Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP

Education Specialist LRM ConsultingNashville, TN

ObjectivesIdentify the causes of rhabdomyolysis.Describe signs and symptoms of rhabdomyolysis.Utilizing a case study, identify management strategies of a patient with renal dysfunction resulting from rhabdomyolysis.

“Rhabdomyolysis was first reported in 1881, in the German literature” (Abbeele, Parker, 1985).“Rhabdomyolysis was first described in the victims of crush injury during the 1940-1941 London, England, bombing raids of World War II” (Craig, 2006).

Rhabdomyolysis accounts for an estimated 8-15% of cases of acute renal failure.the overall mortality rate for patients with Rhabdomyolysis is approximately 5%Rhabdomyolysis is more common in males than in femalesmay occur in infants, toddlers, and adolescents

disintegration of striated muscleresults in the release of muscular cell constituents into the extracellular fluid and the circulationmajor component released is myoglobin

massive amounts of myoglobin are released the binding capacity of the plasma protein is exceededmyoglobin is then filtered by the glomeruli and reaches the tubules, where it may cause obstruction and renal dysfunction

syndrome characterized by muscle necrosis and the release of intracellular muscle constituents into the circulationcreatine kinase (CK) levels are typically markedly elevated, and muscle pain and myoglobinuria may be present

severity of illness ranges from asymptomatic elevations in serum muscle enzymes to life-threatening disease associated with:

extreme enzyme elevationselectrolyte imbalancesacute kidney injury

Rhabdomyolysis is the breakdown of muscle fibers, specifically of the sarcolemma of skeletal muscle, resulting in the release of muscle fiber contents (myoglobin) into the bloodstream.

The sarcolemma is the cell membrane of a muscle cell. The membrane is designed to receive and conduct stimuli

Source: (Muscle Anatomy & Structure, 2007)

when muscle is damaged, a protein pigment - myoglobin is released into the bloodstream and filtered out of the body by the kidneys. broken down myoglobin may block the structures of the kidney, causing damage such as acute tubular necrosis or kidney failure.dead muscle tissue may cause a large amount of fluid to move from the blood into the muscle, leading to hypovolemic shock reduced blood flow to the kidneys.

may result from a large variety of diseases, TRAUMA, or toxic insults to skeletal musclehereditary myopathies

Causes trauma burns compression syndrome infection seizures heat intolerance heat stroke

Causes vascular occlusion prolonged shock electrolyte disorders drugs (cocaine, alcohol,

statins, amphetamine) low phosphate levels shaking chills

Clinical Manifestations muscle tenderness myalgias muscle swelling &

weakness DIC color of urine

• Additionally some possible symptoms include: − Overall fatigue− Joint pain− Seizures− Weight gain

Diagnosisan examination reveals tender or damaged skeletal musclesCreatine Phosphokinase (CK) levels are very highserum myoglobin test is positiveserum potassium may be very high

serum CK begins to rise within 2 to 12 hours following the onset of muscle injury and reaches its maximum within 24 to 72 hoursdecline is usually seen within three to five days of cessation of muscle injury

CK has a serum half-life of about 1.5 days and declines at a relatively constant rate of about 40 to 50 percent of the previous day’s valuepatients whose CK does not decline as expected, continued muscle injury or the development of a compartment syndrome may be present

DiagnosisUrinalysis may reveal protein and be positive for hemoglobin without evidence of red blood cells on microscopic examination Urine myoglobin test is positive

Urine Myoglobinvisible changes in the urine only occur once urine levels exceed from about 100 to 300 mg/dLcan be detected by the urine dipstick at concentrations of only 0.5 to 1 mg/dL half-life of only two to three hours, much shorter than that of CK. rapidly excreted and metabolized to bilirubin, serum levels may return to normal within six to eight hours

Lab Values elevated muscle

enzymes (CK) hyperkalemia hyperphosphatemia hypocalcemia

ComplicationsKidney damageAcute renal failureHyperkalemiaCardiac arrestDisseminated Intravascular CoagulationCompartment syndrome

Treatment volume replacement treat electrolyte

abnormalities protect renal

perfusion alkalinization of urine fasciotomy

• early and aggressive fluids (hydration) may prevent complications by rapidly remove myoglobin out of the kidneys.

