crush injury Flashcards
treatment
Request support at the scene from a medical specialist if there is an established protocol for this in the area.
* Place a tourniquet on the limb(s) if possible.
* Gain IV access (preferably in two sites) and administer a minimum of two litres of 0.9% sodium chloride. Administer further fluid as required.
* Monitor the cardiac rhythm continuously.
* Approximately ten minutes prior to release of the weight:
a) Administer continuous salbutamol nebulised, and
b) Administer 500 ml of 10% glucose IV as a bolus.
* As the weight is being released:
a) Administer 100 ml of 8.4% sodium bicarbonate IV over one minute, and
b) Administer a flush of 0.9% sodium chloride IV via a running line, and
c) Administer 6.8 mmol (1 g) of calcium chloride IV over one minute.
* Administer further doses of 8.4% sodium bicarbonate and calcium chloride if signs of hyperkalaemia (including dysrhythmia) occur.
* Administer 1 g of tranexamic acid IV provided the patient cannot be enrolled in the PATCH study.
Crush injury is also called
traumatic rhabdomyolysis (muscle breakdown).
Release syndrome is a combination of
severe shock, acidosis, hyperkalaemia (raised potassium levels) and dysrhythmia that occurs immediately following release of the weight, when severe crush injury has occurred.
Pathophysiology of crush injury and release syndrome
Crush causes direct injury to muscles. Prolonged crush causes further damage by causing ischaemia. As muscle cells die, acid, cellular proteins (in particular myoglobin) and potassium leak out of cells.
* Acid, myoglobin and potassium may be contained within the limb(s). On release of the pressure, reperfusion occurs and may result in:
ū Many litres of fluid rapidly moving into the crushed area, reducing circulating volume and causing hypovolaemia. This will be exacerbated if there is also uncontrolled bleeding.
ū A rapid release of acid, myoglobin and potassium into the circulation.
* Acid interferes with normal cellular function, particularly in the heart.
* Potassium interferes with normal cardiac conduction and may cause severe dysrhythmia, including cardiac arrest.
* Inflammatory mediators cause an inflammatory response within the lungs that may cause severe pulmonary oedema and impaired oxygenation. If this occurs it usually develops over several hours following release.
* Myoglobin blocks the kidney’s tubules and may cause renal failure.
Several litres of 0.9% sodium chloride should be administered, even if the patient does not appear to be hypovolaemic. This is termed pre-loading. Pre-loading offers protection in three ways:
ū Increased intravascular volume helps dilute the released products.
ū Sodium ions help protect the cardiac cell membranes from the effects of
the potassium.
ū Increased urine flow through the kidneys helps prevent myoglobin
blocking the tubules.
Salbutamol stimulates
beta-2 receptors and causes potassium to move into cells, lowering the potassium concentration in blood.
Glucose stimulates
endogenous insulin production and causes potassium to move into cells, lowering the potassium concentration in blood.
Calcium provides
protection to cardiac cell membranes from potassium.
Sodium bicarbonate provides protection in three ways:
ū Sodium ions help protect cardiac cell membranes from the effects of potassium.
ū The bicarbonate raises blood pH, causing potassium to move into cells which lowers the potassium concentration in blood.
ū The bicarbonate raises urinary pH which reduces myoglobin deposition in kidney tubules.