58 Nursing2003, Volume 33, Number 5 www.nursingcenter.com

WHEN YOU CARE for a traumavictim, monitoring for dangerouscomplications is as important asattending to his injuries. A compli-cation can cause a crippling sec-ondary injury or even take his life.

In this article, I’ll discuss threecommon and potentially devastat-ing trauma complications: rhab-domyolysis, compartment syn-drome, and fat embolism syn-drome (FES). By recognizing theirsigns and symptoms early andintervening correctly, you can pre-vent further disability and death.

Muscle damage leads to rhabdomyolysis

Because trauma usually involvesmuscle damage, rhabdomyolysis—disintegration of muscle tissue—could threaten your patient’s kid-neys and his survival. Damagedmuscle fibers break down andrelease their contents—amongthem, the oxygen-transporting pig-ment myoglobin—into the blood-stream. Although the kidneys filterout myoglobin, the by-products ofits breakdown can reach toxic lev-els and set off a series of eventsthat trigger acute renal failure. (SeeHow Rhabdomyolysis Threatens.)The following circumstances cantrigger rhabdomyolysis:• trauma, including crush injuries,electrical shock, severe burns, andextended immobility

• extreme muscular activity duringstrenuous exercise, status epilepti-cus, and severe dystonia • toxic effects of various sub-stances, including ethanol, ethyleneglycol, isopropanol, methanol,heroin, barbiturates, methadone,cocaine, amphetamines, the streetdrug “ecstasy,” carbon monoxide,snake venom, and tetanus• metabolic abnormalities, such ashypothyroidism, hyperthyroidism,and diabetic ketoacidosis• medication effects, especiallywhen the drug is inadvertentlyintroduced into muscle tissue byintravenous (I.V.) infiltration.Examples include amphotericin B,azathioprine, and cyclosporine.

Classic signs and symptomsThe classic picture of rhabdomy-olysis is profound muscle weak-ness with pain, swelling, stiffnessand cramping, and dark, reddishbrown urine, which is a key char-acteristic of excessive myoglobin.The patient may develop malaise,fever, sinus tachycardia, nausea,and vomiting. Agitation, confu-sion, altered mentation, anddecreased urine production maysignal electrolyte abnormalities.

Your patient’s risk of hyper-kalemia and hyperphosphatemiaincreases as damaged muscle cellsrelease potassium and phosphorus,especially if renal failure develops.

Calcium from blood entering dam-aged muscle tissue may lead tohypocalcemia, but your patientmay not develop adverse reactionsor need treatment because bloodcalcium levels generally don’t droplow enough to cause problems.Hypercalcemia is a risk duringrecovery as soft tissue calcificationresolves and calcium shifts backinto the bloodstream.

Besides electrolyte imbalances,your patient may develop hyper-uricemia as muscle-derived ade-nine nucleotides released duringmuscle injury are converted to uricacid. Thromboplastin releasedfrom the injured myocytes can leadto disseminated intravascular coag-ulation (DIC), a clotting disorderthat may be a late complication ofrhabdomyolysis.

The diagnosis of rhabdomyolysisis made when the patient’s serumcreatine kinase (CK) level increasesto more than five times normal andmyoglobin is present in his urine. Aurine dipstick test showing a posi-tive heme reaction without thepresence of red blood cells indicatesthat myoglobin is present.

Aggressive infusions help Treatment of rhabdomyolysis focus-es on three main goals:• preventing and treating renal dys-function• reversing electrolyte abnormalities

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3deadlyAfter your patient weathers the

initial crisis, stand guard against

these potential problems.

BY CHARLES W. FORT, RN, BSN

How to combat

www.nursingcenter.com Nursing2003, May 59

• correcting the underlying cause.The primary treatment is aggres-

sive administration of I.V. crystal-loid solutions, preferably 0.9% sodi-um chloride. Fluid intake should beadequate to expand intravascularvolume enough to perfuse the kid-neys. If the patient has underlyingcardiac or renal disease, he’ll need apulmonary artery catheter for closemonitoring of his hemodynamicstatus and to prevent overload.

Hyperkalemia, which can triggercardiac arrhythmias, is the mostdangerous electrolyte abnormality.Your patient needs aggressive con-current infusions of sodium bicar-bonate, insulin, and glucose to drivepotassium from his blood back intothe cells. Sodium bicarbonate alsohelps reduce urine acidity to rendermyoglobin more soluble anddecrease cast formation.

