LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0 Advanced Emergency Nursing Journal Vol. 29, No. 2, pp. 145–150 Copyright c 2007 Wolters Kluwer Health | Lippincott Williams & Wilkins Crush Injuries Pathophysiology and Current Treatment Michael Sahjian, RN, BSN, CFRN, CCRN, NREMT-P; Michael Frakes, APRN, CCNS, CCRN, CFRN, NREMT-P Abstract Crush syndrome, or traumatic rhabdomyolysis, is an uncommon traumatic injury that can lead to mismanagement or delayed treatment. Although rhabdomyolysis can result from many causes, this article reviews the risk factors, symptoms, and best practice treatments to optimize patient outcomes, as they relate to crush injuries. Key words: crush syndrome, traumatic rhabdomyolysis RUSH SYNDROME, also known as ology, pathophysiology, diagnosis, and early traumatic rhabdomyolysis, was first re- management of crush syndrome. Cported in 1910 by German authors who described symptoms including muscle EPIDEMIOLOGY pain, weakness, and brown-colored urine in soldiers rescued after being buried in struc- Crush injuries may result in permanent dis- tural debris (Gonzalez, 2005). Crush syn- ability or death; therefore, early recognition drome was not well defined until the 1940s and aggressive treatment are necessary to when nephrologists Bywaters and Beal pro- improve outcomes. There are many known vided descriptions of victims trapped by mechanisms inducing rhabdomyolysis includ- their extremities during the London Blitz ing crush injuries, electrocution, burns, com- who presented with shock, swollen extrem- partment syndrome, and any other pathology ities, tea-colored urine, and subsequent re- that results in muscle damage. Victims of nat- nal failure (Better & Stein, 1990; Fernan- ural disasters, including earthquakes, are re- dez, Hung, Bruno, Galea, & Chiang, 2005; ported as having up to a 20% incidence of Gonzalez, 2005; Malinoski, Slater, & Mullins, crush injuries, as do 40% of those surviving to 2004). Rhabdomyolysis often causes myo- be extricated from structures that collapse in globinuric renal failure, electrolyte distur- both natural and man-made disasters (Better & bances, acidemia, and hypovolemia; its symp- Stein, 1990). Crush injures may also be caused toms have since become known as crush by more common events, including vehicu- syndrome. This article reviews the epidemi- lar crashes, industrial or mining mishaps, and farming incidents, where extremities become pinned in moving machine parts. The clini- From the LIFE STAR/Hartford Hospital, Hartford, Conn. cian must also be alert to the symptoms of rhabdomyolysis in persons with prolonged Corresponding author: Michael Sahjian, RN, BSN, CFRN, CCRN, NREMT-P,LIFE STAR/Hartford Hospital, Hartford, seizures, vigorous exercise, or prolonged im- CT 06102 (e-mail: [email protected]). mobility, and from reactions to medications 145 LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0 146 Advanced Emergency Nursing Journal such as colchicine and the statins. Accord- Return of circulation to the injured and ing to the National Center for Health Statis- ischemic area after rescue also results in tics (2005), the overall incidence of traumatic injury, as reperfusion leads to increased rhabdomyolysis is 0.1 per 10,000 population, neutrophil activity and the release of free making it one of the least common traumatic radicals. Superoxide, the anion form of − injury patterns. However, if not treated ap- oxygen (O2 ) and hydrogen peroxide (H2O2) propriately, it may be lethal. Overall mortality react to form the hydroxyl radical (.OH), from rhabdomyolysis is about 5%, but varies which, in a large enough concentration, widely with the precipitating cause. damages cellular molecules and causes a lipid peroxidation. Lipid peroxidation leads to cell membrane destruction and cell lysis (Civetta, PATHOPHYSIOLOGY Taylor, & Kirby, 1997). This damage leads to Traumatic rhabdomyolysis, as it pertains to a further increase in the absorption of fluid, crush syndrome, results when muscle mass is calcium, and sodium into the damaged cells. compressed, causing direct injury to muscle The amount of fluid that may be rapidly se- fibers. As the tissue is compressed, it is de- questered in the injured muscle can be equal prived of blood flow and becomes ischemic, to the extracellular volume of the patient, eventually leading to cellular death. The time about 12 L in a 75-kg adult (Stewart, 2005). to injury and cell death varies with the crush- This, in part, accounts for one of the main ing force involved; however, skeletal muscle sequelae of crush syndrome, hypovolemia, can often tolerate ischemia for up to 2 hr with- which is discussed later in this article. out permanent injury. In the 2- to 4-hr range, A second effect from pressure and reperfu- some