Approach

The treatment goal is to prevent complications, primarily acute kidney injury (AKI). The mainstay of therapy is aggressive rehydration to promote renal clearance of released intracellular muscular toxins.[2][31][32] Typically, this is initiated with either lactated Ringer’s solution or saline (0.9% or 0.45%).[2] A starting rate of 400 mL/hour with a range of 200 mL/hour to 1000 mL/hour is considered reasonable as goal-directed therapy, with a urine output target of 300 mL/hour.[2][31][33] Potential complications are related to over-hydrating the anuric patient and include fluid retention and congestive heart failure.

Myoglobin is toxic to renal tubules in acidic urine, and some specialists recommend concurrent use of intravenous sodium bicarbonate to alkalinise the urine and prevent crystallisation of uric acid. Some evidence suggests that a urine pH >6.0 is protective.[34][35] This is difficult to achieve without the use of large amounts of bicarbonate and, although some specialists may recommend urine alkalinisation, benefits of its use lack robust evidence-based support.[30][32][35][36] European protocols report limited clinical evidence to support bicarbonate therapy.[31] BAPEN: British consensus guidelines on intravenous fluid therapy for adult surgical patients Opens in new window Should the clinical decision be made to attempt urine alkalinisation, pharmacy consultation should be considered to determine appropriate continuous intravenous therapy mixtures.

The use of diuretic therapy to promote diuresis is unclear. The benefits of diuretic therapies (e.g., mannitol, furosemide) and at what point to administer them have not been prospectively studied. Reports have been spurious and anecdotal, and guidelines do not generally support their use.[2][31][32][37][38][39]

The American Association for the Surgery of Trauma does not recommend the use of either bicarbonate or diuretics for the treatment of rhabdomyolysis, due to a lack of high quality evidence.[2]

Hyperkalaemia and other electrolyte abnormalities (e.g., hyperphosphataemia and hypocalcaemia) are common. Hyperkalaemia from rhabdomyolysis-induced AKI may occur early in the disease process, and should be monitored closely due to the risk of cardiac arrhythmias.[2] Potassium levels >6 mmol/L (>6 mEq/L) require cardiac monitoring. Electrocardiographic changes of hyperkalaemia require treatment with calcium gluconate. Elevated potassium levels should be treated with insulin and glucose infusions, salbutamol inhalation, cation exchange resins, or dialysis as indicated.[2] Other electrolyte abnormalities should be meticulously monitored and corrected as required.[2]

In patients with rhabdomyolysis who develop AKI and need renal replacement therapy (RRT), either continuous RRT (CRRT) or intermittent RRT (e.g., haemodialysis) should be used based on the degree of renal impairment and the clinical status of the patient. There are no recommendations regarding RRT modalities (filtration vs. diffusion), filter type (low vs. high cut-off membranes), or high-flow versus low-flow dialysis.[2] Dialysis corrects refractory metabolic acidosis, hypervolaemia, and electrolyte abnormalities in patients with rhabdomyolysis and AKI.[40] However, there is no evidence to support a role for RRT in the prevention of AKI in patients with rhabdomyolysis without significant renal impairment; utilisation of dialysis should be based on standard indications for AKI refractory to medical management.[2]

Use of this content is subject to our disclaimer