Another approach to normalizehis elevated blood potassium level isto administer sodium polystyrenesulfonate orally or by enema to bindpotassium from his gastrointestinaltract and eliminate it in the stool. Ifthese measures don’t correct hyper-kalemia, he’ll need dialysis.

Although hyperphosphatemiacan contribute to acute renal failure,it usually responds to phosphate-binding antacids.

To help maintain your patient’surine output, you’ll administer adiuretic, such as mannitol (an

osmotic diuretic) or furosemide (aloop diuretic). Mannitol helps pre-serve intravascular volume whileflushing cellular debris through the

kidneys to further prevent myoglobin-protein cast formation.Furosemide works in the loop ofHenle to remove excess fluid from

How rhabdomyolysis threatens

Myoglobin released from damaged muscles enters the bloodand travels to the kidneys, where it’sfiltered in the glomerulus and reab-sorbed in the proximal tubule. As it’sdegraded, toxic metabolites, accelerat-ed by the acidic environment, formmyoglobin-protein casts that clog renaltubules and decrease renal perfusion,which can lead to acute tubular necrosis and renal failure.

complicationst r a u m a

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the body. Because rhabdomyolysisincreases the risk of renal failure,diuretic use must be balanced withfluid administration to preventhypovolemia. Monitor yourpatient’s fluid intake and output toassess for problems. Even if hedevelops severe renal failure andrequires dialysis, chances are goodthat his renal function will return tobaseline within 3 to 4 weeks withproper treatment.

How to care for your patientTo help your patient recover fromrhabdomyolysis, follow these guide-lines.• Administer alkaline crystalloidI.V. solution as ordered—generallyat a rate of 500 ml/hour to maintainurine output of 1 to 2 ml/kg/hour.• Monitor your patient’s urine pHto maintain it between 6 and 7.• Maintain an accurate intake andoutput record. Your patient’s urineoutput may be normal for the first24 to 36 hours, then progressivelydecrease over the next few days asrenal failure develops.• Observe for hypertension andsigns and symptoms of pulmonaryedema and heart failure, which canoccur with fluid overload. Admini-ster diuretics as ordered and docu-ment urine output.• Monitor the patient’s serumpotassium, pH, and muscle enzymelevels, such as CK.• Frequently monitor his pro-thrombin and partial thromboplas-tin times, platelet count, fibrinogen,and D-dimer levels to detect signsof DIC. If he’s bleeding, he mayneed treatment with fresh-frozenplasma, platelets, red blood cell(RBC) transfusion, or cryoprecipi-tate to manage the clotting disorderand anemia. If he isn’t bleeding,continue to monitor him closely;DIC may resolve spontaneously ina few days.• Once your patient’s condition sta-bilizes, ask for a consult to beginphysical therapy to maintain andincrease his weight-bearing ability

and to help him recover from histraumatic injuries.

A pressing problem:Compartment syndrome

Another acute problem associatedwith trauma is compartment syn-drome, which occurs most com-monly with a fracture to an arm orleg. If it isn’t detected and treatedearly, the patient could developparalysis, contractures, or tissuenecrosis that requires amputation.He may even die.

Compartment syndrome occurswhen increasing pressure within amyofascial compartment exceedscapillary perfusion pressure, soblood flow decreases to the tissueswithin. The pressure increasesbecause either the amount of com-partment contents increases or thecompartment itself is compressed.(See How Compartment SyndromeThreatens.)

An increase in compartmentcontents can occur with hemor-rhage, edema, extravasation, orwhen extreme muscular activitycauses muscle tissue within a com-partment to expand. Externalforces that can compress the com-partment include burn eschar, fas-cial defect closure, a tight dressingor cast, a pneumatic splint, or limbcompression during immobility.

Although compartments in thearm, forearm, hand, shoulder, foot,buttock, or thigh can be affected,the four compartments in thelower leg are most commonlyinvolved. Those in the thigh arerarely affected because thigh com-partments are large and excessfluid can move into the pelvis.

