sign in sign up
<<
Home , Crush injury, Crush syndrome, Rhabdomyolysis

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 Pathophysiology and Current Treatment Michael Sahjian, RN, BSN, CFRN, CCRN, NREMT-P; Michael Frakes, APRN, CCNS, CCRN, CFRN, NREMT-P

Abstract , or traumatic , is an uncommon traumatic 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 , , and brown-colored 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, , , com- who presented with , 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, distur- both natural and man-made disasters (Better & bances, acidemia, and ; 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, , vigorous , or prolonged im- CT 06102 (e-mail: [email protected]). mobility, and from reactions to

145 LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0

146 Advanced Emergency Nursing Journal

such as and the . 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, 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 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, sequelae of crush syndrome, hypovolemia, can often tolerate 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 generally sets cells into the circulation. This debris includes in. In addition to ischemic cell damage, direct potassium, phosphorus, and , 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 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 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 of crush injuries is mally receive 25% of cardiac output (Lameire, the development of , 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 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 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 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, , with any muscle breakdown. With rhabdomy- , pulselessness, and 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 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 urine will be higher. Tracking both by hypoperfusion. Vascular access should be serum and urine myoglobin values, although established with two large-bore peripheral sometimes cost prohibitive, is the best way catheters, central venous line, or intraosseous to follow progression and resolution of crush routes. Initial fluid therapy should be di- injury. rected at correcting tachycardia or hypoten- A simple but rapid test for rhabdomyoly- sion with rapid volume expansion using iso- sis can be done with a standard urine dip- tonic solution or lactated stick. The heme portion of myoglobin causes Ringers solution and then slowing to a more a positive reading for blood on the test strip, controlled rate of 1 to 1.5 L/hr as a contin- and heme-positive urine in the absence of uous infusion (Barbera & MacIntyre, 1996; any red blood cells on microscopic exami- Gonzalez, 2005; Gunal et al., 2004; Malinoski nation suggests . However, dip- et al., 2004; Stewart, 2005). The ultimate goal stick findings are positive in only about half of therapy is aimed at achieving a urine output of patients with rhabdomyolysis and the find- of 300 to 400 mL/hr (Malinoski et al., 2004). ings are sometimes intermittent. Accordingly, This aggressive volume expansion can pre- a normal urine dipstick does not rule out the vent the rapid death, sometimes known as res- condition and a laboratory evaluation for myo- cue death, which often accompanies removal globin should be performed in patients sus- from the crushing forces and reperfusion of pected of having crush syndrome. ischemic tissue. LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0

148 Advanced Emergency Nursing Journal

In addition to crystalloid replacement, pressures by mobilizing fluid from the ex- blood or blood products may also be needed travascular to intravascular spaces, which may on the basis of the specific situation. Crush facilitate tissue perfusion and act as a free radi- injuries may result in , ne- cal scavenger, protecting the kidneys from in- cessitating the transfusion of fresh frozen juries incurred by oxidants (Malinoski et al., plasma or . Should there be ongo- 2004). Whenever is administered, a ing active or a marked reduction in chemistry panel and serum osmolality should hemoglobin to 8 or less in healthy individuals, be followed to monitor for electrolyte distur- or below 10 in persons with underlying car- bances, particularly and a rise diac, pulmonary, or cerebrovascular disease, a in osmolality that would indicate dehydra- transfusion of packed red blood cells may be tion. Once has been initiated, potas- needed to optimize oxygen transport. Care- sium levels may fall in spite of the massive ful attention must be paid to ensure that re- release from damaged muscle tissue and nal function is sufficient to provide adequate potassium repletion may be paradoxically re- urine output and prevent pulmonary conges- quired. Loop such as tion from volume replacement. This is es- may acidify the urine and should be avoided. pecially important if resuscitation is started A recent study, however, showed no bene- more than 6 hr postinjury because renal dam- fit of the addition of either sodium bicarbon- age may have already taken place. ate or mannitol to the treatment regimens of Although difficult to achieve, alkalinization patients with posttraumatic rhabdomyolysis of the urine may be beneficial in prevent- and CPK levels of 5,000 international units or ing renal failure and can be started with ini- higher. The use of these therapies offered no tial volume resuscitation. The breakdown of change in overall rates of renal failure, dial- myoglobin results in a nephropathy, causing ysis, or mortality (Brown et al., 2004). The sloughing of the tubular epithelium and the use of both therapies remains controversial formation of casts that obstruct blood flow and additional research is warranted to guide through the kidneys (Criddle, 2003). In alka- practice. lotic urine, myoglobin breakdown has a less Patients who do not respond to hydration toxic effect. Urine alkalinization may be ac- and forced diuresis by producing more than complished by adding 50 mEq of sodium bi- 400 mL of urine per day will almost certainly carbonate to each liter of maintenance fluid. require , as will most patients The therapeutic endpoint is a urine with a pH who present with an initial serum of 6 to 7; the normal value is between 4.6 of more than 1.7 mg/dL (Fernandez et al., and 8 (Better & Stein, 1990; Gonzalez, 2005; 2005; Gunal et al., 2004; Kantarci et al., 2002). Gunal et al., 2004; Stewart, 2005). Should Up to one third of all patients with rhab- systemic alkalosis occur with a pH of more domyolysis will go on to require hemodialysis than 7.5, acetazolamide, an oral that so long it is safe and possible, patients with promotes metabolic by inhibiting significant crush injuries should be triaged carbonic anhydrase in the kidneys, may be directly to centers with onsite, around-the- indicated. clock, hemodialysis capabilities. There is re- Once adequate urine output is accom- search supporting serum CO2, BUN, calcium, plished, the “push” provided by volume ex- creatinine, and a urine dip for blood as the panders may be augmented by a “pull” from most valuable predictors for the development forced diuresis with a 20% mannitol solution, of ARF or the need for hemodialysis. Table 1 with an initial dose of 25 g followed by a describes these relationships. As with any 5 g/hr infusion (Stewart, 2005). The osmotic volume-dependent patient, continuous veno- diuretic effects of the mannitol enhance urine venous may be the best dialy- output and facilitate the clearance of myo- sis option, as it requires the smallest amount globin. Mannitol also reduces compartment of volume to be removed from the patient LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0

