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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
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
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