Rhabdomyolysis Medication

  • Author: Eyal Muscal, MD; Chief Editor: Lawrence K Jung, MD   more...
 
Updated: May 16, 2012
 

Medication Summary

Medical therapy for rhabdomyolysis focuses on restoring adequate intravascular volume. Hydration with isotonic sodium chloride solution (0.9% NaCl) is the cornerstone of rhabdomyolysis therapy. Many clinicians recommend the use of sodium bicarbonate. Use furosemide or other diuretics (such as mannitol in adults) with sufficient hydration if urine output is inadequate. Hyperkalemia should also be addressed.

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Volume Expanders

Class Summary

The use of crystalloid solutions is the cornerstone of rhabdomyolysis therapy.

Sodium chloride 0.9%

 

Aggressive and early hydration with isotonic sodium chloride solution is important for the prevention of pigment-associated renal failure.

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Diuretics, Loop

Class Summary

Loop diuretics promote the excretion of water and electrolytes by the kidneys.

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Furosemide (Lasix)

 

Furosemide increases water excretion by interfering with the chloride-binding cotransport system; this, in turn, inhibits sodium and chloride reabsorption in the ascending loop of Henle and the distal renal tubule. Dosing must be individualized. Depending on the response, administer at increments of 20-40 mg every 6-8 hours until the desired diuresis occurs. When treating infants, titrate in increments of 1 mg/kg until a satisfactory effect is achieved.

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Diuretics, Osmotic Agents

Class Summary

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

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Mannitol (Osmitrol)

 

Mannitol is an 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 intravenously (IV) over 3-5 minutes; this should produce a urine flow of at least 30-50 mL/h over 2-3 hours. In children, assess for adequate renal function by administering a test dose of 200 mg/kg IV over 3-5 minutes; this should produce a urine flow of at least 1 mL/h over 1-3 hours.

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Antidotes, Other

Class Summary

Intracellular potassium transporters are used to decrease serum potassium levels. Insulin causes a transcellular shift of potassium into muscle cells, thereby temporarily lowering serum levels of potassium.

Potassium exchange resins decrease serum potassium levels. Sodium polystyrene sulfonate is an exchange resin that can be used to treat mild-to-moderate hyperkalemia. Each 1 mEq of potassium is exchanged for 1 mEq of sodium.

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Insulin regular human (Humulin, Novolin)

 

Regular human insulin stimulates cellular potassium uptake within 20-30 minutes. Administer with dextrose to prevent hypoglycemia. Monitor blood sugar levels frequently.

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Sodium polystyrene sulfonate (Kayexalate)

 

Sodium polystyrene sulfonate exchanges sodium for potassium and binds it in the gut, primarily the large intestine. It decreases total-body potassium levels. Onset of action after oral administration ranges from 2-12 hours and takes longer after rectal administration.

Sodium polystyrene sulfonate should not be used as first-line therapy for severe life-threatening hyperkalemia. It may be used in the second stage of therapy to reduce total-body potassium levels. The resin is typically mixed in 25% sorbitol before administration.

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Beta2-Agonists

Class Summary

Beta2 -adrenergic agents are used adjunctively to decrease serum potassium levels temporarily. Albuterol and other beta-adrenergic agents induce the intracellular movement of potassium via stimulation of the sodium-potassium adenosine triphosphatase (Na/K-ATPase) pump. Some studies using nebulized albuterol in adults and children indicate that this method of therapy is effective in lowering serum potassium levels, but peak response is unclear. Therefore, nebulized albuterol has not been established as a first-line therapy in severe hyperkalemia.

Albuterol nebulized

 

Nebulized albuterol is an adrenergic agonist that increases plasma insulin concentrations. This increase in insulin may shift potassium into the intracellular space. The onset of the decrease in potassium occurs at about 30 minutes. The duration of action is dose-dependent and is typically between 2 and 5 hours.

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Alkalinizing Agents

Class Summary

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

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Sodium bicarbonate (Neut)

 

Sodium bicarbonate is useful in alkalization of urine to prevent acute myoglobinuric renal failure. Titrate the dose to raise the pH above 6.5-7.0.

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Contributor Information and Disclosures
Author

Eyal Muscal, MD  Assistant Professor, Section of Pediatric Rheumatology, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital

Eyal Muscal, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Rheumatology, and Clinical Immunology Society

Disclosure: Nothing to disclose.

Coauthor(s)

Marietta Morales DeGuzman, MD  Assistant Professor, Department of Pediatrics, Baylor College of Medicine; Consulting Staff, Section of Pediatric Rheumatology, Department of Pediatrics, Texas Children's Hospital, Ben Taub General Hospital

Marietta Morales DeGuzman, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Rheumatology, and Texas Pediatric Society

Disclosure: Nothing to disclose.

Chief Editor

Lawrence K Jung, MD  Chief, Division of Pediatric Rheumatology, Children's National Medical Center

Lawrence K Jung, MD is a member of the following medical societies: American Association for the Advancement of Science, American Association of Immunologists, American College of Rheumatology, Clinical Immunology Society, and New York Academy of Sciences

Disclosure: Nothing to disclose.

Additional Contributors

Sandy Craig, MD, Residency Program Director, Carolinas Medical Center; Associate Professor, Department of Emergency Medicine, University of North Carolina at Chapel Hill School of Medicine

Sandy Craig, MD is a member of the following societies; Alpha Omega Alpha and the Society for Academic Emergency Medicine.

Disclosure: Nothing to disclose.

Herbert S Diamond, MD Adjunct Professor of Medicine, Division of Rheumatology, University of Pittsburgh School of Medicine; Chairman Emeritus, Department of Internal Medicine, Western Pennsylvania Hospital

Herbert S Diamond, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American College of Rheumatology, American Medical Association, and Phi Beta Kappa

Disclosure: Merck Ownership interest Other; Smith Kline Ownership interest Other; Zimmer Ownership interest Other

Lance W Kreplick, MD, FAAEM, MMM 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, FAAEM, MMM, is a member of the following medical societies: American Academy of Emergency Medicine and American College of Physician Executives

Disclosure: Nothing to disclose.

Barry L Myones, MD Associate Professor, Departments of Pediatrics and Immunology, Pediatric Rheumatology Section, Baylor College of Medicine; Director of Research, Pediatric Rheumatology Center, Texas Children's Hospital

Barry L Myones, MD is a member of the following medical societies: American Academy of Pediatrics, American Association of Immunologists, American College of Rheumatology, American Heart Association, American Society for Microbiology, Clinical Immunology Society, and Texas Medical Association

Disclosure: Nothing to disclose.

Tom Scaletta, MD Chair, 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

Disclosure: Nothing to disclose.

Binita R Shah, MD, FAAP, Professor of Clinical Pediatrics and Emergency Medicine, SUNY Health Sciences Center at Brooklyn; Director of Pediatric Emergency Medicine, Departments of Emergency Medicine and Pediatrics, Kings County Hospital Center

Binita R Shah, MD, FAAPis a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Renee Wilson, MD, Clinical Assistant Instructor, Department of Emergency Medicine, SUNY-Downstate and Kings County Hospital

Renee Wilson, MDis a member of the following medical societies: Society for Academic Emergency Medicine

Disclosure: Nothing to disclose

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

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Model of helical domains in myoglobin (protein linked to kidney damage in rhabdomyolysis).
 
 
 
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