r April–June 2007 Vol. 29, No. 2 Crush injuries 149

Table 1. Predictors of acute renal failure tole (Goldberger, 1999). Standard treatment (ARF) and hemodialysis modalities such as calcium, , dextrose, and an exchange resin may temporize the sit- uation; however, may be needed for Initial Initial values definitive treatment. Table 2 provides a re- values predictive of predictive the need for view on the treatment of . of ARF hemodialysis Patients should not be empirically treated with calcium in an effort to blunt the effects Serum CO2 17.24 mEq/L 16.79 mEq/L of potential hyperkalemia. Treatment should BUN 63.47 mg/dL 66.5 mg/dL be based on clinical findings such as anxi- 2+ Ca 7.98 mg/dL NA ety, numbness and tingling, /, Creatinine 5.78 mg/dL 6.86 mg/dL ECG abnormalities suggestive of elevated Urine heme Positive Positive potassium levels, or actual laboratory val- ues. A relative exists because Note. BUN = . the body’s calcium stores are absorbed by hypoxic tissues due to reperfusion and be- (Fernandez et al., 2005; Gunal et al., 2004, cause of a state of re- Kantarci et al., 2002). Potassium is found in sulting from phosphorus loss from damaged high quantity in muscle tissue, and reperfu- cells. Injudicious administration of calcium sion of damaged muscle tissue releases it into intravenously leads to more calcium absorp- the circulation. The risk for significant hyper- tion into the damaged cells, aggravating rhab- kalemia is compounded by any renal impair- domyolysis and resulting in metastatic calci- ment that might occur concomitantly with fication that, with time, can lead to tissue the rhabdomyolysis. Persons suffering with calcification or a deleterious hypercalcemia crush injuries should have continuous car- (Better & Stein, 1990). diac monitoring and electrocardiogaphic eval- Compartment syndrome could be diag- uation for the signs of hyperkalemia such as nosed by direct measurement of pressures tall-peaked T waves, a lengthening PR inter- within the fascia. This is achieved by intro- val, followed by a loss of P waves, and ulti- ducing a transduced needle into the com- mately a widening of the QRS complex into partment space. Pressures normally lie in a a sine wave, which is a precursor to asys- range from 0 to 15 mmHg, and pressures of

Table 2. Treatment of hyperkalemia

Membrane antagonism Calcium directly antagonizes the effects of potassium. is the preferred choice over if there is circulatory compromise, as 10 mL of a 10% solution (1 g) contains three times more elemental calcium than the same volume of calcium gluconate. Cellular shift Treatment with insulin and dextrose forces potassium into the cells and may decrease serum potassium by 1 mEq/L. Administer 10 units of regular insulin IV and 25 g dextrose IV. Exchange resin (Kayexalate) is an exchange resin that enhances potassium clearance across the gastrointestinal tract mucosa. Administer 30 g PO. Albuterol Although no longer widely utilized for the reduction of potassium, albuterol as a continuous nebulizer may be used to lower serum levels by stimulating intracellular uptake of potassium. Hemodialysis Removes potassium from blood. LWW/AENJ LWWJ331-02 April 23, 2007 13:50 Char Count= 0

