![]() ![]() However, upon arrival of the presumed biological father, a thorough history revealed an extensive paternal family history of neonatal cyanosis due to a rare mutation resulting in a hemoglobin M variant. Initial treatment with methylene blue or ascorbic acid was considered. Unconjugated hyperbilirubinemia > 5 mg/dL (442 μmol/L) interfered with laboratory equipment measurement, making accurate methemoglobin levels unattainable despite multiple attempts. No family history was available at the time of transfer to our institution. Given the absence of clear cardiac or pulmonary etiology of persistent cyanosis, hematologic causes such as methemoglobinemia were explored. Investigations to rule out hemolysis and end-organ dysfunction were within acceptable range. Capillary blood gas values were reassuring with normal pH and an elevated pO2. Initial radiographic and echography imaging was normal. Pre- and post-ductal saturations were equal and remained below 85%. Congenital methemoglobinemia is a rare and potentially life-threatening cause of cyanosis in newborns that can be caused by either cytochrome B5 reductase or hemoglobin variants known as Hemoglobin M.Ī term male infant developed cyanosis and hypoxia shortly after birth after an uncomplicated pregnancy, with oxygen saturations persistently 70–80% despite 1.0 FiO2 and respiratory support of CPAP+ 6 cm H2O. The acquired form occurs from exposure to oxidative agents. Methemoglobinemia can be an acquired or congenital condition. ![]()
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