a cohort study. These papers demonstrated that muscle weakness can be persistent in critically ill children, with reduced strength reported even after hospital discharge. A prevalence of approximately 2% has been reported in critically ill children, lower than that reported in adults. This may be related to an under-detection of muscle weakness in critically ill children, as identification of muscle weakness and wasting in critically ill children can be challenging. Some methods that have been used to assess muscle changes in critically ill children include arm muscle circumference derived from triceps skinfold thickness and upper-arm circumference, ultrasound-derived limb and diaphragm muscle size, lean body mass from bioelectrical impedance analysis. Using these methods, various patterns have been reported including increase, decrease and no change in muscle. However, studies have not explored the relationship between muscle changes and function. Evidence suggests that there is heterogeneity in the muscle changes that critically ill children may experience. Future research may need to consider differences in age, illness severity and body composition in interpreting changes in muscle size and strength in critically ill children. Importantly, understanding the role of nutrition and physical rehabilitation in relation to muscle changes and function is an important direction in optimizing long-term outcomes in critically ill children.

Reply to the Letter to Editor Regarding "An Unusual Case of Critical Illness Polyneuromyopathy".

Critical illness myopathy (CIM), critical illness polyneuropathy (CIP), and critical illness polyneuromyopathy (CIPNM) are the group of disorders that are commonly presented as neuromuscular weakness in intensive care unit (ICU) settings. They are responsible for prolonged ICU stay and failure to wean off from mechanical ventilation.1 We report one such case of young female who was admitted with undiagnosed type I diabetes mellitus with diabetic ketoacidosis with severe hypokalemia with sepsis developed acute-onset quadriplegia and diaphragmatic palsy within 72 hours of ICU admission. Detailed investigation led to the diagnosis of critical illness polyneuromyopathy. In view of high morbidity, mortality, and poor prognosis, a guided approach to diagnoses and treatment in earliest possible duration might give better improvement and outcome of the illness. Despite all the odds, our patient showed good clinical improvement and finally got discharged.How to cite this articleMahashabde M, Chaudhary GA, Kanchi G, Rohatgi S, Rao P, Patil R, et al. Reply to the Letter to Editor Regarding “An Unusual Case of Critical Illness Polyneuromyopathy”. Indian J Crit Care Med 2020;24(7):604–605.

An Unusual Case of Critical Illness Polyneuromyopathy.

ABSTRACTCritical illness myopathy (CIM), critical illness polyneuropathy (CIP), and critical illness polyneuromyopathy (CIPNM) are the group of disorders that are commonly presented as neuromuscular weakness in intensive care unit (ICU) settings. They are responsible for prolonged ICU stay and failure to wean off from mechanical ventilation. We report a case of young female who was admitted with undiagnosed type I diabetes mellitus with diabetic ketoacidosis, severe hypokalemia, sepsis developed acute onset quadriplegia, and diaphragmatic palsy within 72 hours of ICU admission. On detailed investigation, CIPNM was diagnosed. In view of high morbidity, mortality, and poor prognosis, a guided approach to diagnose and treat in earliest possible duration might give better improvement and outcome of the illness. Despite all the odds, our patient showed good clinical improvement and finally got discharged.How to cite this articleMahashabde M, Chaudhary G, Kanchi G, Rohatgi S, Rao P, Patil R, et al. An Unusual Case of Critical Illness Polyneuromyopathy. Indian J Crit Care Med 2020;24(2):133–135.

