Crush injury can follow prolonged continuous pressure on muscle tissue. Crush injury can lead to crush syndrome.
Ischaemia reperfusion (when the pressure is released from the crushed limb) is the main mechanism of muscle injury in crush syndrome. There is traumatic rhabdomyolysis.
Muscle injury causes large quantities of potassium, phosphate, myoglobin, creatine kinase and urate to leak into the circulation.
Myoglobin levels in the plasma are normally very low. If a significant amount of skeletal muscle is damaged (>100 g),excess myoglobin is filtered by the kidneys and can cause renal tubular obstruction and renal damage: the excess myoglobin is nephrotoxic.
Intravascular volume depletion and renal hypoperfusion, combined with myoglobinuria, result in renal dysfunction.
Crush syndrome is characterised by:
Hypovolaemic shock (due to sequestration of water in the injured muscle cells).
Hyperkalaemia (release of cellular potassium by the injured muscle cells).
This can also lead to:
Metabolic acidosis (release of cellular phosphate and sulphate by the injured muscle cells).
Acute kidney injury.
Disseminated intravascular coagulation (DIC).
Crush syndrome has been described in numerous settings, most commonly after earthquakes, during war and after explosions that have caused buildings to collapse. It is also seen following industrial accidents, such as those occurring in mining and after road traffic accidents.
The key clinical features of crush syndrome are:
Crushing injury to a large mass of skeletal muscle.
Sensory and motor disturbances in the compressed limbs, which subsequently become tense and swollen. The limb/body part may be pulseless.
Myoglobinuria and/or haemoglobinuria, which may make the urine tea-coloured quite early on.
There may be oliguria with profound hypovolaemic shock.
Nausea, vomiting, confusion and agitation may occur as consequences of disturbed body chemistry; urea, creatinine, uric acid, potassium, phosphate and creatine kinase are elevated. There may also be hypocalcaemia.
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