Abstract
Methemoglobinemia results from the oxidation of the iron in the hemoglobin molecule from the ferrous to the ferric state. Methemoglobinemia may result from congenital deficiencies of enzymes that normally convert methemoglobin (metHb) to hemoglobin, alterations in the hemoglobin molecule itself or, most commonly, from medications or toxins. As metHb cannot carry oxygen, clinical sequelae result when the concentration of metHb is high enough to compromise oxygen delivery to the tissues. With low levels, the patient may be asymptomatic or only symptomatic during periods of increased tissue oxygen demands such as exercise. With higher levels, symptoms may occur at rest. We describe an adolescent with acute leukemia who presented to the operating room for placement of a Broviac catheter for permanent central venous access. Given a persistently low oxygen saturation as measured by pulse oximetry (92% to 94%) with no response to changes in the inspired oxygen concentration and the lack of physical findings on auscultation to explain the low oxygen saturation, the diagnosis of metHb was entertained and confirmed by laboratory analysis.
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