Overview
Mechanism, Triggers, and the Renal Threat
Rhabdomyolysis is skeletal muscle necrosis with leakage of intracellular contents into the bloodstream.
Rhabdomyolysis is skeletal-muscle necrosis with leakage of intracellular contents into the bloodstream. ATP depletion or direct membrane injury causes uncontrolled calcium entry into the myocyte. Calcium activates proteases and phospholipases, the cell swells, and the sarcolemma ruptures. Creatine kinase (CK), myoglobin, potassium, phosphate, uric acid, and other substances then enter the circulation. The released potassium can produce sudden, life-threatening dysrhythmias. Phosphate binds circulating calcium, so hypocalcaemia may occur early; calcium can later move back into the circulation during muscle recovery, producing rebound hypercalcaemia. Do not treat the laboratory value in isolation. Myoglobin is filtered by the kidneys. When renal blood flow is reduced or the urine is acidic and concentrated, myoglobin can form obstructive casts. It also directly injures tubular cells and contributes to renal vasoconstriction. These effects combine to cause acute kidney injury (AKI), particularly when CK is markedly elevated, urine output falls, or dehydration is present. Common settings include crush injury, compartment syndrome, prolonged immobilisation or compression, seizures, extreme exertion, heat illness, and hyperthermic syndromes. Alcohol, cocaine, amphetamines, some prescribed medicines, and infections can also injure muscle. Statin-associated...
