Treatment of methemoglobinemia is done with -

Ans. is 'a' i.e., Methylene blue Methemoglobinemias* Methemoglobin is generated by oxidation of the heme iron moieties to the ferric state, causing a characteristic bluish-brown muddy color resembling cyanosis.* Methemoglobin has such high oxygen affinity that virtually no oxygen is delivered. Levels >50-60% are often fatal.* Congenital methemoglobinemia arises from globin mutations that stabilize iron in the ferric state or from mutations that impair the enzymes that reduce methemoglobin to hemoglobin (e.g., methemoglobin reductase, NADP diaphorase).*Acquired methemoglobinemia is caused by toxins that oxidize heme iron, notably nitrate and nitrite-containing compounds, including drugs commonly used in cardiology and anesthesiology.* Methemoglobin should be suspected in patients with hypoxic symptoms who appear cyanotic but have a PaO2 sufficiently high that hemoglobin should be fully saturated with oxygen.* A history of nitrite or other oxidant ingestions may not always be available; some exposures may be inapparent to the patient, and others may result from suicide attempts.* The characteristic muddy appearance of freshly drawn blood can be a critical clue. The best diagnostic test is methemoglobin assay, which is usually available on an emergency basis.* Methemoglobinemia often causes symptoms of cerebral ischemia at levels >15%; levels >60% are usually lethal.* Intravenous injection of 1 mg/kg of methylene blue is effective emergency therapy.* Milder cases and follow-up of severe cases can be treated orally with methylene blue (60 mg three to four times each day) or ascorbic acid (300-600 mg/d).