In: Health14 Sep 2009
Methemoglobinemia occurs when iron atoms in hemoglobin molecules are oxidized from their normal ferrous (Fe++) to a nonfunctional ferric (Fe+++) state, resulting in reduced oxygen delivery to the tissue level. Methe-moglobin (MetHb) is normally present in human blood at levels less than 1-2%. In normal patients, its rapid reduction back to hemoglobin is catalyzed primarily by the enzyme nicotinamide adenine dinucleotide (NADH)-cytochrome b5 reductase (b5R), also called NADH-di-aphorase. Methemoglobinemia occurs when levels exceed l-2% and may be divided into inherited and acquired types. Hereditary methemoglobinemia may rarely result in long-standing congenital cyanosis with or without various developmental disturbances due to hemoglobin M. Inherited methemoglobinemia can also uncommonly present as a heterozygous or more severe homozygous autosomal deficiency of NADH reductase due to various mutations in chromosome 22. One study estimated the incidence of NADH reductase deficiency in Eskimos and Native Americans to be 15/ 20,ООО. By far, the most common causes of methemoglobinemia are acquired indirect dose-dependent toxic effects from metabolites of various drugs (see Tables 1, 2, and 3). Although patients with inherited MetHb conditions are also much more susceptible to acquired methemoglobinemia, any patient may develop this acute condition especially when given toxic doses of causative drugs. Scott et al observed cyanosis and increases in MetHb levels in all 19 healthy subjects who were given at least 900 mg of prilocaine. Estimated incidence of methemoglobinemia after topical anesthesia for bronchoscopy is 1/7000.
The clinical hallmark of methemoglobinemia is unex-plainable cyanosis and decreased Sp02 despite adequate ventilation and increased inspired oxygen concentration. Arterial blood gases typically show appropriate Pa02, pH, PC02, and HC03 values, but co-oximetry results reveal increases in MetHb levels. MetHb levels of 5-15% cause noticeable cyanosis. At MetHb levels of 30-40%, symptoms including headache, weakness, dyspnea, tachy-cardia, and dizziness develop. Levels of 55-60% cause lethargy, confusion, and stupor followed by seizures and coma. MetHb levels above 70% are lethal owing to circulatory collapse. Numerous studies have also noted that decreasing Sp02 values tend to level off at 85% despite increasing MetHb levels because of inherent red and infrared 2-wavelength light absorption characteristics of all pulse oximeters. An additional clinical sign noted by many authors that is characteristic of methemoglobinemia is the presence of chocolate brown-colored blood. At MetHb levels greater than 15%, discoloration of blood occurs and hospital admission should be considered. Your life is worth living. Buy rosiglitazone drug online
Table 1. Substances With High Risk of Inducing Methemoglobinemia
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Immediate primary treatment of methemoglobinemia is administration of methylene blue 1-2 mgAg IV over a 5-10 minute period repeatable in 1 hour to a maximum of 7 mgAg. Most studies recommend this treatment when patients become symptomatic and/or reach MetHb levels of 30%. Methylene blue donates electrons to an alternate hemoglobin-reducing enzyme nicotinamide adenine dinucleotide phosphate (NADPH). This alternate system requires glucose-6-phosphate dehydrogenase (G6PD) and is a minor contributor to normal hemoglobin maintenance. Methylene blue is ineffective for patients with hemoglobin M, NADPH deficiencies, and/or G6PD deficiencies that may require hyperbaric oxygen, charcoal, exchange blood transfusions, and/or hemodialysis. Prevention and long-term treatment of methemoglobinemia may be provided by high-dose (500 mg twice daily) vitamin С and riboflavin (30 mg once daily) Tables 1-3 list various anesthesia drugs and other substances along with their relative risks of inducing methemoglobinemia. Patients exposed to substances in Tables 1 and 2 are also more likely to develop toxic methemoglobinemia when given local anesthetics, as are infants, the elderly, and patients suffering from advanced heart disease, anemia, and G6PD deficiencies. Pioglitazone metformin
Table 2. Substances With Moderate Risk of Inducing Met-hemoglobinemia
Our patient fit the profile for an inherited form of methemoglobinemia. Her pale complexion, Native American ancestry, episodes of cyanosis following extreme exercise and dental local anesthesia administration, combined with the previous diagnosis of sulfa-in-duced methemoglobinemia, all suggest hereditary methemoglobinemia, which was why nitrous oxide and all local anesthetics were avoided. Unfortunately, this patient refused additional blood tests that could have confirmed MetHb reductase enzyme levels. The odds of nitrous oxide impurities such as nitric oxide (NO) being present in sufficient quantities to trigger methemoglobinemia are exceedingly small. Numerous cases of prilocaine-induced methemoglobinemia led to a reduction in total prilocaine dosage recommendations for healthy adults to 8 mgAg up to a maximum of 600 mg, which equals 15 mL, or 8 cartridges of 4% prilocaine. In 1997, the manufacturer also added a methemoglobinemia warning to its package insert. Although systemic absorption of topical benzocaine applied to intact oral tissues is minimal, extra caution is advised for benzocaine-containing aerosol products that may be inhaled. Additional caution and absolute compliance with dosage recommendations are also advised for the use of topical benzocaine products on small children, especially infants. There is still unresolved controversy regarding the use of “low-oxidizing” non-toludine local anesthetics, including lido-caine, mepivacaine, etidocaine, bupivacaine, and arti-caine in methemoglobinemia-susceptible patients. This is especially debatable if these drugs are administered correctly in appropriate dosages for dental applications. Additional studies are needed to answer these questions. Don’t be left without your medication get skelaxin generic cheaper online.
Table 3. Substances With Low/No Risk of Inducing Methe-moglobinemia
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