Brief review: Nondepolarizing neuromuscular blocking drugs and critical illness myopathy (original) (raw)
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Critical illness neuromuscular disease: clinical, electrophysiological, and prognostic aspects
Archives of Disease in Childhood, 2002
Background: Critical illness neuromuscular disease, which has been recognised as a distinct clinical entity in adults, remains poorly described in children. Aims: To assess retrospectively the clinical, electrophysiological, and prognostic features of the disease. Methods: Retrospective study in a children's university hospital. Results: Five critically ill patients presented with generalised paralysis, associated with long lasting failure to breathe in three. The cause of the generalised paralysis was critical illness neuropathy in two, acute myopathy in two, and mixed neuromyopathy in one. Conclusions: Neuromuscular disease should be suspected in critically ill children with muscle weakness. Because corticosteroids and muscle relaxants appear to trigger some types of intensive care unit neuromuscular disease in children, their use should be restricted or administered at the lowest doses possible.
The myasthenic patient in crisis: an update of the management in Neurointensive Care Unit
Arquivos de Neuro-Psiquiatria, 2013
Myasthenia gravis (MG) is an autoimmune disorder affecting neuromuscular transmission leading to generalized or localized muscle weakness due most frequently to the presence of autoantibodies against acetylcholine receptors in the postsynaptic motor end-plate. Myasthenic crisis (MC) is a complication of MG characterized by worsening muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation. It also includes postsurgical patients, in whom exacerbation of muscle weakness from MG causes a delay in extubation. MC is a very important, serious, and reversible neurological emergency that affects 20-30% of the myasthenic patients, usually within the first year of illness and maybe the debut form of the disease. Most patients have a predisposing factor that triggers the crisis, generally an infection of the respiratory tract. Immunoglobulins, plasma exchange, and steroids are the cornerstones of immunotherapy. Today with the modern neurocritical care, mortality rate of MC is less than 5%.
Muscle atrophy and preferential loss of myosin in prolonged critically ill patients*
Critical Care Medicine, 2012
uscle weakness is a severe complication of prolonged critical illness that hampers weaning from ventilatory support, delays rehabilitation, and is associated with increased risk of death (1-5). Even long after hospital discharge, patients can experience muscle weakness and fatigue, contributing to decreased exercise tolerance and quality of life (5). The severe weakness may originate from a neurogenic and/or myogenic disturbance. The neurologic component, called "critical illness polyneuropathy" in the absence of other neuropathies, comprises axonal degeneration of sensory and motor neurons. The myogenic component may also involve impaired muscle membrane excitability and muscle atrophy, and may coincide with neurologic problems. Both entities share clinical symptoms and electrophysiological signs (6-8). Hence, electrophysiological differential diagnosis of critical illness neuropathy and myopathy is only possible with sophisticated techniques, and ideally requires a conscious and cooperative patient. A biochemical marker of muscle mass or loss during critical illness could theoretically be a tool for characterizing myopathy. Previous studies on muscle biopsies from selected patients with established myopathy revealed a low myofibrillar protein content, loss of myosin and myosin-associated proteins associated with a low ratio of thick-to-thin filaments, and with a very low force-Objective: Muscle weakness contributes to prolonged rehabilitation and adverse outcome of critically ill patients. Distinction between a neurogenic and/or myogenic underlying problem is difficult using routine diagnostic tools. Preferential loss of myosin has been suggested to point to a myogenic component. We evaluated markers of muscle atrophy and denervation, and the myosin/actin ratio in limb and abdominal wall skeletal muscle of prolonged critically ill patients and matched controls in relation to insulin therapy and known risk factors for intensive care unitacquired weakness. Design: Secondary analysis of two large, prospective, singlecenter randomized clinical studies. Setting: University hospital surgical and medical intensive care unit. Patients: Critically ill patients and matched controls. Interventions: Intensive care unit patients had been randomized to blood glucose control to 80-110 mg/dL with insulin infusion or conventional glucose management, where insulin was only administered when glucose levels rose above 215 mg/dL. Measurements and Main Results: As compared with controls, rectus abdominis and vastus lateralis muscle of critically ill patients showed smaller myofiber size, decreased mRNA levels for myofibrillar proteins, increased proteolytic enzyme activities, and a lower myosin/actin ratio, virtually irrespective of insulin therapy. Increased forkhead box O1 action may have played a role. Most alterations were more severe in patients treated with corticosteroids. Duration of corticosteroid treatment, independent of duration of intensive care unit stay or other risk factors, was a dominant risk factor for a low myosin/actin ratio. The immature acetylcholine receptor subunit ␥ messenger RNA expression was elevated in vastus lateralis, independent of the myosin/actin ratio. Conclusions: Both limb and abdominal wall skeletal muscles of prolonged critically ill patients showed downregulation of protein synthesis at the gene expression level as well as increased proteolysis. This affected myosin to a greater extent than actin, resulting in a decreased myosin/actin ratio. Muscle atrophy was not ameliorated by intensive insulin therapy, but possibly aggravated by corticosteroids. (Crit Care Med 2012; 40:79-89) KEY WORDS: critical illness polyneuropathy/myopathy; hyperglycemia; intensive care; insulin; muscle catabolism *See also p. 314.
