EYES DO NOT SEE WHAT MIND DOESN'T SEEK: A PUZZLING CASE OF METHEMOGLOBINEMIA

Abstract

TOPIC: Critical Care TYPE: Medical Student/Resident Case Reports INTRODUCTION: Methemoglobinemia must be considered in the differential diagnosis of hypoxia not improving with supplemental oxygen. CASE PRESENTATION: An 84-year-old male patient with a past medical history of Atrial fibrillation, scleritis, hypertension presented with complaints of fever, chills, shortness of breath for 5 days. Medication history included triamterene/hydrochlorothiazide, Amiodarone, warfarin, ezetimibe, prednisone, and methotrexate. On presentation, the patient was saturating 79% on ambient air and was put on Hiflo nasal oxygen, and saturation improved to 95% on Fi02 100% at 35 l/min. The lab was significant for WBC count of 12.1, procalcitonin 1.06, a chest x-ray revealed bilateral opacities left greater than right with air bronchograms. Chest CT done showed bilateral ground-glass opacities with interposed consolidation. Bronchoscopy was deferred due to the clinical condition of the patient The patient was started on cefepime, doxycycline, methylprednisone, primaquine, and clindamycin for empiric treatment of PCP pneumonia with superimposed bacterial pneumonia and was transferred to ICU for hypotension secondary to sepsis. Pt initially improved clinically and Hiflo was weaned to Fi02 of 50% and maintained saturation above 95%. Over the course of 3-4 days after downgrading to the medical floor, the patient's oxygen requirement uptrend, though a repeat CT scan of the chest showed radiological improvement. An ABG with co-oximetry done showed Po2 of 302 mmHg, saturation of 91 % on Fi02 of 100%, and Methemoglobin content of 7.8%. IV methylene blue infusion was given and the patient's respiratory status improved with the Fio2 requirement coming down. Repeat ABG with co-oximetry showed a methemoglobin level of 2.4%. Repeat labs did not show evidence of hemolysis and G6PD levels were normal. The patient's increased susceptibility to methemoglobinemia would have been due to drug interaction as he is on thiazide diuretic and was started on primaquine increasing the oxidative stress coupled with oxidative stress secondary to sepsis. Primaquine was discontinued and started on atovaquone for PCP treatment. The patient continued to improve clinically. DISCUSSION: Methemoglobinemia can occur after exposure to a number of medications, including primaquine, sulfonamides, nitrates, topical anesthetics. Methemoglobin is the oxidized form of Hb, Oxygen does not bind as easily to the heme subunit with the ferric form of iron. The remaining heme sites have increased affinity for oxygen, resulting in decreased ability to release oxygen to tissues, causing left-shift of the oxygen-hemoglobin dissociation curve leading to tissue hypoxia. A clue to diagnosis is the cyanosis-saturation gap. CONCLUSIONS: An obvious mismatch between the PaO2 (which is >>100 mm) versus the pulse oximetry ( typically ~80-90%), known as the PaO2-saturation gap, is a clue to the diagnosis of methemoglobinemia REFERENCE #1: Gibson QH. The reduction of methemoglobin in red blood cells and studies on the cause of idiopathic methemoglobinemia. Biochem J 1948;42: 13-23. REFERENCE #2: Ohashi K, Yukioka H, Hayashi M, Asada A. Elevated methemoglobin in patients with sepsis. Acta Anaesthesiol Scand 1998;42: 713-716. REFERENCE #3: Beutler E. Methemoglobinemia and other causes of cyanosis. In: Beutler E, Lichtman MA, Coller BS, Kipps TJ, eds. Williams Hematology. 5th ed. New York: McGraw-Hill; 1994: 654-662. DISCLOSURES: No relevant relationships by Santhosh Bayambe, source=Web Response No relevant relationships by Nadish Garg, source=Web Response No relevant relationships by Killol Patel, source=Web Response No relevant relationships by ARCHANA SREEKANTAN NAIR, source=Web Response