skeletal muscle necrosis may cause death either by:
releasing heme pigments such as myoglobin into the circulation which may result in acute renal failure, particularly if there is hypovolaemia and poor renal flow.
releasing potassium and phosphate into the circulation causing hyperkalaemia and hyperphosphataemia
severe hypocalcaemia due to deposition of calcium salts in damaged muscle and decreased bone responsiveness to parathyroid hormone
localised necrosis may also cause odema resulting in compartment syndrome
low likelihood of acute renal failure when peak creatine kinase levels are under 5,000 - 10,000 U/L
A problem that is unique to rhabdomyolysis-induced acute renal failure is the development of hypercalcaemia during the recovery phase in approximately 20 to 30 percent of patients
aetiology
mechanical injury
traumatic crush injury, particularly those trapped in vehicles after motor vehicle accidennts, or in collapsed buildings from earthquakes
prolonged muscle ischaemia from immobilisation such as patients lying comatose for hours before being found
prolonged ischaemia from tourniquets or muscle compression such as during prolonged surgical procedures
near drowning causing prolonged hypoxia &/or vasoconstriction
in the emergent Mx of a limb that is crushed, predict potential of life threatening hyperkalaemia and cardiac arrest on return of circulation once the limb is released
be aware - check CK level in those at risk
treat underlying cause
ensure adequate saline rehydration to prevent renal failure - start early - consider 1-2L/hour iv 0.9% saline initially if fluid overload is not a risk. Adjust to maintain the desired diuresis of approximately 200 to 300 mL/hour.
cardiac monitor and check FBE, U&E, CK
monitor fluid balance and urine output
consider attempted prevention of acute renal failure with forced mannitol-alkaline diuresis in an effort to diminish the renal toxicity of myoglobin.