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Understanding acquired methemoglobinemia

Wesley, Carol MSN/MHA, RN, CCRN, NE-BC

doi: 10.1097/01.NURSE.0000441891.89534.c3

Carol Wesley is vice president of cardiovascular services at Health Quest System in Poughkeepsie, N.Y.

The author has disclosed that she has no financial relationships related to this article.

How is acquired methemoglobinemia treated in adults?—AP, IND.

Carol Wesley, MSN/MHA, RN, CCRN, NE-BC, replies: Methemoglobin, an abnormal hemoglobin that doesn't bind with oxygen, is normally found in the body in quantities of less than 1%. Methemoglobinemia is an uncommon but potentially fatal disease in which normal methemoglobin in the blood increases to levels above 1%.1 Although it can be congenital, most cases are acquired due to exposure to certain chemicals, drugs, or toxins.1 The most common causes are topical anesthetic agents such as benzocaine, lidocaine, and prilocaine; certain antibiotics such as dapsone; and nitrates, such as inhaled nitric oxide.

Signs and symptoms may appear quickly after the oxidizing agent is introduced and progress rapidly if the offending agent isn't removed and treatment isn't administered promptly when indicated. Many patients with preexisting disorders that affect oxygen delivery, such as heart disease, anemia, and pulmonary disease, may develop signs and symptoms at lower methemoglobin levels.

The patient's clinical presentation is a direct result of methemoglobin's inability to carry and deliver oxygen to the tissues. As levels of methemoglobin increase, the severity of signs and symptoms typically increase as well. Methemoglobinemia should be suspected if the patient presents with a normal PaO2 and clinical cyanosis that doesn't improve with supplemental oxygen.

Arterial blood in methemoglobinemia is a chocolate brown color that doesn't change when exposed to oxygen; PaO2 levels will be normal or sometimes higher than normal. Pulse oximetry may not be accurate and shouldn't be used to make the diagnosis.2 ABG analysis may reveal metabolic acidosis related to decreased oxygen delivery.

Diagnosis is made by co-oximetry, which uses various wavelengths of light to differentiate methemoglobin from oxyhemoglobin, deoxyhemoglobin, carboxyhemoglobin, and sulfhemoglobin (which can be mistaken for methemoglobin with older co-oximeters).1 Diagnosis should be confirmed by the Evelyn-Malloy method, which involves adding cyanide, which binds methemoglobin.2 Methemoglobin is then expressed as a percentage of total hemoglobin.1

Treatment depends on the methemoglobin level and severity of signs and symptoms. Asymptomatic patients (with levels less than 20%) usually require only removal of the offending agent.1 After this agent's been removed, symptomatic patients should be treated with I.V. methylene blue, which at low concentrations will convert methemoglobin to hemoglobin. It must be injected very slowly over several minutes to prevent local high concentrations of the compound, which will produce more methemoglobin.3 Although patient response to treatment is rapid, a second dose may be needed in 1 hour if high levels of methemoglobin persist. Monitor patients receiving I.V. methylene blue for adverse reactions, including nausea, headache, dizziness, profuse diaphoresis, confusion, and abdominal and chest pain.3

Acquired methemoglobinemia is a medical emergency that requires prompt recognition and treatment to prevent death.

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1. Denshaw-Burke M.Methemoglobinemia. 2013. Emedicine.
2. Prchal JT.Clinical features, diagnosis, and treatment of methemoglobinemia. UpToDate. 2013.
3. Methylene blue injection, USP 1% [package insert]. AKORN, Lake Forest, IL; June 2011.
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