rhabdomyolysis

Rhabdomyolysis is a clinical syndrome caused by skeletal muscle breakdown with leakage of intracellular constituents into the bloodstream, especially creatine kinase and myoglobin. It can range from asymptomatic enzyme elevation to life-threatening acute kidney injury.

Signs and symptoms include proximal muscle pain and weakness, swelling, and dark brown or reddish urine (myoglobinuria). Some patients have malaise, nausea, or confusion; fever is not common.

Causes are diverse: traumatic injuries and crush injuries, prolonged immobility, strenuous exercise, seizures, overheating; drugs and toxins (statins, fibrates, illicit drugs, alcohol, certain antibiotics); infections, metabolic disorders, and genetic myopathies.

Pathophysiology: damage to muscle cell membranes releases CK, myoglobin, potassium, and phosphate. Myoglobin can cause pigment nephropathy, contributing to acute kidney injury, especially with dehydration and hypotension; electrolyte disturbances such as hyperkalemia can occur.

Diagnosis: high serum CK is central, often markedly elevated (thousands of units per liter). Urinalysis may reveal blood with few red cells due to myoglobinuria. Kidney function and electrolytes should be checked; consider ECG for hyperkalemia.

Management: prompt intravenous isotonic hydration (normal saline) to preserve urine output; correct electrolytes; avoid nephrotoxins. Urinary alkalinization is controversial; renal replacement therapy may be needed for severe AKI or persistent electrolyte disturbances.

Prognosis and prevention: most recover with timely treatment, but severe AKI or complications can occur. Prevention includes ensuring hydration, gradual return to activity after intense exercise, and review of medications that raise risk (notably statins with interacting drugs).