Telltale signs and symptomsClinical signs of compartment syn-drome include:• pain—at rest, with passive exten-sion or flexion, or out of propor-tion to the chief complaint• swelling• tense limb • paresthesia• warm, shiny skin• paresis• loss of two-point discrimination(see Making a Point or Two aboutCompartment Syndrome)• hypoesthesia followed by anes-thesia• complete neuropathy• loss of pulses (a late sign).

If your patient develops theseproblems, elevate the affected limbto the level of his heart and notifyhis primary care provider, whomay order any cast or splintremoved or opened. When thepatient’s awake and cooperative,the results of the clinical examina-

60 Nursing2003, Volume 33, Number 5 www.nursingcenter.com

Gauging compartment pressure

Recognizing progressive increases in intrafascial muscle compartment pres-sures early is important to protect the tissue. One way to measure the pressureis to insert a large-bore needle into the compartment and connect the needleto a saline-filled pressure transducer.

Another method is to use a handheld Stryker intracompartmental pressuremonitor. A needle attached to a prefilled syringe is inserted into the compart-ment for a digital pressure readout. A needle with a side port can be used for aquick reading, or a slit-tipped catheter can be used for continuous monitoring.A brief increase in measured pressure when the compartment is compressedconfirms correct needle placement.

A compartment pressure from 30 to 45 mm Hg is usually the threshold forfasciotomy. However, with systemic hypotension, a lower compartment pres-sure can overcome systolic blood pressure (BP) and capillary perfusion anddamage the tissue, so normalizing systemic BP decreases the risks.

tion are adequate to diagnose com-partment syndrome. If he isn’t, thecare provider may measure intra-compartmental pressure to corrob-orate the diagnosis or to make adefinitive diagnosis. Successivepressures can be used to monitorthe condition of the compartment.(To learn more about pressuremeasurement, see GaugingCompartment Pressure.)

Surgery to relieve the pressureThe definitive treatment for com-partment syndrome is decompres-sive fasciotomy, which should beconsidered if the pressure withinthe compartment exceeds 30 mmHg. By making an incision into thefascia, the surgeon allows the tissuewithin the compartment to ex-pand, which relieves pressure onthe capillaries and restores micro-circulation. During the procedure,the surgeon debrides any necrotictissue. Afterward, he leaves theincision open, covered by a non-constricting dressing.

Typically, the wound begins toclose in 5 to 7 days. The patientmay need skin grafting if thewound is large and doesn’t heal onits own. Potential complications offasciotomy include severe scarringas well as development of chronicpain syndrome and permanentsensory changes that could affectyour patient’s functional abilities.

Managing the problemThe following nursing measures areindicated to manage known or sus-pected compartment syndrome.• Keep the patient N.P.O. with theaffected limb at heart level—nothigher or lower. Although raisingthe limb above heart level usuallyreduces swelling, in compartmentsyndrome it would compromisearterial blood flow and worsenischemia. Keeping the limb belowheart level would increase swellingand raise compartment pressure.• Perform serial examinations toassess for any change in neuromus-cular status, such as paresthesia,paresis, or loss of two-point dis-crimination. • After surgery, use aseptic tech-nique to change your patient’sdressings and assess his wound atleast every 8 hours for odor,swelling, and drainage. Place atowel or linen-saver pad under thelimb to collect serous drainage. • As ordered, obtain culture speci-

mens if you find signs of infection.Monitor the patient’s white bloodcell count, erythrocyte sedimenta-tion rate, and temperature.• Administer antibiotics as ordered.• Continue serial examinations tomonitor for signs of inadequatedecompression. Also assess forsigns and symptoms of rhabdomy-olysis, which may occur as reperfu-sion to damaged muscle cells trig-gers release of myoglobin into thecirculation.

Fracture and FESGenerally associated with large ormultiple bone fractures orintramedullary manipulation dur-ing surgery, FES is a chain of eventsinitiated by the release of fat glob-ules from the bone marrow into thecirculation. If these fat globuleslodge in the pulmonary arteriolesand capillaries, the patient developsrespiratory problems and hypox-emia. (See How Fat EmbolismSyndrome Threatens.) Most com-

www.nursingcenter.com Nursing2003, May 61

How compartmentsyndrome threatens

In the limbs, sheaths of inelastic fasciawrapped around muscle, blood vessels, and nerves form com-partments that support thesestructures. If the volumewithin a compartmentincreases or the compartment itselfshrinks, pressureincreases and thecompartment can’texpand to relievethe pressure.

