Rescue and Salvage of Casualties Suffering from the Crush Syndrome after Mass Disasters

Abstract

Extensive muscle crush injury culminating in the crush syndrome (CS) is often lethal unless promptly and vigorously treated. The causes of death in the CS are extreme hypovolemic shock, hyperkalemia, hypocalcemia, metabolic acidosis, acute myoglobinuric renal failure, and the compartment syndrome. Treatment consists of early massive volume replacement, preferably administered in the field, followed by forced alkaline solute (mannitol) diuresis. With this regimen, it is possible to increase substantially the survival of lives and limbs and to prevent acute myoglobinuric renal failure in patients suffering from the CS. Preliminary experience suggests that intravenous hypertonic mannitol is protective also to the injured muscle and can be used as a noninvasive adjunct in the management of compartment syndrome in humans. Moreover, by preserving muscular integrity, mannitol can conceivably reduce sarcolemmal leakage of the nephrotoxic myoglobin urate and phosphate and thus further defend kidney function. Furthermore, mannitol reduces the plasma pool of these nephrotoxic metabolites by increasing urinary elimination.

The effects of acetaminophen and mannitol on crush injuries in rats: Experimental study

“…[11][12][13][14][15][16][25][26][27][28] In a rat model-based study, radical derivatives of rhabdomyolysis emerging as a result of redox reactions between ferric and ferryl myoglobin was shown to cause serious oxidative damage to kidneys. [29] Several clinical and animal studies have been conducted using a number of active substances that behaved as metal-ion inactivators with the intention of aiding in the recovery of oxidative damage, scavenging free radicals, stimulating physiological enzymatic antioxidant systems, and protecting mitochondrial functions.…”

“…Preferred fluid is isotonic saline for reasons of efficacy and availability. [1,11,13] Sodium bicarbonate, added to half-isotonic solutions, may be effective for alkalizing urine in order to prevent tubular deposition of myoglobin and uric acid, to correct metabolic acidosis, and to reduce hyperkalemia. [11,12] Mannitol may be useful in the expansion of extracellular volume, as well as increasing urine output, and preventing renal tubular cast deposition.…”

The Study of Na+, K+-ATPase Activity of Rat Brain during Crush Syndrome

“…Even, 3-6 months after the crushing of sciatic nerve, several ultrastructural changes and neuronal death are observed, depending upon the time and force of crushing [5]. The development of CS is associated with stress which leads to many biochemical changes in CNS such as: (1) alterations in protein synthesis [15], (2) Changes in alanine-glutamate ratio of brain [16], (3) increase in adenosine deaminase activity [17]. In the present study, we are reporting the changes occurring in Na + , K + -ATPase Activity.…”

“…Serious damage has been observed in the function and structure of kidneys. In most cases, such disturbances lead to a high level of mortality, which is caused by acute heart failure or acute renal insufficiency [3].…”

Management of Patients With Acute Crush Injuries of the Extremities

“…7,8 Alternatively, mannitol treatment can also decompress the compartment, however, this is a slower process and its benefit over surgical intervention has not been fully elucidated. 9,10 In addition to monitoring extremity compartment pressures, pulses, and paresthesias, initial laboratory evaluation must also be completed in a timely manner. With increased blood loss in the affected compartment, periodic evaluation of hemoglobin and hematocrit should be followed to assess ongoing blood loss and volume shifts that could require transfusions or other interventions.…”