Pathophysiology and management of rhabdomyolysis

Abstract Rhabdomyolysis is a potentially life-threatening syndrome characterized by the breakdown of skeletal muscle. It is associated with myalgia, muscle tenderness, swelling, and/or stiffness, accompanied by weakness and raised levels of creatine kinase (CK), myoglobin, phosphate and potassium, sometimes with acute kidney injury (AKI). There are multiple causes of this syndrome, traumatisms and myotoxic effect of drugs being the most frequent in developed countries. The pathophysiology involves direct trauma, as well as energy (ATP) depletion with disruption of sarcolemma integrity and muscle destruction. The sequestration of plasma water leads to hypovolaemic shock, while the release of muscle content, mainly myoglobin and potassium lead to the most severe complications of this syndrome, acute kidney injury/hyperkalaemia. The kidney injury is driven both by renal ischaemia due to vasoconstriction and to the toxic effects of myoglobin. The local oedema produced by the release of muscle content remains trapped within the fascia and can lead to compartment syndrome. Volume repletion with saline is essential to avoid hypovolaemic shock and acute kidney injury (AKI). With respect to compartment syndrome, close monitoring of clinical signs and compartment pressures is essential, since it can evolve to a surgical emergency. The prognosis of rhabdomyolysis is determined by age, baseline conditions and, most importantly, whether or not severe AKI develops.