When the pres-sure exceeds the cap-illary pressure of thetissues, perfusion stopsand the tissues becomeischemic. The ischemia causesfluid shifts and edema, adding tothe pressure. As nerves in the compart-ment are compressed, sensory and motorfunction decrease and severe pain develops. If ischemiacontinues, muscle and nerve tissues die, causing permanentloss of function.

Making a point or twoabout compartment syndrome

To test two-point discrimination,open a paper clip and simultane-ously touch the ends to two pointson your patient’s finger pad. Fromtime to time, touch only one to thearea. Each time you touch the paperclip to his finger pad, ask how manypoints on his finger the clip is touch-ing. The inability to distinguishbetween one and two indicates lossof two-point discrimination.

Fascia Compartmentcontents underpressure

monly, FES affects patients withfractures of the pelvis, femur, tibia,or ribs. As it progresses, patientscould develop acute respiratory dis-tress syndrome (ARDS) or DIC.

Many conditions can causehypoxemia, so a helpful tool to pin-point the FES diagnosis is Gurd’scriteria, named for the physicianwho developed the system. At leastone major and three minor criterialisted below indicate FES.

Major criteria:• petechiae in a vest distribution• hypoxemia with a PaO2 less than60 mm Hg• pulmonary edema• changes in level of consciousness

Minor criteria:• heart rate greater than 110• temperature greater than 103º F(39.4o C)• retinal changes• fat in urine or sputum• unexplained drop in hematocritor platelet count• increasing erythrocyte sedimen-tation rate• jaundice• changes in renal function.

A petechial skin rash is a tell-tale sign that affects half ofpatients with FES, typically 1 to 4days after injury. Commonlyaffecting the conjunctiva, axillae,chest, and neck, the rash doesn’tblanch with pressure and usuallydisappears within 48 hours.Altered mental status with FES isoften significant and caused byhypoxemia and decreased bloodflow to the brain due to microag-gregation in the cerebral vessels.The patient may develop dyspnea,tachypnea (respiratory rate greaterthan 30), tachycardia, fever, anddiffuse crackles on auscultation (alate sign).

Testing, testingCertain assessment measures anddiagnostic tests can gauge thedegree of hypoxemia and systemicchanges affecting your patient.• Perform baseline arterial bloodgases (ABGs) on any patient at

high risk for developing FES.Initially, PaCO2 levels may bebelow normal as hyperventilationblows off carbon dioxide (CO2),but the level may rise above nor-mal as altered respiratory functionretains CO2. The PaO2 level maydrop below 60 mm Hg.• A chest X-ray, although normalin the early stages of FES, canhelp identify or rule out otherpulmonary disorders. Changes onchest X-ray caused by fat emboliare a late sign of FES. If the condi-tion progresses to ARDS, theresults may vary from patchyareas of consolidation to completewhiteout.• A ventilation/perfusion scan isrecommended only if FES isn’tevident from the patient’s history

and clinical symptoms or to ruleout pulmonary emboli from othersources. • Platelet counts can drop as lowas 50,000/mm3 as several factorsconsume circulating platelets.Normal platelet consumption ininjury-related clotting, plateletdilution by the administration ofI.V. crystalloid solution, platelet-poor blood products, and plateletaggregation around fat globules allcontribute to thrombocytopenia.• Hemoglobin levels may drop iftrauma causes the patient to hem-orrhage or if RBCs becometrapped in fatty aggregates.

Although your patient’s serumlipase levels may be elevated andurinalysis may show fat in hisurine, these findings are common

62 Nursing2003, Volume 33, Number 5 www.nursingcenter.com

How fat embolism syndrome threatens

Fat globules from the bone enter the circulation and form emboli in the pulmonary capillaries and arterioles. The body responds by producing lipase tobreak down the fatty globules, but the chemical reaction and the resultant fattyacids irritate the capillary and alveolar walls. As a result of the irritation, fluidleaks into the alveoli; surfactant and functional residual capacity decrease.Engorgement of the pulmonary vessels and increased workload of the rightside of the heart decrease lung compliance and the ventilation/perfusion ratio.All these events reduce oxygenation and trigger hypoxemia.