Acquired neuromuscular weakness In Intensive Care Unit: Review article

A substantial number of patients admitted to the ICU because of an acute illness, complicated surgery, severe trauma, or burn injury will develop a de novo form of muscle weakness during the ICU stay that is referred to as “intensive care unit acquired weakness” (ICUAW). This ICUAW evoked by critical illness can be due to axonal neuropathy, primary myopathy, or both. Underlying pathophysiological mechanisms comprise microvascular, electrical, metabolic, and bioenergetic alterations, interacting in a complex way and culminating in loss of muscle strength and/or muscle atrophy. ICUAW is typically symmetrical and affects predominantly proximal limb muscles and respiratory muscles, whereas facial and ocular muscles are often spared. ICUAW is diagnosed in awake and cooperative patients by bedside manual testing of muscle strength and the severity is scored by the Medical Research Council sum score. In cases of atypical clinical presentation or evolution, additional electrophysiological testing may be required for differential diagnosis. The cornerstones of prevention are aggressive treatment of sepsis, early mobilization, preventing hyperglycemia with insulin, and avoiding the use parenteral nutrition during the first week of critical illness. Future research should focus on new preventive and/or therapeutic strategies for this detrimental complication of critical illness and on clarifying how ICUAW contributes to poor longer-term prognosis.

What is the diagnostic accuracy of single nerve conduction studies and muscle ultrasound to identify critical illness polyneuromyopathy: a prospective cohort study

BackgroundCritical illness polyneuromyopathy (CIPNM) is a major cause of weakness in intensive care unit (ICU) patients, but current diagnostic tests are limited. We evaluated the generalizability and validity of single nerve conduction studies (NCS) and muscle ultrasound testing to identify CIPNM, and we also assessed the ability of muscle ultrasound to prognosticate patient outcomes.MethodsThis was a prospective cohort study of mechanically ventilated medical, cardiac, surgical, and neurosurgical ICU patients. We performed weekly strength testing, NCS, electromyography (EMG), and muscle ultrasound. We calculated the sensitivity, specificity, and other test characteristics of single NCS and muscle ultrasound, and we used multivariable regression models to assess the prognostic ability of muscle ultrasound.ResultsNinety-five patients were enrolled. The incidence of probable CIPNM was 18% and did not differ significantly by type of ICU (p = 0.49). For diagnosing probable CIPNM, the peroneal motor NCS had a sensitivity of 94% (95% confidence interval (CI) 71–100%) and specificity of 91% (95% CI 82–96%), the sural sensory NCS had a sensitivity of 100% (95% CI 80–100%) and specificity of 42% (95% CI 31–54%), and abnormal muscle ultrasound echogenicity had a sensitivity of 82% (95% CI 48–98%) and specificity of 57% (95% CI 43–70%). Abnormal echogenicity was associated with reduced likelihood of discharge to home (9% vs 50%, p = 0.0001), fewer ICU-free days (median 3 (interquartile range 0–15) days vs 16 (9.3–19.3) days, p = 0.0002), and increased ICU mortality (42% vs 12%, p = 0.004).ConclusionsIn a diverse cohort of critically ill patients, single NCS and muscle ultrasound achieved diagnostic accuracy for patients at risk for CIPNM. The routine utilization of these tests could be beneficial for all critically ill patients at risk for CIPNM.

What is in the Myopathy Literature?

This update covers the results of a randomized, placebo-controlled study that provides evidence that lamotrigine is effective in treating nondystrophic myotonias. Next, an overview of adverse effects of immune checkpoint inhibitors is provided, and the association of autoimmune myopathy and these monoclonal antibody therapies is discussed in light of recent reports. Last, the utility of electrodiagnostic testing in patients with intensive care unit weakness is addressed with emphasis on the high sensitivity and specificity of prolonged compound muscle action potential amplitudes in diagnosing critical illness myopathy.

Acquired weakness in intensive care unit

Severe critical illness is often complicated by Intensive Care Unit–Acquired Weakness (ICU-AW), which is associated with increased in and post-ICU mortality, with delayed weaning from mechanical ventilation and with long-term functional. It is related to myopathy and/or sensory-motor axonal polyneuropathy, the latter being associated with a more delayed recovery. Main risk factors of ICU-AW include severity of critical illness, immobilization, hyperglycaemia and more controversial corticosteroids and neuromuscular blocking agents. Pathophysiology of CIP is considered to involve ischemic, metabolic inflammatory processes and impairment of membrane excitability. The mechanisms of CIM involve membrane inexcitability, bioenergetics failure and increased proteolysis. Interestingly, muscle regeneration has not been well investigated in this context, even though its involvement is suggested by the protracted functional consequences of ICU-AW. Recent data suggest that muscle regeneration could be impaired after sepsis, and that Mesenchymal Stem Cells (MSCs) treatment could improve the post-injury muscle recovery. There is no specific treatment of ICU-AW, its prevention relying on early mobilization, discontinuation of sedation and neuromyotoxic drugs whenever possible.

