Methemoglobinemia in Emergency Medicine Clinical Presentation

  • Author: David C Lee, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Jul 27, 2011
 

History

Normal methemoglobin concentrations are 1% (range, 0-3%).

At concentrations of 3-15%, a slight discoloration (eg, pale, gray, blue) of the skin may be present.

At fractions of 15-20%, the patient may be relatively asymptomatic, but cyanosis is likely to be present.

Signs and symptoms at fractions of 25-50% are as follows:

  • Headache
  • Dyspnea
  • Lightheadedness, even syncope
  • Weakness
  • Confusion
  • Palpitations, chest pain

Signs and symptoms at fractions of 50-70% are as follows:

  • Cardiovascular - Abnormal cardiac rhythms
  • CNS - Altered mental status; delirium, seizures, coma
  • Metabolic - Profound acidosis
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Physical

Physical examination findings may include the following:

  • Discoloration of the skin and blood is the most striking physical finding.
  • Cyanosis occurs with the formation of 1.5 g/dL of methemoglobin, as compared to 5 g/dL of deoxygenated hemoglobin.
  • Seizures
  • Coma
  • Dysrhythmias (eg, bradyarrhythmia, ventricular dysrhythmia)
  • Acidosis
  • Cardiac or neurologic ischemia
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Causes

Compromised physiologic cellular defenses against oxidant stress occur in some patients, including the following:

  • Children younger than 4 months may have underdeveloped protective mechanisms (NADH methemoglobin reductase). Infections, especially GI infections, may cause a buildup of systemic oxidants by an overgrowth of gut bacteria.
  • Congenital lack of protective cellular capabilities includes those with the following:
    • Patients with NADH methemoglobin reductase (diaphorase I) deficiency may develop congenital methemoglobinemia.
    • Patients with hemoglobin M disease may have abnormal hemoglobin that is not amenable to reduction.
    • Patients with pyruvate kinase deficiency may have an impaired glycolytic pathway, which results in deficient NADH production.
    • Patients with G-6-PD deficiency may have impaired production of NADPH in the hexose-monophosphate shunt.

Agents that inflict large oxidant stress on patients include the following:

  • Pharmaceutical agents include local anesthetic agents (eg, benzocaine,[1, 2] lidocaine, prilocaine), amyl nitrite, chloroquine, dapsone,[2] nitrates, nitrites, nitroglycerin, nitroprusside, phenacetin, phenazopyridine, primaquine, quinones, and sulfonamides. Dapsone and its hydroxylamine metabolite can cause prolonged methemoglobinemia due to long half-lives.
  • Environmental agents include the following:
    • Aniline dyes
    • Aromatic amines
    • Arsine
    • Butyl nitrite
    • Chlorates
    • Chlorobenzene
    • Chromates
    • Combustion products
    • Dimethyltoluidine
    • Foods containing nitrates or nitrites (including well water)
    • Isobutyl nitrite
    • Naphthalene
    • Nitroaniline
    • Nitrobenzene
    • Nitrofurans
    • Nitrophenol
    • Nitrosobenzene
    • Resorcinol
    • Silver nitrate
    • Trinitrotoluene
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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)

Kathy L Ferguson, DO  Attending Physician, Department of Emergency Medicine, New York Hospital of Queens, Queens, New York

Kathy L Ferguson, DO is a member of the following medical societies: American College of Emergency Physicians and American College of Medical Toxicology

Disclosure: Nothing to disclose.

Specialty Editor Board

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.

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.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

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.

References

  1. Moore TJ, Walsh CS, Cohen MR. Reported adverse event cases of methemoglobinemia associated with benzocaine products. Arch Intern Med. Jun 14 2004;164(11):1192-6. [Medline].

  2. Ash-Bernal R, Wise R, Wright SM. Acquired methemoglobinemia: a retrospective series of 138 cases at 2 teaching hospitals. Medicine (Baltimore). Sep 2004;83(5):265-73. [Medline].

  3. US Food and Drug Administration. FDA Drug Safety Communication: Serious CNS reactions possible when methylene blue is given to patients taking certain psychiatric medications. Available at http://www.fda.gov/Drugs/DrugSafety/ucm263190.htm. Accessed July 27, 2011.

  4. Conkling PR. Brown blood: understanding methemoglobinemia. N C Med J. Mar 1986;47(3):109-11. [Medline].

  5. Ellenhorn MJ, Barceloux DG. Nitrates, nitrites, and methemoglobinemia. In: Medical Toxicology, Diagnosis and Treatment of Human Poisonings. 1988:844-851.

  6. Fitzsimons MG, Gaudette RR, Hurford WE. Critical rebound methemoglobinemia after methylene blue treatment: case report. Pharmacotherapy. Apr 2004;24(4):538-40. [Medline].

  7. Henretig FM, Gribetz B, Kearney T, Lacouture P, Lovejoy FH. Interpretation of color change in blood with varying degree of methemoglobinemia. J Toxicol Clin Toxicol. 1988;26(5-6):293-301. [Medline].

  8. Herman MI, Chyka PA, Butler AY, Rieger SE. Methylene blue by intraosseous infusion for methemoglobinemia. Ann Emerg Med. Jan 1999;33(1):111-3. [Medline].

  9. Howland MA. Methylene blue. In: Goldfrank's Toxicologic Emergencies. 8th ed. 2006:1746-1748.

  10. Price D. Methemoglobin inducers. In: Goldfrank's Toxicologic Emergencies. 8th ed. 2006:1734-1745.

  11. Umbreit J. Methemoglobin--it's not just blue: a concise review. Am J Hematol. Feb 2007;82(2):134-44. [Medline].

 
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Note the chocolate brown color of methemoglobinemia. Tube 1 and tube 2 have a methemoglobin concentration of 70%; tube 3, a concentration of 20%; and tube 4, a normal concentration.
 
 
 
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