Fluid in the alveoli

Fat emboli in pulmonary vessels

Fat from bonemarrow

in patients with orthopedicinjuries who don’t develop FES, sothey’re not diagnostic for FES.

Your role in prevention and managementWhen you care for a patient witha fracture, preventing FES is a keycomponent of his care. The fol-lowing measures can help reducehis risk of FES or prevent furtherfat dissemination, hypoxemia,and hypovolemia if he developsthis dangerous complication.• Move the injured limb as littleand as carefully as possible beforefixation to avoid triggering FES.Early splinting and gentle han-dling are important to prevent therelease of fat globules.• Frequently monitor yourpatient’s respiratory and neuro-logic status for signs of hypox-emia. Monitor his ABGs andplatelet and RBC counts forabnormal values.• Administer supplemental oxygento treat hypoxemia. Oxygen thera-py should aim for a PaO2 of 100mm Hg, but not higher. Yourpatient may need intubation and

mechanical ventilation if he can’tmaintain a PaO2 of 60 mm Hg on40% oxygen delivered by facemask. Positive end-expiratory pres-sure can help improve his func-tional reserve capacity by keepinghis functional alveoli inflated.• As ordered, administer I.V. flu-ids to help flush the fatty acidsout of your patient’s system.Carefully monitor and record hisintake and output. Adequatefluid resuscitation helps preventshock, which is associated with apoor prognosis. Administer crys-talloids and avoid colloids toprevent protein leakage into theinterstitial space, which increasespulmonary edema. • Encourage your patient tocough and coach him in deep-breathing exercises and incentivespirometry. These measures openand stabilize atelectatic areas ofthe lung and improve lung capac-ity and ventilation.

Protecting against disabilityThrough diligent assessment andcare, you can minimize the risks ofthree dangerous complications of

trauma and help protect yourpatient against long-termdisability.

SELECTED REFERENCESCarriere, S., and Elsworth, T.: “Found Down:Compartment Syndrome, Rhabdomyolysis, andRenal Failure,” Journal of Emergency Nursing.24(3):214-217, June 1998.

Dalsimer, D.: “Case Report of Delayed OnsetCompartment Syndrome,” The American Journal ofEmergency Medicine. 12(2):176-177, March 1994.

D’Heere, M., et al.: “Fat Embolism Syndrome,”Journal of Trauma Nursing. 6(3):73-76, July-September 1999.

Maher, A., et al. (eds): Orthopaedic Nursing, 3rdedition. Philadelphia, Pa., W.B. Saunders Co.,2002.

Meister, J., and Reddy, K.: “Rhabdomyolysis: AnOverview,” The American Journal of Nursing.102(2):75-79, February 2002.

Miller, P., and Kane, J.: “Compartment Syn-drome and Rhabdomyolysis,” in The TraumaManual, 2nd edition, A. Peitzman, et al.(eds).Philadelphia, Pa., Lippincott Williams &Wilkins, 2002.

Charles W. Fort is a trauma program staff-developmentspecialist at Christiana Care Health System inWilmington, Del.

www.nursingcenter.com Nursing2003, May 63

National Association of Orthopaedic Nurseshttp://www.orthonurse.org

Wheeless’ Textbook of Orthopaedicshttp://wheeless.orthoweb.be

Last accessed on April 2, 2003.

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How to combat 3 deadly trauma complicationsInstructions:• Read the article beginning on page 58.• Take the test, recording your answers in the test answerssection (Section B) of the CE enrollment form. Each question has only one correct answer.• Complete registration information (Section A) and courseevaluation (Section C).• Mail completed test with registration fee to: LippincottWilliams & Wilkins, CE Dept., 16th Floor, 345 Hudson St., NewYork, NY 10014.• Within 3 to 4 weeks after your CE enrollment form is received,you will be notified of your test results.• If you pass, you will receive a certificate of earned contacthours and an answer key. If you fail, you have the option oftaking the test again at no additional cost.• A passing score for this test is 15 correct answers.• Need CE STAT? Visit http://www.nursingcenter.com forimmediate results, other CE activities, and your personalized CEplanner tool. • No Internet access? Call 1-800-933-6525, ext. 331 or ext. 332,for other rush service options.• Questions? Contact Lippincott Williams & Wilkins: (212) 886-1331 or (212) 886-1332.

