If multiple compartments are involved and a significant amount of muscle infarction is present, the patient may develop crush syndrome, which refers to the systemic effects of myonecrosis on the renal and cardiovascular systems. Myonecrosis causes the release of myoglobin, which is deposited in the distal convoluted tubules, ultimately occluding them and causing acute myoglobinuric renal failure. Third-space fluid loss occurs rapidly, leading to further hypotension and shock. The myonecrosis causes acidosis and hyperkalemia. Because the excessive potassium released from the damage muscle is not excreted in the presence of renal failure, cardiac arrhythmias may occur.

The most common cause of crush syndrome is prolonged compression of a limb (>12 hours) after alcohol or drug intoxication and stupor. Occasionally, trauma resulting from entrapment in debris produces the same effects. The presenting signs are hyperkalemia, acidosis, disorientation or coma, possibly cardiac arrhythmias, hypotension, renal failure, and swollen, tense limbs with pressure sores. Results of laboratory studies are typically very abnormal. Concentration of creatinine phosphokinase is usually greater than 10,000 IU, and serum levels of creatinine, blood urea nitrogen, and potassium are also elevated. The finding of myoglobinuria confirms the diagnosis.

The three main causes of compartment syndrome are increased accumulation of fluid, decreased volume (compartment constriction), and restricted volume expansion secondary to external compression (see Plate 7-12). Although compartment syndrome develops most frequently in the four compartments of the leg, it can also occur in the forearm, hand, arm, shoulder, foot, thigh, buttocks, and back.

INCREASED ACCUMULATION OF FLUID

The most common mechanism of compartment syndrome is increased fluid content in the compartment. The most common cause is a fracture, with the tibia the most often fractured bone. It is important to note that compartment syndrome can still occur after open fractures (particularly of the tibia) and that the soft tissue disruption does not offer adequate decompression of the compartment. It can also be seen after severe contusion of the limb with no fracture.

Injury to a major blood vessel may produce compartment syndrome by three mechanisms: (1) bleeding into the compartment, (2) partial occlusion of the artery secondary to spasm or intimal tear with inadequate collateral circulation, and (3) postischemia swelling after circulation is restored. Postischemia swelling and compartment syndrome result if repair of the artery and restoration of the circulation are delayed more than 6 hours.