Critical illness myopathy: what is happening?

Friedrich, Oliver

doi:10.1097/01.mco.0000232900.59168.a0

Cited by 47 publications

(31 citation statements)

References 84 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…This therapy is currently the only pharmacological intervention that has been shown to be effective in prevention of ICUAW. The mechanisms for this are unclear, but it is thought that treatment with insulin helps to combat insulin resistance and, thereby, protects against bioenergetic failure [105]. Insulin therapy upregulates GLUT4 and hexokinase, resulting in increased insulin-controlled uptake of glucose into skeletal muscle and, therefore, more availability for mitochondrial function.…”

Section: Bioenergenetic Failure Oxidative Stress and Glycaemic Controlmentioning

confidence: 99%

See 1 more Smart Citation

Molecular mechanisms of intensive care unit-acquired weakness

Bloch¹,

Polkey²,

Griffiths³

et al. 2011

Eur Respir J

View full text Add to dashboard Cite

Intensive care unit-acquired weakness (ICUAW) is an increasingly recognised and important clinical consequence of critical illness. It is associated with significant morbidity and mortality. The aetiology of this disease is not well understood. The purpose of this article is to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and aetiology.Key features of the disease are loss of muscle mass resulting from a shift in the dynamic balance of muscle protein synthesis and breakdown and a reduction in force-generating capacity. These alternations are secondary to neuropathy, disruption of the myofilament structure and function, a disrupted sarcoplasmic reticulum, electrical inexcitability and bioenergenetic failure.As knowledge and understanding of ICUAW grows, potential therapeutic targets will be identified, hopefully leading to multiple strategies for prevention and treatment of this important condition.

show abstract

Section: Bioenergenetic Failure Oxidative Stress and Glycaemic Controlmentioning

confidence: 99%

“…This condition is termed bioenergenetic failure [105]. Glucose is a primary source of energy used by muscle.…”

Section: Bioenergenetic Failure Oxidative Stress and Glycaemic Controlmentioning

confidence: 99%

Molecular mechanisms of intensive care unit-acquired weakness

Bloch¹,

Polkey²,

Griffiths³

et al. 2011

Eur Respir J

View full text Add to dashboard Cite

show abstract

“…Atrophy and loss of myosin both cause weakness due to loss of force generation following muscle fiber action potentials. The causes of muscle atrophy and loss of myosin are complex and are still poorly understood [5,39] and while very important, will not be discussed further. The third factor is loss of the ability of muscle fibers to generate action potentials, which results in electrical inexcitability of muscle [29,30,40].…”

Section: Mechanisms Underlying Acquired Paresis In Cimmentioning

confidence: 99%

Mechanisms of Neuromuscular Dysfunction in Critical Illness

Khan

Harrison

Rich

2008

Critical Care Clinics

View full text Add to dashboard Cite

The development of neuromuscular dysfunction (NMD) during critical illness is increasingly recognized as a cause of failure to wean from mechanical ventilation and is associated with significant morbidity and mortality. At times it is difficult to identify the presence of NMD and distinguish the etiology of the weakness in patients with critical illness, but subtle clinical findings and bedside electrophysiological testing are helpful in establishing the diagnosis. The purpose of this review is to describe the clinical spectrum of acquired neuromuscular weakness in the setting of critical illness, provide an approach to diagnosis, and to discuss its pathogenesis. Finally, we propose defective sodium channel regulation as a unifying mechanism underlying NMD in critically ill patients.

show abstract

“…Corticosteroids may also play an important role in muscle wasting in CIM [78]. Muscle wasting [54,79] represents a depletion of muscle proteins due to hypercatabolic conditions.…”

Section: Risk Factors and Pathophysiologymentioning

confidence: 99%

Neurological Sequelae of Sepsis: II) Neuromuscular Weakness

Axer¹

2011

TOCCMJ

View full text Add to dashboard Cite

Abstract:Critical illness polyneuropathy (CIP) and critical illness myopathy (CIM) have been established as separate entities of muscular weakness in critically ill patients, although both may be associated to each other in some respects. Both are associated to systemic inflammatory response syndrome, sepsis, and severe sepsis. Major signs of nerve and muscle disturbances in critically ill patients are muscle weakness and problems of weaning from the ventilator. Electroneurographic measurements help to detect CIP early in the course of the disease, while muscle biopsy seems to date the diagnostic tool of choice to detect CIM. Sepsis therapy is the major target to prevent the development of CIP and CIM. However, no specific therapy of CIP and CIM has been established in the past. Therefore, management of patients with CIP and CIM is mainly supportive. Neuromuscular weakness cause elongated times of ventilation, elongated hospital stay, elongated times of rehabilitation, and increased mortality. This review provides an overview of clinical and diagnostic features of CIP and CIM, and summarizes current pathophysiological and therapeutic concepts.

show abstract

Critical illness myopathy: what is happening?

Abstract: The search for pathomechanisms is an important task for both clinical and basic sciences. Targets for treatment or prevention of critical illness myopathy include systemic inflammatory response, increased proteolysis and reduced antioxidative capacitance in critically ill patients.

Cited by 47 publications

References 84 publications

Molecular mechanisms of intensive care unit-acquired weakness

Molecular mechanisms of intensive care unit-acquired weakness

Mechanisms of Neuromuscular Dysfunction in Critical Illness

Neurological Sequelae of Sepsis: II) Neuromuscular Weakness

Contact Info

Product

Resources

About