crush injury Flashcards

1
Q

treatment

A

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.

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2
Q

Crush injury is also called

A

traumatic rhabdomyolysis (muscle breakdown).

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3
Q

Release syndrome is a combination of

A

severe shock, acidosis, hyperkalaemia (raised potassium levels) and dysrhythmia that occurs immediately following release of the weight, when severe crush injury has occurred.

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4
Q

Pathophysiology of crush injury and release syndrome

A

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.

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5
Q

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:

A

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.

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6
Q

Salbutamol stimulates

A

beta-2 receptors and causes potassium to move into cells, lowering the potassium concentration in blood.

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7
Q

Glucose stimulates

A

endogenous insulin production and causes potassium to move into cells, lowering the potassium concentration in blood.

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8
Q

Calcium provides

A

protection to cardiac cell membranes from potassium.

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9
Q

Sodium bicarbonate provides protection in three ways:

A

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.

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