eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Rhabdomyolysis: Treatment & Medication

Author: Sandy Craig, MD, Adjunct Associate Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Carolinas Medical Center
Contributor Information and Disclosures

Updated: Oct 1, 2009

Treatment

Prehospital Care

Vigorous hydration with isotonic crystalloid is the cornerstone of therapy for rhabdomyolysis. Retrospective studies of patients with severe crush injuries resulting in rhabdomyolysis suggest that the prognosis is better when prehospital personnel provide fluid resuscitation.40 Support of the intravascular volume increases the glomerular filtration rate (GFR) and oxygen delivery and dilutes myoglobin and other renal tubular toxins.

  • Immediately obtain intravenous access with a large-bore catheter.
  • Administer isotonic crystalloid 500 mL/h and then titrate to maintain a urine output of 200-300 mL/h.
  • Because injured myocytes can sequester large volumes of extracellular fluid, crystalloid requirements may be surprisingly large.

Emergency Department Care

Assess ABCs and support as needed. Treat any underlying conditions, such as trauma, infection, or toxins. General recommendations for the treatment of rhabdomyolysis include fluid resuscitation and prevention of end-organ complications.

  • Patients with CK elevation in excess of 2-3 times the reference range, appropriate clinical history, and risk factors should be suspected of having rhabdomyolysis. Administer isotonic crystalloid 500 mL/h and titrate to maintain a urine output of 200-300 mL/h. (Consider central venous pressures or Swan-Ganz catheterization in patients with cardiac or renal disease. These invasive studies can assist in the assessment of the intravascular volume.) Repeat CK assay every 6-12 hours in order to determine peak CK level.
  • Acute renal failure develops in 30-40% of patients with rhabdomyolysis. Suggested mechanisms include precipitation of myoglobin and uric acid crystals within renal tubules, decreased glomerular perfusion, and the nephrotoxic effect of ferrihemate (formed upon dissociation of myoglobin in the acidic environment of the renal parenchyma). In a 1988 review, Ward suggested that predictors for the development of renal failure include peak CK level more than 6000 IU/L, dehydration (hematocrit >50, serum sodium level >150 mEq/L, orthostasis, pulmonary wedge pressure <5 mm Hg, urinary fractional excretion of sodium <1%), sepsis, hyperkalemia or hyperphosphatemia on admission, and the presence of hypoalbuminemia. Acute renal failure has occasionally developed in severely dehydrated patients with peak CK level as low as 2000 IU/L. To prevent renal failure, many authorities advocate urine alkalinization, mannitol, and loop diuretics.
    • Urinary alkalinization to prevent the development of acute renal failure in patients with rhabdomyolysis has been supported by animal studies and retrospective human studies, although prospective randomized human studies are lacking.
    • Urinary alkalinization is recommended for patients with rhabdomyolysis and CK levels in excess of 6000 IU/L. Alkalinization should be considered earlier in patients with acidemia, dehydration, or underlying renal disease. A suggested regimen is 0.5 isotonic sodium chloride solution with one ampule of sodium bicarbonate administered at 100 mL/h and titrated to a urine pH higher than 7.
    • After establishing an adequate intravascular volume, mannitol may be administered to enhance renal perfusion.
    • Loop diuretics may be used to enhance urinary output in oliguric patients, despite adequate intravascular volume.
  • Treatment of hyperkalemia consists of intravenous sodium bicarbonate, glucose, and insulin; oral or rectal sodium polystyrene sulfonate (Kayexalate); and hemodialysis. Administer intravenous calcium chloride for patients who are hemodynamically compromised and hyperkalemic.
  • Hypocalcemia is noted early in the course of rhabdomyolysis and generally is not of clinical significance. Calcium supplementation is not recommended.
  • Compartment syndrome requires immediate orthopedic consultation for fasciotomy.
  • DIC should be treated with fresh frozen plasma, cryoprecipitate, and platelet transfusions.
  • Hyperuricemia and hyperphosphatemia rarely are of clinical significance and rarely require treatment.

Consultations

  • Nephrologist: Indications for hemodialysis include hyperkalemia that is persistent despite therapy, severe acid-base disturbances, refractory pulmonary edema, and progressive renal failure.
  • Orthopedist: Consult an orthopedist in cases of suspected compartment syndrome.

Medication

Medical therapy for rhabdomyolysis focuses on restoring adequate intravascular volume using isotonic crystalloid. Adjunctive measures that may decrease the incidence of acute myoglobinuric renal failure include urinary alkalinization and osmotic and loop diuresis.

Alkalinizing agents

Sodium bicarbonate is administered IV to alkalinize urine in patients with rhabdomyolysis. This may prevent toxicity caused by the presence of myoglobin in acidic urine and crystallization of uric acid.


Sodium bicarbonate (Neut)

Useful in alkalization of urine to prevent acute myoglobinuric renal failure. Titrate dose to increase pH to >7.

