Crush injury
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. [1]
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.
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.
These systemic effects are caused by a traumatic rhabdomyolysis (muscle breakdown) and the release of potentially toxic muscle cell components and electrolytes into the circulatory system. Crush syndrome can cause local tissue injury, organ dysfunction, and metabolic abnormalities, including acidosis, hyperkalemia, and hypocalcemia.
These conditions differ from compartment syndrome, but the same sort of injuries can produce the latter.
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. 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 an intensive care unit may be appropriate.
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. Alkalinization of urine is critical; administer IV sodium bicarbonate until urine pH reaches 6.5 to prevent myoglobin and uric acid deposition in kidneys
"To prevent Hyperkalemia/Hypocalcemia: Consider administering 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 and D5O 1-2 ampules IV bolus; kayexalate 25-50g with sorbitol 20% 100mL PO or PR." Even so, cardiac arrythmias may develop; electrocardiographic monitoring is advised, and specific treatment begun promptly.
"Treat open wounds with antibiotics, tetanus toxoid, and debridement of necrotic tissue "Apply ice to injured areas and monitor for the 5 P’s: pain, pallor, parasthesias, pain with passive movement, and pulselessness