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Methaemoglobinaemia

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  • Methaemoglobin formed by oxidation of iron in circulating haemoglobin from Fe2+ to Fe3+.
  • Met-Hb unable to bind and transport oxygen
  • Shifts oxy-Hb dissociation curve to left - interferes with off-loading of oxygen in peripheral tissues
  • Reduced cytochrome b5 reacts with circulating met-Hb to form Hb and oxidized cytochrome b5. Reduced cytochrome b5 is regenerated by methaemoglobin reductase

Aetiology

  • hereditary
  • idiopathic
  • toxin or drug induced
    • amyl nitrite, butyl nitrite, methyl nitrite, isobutyl nitrite, sodium nitrite
    • bromates
    • aniline dyes
    • benzocaine, bupivicaine, lidocaine, prilocaine
    • chlorates
    • chloroquine, primaquine
    • dapsone
    • flutamide
    • herbicides & pesticides
    • isosorbide dinitrate, nitroglycerin, nitroprusside, nitric oxide
    • Loxosceles gaucho venom
    • metoclopramide
    • nitroethane, nitrobenzene
    • petrol octane booster
    • phenacetin
    • phenazopyridine
    • potassium ferricyanide
    • silver nitrate
    • sulfonamides

Clinical features

  • mild (met-Hb <15%)
    • usually asymptomatic despite cyanosis
    • patients with critical coronary artery disease may develop angina or MI
  • moderate
    • dyspnoea
    • headache
    • weakness
  • severe
    • confusion
    • seizures
    • death

Investigations

  • co-oximetry gives met-Hb concentration. Met-Hb level falsely elevated in presence of methylene bluc
  • pulse oximetry unreliable

Treatment

  • gastric lavage and activated charcoal
  • methylene blue
    • consider in symptomatic patients with drug or toxin-induced methaemoglobinaemia (converts met-Hb to Hb)
    • 1-2 mg/kg IV over 5 min usually results in reduction in met-Hb within 30-60 min
    • repeat after 60 min if necessary
    • additional repeat doses may be required in patients who have received a long-acting oxidant drug such as dapsone but excessive doses may paradoxically increase oxidant stress and methaemoglobinaemia
    • contra-indications:
      • glucose-6-phosphate dehydrogenase (G6PD) deficiency
      • renal failure
      • reversal of nitrite-induced methaemoglobinaemia during treatment of cyanide poisoning
    • failure to respond suggests methaemoglobin reductase deficiency, G6PD deficiency or sulfhaemoglobinaemia
  • in severe cases consider exchange transfusion and hyperbaric oxygen

Further reading

Mokhlesi B. Adult toxicology in critical care. Part II: specific poisonings. Chest 2003; 123:897-952


 

©Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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