A Review on Methaemoglobinaemia: From Diagnosis to Treatment

Abstract

The first case of methaemoglobinaemia was reported by Sloss and Wybauw in 1912. Methaemoglobin is a derivative of normal haemoglobin in which the iron of the haem complex has been oxidized from the ferrous to the ferric form. Methaemoglobin does not combine with oxygen and thus does not take part in oxygen transport. In normal red cells, methaemoglobin is continually being formed by the auto-oxidation of haemoglobin, but it is reduced as soon as it is formed; thus the concentration of methaemoglobin in the red blood cells under normal conditions is less than one percent of total haemoglobin. The term methaemoglobinaemia is used to describe the excess accumulation of methaemoglobin in the red blood cell. Methaemoglobin lacks the capacity to carry oxygen, and methaemoglobinaemia causes symptoms and signs of hypoxia. Toxic methaemoglobinaemia occurs when a drug or other toxic substance oxidizes haemoglobin and the patient is likely to show cyanosis. Methaemoglobinaemia has a wide spread among industrial workers worldwide where they make use of toxic chemicals, also among fertilizer company workers. Methaemoglobin can be identified spectroscopically by its absorption band in the red part of the spectrum at 630nm; this band disappears on the addition of yellow ammonium sulphide. Methaemoglobin levels are best measured using the change of absorbance of methaemoglobin of 630nm that occurs when cyanide is added, converting the methaemoglobin to cyanmethaemoglobin. Treatment consists of slow intravenous injection of methylene blue; the recommended does is 2mg/kg bodyweight for infants, 1.5mg/kg bodyweight for older children, and 1mg/kg bodyweight for adults, in a 1% sterile aqueous solution.