Dyshemoglobinemia Dealings

Overview

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).

Causes

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).

Detection

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).

Treatment

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).


Reference List

1. Tintinalli JE, Kelen GD, Stapcynski JS. Emergency Medicine: A Comprehensive Study Guide. Columbus, OH: McGraw-Hill Professional, 2003.
2. Lambert M, Sonnet J, Mahieu P, Hassoun A. Delayed sulfhemoglobinemia after acute dapsone intoxication. J Toxicol Clin Toxicol 1982;19:45-50.
3. Devlin TM. Textbook of Biochemistry with Clinical Correlations. Philadelphia: Wiley-Liss, 2002.
4.Shperling IA, Novitskii VV, Riazantseva NV et al. [Mechanisms underlying changes in functional properties of red cells in acute action of carbon monoxide]. Patol Fiziol Eksp Ter 2008;18-20.
5. Rusca M, Oddo M, Schaller MD, Liaudet L. Carboxyhemoglobin formation as an unexpected side effect of inhaled nitric oxide therapy in severe acute respiratory distress syndrome. Crit Care Med 2004;32:2537-9.
6. Ren X, Dorrington KL, Robbins PA. Respiratory control in humans after 8 h of lowered arterial PO2, hemodilution, or carboxyhemoglobinemia. J Appl Physiol 2001;90:1189-95.
7. Flexman AM, Del VG, Schwarz SK. Dark green blood in the operating theatre. Lancet 2007;369:1972.
8. Martin DG, Watson CE, Gold MB, Woodard CL, Jr., Baskin SI. Topical anesthetic-induced methemoglobinemia and sulfhemoglobinemia in macaques: a comparison of benzocaine and lidocaine. J Appl Toxicol 1995;15:153-8.
9. Sinex JE. Pulse oximetry: principles and limitations. Am J Emerg Med 1999;17:59-67.
10. Michaelis G, Biscoping J, Salzer A, Hempelmann G. [Effect of dyshemoglobinemia (methemoglobinemia and carboxyhemoglobinemia) on accuracy of measurement in pulse oximetry in operations of long duration]. Anasth Intensivther Notfallmed 1988;23:102-8.
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