Rhabdomyolysis is a condition where skeletal muscle tissue breaks down and releases breakdown products into the blood. This is usually triggered by an event that causes the muscle to break down, such as extreme underuse or overuse or a traumatic injury.
The muscle cells (myocytes) undergo cell death (apoptosis). The cell death results in muscle cells releasing:
- Myoglobin (causing myoglobinurea)
- Creatine kinase
Potassium is the most immediately dangerous breakdown product, as hyperkalaemia can cause cardiac arrhythmias that can potentially result in a cardiac arrest.
These breakdown products are filtered by the kidney and cause injury to the kidney. Myoglobin in particular is toxic to the kidney in high concentrations. This results in acute kidney injury. The acute kidney injury causes the breakdown products to further accumulate in the blood.
Anything that causes significant damage to muscle cells can cause rhabdomyolysis:
- Prolonged immobility, particularly frail patients that fall and spend time on the floor before being found
- Extremely rigorous exercise beyond the person’s fitness level (e.g. ultramaraton, triathalon, crossfit competition)
- Crush injuries
Signs and Symptoms
- Muscle aches and pain
- Confusion (particularly in elderly frail patients)
- Red-brown urine
Creatine Kinase (CK) blood test is a key investigation in establishing the diagnosis. It will be in the thousands to hundreds of thousands of Units/L. CK typically rises until 12 hours, then remains elevated for 1-3 days, then falls gradually. A higher CK increases the risk of kidney injury.
Myoglobinurea is myoglobin in the urine. It gives urine a red-brown colour. This will cause a urine dipstick to be positive for blood.
Urea and electrolytes (U&E) blood tests for acute kidney injury and hyperkalaemia.
ECG is important in assessing the heart’s response to hyperkalaemia.
Suspect rhabdomyolysis in patients with trauma, crush injury, prolonged immobilisation or excessive exercise.
IV fluids are the mainstay of treatment. The aim is to rehydrate the patient and encourage filtration of the breakdown products.
Consider IV sodium bicarbonate. This aims to make the urine more alkaline (pH ≥ 6.5), reducing the toxicity of the myoglobin on the kidneys. The evidence on this is not clear and there is some debate about whether to use it.
Consider IV mannitol. This aims to increase the glomerular filtration rate to help flush the breakdown products and to reduce oedema surrounding muscles and nerves. Hypovolaemia should be corrected before giving mannitol. The evidence on this is not clear and there is some debate about whether to use it.
Treat complications, particularly hyperkalaemia. Hyperkalaemia can be immediately life threatening as it can cause arrhythmias (particularly ventricular fibrillation).
Last updated April 2019