Crush Syndrome and Rhabdomyolysis
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Direct answer
Crush syndrome is a form of traumatic rhabdomyolysis in which prolonged compression of muscle is followed by release, freeing myoglobin, potassium and phosphate into the circulation. Its hallmark is acute kidney injury from pigment nephropathy, with hyperkalaemia that can be fatal. Early and aggressive intravenous fluid resuscitation, with monitoring of urine output, is the cornerstone of treatment.
What you must remember
- Mechanism: compression of muscle for hours, as in a collapsed building, causes ischaemic necrosis; the damage becomes apparent on release of the limb.
- Released products: myoglobin, potassium, phosphate, urate and creatine kinase enter the blood, producing hyperkalaemia, hyperphosphataemia, hyperuricaemia and hypocalcaemia.
- Renal injury: myoglobin precipitates in tubules, causing dark, red-brown urine that is positive on dipstick for blood but has no red cells on microscopy.
- Laboratory clue: a very high creatine kinase, often in the tens of thousands, supports the diagnosis and tracks severity.
- Fluids: early, large-volume crystalloid resuscitation to keep urine output adequate is the key intervention.
- Adjuncts: urinary alkalinisation with sodium bicarbonate has been used, but its benefit is debated, so books differ on its role.
- Compartment syndrome: fasciotomy is needed when a compartment is tense, as it may coexist with rhabdomyolysis.
A pathway from compression to renal recovery
The sequence matters because the most dangerous moment is often the release of the limb, not the compression itself. The steps below follow the usual course in a crush injury, from the trapped limb to the kidney and the local wound. Each stage carries its own hazard, so the sequence is also a checklist for the rescuer and the surgeon.
- Compression: a limb is trapped and muscle becomes ischaemic over hours, often in earthquakes or collapsed structures.
- Release: removing the weight lets toxic products from necrotic muscle enter the bloodstream, and this is the highest-risk point for sudden hyperkalaemia and arrhythmia.
- Early fluids: intravenous crystalloid is started at once, before or during extrication, to keep the kidneys perfused and dilute pigment.
- Monitoring: urine output, serum potassium, phosphate, calcium and creatine kinase are checked, with cardiac monitoring when potassium is high. A falling urine output despite fluids signals that the kidney is at risk.
- Renal support: if oliguria or hyperkalaemia persists despite fluids, dialysis is considered.
- Local care: a compartment syndrome is treated by fasciotomy, and necrotic tissue is debrided once the patient is stable.
Where the exam tries to catch you
Most lost marks come from treating the kidney as a separate problem or from ignoring the release phase.
- Trap: a dark urine with red blood cells on microscopy is simply haematuria. Correct: myoglobinuria gives dipstick-positive blood with no red cells on microscopy, which points to rhabdomyolysis.
- Trap: the fluid goal is to limit volume because the patient is at risk of pulmonary oedema. Correct: early large-volume crystalloid is given to protect the kidneys, with close monitoring for overload.
- Trap: hyperkalaemia after release is treated only after the limb is salvaged. Correct: potassium is a life-threatening emergency, so cardiac monitoring and treatment are given immediately.
Frequently asked questions
What is the classic urine finding in crush syndrome?
The classic urine finding in crush syndrome is dark, red-brown urine that is positive on dipstick for blood without red cells on microscopy. This reflects myoglobinuria from breakdown of muscle, which is typical of rhabdomyolysis.
Why is hyperkalaemia dangerous in crush syndrome?
Hyperkalaemia in crush syndrome is dangerous because potassium is released from necrotic muscle, especially at the moment the limb is released. It can cause fatal cardiac arrhythmias, so cardiac monitoring and urgent treatment are needed.
What is the main treatment of crush syndrome?
The main treatment of crush syndrome is early, aggressive intravenous crystalloid resuscitation to maintain urine output and flush myoglobin. Potassium control, dialysis for refractory renal failure and fasciotomy for compartment syndrome are added as needed.
Is sodium bicarbonate proven in crush syndrome?
Sodium bicarbonate for alkalinising the urine is used in crush syndrome, but its benefit is not firmly established. Textbooks differ on its role, so fluids remain the core therapy in the exam answer.
What does the creatine kinase level show in crush syndrome?
Creatine kinase is markedly raised in crush syndrome and reflects the extent of muscle breakdown. A very high value supports the diagnosis of rhabdomyolysis and helps predict the risk of acute kidney injury.