Weakness In Intensive Care Unit Patients Research Articles

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

ABSTRACTIntroductionCritical 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.MethodsThe 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.ResultsAll 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%.ConclusionMuscle STIR imaging may help to differentiate between CIMN and GBS.How to cite this articleMaramattom 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.

Critical illness myopathy in a cervical spine-injured patient.

Neuromuscular weakness acquired in the intensive care unit (ICU) causes significant impairment in critically ill patients. The spectrum of critical illness neuromuscular disease includes critical illness myopathy, critical illness polyneuropathy or both, and occurs in approximately one-third of patients admitted to the ICU and those who are ventilated for at least 7 days. Recognized risk factors include sepsis, systemic inflammatory response syndrome, multi-organ failure, neuromuscular blocking agents and corticosteroids, however the absence of predisposing factors should not preclude critical illness neuromuscular disease. A 23-year-old male suffered a cervical spine injury and was admitted to the ICU. Two weeks post admission, he lost all power in his upper limbs, neck and face. Nerve conduction studies and needle electromyography were performed 4 weeks and 3 months after the injury, suggesting that myopathy was the likely cause of weakness. The definitive diagnosis of critical illness myopathy was based on muscle biopsy demonstrating myosin filament loss. Evaluation of new-onset weakness in ICU patients is essential to distinguish neurological causes from complications of critical illness. Signs and symptoms of critical illness neuromuscular disease must be identified early to encourage recovery, promote rehabilitation, and reduce morbidity and mortality.

Electrophysiology of neuromuscular disorders in critical illness

Neuromuscular disorders, predominantly critical illness myopathy (CIM) and critical illness polyneuropathy (CIP) occur in approximately one-third of patients in intensive care units. The aim of this study was to review the important role of electrophysiology in this setting. In CIM, sarcolemmal inexcitability causes low amplitude compound muscle action potentials (CMAPs) that may have prolonged durations. Needle electrode examination usually reveals early recruitment of short duration motor unit potentials, often with fibrillation potentials. In CIP, the findings are usually those of a generalized axonal sensorimotor polyneuropathy. Direct muscle stimulation aids in differentiating CIP and CIM and in identifying mixed disorders along with other electrodiagnostic and histopathologic studies. Identifying evolving reductions in fibular CMAP amplitudes in intensive care unit (ICU) patients predicts development of neuromuscular weakness. Knowledge of the various neuromuscular disorders in critically ill patients, their risk factors, and associated electrodiagnostic findings can lead to development of a rational approach to diagnosis of the cause of neuromuscular weakness in ICU patients.

Time Resolved Analyses of Gene Expression in a Rodent Icu Model

Intensive care unit (ICU) patients commonly develop severe skeletal muscle wasting that aggravate the recovery from the primary disease and weaning from respirator. The modern treatment in anesthesiology and intensive care can progress in Acute Quadriplegic Myopathy (AQM). This study aims at improving our understanding of the mechanisms underlying the muscle wasting and weakness in ICU patients with AQM. Specific interest is focused on duration-dependent effects on intracellular signaling and myofibrillar gene and protein expression. For that reason, a unique experimental rat model mimicking ICU such as mechanical ventilation, muscle unloading, neuromuscular blocking agents (NMBA) administration and monitoring at different time points from 6h to 14 days, was used. Gene expression profile was analyzed in gastrocnemius muscle, showing an increased expression in the muscle-specific ubiquitin ligases, atrogin-1 and MuRF-1 after 6 h, as well as other genes involved in translational repression, authophagic/lysosomal genes (LC3b, cathepsins), oxidative stress response and up-regulation of pro-apoptosis signaling, except caspase-3 that increased after 9 days of intervention. Metalloproteins, GST, cystatins and cell cycle repressors were up-regulated in the early stages in response to oxidative stress and cellular damage among other genes, while LIM and sarcomeric proteins, collagen, extracellular matrix transcripts, carbohydrate metabolism, mitochondrial genes and the muscle-specific calpain-3 were down-regulated mainly after 5 days. These results suggest a very complex, unique and highly temporally coordinated activation of protein synthesis, degradation, protective mechanisms and intracellular signaling activation at different time points during ICU conditions.

Methodologies for Performing Non-Invasive Stimulated Muscle Force Assessment in Critically Ill Patients

Objective: To optimize the assessment of muscle weakness in critically ill patients in the intensive care unit (ICU) by development non-invasive, reproducible assessment devices and application protocols. Methods: For over 5years we evaluated weakness in ICU patients by employing a prototype non-invasive muscle force assessment system. We determined peak torques, peak rates of torque development and decay of the ankle dorsiflexors after supramaximal peroneal nerve stimulation. We continue to test modifications of our devices (i.e. different stabilizing boots, extendable leg support systems, electrodes) so to optimize this important clinical assessment. Results: Measurements were performed in over 30 severely ill adult patients. During their illnesses, one observed dramatic reductions in stimulated torques, and during the recovery period, values increased to 70–80% of initial values. In those patients who died, the values continuously decreased until death. Throughout these investigations, several technical problems arose: i) the current device could not be used on patients in a prone position; ii) the mechanism used to adjust and lock ankle slipped; iii) edema made nerve stimulation difficult (altered skin conductance and difficult to maintain electrode position); iv) device was bulky for positioning (e.g., weight), and∕or v) stimulus parameters could not be readily adjusted. Discussion: Stimulated muscle force assessment can be used to study ICU patients’ forces. Nevertheless, next generation force assessment systems should be smaller, lighter, more portable, with a simple angle adjustment means, easier to use with a computer-controlled stimulator and include EMG recordings.

Myopathy in critically ill patients.

To review myopathic changes occurring during intensive care treatment in the light of recent information about manifestation, clinical settings, pathophysiology, and histomorphologic changes. The computerized MEDLINE database, bibliography of pertinent articles, and the author's personal files. Studies were selected according to their relevance to myopathic complications in critically ill patients. All applicable data were extracted. Myopathic changes occur frequently in patients treated in the intensive care unit (ICU). Three main types have been identified: critical illness myopathy, myopathy with selective loss of myosin filaments, and acute necrotizing myopathy of intensive care. These histologic types probably represent variable expressions of a toxic effect not yet identified. Candidates for such myotoxic effects are the mediators of the systemic response in sepsis and high-dose administration of corticosteroids and muscle relaxants. The influence of these latter agents appears to be particularly important in the pathogenesis of myosin loss and myonecrosis. Experimental studies suggest that axonal damage attributable to critical illness neuropathy can be an additional factor triggering myopathies in the ICU. Muscle membrane inexcitability was recently identified as an alternative mechanism of severe weakness in ICU patients. Myopathic changes are surprisingly frequent in critically ill patients. The clinical importance of this finding is still unknown, but it is likely that weakness caused by myopathy prolongs ICU stay and rehabilitation. Because corticosteroids and muscle relaxants appear to trigger some types of ICU myopathy, they should be avoided or administered at the lowest doses possible. Sepsis, denervation, and muscle membrane inexcitability may be additional factors. Studies addressing the pathophysiology of myopathy in critically ill patients are urgently needed.

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.