Any mechanism that causes the entrapment and compression of muscle tissue is a crush injury that can eventually lead to both crush syndrome and compartment syndrome. Time under compression and the integrity of the myofascial compartment are the primary factors leading to the development of either or both pathology.
Crush syndrome is simply rhabdomyolysis induced by trauma. There is a compromise in the vasculature caused by a compressive outside force, which causes a failure of perfusion to the muscle cells in the affected area. This results in anaerobic metabolism, Na-K pump failure, and cell lysis as in any prolonged ischemic state. The cell breakdown causes a relative hyperkalemia, hypocalcemia, and hyperphosphatemia, as seen any any state of hypoperfusion/shock. However, there are some additional components to consider because we are dealing with the breakdown of muscle tissue. Skeletal muscle contains large quantities of the protein myoglobin, which, when released by lysed cells, must be excreted by the kidneys. Without treatment, this myglobin interacts with acidified urine in the kidneys, creating a gel which occludes flow though the kidneys, and thereby acute renal failure. Additional components of crush syndrome are hypovolemia secondary to fluid shifting out of the intravascular space (“third spacing”), and DIC.
It is important to note that while crush syndrome typically manifests after four to six hours of compression, it has been seen in as little as 20 minutes.
Field management of crush syndrome has the following objectives:
- Isolate the extremity from systemic circulation prior to release to prevent release of myoglobin, potassium, phosphate, and thromboxane. This isolation effectively halts systemic crush syndrome from occurring.
- Fluid resuscitation to support the kidneys and treat hypovolemia secondary to hemorrhage and third-spacing. This is balanced against the evidence in support of permissive hypotension. Ideally, bleeding is controlled prior to crystalloid administration.
- Alkilinization of the urine, usually via sodium bicarbonate administration.
- Management of arrhythmia emerging from hyperkalemia. Note that calcium administration, while indicated in the setting if EKG changes, should be undertaken with caution due to the potential for precipitation in the injured extremities.
Compartment syndrome in the setting of crush injury occurs when there is microvascular compromise resulting in bleeding into an intact myofascial compartment. Notably however, any increase in intra-compartment pressure can lead to compartment syndrome. Chronic exertional compartment syndrome is a sports injury arising from overuse, and most commonly affects the lower leg. Anyone who has suffered pain in the calves for a number of days following a run has probably experienced this type of compartment syndrome. Regardless of the cause, compartment syndrome can progress to crush syndrome, as the muscle tissue swells inward producing a compressive force on the tissues. A presumptive field diagnosis may be made on the basis of the P’s of arterial obstruction (five to seven depending on the reference): Pain out of proportion to the injury, pallor, pulselesness, paresthesia, paralysis, poikelothermia, and a purple/mottled color. Definitive diagnosis is based on compartment pressure monitoring, and management is via surgical fasciotomy.
Further reading on these issues:
Crush Injuries Pathophysiology and Current Treatment