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Deborah Beer is a staff nurse in the surgical intensive care unit at Robert Wood Johnson University Hospital, New Brunswick.
To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 809-2273 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.
The case study (shaded box) describes the development of acquired methemoglobinemia in a 73-year-old woman after trans-esophageal echocardiography in which a topical anesthetic containing benzocaine was used.
ACQUIRED METHEMOGLOBINEMIA
Pathophysiology
Hemoglobin consists of 4 heme groups, each containing an iron atom. Each atom is capable of binding with oxygen only if the iron is in the reduced or ferrous state (Fe2+). Removal of an electron (oxidation) from a reduced iron atom produces the ferric state (Fe3+; Figure 1
), and methemoglobin results. This abnormal hemoglobin (ie, methemoglobin) is incapable of binding with oxygen.1–9
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), may cause an increase in the oxidation of hemoglobin that overwhelms these internal mechanisms.1–9
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). Therefore, less oxygen is available for tissues. This inability to transport oxygen causes the clinical manifestations of methemoglobinemia: cyanosis, hypoxia, dizziness, nausea, stupor, coma, metabolic acidosis, and eventually cardiovascular collapse. The color of blood is notably chocolate-brown because of the increased concentration of methemoglobin (>0.15).1–9
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).
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Co-oximeters measure the light absorption of blood at numerous ultraviolet wavelengths. Therefore, these machines can determine the amounts of oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and methemoglobin. Pulse oximeters measure ultraviolet absorption at only 2 wavelengths and can therefore only differentiate oxyhemoglobin from deoxyhemoglobin.5,12,13
Methemoglobinemia cannot be detected with standard blood gas analysis. In blood gas analysis, PO2 and pH are measured, and oxygen saturation is calculated on the basis of these values. In patients with methemoglobinemia, PaO2 determined by using arterial blood gas analysis is falsely elevated, and pulse oximetry measurements are inaccurate.2,6,7,9 Co-oximetry determines the true amount of oxygen saturation, which is much lower than the calculated oxygen saturation.6,9
Pulse oximeters use light at wavelengths of 660 nm (red) and 940 nm (infrared) to generate a ratio of deoxyhemoglobin to oxyhemoglobin.5,8,10,11 Methemoglobin is detected by both the oxyhemoglobin (940 nm) and the deoxyhemoglobin (660 nm) sensors. At low levels (<0.20), methemoglobin is detected primarily by the deoxyhemoglobin sensor, and a pulse oximeter may indicate a falsely low oxygen saturation. At high levels of methemoglobin (>0.70), detection by the oxyhemoglobin sensor predominates, and a pulse oximeter may indicate a falsely high oxygen saturation.5,6 As a further complication, methylene blue is also detected by the deoxyhemoglobin sensor. This situation may lead to falsely low values for oxygen saturation after treatment with methylene blue.5
Treatment
Treatment of methemoglobinemia includes removal of the oxidizing agent and intravenous administration of methylthionine chloride (methylene blue).1–9 Methylene blue reacts within red blood cells to form leukomethylene blue, which acts as a reducing agent (electron donor) of oxidized hemoglobin, converting the ferric ion (Fe3+) back to its oxygen-carrying ferrous (Fe2+) state1–9 (Figure 3). The dose of methylene blue for adults is 1 to 2 mg/kg of a 1% solution administered intravenously during 5 minutes.1–9
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Doses of methylene blue should not exceed 7 mg/kg because of its oxidizing properties at high doses. Methylene blue can cause the oxidation of hemoglobin, thereby increasing the formation of methemoglobin and worsening of the methemoglobinemia.1–3,6
Adverse Effects of Methylene Blue
Adverse effects associated with administration of methylene blue include anemia, nausea , vomiting, diarrhea , a burning sensation in the mouth or warmth in the stomach, dyspnea, restlessness, and sweating.1,2 Urine, feces, saliva, skin, and mucous membranes may be blue.1,2 Doses greater than 15 mg/kg have actually caused methemoglobinemia.1 Use of the agent is reserved for patients who have indications of hypoxia and methemoglobin levels greater than 0.30.1,2,4
Lack of response to methylene blue suggests the congenital form of methemoglobinemia in which a deficiency of the intrinsic mechanisms of glucose-6-phosphate dehydrogenase or NADPH (the reduced form of nicotinamide-adenine dinucleotide phosphate) methemoglobin reductase exists. In these patients, or any patient not responding to methylene blue, transfusions of packed red blood cells are necessary to increase the amount of nonionized hemoglobin, thereby allowing increased oxygen binding and transportation.1,4
CONCLUSION
Methemoglobinemia should be considered in patients with cyanosis that is refractory to oxygen administration, especially after administration of topical anesthetics. Acquired methemoglobinemia, although rare, can be fatal, and anyone using chemicals or medications that may lead to the development of methemoglobinemia should be aware of the potential for this complication. With topical anesthetics used in an ever-increasing number of procedures at the bedside and in outpatient settings, education of staff should include recognition and treatment of this potential life-threatening adverse event. The availability of methylene blue in all areas where these procedures are performed is essential to ensure prompt management of methemoglobinemia.
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This article has been cited by other articles:
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  E. Wolak, F. L. Byerly, T. Mason, and B. A. Cairns Methemoglobinemia in Critically Ill Burned Patients Am. J. Crit. Care., March 1, 2005; 14(2): 104 - 108. [Full Text] [PDF]
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