The symptoms of patients suffering from methemoglobinemia can vary depending in large part on the total hemoglobin level that the patient normally has. It is essential to remember that methemoglobin levels are reported by most laboratories as a percentage of total hemoglobin. In the face of acute methemoglobinemia, the level at which antidotal therapy is considered essential is generally approximately 20% to 30% methemoglobin.
There are indeed patients who suffer from congenital forms of methemoglobinemia, and who can tolerate high systemic methemoglobin concentrations without ever developing significant symptomatology. In fact, many patients will do quite well with meticulous supportive care only. It is important to remember, however, that not all patients require an antidote for methemoglobinemia. Once the diagnosis of significant methemoglobinemia has been made, treatment should begin without delay. Procalcitonin: Risk Assessment in COVID-19 Bacterial Co-Infection.Current Procalcitonin Utilization and Publications.The Physician Grind EMN with Zahir Basrai, MD.EM Board Bombs with Blake Briggs, MD, and Iltifat Husain, MD.In cases of severe intoxication by methemoglobin formers such as nitrite, larger doses of methylene blue than generally recommended, may be of considerable therapeutic value. High concentrations of either dye did not result in appreciable production of methemoglobin. Tolonium chloride provided approximately equivalent protection at 8.8 mg/kg but may be more toxic than methylene blue. Methylene blue increased in effectiveness as the dose was increased up to 22 mg/kg. Tolonium chloride (toluidine blue) another structurally related dye was also evaluated using the same parameters. Methylene blue was evaluated as a nitrite toxicosis antidote using methemoglobin reduction and lethality protection as evaluation parameters. It is usually used only in low dosage (4mg/kg) because of its purported enhancement of methemoglobin formation in high dosages. Methylene blue is widely accepted as an antidote for nitrite toxicosis because of its ability to stimulate reduction of methemoglobin (ferrihemoglobin) to hemoglobin.
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