Emergency War Surgery NATO Handbook: Part III: General Considerations of Wound Management: Chapter XVII: Crush Injury
United States Department of Defense
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A clear history of crush injury is not always available in wartime, and the syndrome sometimes develops insidiously in patients who appear well when they first present. Crush injuries of the trunk and buttocks can be overlooked if a complete physical examination is not performed.
Although the compressed region may appear normal when it is released from pressure, paralysis caused by the compression is sometimes present. Erythema may appear at the margin of the affected area early after release, and the adjacent skin may blister. These signs are sometimes the first evidence of damage.
Shortly after release from compression, swelling caused by extravasation of plasma appears in the part. The loss of plasma initiates or aggravates oligemic shock, and the patient's condition rapidly deteriorates. The blood pressure, which was at first maintained by vasoconstriction, falls rapidly as plasma loss continues. The damaged part, which is usually a limb, becomes swollen, tense, and hard. If it is incised, serous fluid oozes from it. The distal pulses tend to disappear. When the fascia is opened, swollen or friable muscle, which in the later stages is very pallid, bulges out. Later symptoms and signs may include anorexia, hiccups, dryness of the tongue, and drowsiness or mental disturbances as the blood urea and blood pressure mount.
In favorable cases, diuresis ensues 6-8 days after injury and the patient improves clinically, although renal dysfunction may persist for months. In less favorable cases, death may occur promptly from shock or from pulmonary edema, aggravated by the unwise forcing of fluids in the presence of renal shutdown.
Later death may be attributable to cardiac arrest caused by the hyperkalemia of uremia. In untreated cases, renal insufficiency almost always occurs within a few hours of release of compression.
Laboratory findings reveal an elevated hematocrit reflecting the state of hemoconcentration. Serum potassium and uric acid levels are elevated. The blood area nitrogen levels are unchanged. Free myoglobin may be detected. The serum creatinine phosphokinase (CPK) is markedly elevated to at least five times normal. The first urine specimen, because it was collected in the bladder before injury, may be normal. Later, urine becomes dark due to the presence of myoglobin. It will have an acid pH.
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