Essay On Rhabdomyolysis

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Rhabdomyolysis Pathophysiology, Risk Factor, Manifestations, and treatment
Rhabdomyolysis is potentially life-threatening disease that rapidly breaks down the muscle fibers that causes the release of intracellular contents into the extracellular space and bloodstream. Physical interruptions in the sarcolemma membrane, called delta lesions, suggest that the sarcolemma membrane is the route through which muscle constituents are released (McCance & Huether, 2014).
Rhabdomyolysis is an increase in intracellular free ionized calcium due to either cellular energy depletion, or direct plasma membrane rupture. The increased intracellular calcium activates several proteases, intensifies skeletal muscle cell contractility, induces mitochondrial dysfunction, and increases the production of reactive oxygen species, ultimately resulting in skeletal muscle cell death (Giannoglou,
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Rhabdomyolysis can cause serious complications such as hyperkalemia, metabolic acidosis, acute renal failure, and cardiac arrest. Signs and symptoms of these complication complications are confusion, delirium, agitation, and seizures. The major laboratory findings are Increased myoglobin and creatinine phosphokinase because of muscular cell death.
Treatment
The main treatment for rhabdomyolysis is to preserve renal function and prevent kidney failure. Rapid intravenous hydration maintains adequate kidney flow (McCance & Huether, 2014). Other treatment includes hemodialysis, and identifying and treating the cause of the rhabdomyolysis. Other treatments, such as using mannitol to cause an osmotic diuresis or bicarbonate to alkalinize the urine, have not been shown to consistently improve outcomes (McCance & Huether, 2014). The most important and clinically useful measurement in rhabdomyolysis is serum creatinine kinase (CK) level (McCance & Huether,

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