- Traumatic
- Crush injuries
- Blunt trauma
- Burns including electrocution
- Atraumatic
- Infection esp. Legionella, tetanus
- Drugs e.g. cocaine
- Prolonged immobilisation inc. for surgery
- Alcohol (see below)
- Immune-mediated e.g. polymyositis, dermatomyositis
Rhabdomyolysis
Rhabdomyolysis
- Rhabdomyolysis results from the breakdown of striated muscle
- Muscle degradation leads to elevated intra-cytoplasmic calcium
- This causes release of myocyte constituents into the blood, leading to AKI and hyperkalaemia
Acute kidney injury
- Myoglobin precipitates in the renal tubules and obstructs them
- Release of the Fe2+ from haem causes:
- Generation of hydroxyl radicals and free-radical-mediated injury
- Lipid peroxidation by both hydroxyl radicals and haem itself, leading to tubular membrane dysfunction
- Renal blood flow becomes impaired by:
- Vasoconstriction, as nitric oxide is scavenged by myoglobin
- Reduced renal blood flow e.g. due to shock following trauma, burns etc.
Alcohol-induced rhabdomyolysis
- Alcohol is involved in 20% of cases of rhabdomyolysis
- Alcohol-induced coma leads to prolonged immobilisation, muscle compression and ischaemia
- This causes direct calcium influx and the same pathophysiological mechanism as above
- Furthermore, alcohol damages cell sarcolemma, increasing sodium permeability
- This activates the sodium-calcium exchange pump
- This further contributes to increasing cytosolic calcium
- Presents as a spectrum, from asymptomatic through to hypovolaemic shock, AKI and life-threatening electrolyte imbalance
- Malaise
- Myalgia
- Fever
- Tachycardia
- Dark-coloured urine from myoglobinuria
- Creatinine kinase (CK)
- Is the most sensitive test for rhabdomyolysis
- Levels may be greatly elevated
- Values >5000 units/L are associated with a >50% incidence of AKI
- Urea and creatinine - raised due to acute kidney injury
- Potassium - elevated due to release from myocytes
- Phosphate - elevated due to release from myocytes
- Uric acid - elevated due to release from myocytes
- Blood gas may demonstrate hyperlactataemia ± lactic acidosis
- Urine dipstick cannot differentiate between haematuria, haemoglobinuria or myoglobinuria
- USS: reduced compartment perfusion
- CT or MRI: muscle oedema
Fluid management
- Commence prompt fluid therapy (ideally within 6hrs)
- Aim for a urine output >300ml/hr
- May need to use mannitol to achieve UO
Management of electrolytes and acid/base balance
- Manage hyperkalaemia as standard
- If systemic acidosis can use sodium bicarbonate to correct the acidosis
- No robust evidence for benefit in rhabdomyolysis-induced AKI
- Many still use it for forced alkaline diuresis
- Do not routinely replace calcium, which may exacerbate the pathophysiological mechanism i.e. calcium accumulation in muscular tissue
Renal replacement therapy
- CVVHDF
- Dialysis using a high-permeability membrane filter to improve removal of myoglobin