Crush Syndrome: A Case Study

Pathophysiology

Crush syndrome involves a series of metabolic changes that occur from a prolonged, highly compressive injury to skeletal muscle. Generally, in the two to four-hour range, some reversible cell damage occurs. By six hours, irreversible tissue death is evident². The more skeletal muscle mass involved, the greater the potential complications could be.

Direct injury from the crushing force causes skeletal cell membrane fracture and the opening of calcium, sodium, and potassium channels. This leads to high volumes of sodium rushing into the cell, pulling extracellular and intravascular fluid along with it. Stagnated blood flow due to compression causes a local histamine release. The resultant capillary dilation contributes to intravascular volume loss.

The intracellular water level thus dramatically increases and combined with the direct injury, the cell membrane ruptures. Intracellular contents spill into the surrounding tissue and bloodstream; most notably myoglobin, uric acid, and phosphate. The high extracellular phosphate levels accelerate the calcium influx, quickly resulting in an excessive intracellular concentration. A hyperactivation of lysosomes ensues, increasing the concentration of digestive enzymes inside the cell and hastening the cellular membrane breakdown.

Once the local supply of oxygen runs out due to lack of blood flow, energy production (ATP) diminishes and lactic acid levels increase. The increased uric acid level, combined with lactic acid pulls massive amounts of intracellular potassium into the extracellular space and bloodstream. Lack of available ATP leads to the shutdown of the sodium-potassium pump. Now, no mechanism exists to remove excess intracellular sodium, nor retrieve the excess extracellular potassium.

To sum it up: The compressed tissue is now comprised of dead cells. The local bloodstream is volume-depleted with excessively low calcium and sodium levels and contains a high concentration of potassium. It is acidotic and filled with myoglobin and other toxins that will cause multisystem organ damage.

Management

The good news is, while the patient is trapped, the consequences are localized. The major problem is not recognizing the systemic potential effects after extrication. Properly prepping the patient before removing the compressive force is essential. Initial management is similar to other trauma patients. Address any airway, oxygenation and ventilation issues, but the priorities are IV establishment and medication administration. Fluid, ideally normal saline, should be aggressively infused to correct hypovolemia and counteract acute renal failure from increased levels of intravascular myoglobin. Typically, this is a 1-2 liter bolus, then infused at 1 to 1.5 L/hr³. Per medical control, sodium bicarbonate, calcium, and nebulized albuterol should be administered to counteract metabolic acidosis, hypocalcemia, and hyperkalemia. If the injury is isolated to an extremity that is accessible, consider placing a tourniquet above the injured site prior to extrication.

Summary

Crush syndrome is frequently observed because of prolonged entrapment, although cases resulting from brief entrapment have also been reported. Reperfusion of ischemic tissues spreads cellular toxins into the circulatory system. The goal of treatment is to anticipate crush syndrome and try to counteract its complications as best as possible.

References

1. Gonzalez, D. (2005). Crush syndrome. Critical Care Medicine, 33, 34-41.

2. Sahjian, M., Frakes, M. (April/June 2007) Crush Injuries: Pathophysiology and Current Treatment. Advanced Emergency Nursing Journal, Volume 29 (2), 145 – 150.

3. Barbera, J. A., & MacIntyre, A. (1996). Urban search and rescue. Emergency Medicine Clinics of North America, 14, 399-412.