Crush injuries can result in acute compartment syndrome (ACS). Most often associated with long bone fractures, ACS results from internal tissue pressure against the surrounding fascia exceeding 8 mmhg and impedes vascularization and nerve transmissions (Sheridan & Matsen, 1976). Tissue necrosis can occur when the tissue pressure approaches that of diastolic pressure (Riede, Schmid, & Romero, 2007). When ACS occurs with dressings, splints, or casts, treatments include loosening or removing the dressing, splint, or cast; begin supplemental oxygen, provide analgesia, and position the extremity level with the trunk (do not elevate). The patient should be evaluated for surgical fasciotomy and potential treatment with hyperbaric oxygen (Riede, Schmid, & Romero, 2007; Strauss et al., 1986).
Evaluation of kidney damage in the patient with a crush injury is important as acute tubular necrosis can develop secondary to hypovolemia and increased circulating levels of myoglobin (resulting from rhabdomyolysis from injured muscles) (Bartal et al., 2011). Input and output (I&O) measurement therefore is important. Hyperkalemia, which is often present in crush injury patients, results from intracellur potassium released from the injured tissues and muscles. Intravenous fluids containing potassium (lactated Ringer’s) should be avoided (Bartal et al., 2011).