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Rhabdomyolysis means a breakdown of striated muscle, allowing myoglobin, muscle enzymes, potassium, and other intracellular constituents to leak in to the blood. It has a long and varied list of causes including infections, drugs (including statins), trauma, reperfusion injury, and genetic myopathies. Rhabdomyolysis has also been reported in athletes, particularly long distance runners and body builders. Severe or unaccustomed exercise in high temperatures is particularly risky for polo ponies and race horses as well as humans. In severe cases, the resulting hyperkalaemia, hypocalcaemia and renal failure can be fatal. Milder rhabdomyolysis is easy to miss because the tell tale physical sign—severe myoglobinuria causing tea coloured urine—occurs only after 100g muscle has been destroyed. Once recognised, the aim of treatment is to protect renal function (myoglobin is a renal toxin) and restore normal plasma biochemisty, especially potassium. Intravenous saline and sometimes mannitol are used to expand the intravascular volume and increase urine output to more than 200ml/hr. Frequent monitoring of plasma biochemistry is essential. If acute renal failure ensues despite these measures, continuous haemofiltration or haemodialysis may be required until renal function recovers. There are no randomised trials evaluating the management of rhabdomyolysis. But the fundamental principles have been agreed by consensus. Prognosis is excellent for uncomplicated cases once the cause has been identified, and reversed wherever possible.