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Rhabdomyolysis and multiple system organ failure with streptokinase

BMJ 1995; 311 doi: https://doi.org/10.1136/bmj.311.7018.1472 (Published 02 December 1995) Cite this as: BMJ 1995;311:1472
  1. H E MONTGOMERY, Drs,
  2. C W MCINTYRE,
  3. M K ALMOND,
  4. K DAVIES,
  5. C W PUMPHREY,
  6. D BENNETT
  1. Hatter Institute for Cardiovascular Research, University College Hospital, London WC1E 6AU)
  2. Renal Unit, Southend General Hospital, Essex)
  3. Department of Rheumatology, Hammersmith Hospital, London W12 0NN
  4. Cardiology and Intensive Care Units, St George's Hospital, London SW17

    Write: We report two cases of rhabdomyolysis and multiple system organ failure with streptokinase treatment.

    A 47 year old normotensive (110/70 mm Hg) man with normal renal function suffered an inferoposterior myocardial infarction treated with oral aspirin (300 mg). Lumbar pain accompanied intravenous streptokinase (1.5x106 units over one hour). At three hours renal, respiratory, and high output circulatory failure with fever ensued despite inotropes and fluids. At 17 hours his temperature was 39.2°C, blood pressure 70/40 mm Hg, urea 22 mmol/l, creatinine 400 μmol/l; urine red+ and white cells+ and cellular and hyaline casts+; PaO2 5.5 kPa breathing 60% O2, and a chest x ray film was suggestive of the adult respiratory distress syndrome. His cardiac output was 9.8 l/min, systemic vascular resistance 410 dyn.s/cm-5, and pulmonary capillary wedge pressure 15 mm Hg. Transthoracic echocardiography showed no aortic dissection; erythrocyte sedimentation rate was 102 millimetres in the first hour; no cryoglobulins were detected; rhabdomyolysis and complement consumption were noted (figure). Radial immunodiffusion assay,1 showed steptokinase IgG (titres of 40 before streptokinase and 320 at one week). Screens for infection were all negative. Flaccid tetraparesis developed. He never suffered bruising or rashes, and died on day 17.

    A 62 year old man suffered an acute anterior myocardial infarction, treated as above. Without hypotension, acute renal failure and rhabdomyolysis occurred by day 3 (urea 63.1 mmol/l, creatinine 787 μmol/l, corrected calcium 2.67 mmol/l, phosphate 3.75 mmol/l, uric acid 1.15 mmol/l, creatine kinase 5231 IU/l, creatine kinase MB fraction <2% on day 3, aspartate aminotransferase 2426 IU/l). Urine analysis showed blood++, protein++. Screens for infection were negative. A chest x ray film showed pulmonary oedema. Renal tract ultrasound was normal. Creatine kinase was >5000 IU/l for 7 days and was raised to day 15. He died on day 23. Postmortem examination showed acute tubular necrosis with red cell and pigmented granular casts. Skeletal muscle (three groups) showed foci of muscle fibre degeneration, regeneration, and calcification consistent with rhabdomyolysis.

    We postulate an immunopathogenic mechanism, possibly through sensitisation by rheumatic fever, in the first case. Streptokinase IgG titre rose, with complement consumption atypical of streptokinase infusion or mild reactions.1 Reaction to streptokinase has caused immune complex-mediated acute renal failure,2 adult respiratory distress syndrome,3 and severe back pain before,4 and rhabdomyolysis due to cholesterol microembolisation.5 Our patients had no rash or urinary cholesterol crystals. Neuropathy and streptokinase treatment have not been associated. Adverse reactions to streptokinase may mimic cardiogenic shock in producing hypotension, pulmonary oedema, renal failure, and a high serum creatine kinase concentration.

    Figure1

    Serum complement and muscle enzymes against time after streptokinase infusion. Serum complement (C3 and C4) are expressed as percentage of normal human pool

    References

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