China
Africa
Explore chapters and articles related to this topic
Carbon Monoxide Poisoning, Methemoglobinemia, and Sulfhemoglobinemia
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
While sulfhemoglobinemia is probably a relatively nontoxic syndrome in individuals with hemoglobin A, it may prove to be a surprisingly toxic syndrome in individuals with Hb S—especially in comparison to methemoglobinemia, which would be expected to ameliorate sickling. The presence of sulfurated subunits will shift the conformation of Hb S tetramers toward the unliganded, polymerizing T form even in the presence of high pO2. Microvascular occlusion could be exacerbated by the fact that these tetramers remain in the polymerizing conformation in both the arterial and venous circulations.
Red Cells Containing Low-Oxygen-Affinity or M Hemoglobins
Published in Ronald L. Nagel, Genetically Abnormal Red Cells, 2019
While sulfhemoglobinemia is probably a relatively nontoxic syndrome in individuals with hemoglobin A, it may prove to be a surprisingly toxic syndrome in individuals with Hb S — especially in comparison to methemoglobinemia which would be expected to ameliorate sickling.82 The presence of sulfurated subunits will shift the conformation of Hb S tetramers toward the unliganded, polymerizing T form, even in the presence of high PO2. Microvascular occlusion could be excerbated by the fact that these tetramers remain in the polymerizing conformation in both the arterial and venous circulation. We have shown that a solution of HbS that is half sulfurated does gel at atmospheric PO2 in concentrations found in red blood cells.
Fatal Sodium Nitrite Poisoning: Key Considerations for Prehospital Providers
Published in Prehospital Emergency Care, 2021
Matthew R. Neth, Jennifer S. Love, B. Zane Horowitz, Michael D. Shertz, Ritu Sahni, Mohamud R. Daya
Methylene blue (methylthioninium chloride) is the treatment of choice for symptomatic methemoglobinemia. It works by accelerating the enzymatic reduction of ferric (Fe3+) iron to the ferrous (Fe2+) state through its metabolic product leukomethylene blue, ultimately converting methemoglobin to hemoglobin (41,42). The usual dose of methylene blue is 1 to 2 mg/kg of a 1% solution IV administered over five minutes (41). The dose can be repeated in 30 to 60 minutes if the patient is still symptomatic or methemoglobin levels are greater than 30% (41). The maximum total dose of methylene blue is 7 mg/kg, in most situations, but more may be needed in severe cases. There is the possibility that oxidation back to methemoglobin will reoccur at higher doses of methylene blue (41). Methylene blue is ineffective in patients with G6PD deficiency, NADPH methemoglobin reductase deficiency, sulfhemoglobinemia, and hemoglobin M disease (41,42). Recent evidence suggests that methylene blue may also inhibit the downstream effect of nitric oxide and may assist in the treatment of refractory distributive shock (43).