Patients with methemoglobinemia require optimal supportive measures to ensure oxygen delivery and the administration of appropriate antidotal therapy if indicated. In general, gastric decontamination is limited, because there often is a substantial time interval between exposure to the toxic agent and the development of methemoglobin. If a source of continuing exposure exists, decontamination is indicated, and in most stable patients a single dose of activated charcoal is likely sufficient. Antidotal therapy with methylene blue is reserved for patients with documented methemoglobinemia or a high clinical likelihood of the disease. Highly unstable patients should receive methylene blue, but may require transfusion or exchange transfusion to produce an immediate enhancement of oxygen delivery.

Methylene blue serves to indirectly accelerate the enzymatic reduction of methemoglobin by NADPH-methemoglobin reductase, a normally minor enzymatic pathway. In this capacity, methylene blue is reduced to leucomethylene blue, which itself is capable of directly reducing the oxidized iron back to its oxygen carrying form ( Fig. 183-1). The initial dose of methylene blue is 1 to 2 mg/kg intravenously (0.1 mL/kg of the 1% solution, about 7 mL in an adult) and its effect should be seen with 20 min. As the methemoglobin concentration falls, the most severe signs and symptoms will resolve first. Resolution of the cyanosis is a late finding, occurring only after the concentration of methemoglobin falls below 1.5 g/dL. Repeat dosing of methylene blue may be acceptable if needed, but high doses of methylene blue (<7 mg/kg) may actually induce methemoglobin formation. Treatment failures may result if the patient is deficient in glucose-6-phosphate dehydrogenase (G6PD), because this enzyme is critical in the production of NADPH within the hexose monophosphate shunt (see Fig 183-1).7 Because this group of patients does not lack NADH

cytochrome-b5 reductase, they are not at increased risk of developing methemoglobinemia, and they only lack the ability to respond to methylene blue. The concomitant occurrence of methemoglobinemia and hemolysis is not unexpected because both occur through similar oxidative mechanisms, and it is the rule for some agents such as chlorates. However, hemolysis may impede a response to methylene blue, which requires an intact erythrocyte to be effective. Oxidant drugs with long

serum half-lives, such as dapsone (T2 ~50 h) produce prolonged oxidant stress to the red blood cell. Although not a true treatment failure, exposed patients may require repetitive dosing of methylene blue. In rare instances, patients may be deficient in NADPH-methemoglobin reductase, the required enzyme for methylene blue activation. Lastly, treatment failure may occur in patients with sulfhemoglobinemia, which is clinically indistinguishable from methemoglobinemia, but which is not responsive to methylene blue (see below). Patients that do not respond to methylene blue should be treated supportively. If clinically unstable, the use of blood transfusions or exchange transfusions is indicated. In the event that the newly administered red blood cell hemoglobin undergoes oxidation, it will likely respond appropriately to methylene blue.

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