Crush injury

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	To oppose or discuss a nomination, please go to CZ:Proposed for deletion and follow the instructions. For the monthly nomination lists, see Category:Articles for deletion. Crush injury is compression of extremities or other parts of the body that causes muscle swelling and/or neurological disturbances in the affected areas of the body, while crush syndrome is localized crush injury with systemic manifestations. Typically affected areas of the body include lower extremities (74%), upper extremities (10%), and trunk (9%). They typically are caused by building collapse from explosives, or earthquake and other natural disasters, or construction accidents. They also can be caused by cave-ins. Explosion-caused crush injury is quaternary blast injury. Victims of crushing damage present some of the greatest challenges in field medicine, and may be among the few situations where a physician is needed in the field. The most drastic response to crushing under massive objects may be field amputation. Even if it is possible to extricate the patient without amputation, appropriate physiological preparation is mandatory: where permissive hypotension is the standard of field care for most trauma, it can be lethal if crush toxins are suddenly released into a small volume of circulating fluid. Systemic effects The most devastating systemic effects can occur when the crushing pressure is suddenly released, without proper preparation of the patient, causing reperfusion syndrome. Without proper preparation, the patient, with pain control, may be cheerful before extrication, but die shortly thereafter. This sudden decompensation is called the "smiling death." These systemic effects are caused by a traumatic rhabdomyolysis. As muscle cells die, they absorb sodium, water and calcium; the rhabdomyolysis releases potassium, myoglobin, phosphate, thromboplastin, creatine and creatine kinase. Compartment syndrome can be secondary to crush syndrome. Monitor for the classic 5 P’s: pain, pallor, parasthesias, pain with passive movement, and pulselessness. Field management As mentioned, permissive hypotension is unwise. Especially if the crushing weight is on the patient more than 4 hours, but often if it persists more than one hour, careful fluid overload is wise, as well as the administration of intravenous sodium bicarbonate. The San Francisco emergency services protocol calls for a basic adult dose of a 2 L bolus of normal saline followed by 500 ml/hr, limited for "pediatric patients and patients with history of cardiac or renal dysfunction." If the patient cannot be fluid loaded, this may be an indication for a tourniquet to be applied. Initial hospital management The clinician must protect the patient against hypotension, renal failure, acidosis, hyperkalemia and hypokalemia. Admission to a intensive care unit, preferably one experienced in trauma medicine, may be appropriate; even well-seeming patients need observation. Treat open wounds as surgically appropriate, with debridement, antibiotics and tetanus toxoid; apply ice to injured areas. Intravenous hydration of up to 1.5 L/hour should continue to prevent hypotension. A urinary output of at least 300 ml/hour should be maintained with IV fluids and mannitol, and hemodialysis considered if this amount of diuresis is not achieved. Use intravenous sodium bicarbonate to keep the urine pH at 6.5 or greater, to prevent myoglobin and uric acid deposition in kidneys. To prevent hyperkalemia/hypocalcemia, consider the following adult doses: calcium gluconate 10% 10cc or calcium chloride 10% 5cc IV over 2 minutes sodium bicarbonate 1 meq/kg IV slow push regular insulin 5-10 U 50% glucose1-2 ampules IV bolus kayexalate 25-50g with sorbitol 20% 100mL by mouth or rectum. Even so, cardiac arrythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly. References