Sulfhemoglobinemia is a rare condition in which there is excess sulfhemoglobin (SulfHb) in the blood. 



The pigment is a greenish derivative of hemoglobin.



 Sulfhemoglobinemia cannot be converted back to abnormal, functional hemoglobin. 



It causes cyanosis even at low blood levels.



Complications of sulfhemoglobinemia :


cyanosis, hypoxemia, methemoglobinemia and hypoxia.



Causes include sulfur medications and hydrogen sulfide, produced by intestinal bacteria such as Morganella morganii



The hemoglobin molecule has the ability to bind irreversibly to any substance containing a sulfur atom.



When hydrogen sulfide, or sulfide ions, and ferric ions combine in the blood, the blood is incapable of carrying oxygen.



Sulfhemoglobinemia can lead to an oxygen saturation gap greater than 5%.



Sulfhemoglobinemia decreases the ability of oxygen molecules to bind to heme proteins, shifting the oxygen dissociation curve to the right and leading to increased release of oxygen in the peripheral tissues.



There are    few clinical symptoms with self hemoglobinemia since oxygen is released into the peripheral tissues.



Symptoms include a blue or green discoloration of the blood, skin, and mucous membranes.



Findings include cyanosis, greater than 5 grams per cent of deoxyhemoglobin, or 1.5 grams per cent of methemoglobin, or 0.5 grams per cent of sulfhemoglobin.



It can be caused by taking medications that contain sulfonamides under certain conditions.



Sulfhemoglobinemia is usually drug induced: sulphonamides such as sulfasalazine, phenazopyridine, sumatriptan, and occupational exposure to sulfur compounds.



Sulfhemoglobinemia generally resolves itself with red blood cell turnover.



In severe cases blood transfusions may be necessary,


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