Editorials

Rhabdomyolysis

BMJ 2003; 327 doi: https://doi.org/10.1136/bmj.327.7407.115 (Published 17 July 2003) Cite this as: BMJ 2003;327:115

This article has a correction. Please see:

  1. Russell Lane, consultant neurologist (r.lane@imperial.ac.uk),
  2. Malcolm Phillips, consultant nephrologist
  1. Charing Cross Hospital and Imperial College, London W6 8RF

    Has many causes, including statins, and may be fatal

    The dramatic title—Rhabdomyolysis: the hidden killer—given to a recent review of this condition emphasised that dissolution of striated muscle fibres, with leakage of muscle enzymes, myoglobin, potassium, calcium, and other intracellular constituents, can occur in anyone under particular circumstances and that the consequences can be severe and sometimes fatal.1 There are no prospective studies of the incidence of rhabdomyolysis and many mild cases probably go unrecognised.

    Rhabdomyolysis is defined as an acute increase in serum concentrations of creatine kinase to more than five times the upper normal limit—and when myocardial infarction has been excluded as a cause (CK-MB fraction less than 5%). Visible myoglobinuria (tea or cola coloured urine) occurs when urinary myoglobin exceeds 250 μg/ml (normal < 5 ng/ml), corresponding to the destruction of more than 100 g of muscle.2 3 Myoglobinuria can be inferred by a positive urine dipstick test for haem, in the absence of red cells on microscopic examination of urine.

    The causes of …

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