• administer isotonic crystalloid fluids (Normal Saline or Lactated Ringer’s)

• give as much fluid as you would give a severely burned patient.

studies of patients with severe crush

injuries resulting in Rhabdomyolysis

suggest that the prognosis is better

when prehospital personnel provide

FLUID RESUCITATION!

medicines that may be prescribed include diuretics and sodium bicarbonate.hyperkalemia should be treated if presentkidney failure should be treated as appropriate

if urinary flow is >20 mL/hour add mannitol to the intravenous alkaline solution providing an increase in urine output is demonstrated following a test dosesuggested test dose is 60 mL of a 20 percent solution of mannitol administered intravenously over three to five minutes

if urine output increases by at least 30 to 50 mL/h above baseline levels in response to the test dose, 50 mL of 20 percent mannitol (1 to 2 g/kg per day [total, 120 g], may be given at a rate of 5 g/hour. mannitol is contraindicated in patients with oliguria

The outcome varies depending on the extent of kidney damage.

Source: Silberber, 2007

Renal Failure Index (RFI)RFI = UNa x SCr/UCrIntrepretation

RFI < 1 (prerenal failure)RFI > 1 (intrarenal failure)

Fraction Excreted Sodium (FENa)

FENa = Una X PCr / Pna X Ucr x 100Intrepretation

FENa < 1 (prerenal failure)FENa > 1 (intrarenal failure)

Renal Failure Index (RFI)RFI = UNa x SCr/UCrExampleRFI > 1 UNa>40 mEq/L FENa > 2-3% UCr/SCr<20

Renal BiomarkersUrine interleukin – 18 (IL – 18)Urine or blood NGAL

neutrophil gelatinase – associated lipocalin

Increase 24 to 48 hours earlier than creatinine

IntrinsicDiagnostics

BUN/Creatinine ratioRFI/FENaurinalysis

Treatmentunderlying causeprevention on injury

high risk patienthydrationlimit exposure

Management Principlesmaintain fluid balancemanage hyperkalemia• glucose & insulin• sodium bicarbonate• calcium gluconate• albuterol

Clinical Manifestationshyperkalemiahypocalcemiahypermagnesemiahyperphosphatemiaacid – base imbalance

hypocalcemia occurs in up to two-thirds of patients with significant rhabdomyolysis

increase in serum phosphate deposition of calcium phosphate into injured muscledecreased bone responsiveness to parathyroid hormone

Management Principlescontrol hypertension in presence of encephalopathybicarbonate for severe acidosis (pH < 7.2)manage anemia

Renal Replacement Renal Replacement TherapiesTherapies

TreatmentReplacement Therapies

acidosisHCO3 < 10 mEq/LK+ > 6.5 mEq/Lneed high protein dietdeteriorating

Treatment:Types

hemodialysiscontinuous renal replacement therapy

Treatmentfluid balanceanticoagulationprevent clottingprevent blood lossultrafiltration

Case Study 20 – year old male with friends “doing

drugs – cocaine” police break up party – male runs from

police but collaspes – states legs became so weak that he fell

admitted to ED – lower extremity weakness and severe pain in legs

Case StudySerum Electrolytes ABGs

Na 141K 6.7Cl 104CO2 7Creatinine 4.5BUN 20Ca 5.0Mg 2.0PO4 11.2

pH 7.11PaCO2 27PaO2 97SaO2 98%HCO3 7

Case Study

Serum Enzymes Hematology Values Clotting Profile

CK 4,780LDH 812

Hct 30WBC 18,400

PT 28PTT >180Platelets 80,000

Case Study

Urinalysis Sediment Urine Chemistries

Color Reddish brownSG 1.008pH 5.0

RBC 0-1WBC 4-5Casts granular & epithelial

Urine Na 42Urine Osm 280

wide variety of situations that cause rhabdomyolysisfocus is fluid resuscitation and surgical intervention if compartment syndrome developsARF is a common consequence – treat as you would any type of intrinsic ARF