Rhabdomyolysis - emergency and nephrology overview
Rhabdomyolysis is the acute breakdown of skeletal muscle with release of intracellular contents (creatine kinase [CK], myoglobin, potassium, phosphate, urate and enzymes) into the circulation.
These substances produce systemic derangement and can cause acute kidney injury (AKI) through tubular obstruction, direct tubular toxicity and intrarenal vasoconstriction.
Major immediate risks are life‑threatening hyperkalaemia, metabolic disturbance, hypovolaemia, compartment syndrome and, in severe cases, disseminated intravascular coagulation (DIC) and multiorgan failure.
Pathophysiology (concise)
- Sarcolemmal disruption (trauma, ischaemia, toxins, exertion, seizures, heat) leads to intracellular Ca2+ influx, sustained contraction, protease activation and necrosis.
- ATP depletion and hypoxia exacerbate muscle injury.
- Cell membrane pump failure releases potassium, phosphate, CK, urate and myoglobin into the blood.
- Myoglobin injures the kidney by:
- tubular obstruction (myoglobin casts, worse in acidic urine),
- direct cytotoxicity from heme products,
- intrarenal vasoconstriction (nitric oxide scavenging).
- Systemic consequences include hyperkalaemia, hyperphosphataemia, early hypocalcaemia (with potential delayed hypercalcaemia), metabolic acidosis and raised urate.
Common causes (ED‑relevant)
- Traumatic/crush injury, prolonged compression or “long‑lie”