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1. Which of the following best describes rhab-domyolysis?a. It causes kidney tissue to disintegrate.b. The kidneys can’t filter out myoglobin, so levels

become toxic.c. It results in pulmonary failure.d. Damaged muscle fibers break down and

release myoglobin.

2. The most dangerous electrolyte imbalanceassociated with rhabdomyolysis is a. hyperuricemia. c. hyperkalemia.b. hypercalcemia. d. hyperphosphatemia.

3. The classic clinical picture of rhabdomyoly-sis includesa. paresthesia.b. hypoesthesia.c. profound muscle weakness with pain.d. anesthesia.

4. A key characteristic of excessive myoglobinisa. swelling.b. dark, reddish brown urine.c. stiffness.d. cramping.

5. Thromboplastin released from injuredmyocytes can lead toa. DIC. c. status epilepticus.b. hyperthyroidism. d. diabetic ketoacidosis.

6. The diagnosis of rhabdomyolysis is madewhen myoglobin is present in the urine andthe serum CK level increases more thana. two times normal. c. four times normal.b. three times normal. d. five times normal.

7. The primary treatment for rhabdomyolysisis aggressive I.V. administration of a. mannitol. c. crystalloid solutions.b. insulin and glucose. d. furosemide.

8. How does administration of sodium bicar-

bonate affect rhabdomyolysis?a. It increases urine pH to between 4 and 5.b. It helps reduce urine acidity.c. It renders myoglobin insoluble.d. It increases cast formation.

9. Which statement correctly describes com-partment pressure in compartment syndrome?a. It’s less than capillary perfusion pressure.b. An increase enhances blood flow to tissues in

the compartment.c. Increased compartment contents or compres-

sion of the compartment increase the pressure.d. The pressure decreases when muscle in the

compartment expands.

10. Which area does compartment syndromemost commonly affect?a. lower leg c. armb. buttock d. shoulder

11. What’s the most common cause of com-partment syndrome?a. prolonged immobilityb. carbon monoxide toxicityc. cyclosporine infiltration into muscled. extremity fracture

12. Which of the following is a sign of com-partment syndrome?a. anesthesia followed by hypoesthesiab. a tense limbc. decreased urine productiond. altered mentation

13. What’s needed to diagnose compartmentsyndrome in an unconscious patient?a. pulmonary artery catheterizationb. urine dipstick testc. serum CK leveld. intracompartmental pressure measurement

14. The definitive treatment for compartmentsyndrome isa. elevation of the affected extremity.

b. removing or opening any cast or splint.c. decompressive fasciotomy.d. administration of I.V. crystalloid solution.

15. How should you manage known or sus-pected compartment syndrome?a. Elevate the affected limb above heart level.b. Administer sodium polystyrene sulfonate.c. Keep the affected limb below heart level.d. Assess for inadequate decompression.

16. Fractures of which area most commonlytrigger FES?a. pelvis c. radiusb. ulna d. scapula

17. Major criteria for FES include a. heart rate greater than 110.b. unexplained drop in platelet count.c. jaundice.d. petechiae in a vest distribution.

18. Which of the following may help preventFES in a patient with a fracture?a. Perform passive extension and flexion exercises

before fixation of the injured limb.b. Administer supplemental oxygen to treat hypox-

emia.c. Administer I.V. colloid solutions.d. Avoid administration of I.V. crystalloid solu-

tions.

19. Which pressure range is the usualthreshold for fasciotomy in compartmentsyndrome?a. 0-5 mm Hg c. 20-25 mm Hgb. 10-15 mm Hg d. 30-45 mm Hg

20. What’s a pathophysiologic change associ-ated with FES? a. decreased sensory and motor functionb. decreased lung compliancec. myoglobin-protein cast formationd. perfusion abnormalities leading to tissue

ischemia

How to combat 3 deadly trauma complicationsGENERAL PURPOSE To provide an overview of the manifestations and treatment of rhabdomyolysis, compartment syndrome, and FES. LEARNING OBJECTIVES After readingthe preceding article and taking this test, you should be able to: 1. Identify pathophysiologic changes associated with rhabdomyolysis, compartment syndrome, and FES. 2. Identifyclinical manifestations of and diagnostic testing for these conditions. 3. Indicate management strategies for patients with rhabdomyolysis, compartment syndrome, and FES.

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