reversible cell damage occurs, and by sion is the release of debris from the damaged 6 hr irreversible tissue necrosis generally sets cells into the circulation. This debris includes in. In addition to ischemic cell damage, direct potassium, phosphorus, and myoglobin, the injury from the crushing forces causes cell latter is responsible for the ARF that can occur membrane failure and the opening of intracel- with the syndrome. Myoglobin, an oxygen- lular sodium and calcium channels. The open- binding molecule, contains a heme group and ing of these channels results in the shift of a globin group that disassociate into globin calcium and sodium into hypoxic cells. This and ferrihemate when released into the cir- damages myofibril proteins and results in both culation, especially in an acidic environment worsened cell membrane dysfunction and the such as that of hypoperfusion. Myoglobin and release of ATP-inhibiting nucleases. The re- myoglobin breakdown products, particularly sultant pressure-induced reduction in aerobic in the presence of acidic urine (pH < 5.4), metabolism is further compounded by the is- have a toxic effect on the renal tubules and chemia of reduced blood flow. react with the Tamm-Horsefall proteins in the Crush injury also causes hypovolemia by renal tubules to form casts (Stewart, 2005). hemorrhagic volume loss and the rapid shift Recent literature implicates free radical for- of extracellular volume into the damaged tis- mation as worsening cast-induced renal tox- sues. Acute renal failure (ARF) is caused by icity (Malinoski et al., 2004). hypoperfusion of the kidneys, which nor- Another complication of crush injuries is mally receive 25% of cardiac output (Lameire, the development of compartment syndrome, 2005). This hypoperfusion compounds the which occurs when pressures increase within toxicity caused by cast formation and me- a fascia-encased region, classically a mus- chanical blockage of the nephrons by myo- cle group or the abdomen. The fascia pro- globin, and underscores the importance of vides a nonexpandable space, and, as fluid early, vigorous volume resuscitation to im- is sequestered, the pressure within the com- prove urine flow, which dilutes and clears partment rises. With the rise in pressure, toxins. the microvascular circulation is compromised LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0 r April–June 2007 Vol. 29, No. 2 Crush injuries 147 leading to tissue ischemia. The signs and Creatine phosphokinase (CPK) is another symptoms of compartment syndrome in an marker of muscle damage and laboratory test- extremity include pain out of proportion to ing is commonly available. CPK is released the injury or with passive motion, pallor, with any muscle breakdown. With rhabdomy- paresthesia, pulselessness, and paralysis of olysis, the levels are tremendously high, often the affected extremity. Attempts should be in excess of 30,000 units/L and correlate with made to intervene before there is a loss of the amount of muscle damaged (Fernandez pulses, an ominous finding that will almost al- et al., 2005; Stewart, 2005). Although crush ways reflect irreversible tissue necrosis. Com- injury can produce spectacularly high CPK partment syndrome may also occur in the ab- values, the incidence of renal failure becomes domen. To monitor abdominal compartment significant at a threshold of only 5,000 units/L. syndrome, bladder pressures may be obtained This level should prompt aggressive evalua- through an indwelling urinary catheter. Pres- tion and intervention (Brown, Rhee, Evans, sures higher than 25 mmHg often warrant sur- Demetriades, & Velmahos, 2004). As the half- gical decompression. life of CPK is about 1.5 days and that of myo- globin is about 3 hr, tracking both CPK and myoglobin values is beneficial when trying to DIAGNOSIS guide treatment decisions. The release of myoglobin into the circula- tion should be considered whenever there MANAGEMENT is significant muscle injury. Normal serum values vary depending on the laboratory re- The most important prehospital treatment sults, but are usually less than 85 ng/mL. goal should be the removal of the crush- With significant muscle damage, it is possible ing forces. Initial treatment, whether out-of- for the value to rise astronomically, perhaps hospital or in-hospital, begins with the ini- more than 150,000 ng/mL (Stewart, 2005). tiation of intravenous hydration. Subsequent The serum myoglobin levels may be initially treatment should be aimed at restoring end- higher in comparison to urine values, but as organ perfusion and preventing renal fail- myoglobin is cleared from the body, these val- ure by volume expansion. Volume expansion ues will flip and the amount of myoglobin also aids in correcting the acidemia caused in the