Dyshemoglobinemias are mainly caused by exposure to exogenous xenobiotics although it can be hereditary (1). The occurrence is result of altered hemoglobin (Hb) preventing its normal function of carrying oxygen (1). The anemia, hypoxia, cyanosis and associated problems can be life-threatening (2).
Acquired methemoglobinimeas occur when dysfunctional hemoglobin form methemoglobin, whereas mutated amino acids make up a wall against heme or form the site involved in binding oxygen (3).
Carboxyhemoglobinemia is a form that results of exposure to carbon monoxide or nitrous oxide poisoning (4-6). It can occur as a result of overexposure to automobile exhaust, smoke from a fire or tobacco or nitrous oxide (4-6).
Sulfhemoglobinemia is a serious form that can occur when overexposed to sulfonamides or sulfur compounds such as when taking certain drugs (2;7;8).
Pulse oximetry is a non-invasive way to detect dyshemoglobinemia through monitoring the oxygenation of the blood (9;10). Invasive approaches of carbon monoxide oximetry or blood gas analysis also exist (10;11). Symptoms include cognitive changes, headache, fatigue, dizziness and syncope (12). If methemoglobinemia is greater, then dysrhythmias, seizures or coma can occur (12).
An obvious measure is to eliminate exposure to the causal agent. Oxygen therapy can be used to increase oxygen carried by normal hemoglobin and, in extreme cases, blood transfusions may be necessary (12).
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11. Akhtar J, Johnston BD, Krenzelok EP. Mind the gap. J Emerg Med 2007;33:131-2.
12. Masimo corporation. Demystifying Methemoglobinemia. Available at: http://www.masimo.com/pdf/whitepaper/LAB4280A.PDF