Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Critical illness myopathy (CIM) which is common after sepsis and multiorgan failure also has been described after organ transplantation. Prior reports of CIM after lung transplantation have not recorded a necrotizing myopathy. We present a 42-year-old man who developed a necrotizing critical illness myopathy following bilateral orthotopic lung transplantation. In addition we provide pathological confirmation that the ventral roots, spinal cord and the rest of the neuraxis are preserved in this condition. Extensive muscle necrosis is documented.
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PMID:Flaccid quadriplegia due to necrotizing myopathy following lung transplantation. 1562 Nov 61

Myopathies occurring in critically ill patients have gained increasing interest during the past years. For the patient, they represent a crucial factor for prolonged intensive care unit treatment and secondary complications. Critical illness myopathies (CIMs) seem to be related to various pathogenic factors. Among those, the septic inflammatory response syndrome seems to play a major role. It has been suggested that, similar to sepsis-related multiorgan failure, CIM might be considered a failure of the organ muscle. Muscle function might be impaired by proposed "myotoxic" humoral factors. These could be endogenously produced during the innate immune response to sepsis. This article follows up recent evidence for such active fractions in the blood serum of CIM patients. To explain muscle weakness in CIM, serum fractions acutely modified membrane excitability and subcellular Ca2+ regulation in an animal model. From the differential serum effects, early-phase CIM seems to involve a reduction in the overall force generation in muscle but also a compensation by the membrane, increasing the excitability. Different animal models will help to elucidate the underlying mechanisms accounting for the specific proteolytic activities found in different forms of CIM. CIM represents a systemic rather than a local disorder. Humoral factors might initiate the local reaction of skeletal muscle clinically seen as muscle weakness, altered excitability, and proteolysis of contractile proteins. Establishing the interactions in the excitation-contraction cascade in CIM is a challenging task, not only to clarify its pathomechanism but also to deduce clinical interventions.
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PMID:Understanding critical illness myopathy: approaching the pathomechanism. 1598 71

Critical illness myopathy, neuropathy, and neuromyopathy are frequently encountered in the intensive care unit, particularly in the setting of sepsis and the systemic inflammatory response syndrome. A multidisciplinary approach is important to optimize management and minimize debility associated with these neuromuscular disorders. This article reviews the underlying pathophysiology, risk factors, clinical presentation, electrodiagnostic evaluation, management, and prognosis of these disorders.
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PMID:Critical illness neuromyopathy. 1819 52

Critical illness myopathy (CIM) is characterized by a preferential loss of the motor protein myosin, muscle wasting, and impaired muscle function in critically ill intensive care unit (ICU) patients. CIM is associated with severe morbidity and mortality and has a significant negative socioeconomic effect. Neuromuscular blocking agents, corticosteroids, sepsis, mechanical ventilation, and immobilization have been implicated as important risk factors, but the causal relationship between CIM and the risk factors has not been established. A porcine ICU model has been used to determine the immediate molecular and cellular cascades that may contribute to the pathogenesis prior to myosin loss and extensive muscle wasting. Expression profiles have been compared between pigs exposed to the ICU interventions, i.e., mechanically ventilated, sedated, and immobilized for 5 days, with pigs exposed to critical illness interventions, i.e., neuromuscular blocking agents, corticosteroids, and induced sepsis in addition to the ICU interventions for 5 days. Impaired autophagy as well as impaired chaperone expression and protein synthesis were observed in the skeletal muscle in response to critical illness interventions. A novel finding in this study is impaired core autophagy machinery in response to critical illness interventions, which when in concert with downregulated chaperone expression and protein synthesis may collectively affect the proteostasis in skeletal muscle and may exacerbate the disease progression in CIM.
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PMID:Impaired autophagy, chaperone expression, and protein synthesis in response to critical illness interventions in porcine skeletal muscle. 2357 37

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. 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.
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PMID:An Unusual Case of Critical Illness Polyneuromyopathy. 3220 46

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.
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PMID:Reply to the Letter to Editor Regarding "An Unusual Case of Critical Illness Polyneuromyopathy". 3296 53