<prompt> Treatment of methemoglobinemia is done with -Methylene blueHydroxyureaFava beansExchange tranfiision  <response>: 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 mgkg 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 mgd. 