Intensive Care Unit Acquired Weakness and Recovery From Critical Illness
Marwa Ali Mohammed;
Abstract
Intensive Care Unit Acquired Weakness (ICUAW) is syndrome of generalized limb weakness that develops while the patient is critically ill and for which there is no alternative explanation other than the critical illness itself.
ICUAW is clinically detected weakness in critically ill patients in whom there is no etiology other than critical illness. Patients with ICUAW are then classified into those with critical illness polyneuropathy (CIP), critical illness myopathy (CIM), critical illness neuromyopathy (CINM). Those with (CIM) are further subclassified histologically into: cachectic myopathy, thick filament myopathy, and necrotizing myopathy.
Reasons for the development of muscle weakness are multifactorial, including premorbid conditions (for example, malignancy), as well as conditions that the patient may developed in the ICU, such as systemic inflammation, prolonged ventilation, and prolonged bed rest. The occurrence of ICUAW varies considerably depending on the patient case, diagnostic method used, and the timing of examination.
The muscles of patients with ICUAW demonstrate a range of alterations, muscle strength depends on the force-generating capacity of the muscle and the muscle mass, and both are thought to be affected in ICUAW. Clinically, this manifests as muscle wasting preceded by abnormal. Muscle electrophysiology. A key feature of the disease is a marked loss of thick myosin filaments with disruption to the actin: myosin ratio and a disruption of the myofilament organisation of the tissue. Other mechanisms that contribute to the loss of power include neuropathy, a reduction in energy generation by the muscle through insulin resistance and mitochondrial dysfunction, dysregulation of calcium handling and electrical inexcitability.
ICUAW is clinically detected weakness in critically ill patients in whom there is no etiology other than critical illness. Patients with ICUAW are then classified into those with critical illness polyneuropathy (CIP), critical illness myopathy (CIM), critical illness neuromyopathy (CINM). Those with (CIM) are further subclassified histologically into: cachectic myopathy, thick filament myopathy, and necrotizing myopathy.
Reasons for the development of muscle weakness are multifactorial, including premorbid conditions (for example, malignancy), as well as conditions that the patient may developed in the ICU, such as systemic inflammation, prolonged ventilation, and prolonged bed rest. The occurrence of ICUAW varies considerably depending on the patient case, diagnostic method used, and the timing of examination.
The muscles of patients with ICUAW demonstrate a range of alterations, muscle strength depends on the force-generating capacity of the muscle and the muscle mass, and both are thought to be affected in ICUAW. Clinically, this manifests as muscle wasting preceded by abnormal. Muscle electrophysiology. A key feature of the disease is a marked loss of thick myosin filaments with disruption to the actin: myosin ratio and a disruption of the myofilament organisation of the tissue. Other mechanisms that contribute to the loss of power include neuropathy, a reduction in energy generation by the muscle through insulin resistance and mitochondrial dysfunction, dysregulation of calcium handling and electrical inexcitability.
Other data
| Title | Intensive Care Unit Acquired Weakness and Recovery From Critical Illness | Other Titles | إعتلال العضلات والأعصاب المكتسب في وحدة الرعاية المركزة | Authors | Marwa Ali Mohammed | Issue Date | 2017 |
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