Jpma the Journal of the Pakistan Medical Association, 2010
Critical illness myopathy (CIM) is a syndrome of widespread muscle weakness and neurological dysfunction which can develop in critically ill patients receiving intensive care. CIM are often distinguished largely on the basis of specialized electrophysiologic testing or muscle and nerve biopsy and its causes are unknown, though they are thought to be a possible neurological manifestation of systemic inflammatory response syndrome usually developing in patients after a brief period of stay in the Intensive Care Unit (ICU). This case report aims to analyze the Clinical feature, diagnosis and treatment of CIM of 60 years old male case with Chronic Obstructive Lung disease (COPD) admitted to the intensive care. Health professionals working at critical care unit should be aware that any ICU patient may develop CIM.
Undiagnosed myopathy before surgery and safe anaesthesia table
Acta myologica : myopathies and cardiomyopathies : official journal of the Mediterranean Society of Myology / edited by the Gaetano Conte Academy for the study of striated muscle diseases, 2013
Patients with muscle pathology are a challenge for anaesthesiologists because of possible life-threatening general anaesthesia complications. A review of the current medical literature on the issue clearly indicates that increasing awareness by anaesthesiologists in recent years has led to a reduction in the occurrence of adverse events in patients with diagnostically well-defined muscle disease. On the other hand, the current emerging aspect is that the great majority of complications concern subjects with clinically non-overt (silent to mildly symptomatic) and thus undiagnosed myopathy. With a view to improving prevention of possible critical anaesthesia complications in such patients, we present a "Safe Anaesthesia Table", listing both the anaesthetic drugs to be avoided and those considered harmless for myopathic patients, irrespective of age and type of pathology. In addition, a brief outline about the clinical aspects suggestive of a possible muscle pathology is also...
Neuromuscular Disorders in Critically Ill Patients: Review and Update
Journal of Clinical Neuromuscular Disease, 2011
Neuromuscular disorders that are diagnosed in the intensive care unit (ICU) usually cause substantial limb weakness and contribute to ventilatory dysfunction. Although some lead to ICU admission, ICU-acquired disorders, mainly critical illness myopathy (CIM) and critical illness polyneuropathy (CIP), are more frequent and are associated with considerable morbidity. Approximately 25% to 45% of patients admitted to the ICU develop CIM, CIP, or both. Their clinical features often overlap; therefore, nerve conduction studies and electromyography are particularly helpful diagnostically, and more sophisticated electrodiagnostic studies and histopathologic evaluation are required in some circumstances. A number of prospective studies have identified risk factors for CIP and CIM, but their limitations often include the inability to separate CIM from CIP. Animal models reveal evidence of a channelopathy in both CIM and CIP, and human studies also identified axonal degeneration in CIP and myosin loss in CIM. Outcomes are variable. They tend to be better with CIM, and some patients have longstanding disabilities. Future studies of well-characterized patients with CIP and CIM should refine our understanding of risk factors, outcomes, and pathogenic mechanisms, leading to better interventions.