Hussam Mustafa Rawas^1,, Mazen Alaadeen Nassar¹, Ammar Adnan AbuSeer², Abdullah Hussain Khan², Haytham Abdulsalam Nasrulden³, Lamees Abdulelah subhi², Saleh Tariq Baaziz³, Moatz Obaidulrahman Alhandi⁴

Background: Muscle weakness is common in the surgical intensive care unit (ICU). Low muscle mass at ICU admission is a significant predictor of adverse outcomes. The consequences of ICU-acquired muscle weakness depend on the underlying mechanism. Severe perioperative acquired weakness that is associated with adverse outcomes (prolonged mechanical ventilation, increases in ICU length of stay, and mortality) occurs with persistent (time frame: days) activation of protein degradation pathways, decreases in the drive to the skeletal muscle, and impaired muscular homeostasis. Methods: In this article, we review the current state-of-the-art of the basic pathophysiology of nerve and muscle weakness after critical illness and explore the current literature on ICUAW with a special emphasis on the most important mechanisms of weakness. In addition to review our understanding of the molecular pathogenesis of ICUAW in the context of current knowledge of clinical risk factors and etiology. Results: ICU-AW can be caused by a critical illness polyneuropathy, acritical illness myopathy, or muscle disuse atrophy, alone or in combination. Its diagnosis requires both clinical assessment of muscle strength and complete electrophysiological evaluation of peripheral nerves and muscle Conclusion: ICU-AW can be prevented by early treatment of the underlying disease, goal-directed therapy, restrictive use of immobilizing medications, optimal nutrition, activating ventilatory modes, early rehabilitation, and preventive drug therapy.

muscle weakness, ICU-acquired weakness