Adult

1 ampule (44 mEq) of sodium bicarbonate is added to 1 L of 0.45 NS and infused at 100 mL/h IV

Pediatric

1.9 mEq/kg IV q1-2h prn

Urinary alkalinization, induced by increased sodium bicarbonate concentrations, may cause decreased levels of lithium, tetracyclines, chlorpropamide, methotrexate, and salicylates; increases levels of amphetamines pseudoephedrine, flecainide, anorexiants, mecamylamine, ephedrine, quinidine, and quinine

Documented hypersensitivity; alkalosis; hypernatremia; hypocalcemia; severe pulmonary edema; unknown abdominal pain

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Can cause alkalosis, decreased plasma potassium, hypocalcemia, and hypernatremia; caution in electrolyte imbalances, such as in patients with CHF, cirrhosis, edema, corticosteroid use, or renal failure; when administering, avoid extravasation because can cause tissue necrosis

Osmotic diuretics

These agents increase osmolarity of glomerular filtrate and induce diuresis. They hinder tubular reabsorption of water, causing sodium and chloride excretion to increase.


Mannitol (Osmitrol)

Alternative diuretic used when urine output is inadequate despite aggressive fluid therapy.
Initially assess for adequate renal function in adults by administering a test dose of 200 mg/kg IV over 3-5 min. Should produce a urine flow of at least 30-50 mL/h over 2-3 h.
In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 min. It should produce a urine flow of at least 1 mL/h over 1-3 h.

Adult

1.5-2 g/kg IV as 20% solution (7.5-10 mL/kg) or as 15% solution (10-13 mL/kg) over a period as short as 30 min

Pediatric

0.5-1 g/kg IV initial; followed by 0.25-0.5 g/kg IV q4-6h maintenance dose

Documented hypersensitivity; anuria; severe pulmonary congestion; progressive renal damage; severe dehydration; active intracranial bleeding; progressive heart failure

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Carefully evaluate cardiovascular status before rapid administration of mannitol because a sudden increase in extracellular fluid may lead to fulminating CHF; avoid pseudoagglutination, when blood given simultaneously, add at least 20 mEq of sodium chloride to each liter of mannitol solution; do not give electrolyte-free mannitol solutions with blood

Loop diuretics

These agents elicit a loss of free water, increasing diuresis.


Furosemide (Lasix)

Increases water excretion by interfering with the chloride-binding cotransport system, resulting in inhibition of sodium and chloride reabsorption in the ascending loop of Henle and distal renal tubule.
Individualize doses. Depending on response, administer at increments of 20-40 mg q6-8h until desired diuresis occurs. When treating infants, titrate with 1-mg/kg/dose increments until a satisfactory effect is achieved.

Adult

20-40 mg IV q2h prn to maintain urine output; may increase dose by 20 mg q2h prn to desired response

Pediatric

1-2 mg/kg IV q6h; titrate to desired urine output; not to exceed 6 mg/kg/d

Metformin decreases concentrations; interferes with hypoglycemic effect of antidiabetic agents and antagonizes muscle relaxing effect of tubocurarine; auditory toxicity appears to be increased with coadministration of aminoglycosides and furosemide; hearing loss of varying degrees may occur; anticoagulant activity of warfarin may be enhanced when taken concurrently with this medication; increased plasma lithium levels and toxicity are possible when taken concurrently with this medication

Documented hypersensitivity; hepatic coma; anuria; state of severe electrolyte depletion

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Perform frequent serum electrolyte, carbon dioxide, glucose, creatinine, uric acid, calcium, and BUN determinations during first few months of therapy and periodically thereafter

More on Rhabdomyolysis

Overview: Rhabdomyolysis
Differential Diagnoses & Workup: Rhabdomyolysis
Treatment & Medication: Rhabdomyolysis
Follow-up: Rhabdomyolysis
References

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Further Reading

Contributor Information and Disclosures

Author

Sandy Craig, MD, Adjunct Associate Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill, Carolinas Medical Center
Sandy Craig, MD is a member of the following medical societies: Alpha Omega Alpha and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

Lance W Kreplick, MD, MMM, FAAEM, FACEP, Medical Director of Hyperbaric Medicine, Fawcett Wound Management and Hyperbaric Medicine; Consulting Staff in Occupational Health and Rehabilitation, Company Care Occupational Health Services; President and Chief Executive Officer, QED Medical Solutions, LLC
Lance W Kreplick, MD, MMM, FAAEM, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Tom Scaletta, MD, President, Emergency Excellence (EmEx) (www.emergencyexcellence.com); Assistant Professor of Emergency Medicine, Rush Medical College, Cook County Hospital; Chairperson, Department of Emergency Medicine, Edward Hospital; Past-President, American Academy of Emergency Medicine
Tom Scaletta, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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