Rhabdomyolysis
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Introduction

Rhabdomyolysis is the result of breakdown of muscle tissue, with the subsequent release of muscle products into the bloodstream.

Aetiology

Causes
  • Trauma – most common
  • Prolonged immobilisation
  • Drug reactions – e.g. statins, fibrates, alcohol, ecstacy, heroin, carbon monoxide, neuroleptic malignant syndrome
  • Infection – coxackie, EBV, influenza
  • Metabolic disorders
  • Genetic muscular disorders – e.g. McArdle’s disease, Duchenne’s muscular dystrophy
 

Pathology

The breakdown of muscle tissue release several products into the blood, including:
  • Myoglobin
  • Potassium – resulting in hyperkalaemia
  • Creatinine kinase (CK)
  • Phopsphate urate
 

Signs & Symptoms

  • Often associated with the cause
  • Muscle aches
  • Oedema
  • Red-brown urine
 

Complications

Investigations

  • Bloods
    • ↑CK > 1000iU/L
    • U+E’s – hyperkalaemia
  • Urine Dipstick
    • +ve for haemoglobin, but absence of red cells on microscopy – due to myoglobin

Treatment

  • URGENT – treat hyperkalaemia (if >6.5mmol/L, or ECG changes)
    • Untreated, it can cause VENTRICULAR FIBRILLATION
      • Other ECG changes include; ‘tented T waves’, flat p waves, increased PR interval, wide QRS – which can get wider and wider, resulting in VT and VF
    • Treatment
      • IV calcium gluconate – this provides cardioprotection but does not alter serum potassium concentration
      • Insulin + glucose – e.g. 20U insulin + 50g glucose 50% IV. Insulin is taken up into cells in conjunction with potassium, thus, serum K is lowered
      • Nebulised salbutamol – also moves K into cells
      • Polysytrene sulfonate resin – 15g/8h in water, or can be given as an enema if vomiting present (can cause vomiting)
      • Dialysisrarely needed
  • IV fluids
    • Reduce the risk of ARF
    • Keep urine output at >300ml/hour until myoglobinurea is resolved
    • 1.5L/hour may be required
  • IV sodium bicarbonate
    • Can be useful to increase the urine pH >6.5, which makes myoglobin less toxic
  • With treatment, most patients make a full recovery (as the cause is usually identifiable and resolvable), without any long-term effects

References

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Dr Tom Leach

Dr Tom Leach MBChB DCH EMCert(ACEM) currently works as a GP Registrar and an Emergency Department CMO in Australia. He is also a Clinical Associate Lecturer at the Australian National University. After graduating from his medical degree at the University of Manchester in 2011, Tom completed his Foundation Training at Bolton Royal Hospital, before moving to Australia in 2013. He started almostadoctor whilst a third year medical student in 2009. Read full bio

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