Sulfhemoglobinemia is less common than methemoglobinemia. Although patients with sulfhemoglobinemia have a clinical presentation similar to those with methemoglobinemia, the disease process itself is substantially less concerning.8 Although the reduction in the patients oxygen carrying capacity is quantitatively similar, the patient's oxygen dissociation curve is shifted rightward, not leftward as in methemoglobinemia, favoring the release of hemoglobin-bound oxygen to the tissue. Because the pigmentation of the blood by sulfhemoglobin is substantially more intense than other colored hemoglobin species, only 0.5 g/dL of sulfhemoglobin is needed to produce a cyanosis equivalent to that produced by 1.5 g/dL of methemoglobin. At the level of the hemoglobin molecule, sulfhemoglobin occurs by oxidation of the porphyrin ring. Many of the responsible agents are identical to those that induce methemoglobin, and the agents do not need to contain sulfur. The diagnosis is difficult to confirm, because standard co-oximetry does not differentiate sulfhemoglobin from methemoglobin because of similar spectral absorbances. The addition of cyanide to the laboratory sample differentiates the two hemoglobin species, because cyanide binds to methemoglobin and changes its spectrophotometric pattern. Thus, if the addition of cyanide to this sample fails to eliminate the methemoglobin peak, the diagnosis of sulfhemoglobinemia is confirmed. Sulfhemoglobin is not reduced by treatment with methylene blue, and generally patients require only supportive care, although transfusions may be necessary for severe toxicity.
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