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Life in the Fast Lane • LITFL • Medical Blog

Emergency medicine and critical care medical education blog

Critical Care Compendium | Methaemoglobinaemia

Methaemoglobinaemia

by Chris Nickson, Last updated September 15, 2014

Reviewed and revised 14 September 2014

OVERVIEW

  • Methaemoglobinaemia is the state of excessive methaemoglobin in the blood
  • methaemoglobin is an altered state of Hb where ferrous ions (Fe2+) of haem are oxidised to the ferric state (Fe3+) and rendered unable to bind O2
  • normal level is < 1.5%

CAUSES

Congenital

  • cytochrome b5 reductase deficiency
  • haemoglobin M disease

Acquired (toxin/drugs)

  • aniline dyes
  • benzene derivatives
  • chloroquine
  • dapsone
  • prilocaine
  • metoclopramide
  • nitrites (nitroglycerin, NO, sodium nitroprusside)
  • sulphonamides

CLINICAL FEATURES

  • cyanosis
  • symptoms and signs of decreased oxygen delivery e.g. chest pain, dyspnea, altered metal state, end organ damage
  • SpO2 reading 85-90%
  • blood samples typically have a chocolate brown hue
  • Normal PaO2

INVESTIGATIONS

  • confirmation via ABG (co-oximetry +/- specific assay + history of exposure)
  • high metHb

MANAGEMENT

Resuscitation

  • high flow O2 (to ensure available Hb is saturated well)

Specific therapy

  • congenital
    — avoid precipitants
  • cessation of precipitants
  • methylene blue (1-2mg/kg over 5 minutes) provides an artificial electron acceptor to facilitate the reduction of MetHb via the NADPH-dependent pathway; give if:
    — symptomatic
    — consider if asymptomatic with >20% MetHb, or >10% if risk factors such as anaemia or ischemic heart disease
  • repeat methylene blue at 30-60 min if inadequate response
  • alternatives to methylene blue:
    —ascorbic acid (if methylene blue contra-indicated, e.g. G6PD deficiency)
    — exchange transfusion
    — hyperbaric oxygen

Supportive care and monitoring

REASONS FOR FAILURE OF METHYLENE BLUE

Consider the following if MetHb levels do not fall with methylene blue:

  • massive ongoing exposure to an oxidising agent
  • sulfhaemoglobinemia (e.g. dapson, sulfonamides)
  • G6PD deficiency
  • methaemoglobin reductase deficiency
  • abnormal haemoglobin
  • excessive methylene blue (paradoxical effect in high doses)

References and Links

  • CCC — Methylene blue

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About Chris Nickson

FCICM FACEM BSc(Hons) BHB MBChB MClinEpid(ClinTox) DipPaeds DTM&H GCertClinSim

Chris is an Intensivist at the Alfred ICU in Melbourne and is an Adjunct Clinical Associate Professor at Monash University. He is also the Innovation Lead for the Australian Centre for Health Innovation and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He has a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives. After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia's Northern Territory, Perth and Melbourne. He has since completed further training in emergency medicine, clinical toxicology, clinical epidemiology and health professional education. He coordinates the Alfred ICU's education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the 'Critically Ill Airway' course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of Lifeinthefastlane.com, the RAGE podcast, the Resuscitology course, and the SMACC conference. His one great achievement is being the father of two amazing children. On Twitter, he is @precordialthump.

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