Methaemoglobin Interpreter
Methaemoglobin Interpreter
Band a co-oximetry methaemoglobin percentage against the thresholds for cyanosis, symptoms and methylene blue, and see why the pulse oximeter sticks near 85%.
Methaemoglobin level
1 input → % MetHbMethaemoglobin 26% by co-oximetry in a patient given topical benzocaine, cyanosed and unresponsive to oxygen
How the level is read
Normal < 1% · cyanosis from about 10% · methylene blue above 20–30%, or lower if symptomatic
Methylene blue 1–2 mg/kg intravenously over 5 minutes
- co-oximetry
- the only reliable measurement — a pulse oximeter reads towards 85% regardless of the true saturation, and the arterial blood gas PaO₂ is normal because dissolved oxygen is unaffected
- 10%
- the level from which cyanosis typically appears, with chocolate-brown blood around 15% and cyanosis that does not improve with oxygen
- 20–30%
- the usual threshold for methylene blue, or a lower level in a symptomatic patient
- G6PD deficiency
- methylene blue is ineffective and can precipitate haemolysis; ascorbic acid or exchange transfusion is used instead
Worked example
Methaemoglobin 26% by co-oximetry in a patient given topical benzocaine, cyanosed and unresponsive to oxygen
26.0% lies between 20 and 30 → methylene blue usually indicated
Cyanosis appears from about 10% and chocolate-brown blood around 15%, both consistent with this level
Methylene blue 1–2 mg/kg intravenously over 5 minutes, after checking for G6PD deficiency
The pulse oximeter reading of 85% is uninformative here and must not be used to track the response
Methaemoglobin percentage and typical features
| MetHb | Interpretation | Typical features |
|---|---|---|
| < 1% | Normal | None |
| 1 – 10% | Usually asymptomatic | None, or mild discolouration |
| 10 – 20% | Cyanosis, mild symptoms | Cyanosis unresponsive to oxygen; chocolate-brown blood around 15% |
| 20 – 30% | Methylene blue usually indicated | Anxiety, light-headedness, headache, tachycardia |
| 30 – 50% | Marked symptoms | Tachypnoea, confusion, loss of consciousness |
| > 50% | Life-threatening | Seizures, dysrhythmias, acidosis, coma; above 70% often fatal |
Common triggers of acquired methaemoglobinaemia
| Agent | Setting |
|---|---|
| Dapsone | Prolonged therapy; the commonest drug cause, and often recurrent because of its long half-life |
| Benzocaine and prilocaine | Topical and local anaesthesia, including throat sprays and endoscopy |
| Nitrates and nitrites | Well water, cured meats, inhaled nitrites, nitric oxide, nitroglycerin |
| Aniline dyes | Industrial exposure, dyed textiles, marking inks |
| Chloroquine, metoclopramide, sulfonamides | Less common drug causes |
Cyanosis that will not lift with oxygen
Methaemoglobin is haemoglobin whose iron has been oxidised from the ferrous to the ferric state, which cannot carry oxygen and which shifts the dissociation curve so that the remaining normal haemoglobin releases oxygen less readily. Normal levels are below 1%. The clinical signature is cyanosis that does not improve with high-flow oxygen, chocolate-brown arterial blood, and an arterial blood gas whose calculated saturation looks normal because the PaO₂ is unaffected. Only co-oximetry measures it directly.
The pulse oximeter behaves in a characteristic way. Methaemoglobin absorbs both wavelengths used by the device almost equally, so as the level rises the displayed saturation is dragged towards roughly 85% and stays there whatever the true oxygenation. A saturation stuck near 85% in a cyanosed patient who is not responding to oxygen is a strong pointer, and the oximeter cannot then be used to follow the response to treatment.
Cyanosis appears from about 10%, and chocolate-brown blood around 15%. Roughly 20% produces anxiety, light-headedness and headache; 30 to 50% brings tachypnoea, confusion and loss of consciousness; and approaching 50% seizures, dysrhythmias, metabolic acidosis, coma and death follow, with levels above 70% often fatal. Most cases are acquired: dapsone, local anaesthetics such as benzocaine and prilocaine, nitrates and nitrites, and aniline dyes account for the bulk of them.
Methylene blue is indicated above 20 to 30%, or at a lower level in a symptomatic patient, at 1 to 2 mg/kg intravenously over 5 minutes. The important caution is G6PD deficiency, in which methylene blue is ineffective because the reduction pathway it exploits depends on NADPH, and in which it can precipitate haemolysis; ascorbic acid or exchange transfusion is used instead. Methylene blue also crosses the placenta, and animal and case data show foetal harm, so it is avoided in pregnancy unless the methaemoglobinaemia is itself life-threatening and no alternative is available. Poisoning management is time-critical and directed by a poisons centre or clinical toxicology service, and this interpreter supports that advice rather than replacing it.
Frequently asked questions
What methaemoglobin level needs methylene blue?
Above 20 to 30%, or a lower level in a symptomatic patient. The dose is 1 to 2 mg/kg intravenously over 5 minutes. Levels below about 10% are usually asymptomatic and treated by removing the trigger.
Why does the pulse oximeter read 85%?
Methaemoglobin absorbs the two wavelengths a pulse oximeter uses almost equally, so the displayed saturation is dragged towards roughly 85% and stays there regardless of the true oxygenation. It cannot be used to follow the response to treatment.
What causes acquired methaemoglobinaemia?
Most often dapsone, local anaesthetics such as benzocaine and prilocaine, nitrates and nitrites, and aniline dyes. Removing the agent matters as much as the antidote, and dapsone in particular outlasts a single dose of methylene blue so rebound is expected.
What if the patient has G6PD deficiency?
Methylene blue is ineffective, because the pathway it exploits depends on NADPH, and it can precipitate haemolysis. Ascorbic acid or exchange transfusion is used instead.
Do I need to involve a poisons centre?
Yes. Poisoning management is time-critical and directed by a poisons centre or clinical toxicology service, particularly when methylene blue is contraindicated or the level fails to fall. This interpreter supports that advice and never replaces it.
Related calculators
References
- Ludlow JT, Wilkerson RG, Nappe TM. Methemoglobinemia. In: StatPearls. Treasure Island (FL): StatPearls Publishing.
- Wright RO, Lewander WJ, Woolf AD. Methemoglobinemia: etiology, pharmacology, and clinical management. Ann Emerg Med. 1999;34(5):646–656.
- Methemoglobinemia. In: Merck Manual Professional Edition. Merck & Co.