Contributing factors for acquired muscle weakness in intensive care unit

Introduction: One of the complications of intensive care unit (ICU) admission is neuromuscular dysfunction because of critical illness, which may lead to disuse atrophy. Many of critically ill patients have severe muscle weakness, which has been termed ICU-acquired weakness (ICU-AW). ICU-AW has many consequences on patients’ outcome. The aim of the study was to determine contributing factors for occurrence of acquired muscle weakness in intensive care units. Setting: The study was conducted in four general ICUs in two selected Hospitals in Makkah in KSA. Subjects: Hundred patients were included in the study. Materials and Method: Tool one: factors contributing to ICU-AW assessment tool. Tool two: indicators of ICU-AW in critically ill patients. Results: Forty-two patients were diagnosed ICU-AW. Differences between the ICU-AW group and the no ICU-AW group in: sex, diagnosis on admission and APACHE II were not statistically significant. Age in the ICU-AW group was higher than in no ICU-AW group [59±14 vs. 53±11 years, p = .0183] which was significant statistical difference. Conclusion: The contributing factors for ICU-AW are immobility, patients’ age, level of consciousness, parenteral nutrition, and glucocorticoid & insulin therapy.

Drug-induced cortisol deficiency as a cause of intensive care unit weakness

Drug-induced cortisol deficiency as a cause of intensive care unit weakness

Generalized Paralysis in the Intensive Care Unit: Emphasis on the Complications of Neuromuscular Blocking Agents and Corticosteroids

Generalized weakness in intensive care unit (ICU) patients is increasingly recognized as a frequent complication and a common cause of prolonged ventilator dependency. Intravenous corticosteroids and neuromuscular blocking agents, sepsis, and multiorgan failure have been strongly implicated in the ICU paralysis syndromes, but the pathophysiology of these disorders is poorly understood. The combination of neuromuscular blocking agents and corticosteroids may induce three distinct syndromes of generalized weakness in ICU patients: acute myopathy, prolonged neuromuscular blockade, and critical illness polyneuropathy. More than one syndrome may occur simultaneously, and the distinctions may be difficult in a particular patient, but a specific diagnosis usually can be established after careful clinical, electrodi-agnostic, and histological evaluation. Acute myopathy with generalized weakness, preserved eye movements, elevated creatine kinase levels, and myopathic motor units on electromyography (EMG) have developed in asthmatics requiring neuromuscular blockers and steroids. Muscle biopsy has shown distinctive changes, with fiber atrophy, scattered necrosis, and thick (myosin) filament depletion on ultrastructural studies. Patients who have had a prolonged ICU stay or sepsis with failure to wean from the ventilator, distal weakness, and areflexia probably have critical illness polyneuropathy. EMG in these patients has demonstrated reduced or absent motor and sensory potentials with neurogenic motor units. Prolonged neuromuscular blockade most commonly has occurred in patients with renal failure who received prolonged infusions of neuromuscular blockers. Severe flaccid, areflexic paralysis with normal sensation, facial weakness, and ophthalmoparesis persists for days or weeks after the neuromuscular blockers have been discontinued. Repetitive nerve stimulation has shown a decrement of the compound muscle action potential, and it establishes a disorder of neuromuscular transmission in most patients. We critically examine the clinical, electrophysiological, and pathological features of each of these syndromes, and we summarize current understanding of the pathophysiology of these disorders and the relationship to neuromuscular blocking agents and corticosteroids.