By damaging cell membrane integrity, acute rhabdomyolysis leads to electrolyte shifts according to the concentration gradients and the liberation of intracellular substances. Diagnosis is confirmed by the presence of a high serum creatinkinase activity (CK) and myoglobinuria. For clinical purposes myoglobinuria is demonstrated by a blood-positive dipstick in the absence of hematuria or hemoglobinuria. Rhabdomyolysis is usually acquired and is rarely due to hereditary enzyme defects. The authors report on 61 patients admitted in the last 15 years with rhabodomyolysis. In the past 4 1/2 years the diagnosis was suggested by CK greater than 5000U/1 in 49 patients, representing 1.6% of all admissions in the departments of medicine and surgery. Originally described in crush situations, rhabdomyolysis has been observed with increasing frequency as a consequence of muscular stress and self crush due to coma or hemi- and paraplegia during the last decades. 24% of the patients with this diagnosis had had an intoxication, and in 70% there were multiple simultaneous causes. Autoimmune diseases, infections of bacterial, viral and fungal origin, endocrinopathies, and thermic and ischemic injuries can also provoke rhabdomyolysis. As a consequence of fluid shift into the damaged muscle a compartment syndrome may lead to vascular or neural defects. In 80% of cases there is initial hypocalcemia, turning later into hypercalcemia. Other frequent electrolyte disorders accompanying rhabdomyolysis are hyperkalemia, hyperphosphatemia and a widened anion gap. 6 of 13 patients showed the typical blood changes found in patients with disseminated intravascular coagulation. Acute renal failure developed in 30 patients, 15 of whom underwent dialysis or hemofiltration.(ABSTRACT TRUNCATED AT 250 WORDS)