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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