Definition and concepts

Crush injury is the anatomical injury associated with direct trauma due to a compressive force. Extended entrapment with compression may cause crush syndrome, traumatic rhabdomyolysis, or compartment syndrome. Crush syndrome is the systemic manifestation of skeletal muscle injury from extended compression. Crush injury-induced traumatic rhabdomyolysis is one form of rhabdomyolysis; however, prolonged immobilization of an individual against a surface (e.g. due to altered level of consciousness) and agitated delirium can cause rhabdomyolysis without external trauma. Compartment syndrome is the increase in pressure within a fascial compartment eventually compromising venous outflow then arteriolar inflow with progressive capillary leak and edema leading to skeletal muscle injury that can progress to rhabdomyolysis. All three of these clinical entities may be encountered by EMS physicians, potentially in the same patient.

Pathophysiology of crush injuries

The systemic manifestations of crush syndrome are due to ischemia/reperfusion injury of skeletal muscle and the intense local and systemic inflammatory response due to the physiological, biochemical, and immunological changes that accompany the ischemic and reperfusion periods [1]. Ischemia/reperfusion injury is encountered in EMS practice in acute stroke, head injury, myocardial infarction, and crush injury with crush syndrome. Reactive oxygen species and activated neutrophils are the main contributors to local and systemic effects of ischemia reperfusion. Oxygen is the substrate initiating this response and is provided upon reperfusion. All tissue is sensitive to ischemia reperfusion but skeletal muscle injury can cause major systemic complications.

From the EMS perspective, the critical factors placing a patient at risk of crush syndrome are mass of muscle injured and ischemia time. The critical muscle mass necessary to put an entrapped patient at risk for crush syndrome is poorly defined, but qualitatively requires more than that of a hand or foot. Critical ischemia time is better defined but variable. At body temperature, critical ischemia time (the maximum time a tissue can tolerate ischemia and remain viable) of skeletal muscle is 4 hours [2]. However, critical ischemia time can be shorter when direct trauma is the cause of ischemia rather than just vascular occlusion.

The compression-stretch myopathy and ischemia of crush injury with muscle compression result in sarcolemma membrane leak and the release of myoglobin, urate, potassium, and phosphate out of muscle cells. Water, calcium, and sodium leak into muscle cells. Fluid and electrolyte shifts, myoglobinuria, and hyperkalemia then contribute to the systemic manifestations of crush syndrome after muscle compression is relieved and perfusion is reestablished. Large volumes of intravascular fluid shift into the injured muscle, leading to hypovolemia and hypotension. Hyperkalemia and metabolic acids cause bradydysrhythmias and reduced cardiac output while uric acid from muscle purines and myoglobin cause acute renal injury. From a clinical management perspective, the early consequences of crush syndrome are hypovolemia, hyperkalemia, and metabolic acidosis and the late consequence is acute renal failure due to myoglobinia and uricosuria.

Clinical setting

Because the compression-stretch myopathy and reperfusion injury of crush injury that goes on to become crush syndrome requires muscle compression of the order of hours rather than minutes, the clinical setting of EMS patients in which crush syndrome is to be suspected will be somewhat unique. Mostly these patients will be entrapped in some way, requiring disentanglement and extrication involving technical rescue, or may require a search operation before extrication is possible. In single-patient or small multicasualty incidents this may involve traffic collisions, industrial, construction or machinery incidents, explosions, structural collapse, debris flows, and below-grade or confined space entrapments.

Although the critical mass of skeletal muscle necessary to cause the systemic effects of crush syndrome is uncertain, the clinical setting would likely involve entrapment of an extremity, possibly as far as the shoulder, hip, or gluteus. Torso compression associated with traumatic asphyxia would be rapidly fatal.

In the large multicasualty or mass casualty/disaster setting, crush syndrome is associated with structural collapse due to earthquakes, floods, tornadoes, hurricane/tropical cyclones, or events of war. Because substantial time might pass before survivors are found in search operations following a disaster, crush syndrome can be a major contributor to delayed morbidity and mortality. Crush syndrome that leads to acute renal failure has been reported to be the second most frequent cause of mortality following disasters, after direct trauma [3–5].