150 Advanced Emergency Nursing Journal

more than 30 mmHg often require surgical cated. Further research is required as to the decompression with a . Pressures benefit of antioxidant therapy, routine alka- in the abdomen can be determined by lization of the urine, and the administration measuring the pressure within the bladder of APC. through an indwelling urinary catheter. Pa- tients with bladder pressures of more than 25 REFERENCES mmHg should be considered potential can- Barbera, J. A., & MacIntyre, A. (1996). Urban search and didates for surgical decompression if there rescue. Clinics of North Amer- is clinical evidence of organ dysfunction as ica, 14, 399–412. well. Higher diastolic blood pressures allow Better, O. S., & Stein, J. H. (1990). Early management perfusion, and another course followed is to of shock and prophylaxis of acute renal failure in treat when any compartment pressures rise to traumatic rhabdomyolysis. New England Journal of Medicine, 322, 825–829. within 20 points of diastolic blood pressure Brown, C. V., Rhee, P., Evans, K., Demetriades, D., & (Malinoski et al., 2004). Velmahos, G. C. (2004). Preventing renal failure in pa- tients with rhabdomyolysis: Do and man- INVESTIGATIVE THERAPY nitol make a difference? Journal of Trauma, 56, 1191– 1196. Activated protein C (APC) has been shown to Civetta, J., Taylor, R., & Kirby, R. (1997). Critical care (3rd regulate and in sep- ed.). Philadelphia: Lippincott-Raven. sis and there is belief that the administration Criddle, L. M. (2003). Rhabdomyolysis: Pathophysiology, recognition, and management. Critical Care Nurse, of APC in any disease state that activates this 23, 14–30. response, such as ischemia-reperfusion, may Fernandez, W. G., Hung, O., Bruno, R., Galea, S., & benefit from its administration (Levi, Choi, Chiang, W. (2005). Factors predictive of acute renal Schoots, Schultz, & van der Poll, 2004). APC failure and need for hemodialysis among ED patients is a physiologic that degrades with rhabdomyolysis. American Journal of Emer- gency Medicine, 23, 1–7. clotting factors that cause thrombus forma- Goldberger, A. L. (1999). Clinical : A tion in the microvasculature and exacerbate simplified approach. St. Louis: CV Mosby. ischemia. Another study has shown that there Gonzalez, D. (2005). Crush syndrome. Critical Care may be improved outcomes with the admin- Medicine, 33, 34–41. istration of free radical scavengers and antiox- Gunal, A. I., Celiker, H., Dogukan, A., Ozalp, G., Kirciman, E., & Simeskli, H. (2004). Early and vigorous fluid re- idants, as they might reduce tissue necrosis suscitation prevents acute renal failure in the crush and improve renal function (Malinoski et al., victims of catastrophic earthquakes. Journal of the 2004). American Society of , 15, 1862–1867. Kantarci, G., Vanholder, R., Tugular, S., Akin, H., Koc, CONCLUSION M., & Ozener, C. (2002). Acute renal failure due to crush syndrome during Marmara earthquake. Ameri- Crush injuries can result in rhabdomyolysis, can Journal of Diseases, 40, 682–689. electrolyte abnormalities, and hypovolemia, Lameire, N. (2005). The pathophysiology of acute renal failure. Critical Care Clinics, 21, 197–210. potentially causing ARF.The treatment modal- Levi, M., Choi, G., Schoots, I., Schultz, M., & van der ity of choice is early rehydration with crystal- Poll, T. (2004). Beyond : Activated protein C and loids, initiated even before extrication is com- ischemia-. Critical Care Medicine, plete. Volume expansion improves outcomes 32, S309–S312. from all complications of crush syndrome and Malinoski, D. J., Slater, M. S., & Mullins, R. J. (2004). Crush injury and rhabdomyolysis. Critical Care Clinics, 20, is a life-saving intervention. It is crucial to 171–192. monitor laboratory studies and be prepared to National Center for Health Statistics. (2005). Health, treat electrolyte disturbances. After urine pro- United States, 2004 (DHHS Publication No. 2005- duction has been verified, forced diuresis in 0152). Washington, DC: U.S. Government Printing conjunction with intravenous hydration may Office. Stewart, C. (2005). EMR textbook: Crush injuries. Re- reduce the need for dialysis. If compartment trieved February 4, 2007, from http://www.wnysmart. syndrome is suspected, it should be moni- org/References/Medical%20Subjects/Crush%20Injury. tored and treated with a fasciotomy as indi- pdf