Lithium Toxicity Treatment & Management

  • Author: David C Lee, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Nov 18, 2010
 

Prehospital Care

Stabilize life-threatening conditions and initiate supportive therapy according to local EMS protocols.

Obtain intravenous access with isotonic sodium chloride solution.

Monitor cardiac function to assess rhythm disturbances.

Obtain all pill bottles available to the patient.

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Emergency Department Care

Supportive therapy is the mainstay of treatment of lithium toxicity. Airway protection is crucial due to emesis and risk of aspiration. Seizures can be controlled with benzodiazepines, phenobarbital, or propofol.

GI decontamination

Gastric lavage may be attempted if the patient presents within one hour of ingestion.

Lithium is a monovalent cation that does not bind to charcoal; therefore, activated charcoal has no role. However, activated charcoal might be considered in the case of exposure to co-ingestants. The clinician also has to be aware that acute lithium toxicity can produce vomiting and precipitate aspiration of activated charcoal.

Whole-bowel irrigation with polyethylene glycol lavage can be effective in preventing absorption from extended-release lithium.

Because of its similarity to potassium, the use of sodium polystyrene sulfonate has been proposed as a method of eliminating lithium.[1] However, hypokalemia has been reported and studies have still not shown definite evidence of benefit. One retrospective review showed a possible decrease in lithium half-life with administration of sodium polystyrene sulfonate in patients presenting with chronic lithium toxicity.[2] However, it is unknown if this was clinically relevant or if patient outcome was improved.

Enhanced elimination

The mainstay of treatment is fluid therapy. The goal of saline administration is to restore glomerular filtration rate (GFR), normalize urine output, and enhance lithium clearance.

Lithium is readily dialyzed because of water solubility, low volume of distribution, and lack of protein binding.

Hemodialysis is indicated for patients who have renal failure and are unable to eliminate lithium. It is also indicated in patients who cannot tolerate hydration such patients with congestive heart failure (CHF) or liver disease. Hemodialysis should be considered in patients who develop severe signs of neurotoxicity such as profound altered mental status and seizures. An absolute level of 4 mEq/L in acute toxicity and a level of 2.5 mEq/L in chronic toxicity in patients with symptoms should also be considered for hemodialysis (GF), although guidelines for hemodialysis based on levels alone are controversial.

Because postdialysis rebound elevations in lithium levels have been documented, continuous venovenous hemofiltration (CVVH) has been advocated.[3, 4]

Patients who are already on peritoneal dialysis should continue with it while awaiting hemodialysis or CVVH.

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Consultations

Consult renal service personnel for hemodialysis in severe intoxications.

Consult psychiatric service personnel for patients with intentional overdose.

Consult the poison control center and a medical toxicologist regarding appropriate treatment.

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Contributor Information and Disclosures
Author

David C Lee, MD  Research Director, Department of Emergency Medicine, Associate Professor, North Shore University Hospital and New York University Medical School

David C Lee, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

Amit Gupta, MD  Department of Emergency Medicine, Staten Island University Hospital

Amit Gupta, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

Specialty Editor Board

Mark S Slabinski, MD, FACEP, FAAEM  Vice President, EMP Medical Group

Mark S Slabinski, MD, FACEP, FAAEM is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, and Ohio State Medical Association

Disclosure: Nothing to disclose.

John T VanDeVoort, PharmD  Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH  Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Society for Academic Emergency Medicine, Undersea and Hyperbaric Medical Society, and Wilderness Medical Society

Disclosure: Nothing to disclose.

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

Asim Tarabar, MD  Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, James G Linakis, PhD, MD, to the development and writing of this article.

References

  1. Linakis JG, Savitt DL, Wu TY, Lockhart GR, Lacouture PG. Use of sodium polystyrene sulfonate for reduction of plasma lithium concentrations after chronic lithium dosing in mice. J Toxicol Clin Toxicol. 1998;36(4):309-13. [Medline].

  2. Ghannoum M, Lavergne V, Yue CS, Ayoub P, Perreault MM, Roy L. Successful treatment of lithium toxicity with sodium polystyrene sulfonate: a retrospective cohort study. Clin Toxicol (Phila). Jan 2010;48(1):34-41. [Medline].

  3. Menghini VV, Albright RC Jr. Treatment of lithium intoxication with continuous venovenous hemodiafiltration. Am J Kidney Dis. Sep 2000;36(3):E21. [Medline].

  4. van Bommel EF, Kalmeijer MD, Ponssen HH. Treatment of life-threatening lithium toxicity with high-volume continuous venovenous hemofiltration. Am J Nephrol. Sep-Oct 2000;20(5):408-11. [Medline].

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  16. Juurlink DN, Mamdani MM, Kopp A, Rochon PA, Shulman KI, Redelmeier DA. Drug-induced lithium toxicity in the elderly: a population-based study. J Am Geriatr Soc. May 2004;52(5):794-8. [Medline].

  17. Lee DC, Klachko MN. Falsely elevated lithium levels in plasma samples obtained in lithium containing tubes. J Toxicol Clin Toxicol. 1996;34(4):467-9. [Medline].

  18. Ng YW, Tiu SC, Choi KL, Chan FK, Choi CH, Kong PS. Use of lithium in the treatment of thyrotoxicosis. Hong Kong Med J. Aug 2006;12(4):254-9. [Medline].

  19. Rosenqvist M, Bergfeldt L, Aili H, Mathe AA. Sinus node dysfunction during long-term lithium treatment. Br Heart J. Oct 1993;70(4):371-5. [Medline].

  20. Scharman EJ. Methods used to decrease lithium absorption or enhance elimination. J Toxicol Clin Toxicol. 1997;35(6):601-8. [Medline].

  21. Timmer RT, Sands JM. Lithium intoxication. J Am Soc Nephrol. Mar 1999;10(3):666-74. [Medline].

  22. Zimmerman JL. Poisonings and overdoses in the intensive care unit: general and specific management issues. Crit Care Med. Dec 2003;31(12):2794-801. [Medline].

 
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