Acquired<unk>  may be acquired. Classical drug causes of<unk>  include various antibiotics (trimethoprim, sulfonamides, and dapsone), local anesthetics (especially articaine, benzocaine, prilocaine, and lidocaine), and aniline dyes, metoclopramide, rasburicase, umbellulone, chlorates, bromates, and nitrites. Nitrates are suspected to cause<unk> . In otherwise healthy individuals, the protective enzyme systems normally present in red blood cells rapidly reduce the<unk> moglobin back to hemoglobin and hence maintain<unk> moglobin levels at less than one percent of the total hemoglobin concentration. Exposure to exogenous oxidizing drugs and their<unk> olites (such as benzocaine, dapsone, and nitrates) may lead to an increase of up to a thousandfold of the<unk> moglobin formation rate, overwhelming the protective enzyme systems and acutely increasing<unk> moglobin levels. Infants under 6 months of age have lower levels of a key<unk> moglobin reduction enzyme (NADH-cytochrome b5 reductase) in their red blood cells. This results in a major risk of<unk>  caused by nitrates ingested in drinking water, dehydration (usually caused by gastroenteritis with diarrhea), sepsis, or topical anesthetics containing benzocaine or prilocaine. Nitrates used in agricultural fertilizers may leak into the ground and may contaminate well water. The current EPA standard of 10 ppm nitrate-nitrogen for drinking water is specifically set to protect infants. Benzocaine applied to the gums or throat (as commonly used in baby teething gels, or sore throat lozenges) can cause<unk> . Genetic The congenital form of<unk>  has an autosomal recessive pattern of inheritance. Due to a deficiency of the enzyme diaphorase I (cytochrome b5 reductase),<unk> moglobin levels rise and the blood of<unk>  patients has reduced oxygen-carrying capacity. Instead of being red in color, the arterial blood of<unk>  patients is brown. This results in the skin of Caucasian patients gaining a bluish hue. Hereditary<unk>  is caused by a recessive gene. If only one parent has this gene, offspring will have normal-hued skin, but if both parents carry the gene, there is a chance the offspring will have blue-hued skin. Another cause of congenital<unk>  is seen in patients with abnormal hemoglobin variants such as hemoglobin M (HbM), or hemoglobin H (HbH), which are not amenable to reduction despite intact enzyme systems.<unk>  can also arise in patients with pyruvate kinase deficiency due to impaired production of NADH – the essential cofactor for diaphorase I. Similarly, patients with glucose-6-phosphate dehydrogenase deficiency may have impaired production of another co-factor, NADPH.
Methemoglobinemia
Argyria
Sulfhemoglobinemia
Heart failure
Hyperaemia
Hypoxemia
Organic acidemia
Hypercapnia