Methemoglobinemia

Incidence within USA: Rare

Gender prevalence: None

Socioeconomic or ethnic prevalence: None

Inadequate O ₂ carriage and delivery to tissues.

Hemolysis may be induced by methylene blue, especially in pts with G6PD deficiency.

Percent of MetHb. Symptoms vary and depend on the level of MetHb present: Cyanosis appears when MetHb reaches 10–20%. Tachycardia and tachypnea can appear when MetHb reaches 20–50%. CV collapse, coma, and seizures can occur when MetHb reaches 50–70%. Death may occur at MetHb levels >70%

MetHb is produced when Hb is oxidized and Fe ²⁺ is converted to Fe ³⁺ so that Hb cannot bind O ₂ , and the O ₂ -Hb dissociation curve is shifted to the left.

Hereditary forms due to cytochrome b5 reductase deficiency or abnormal hemoglobin M.

Acquired methemoglobinemia is largely due to oxidizing medications, including local anesthetics (benzocaine, prilocaine), antibiotics (dapsone), and nitrites. Toxic dosages can vary between individuals. Other medications and drugs (e.g., cocaine) have also been known to cause methemoglobinemia.

Endogenous mechanisms (NADH-MetHb reductase and NADPH-MetHb reductase) normally maintain MetHb levels to <1%. Oxidizing agents convert Hb to MetHb and can overwhelm protective mechanisms, resulting in toxic methemoglobinemia.

Diagnosis:

• An ABG with co-oximetry (spectrophotometry), which uses multiple wavelengths of light to determine the amount of normal versus abnormal Hb (e.g., MetHb, COHb), is necessary.

• Keys to diagnosis are a discrepancy between pulse oximeter saturation and measured Pao ₂ (Spo ₂ <90% while Pao ₂ >70 mm Hg) and hypoxia that does not improve with increasing FIO ₂ .

• “Chocolate brown” blood may be seen.