Methemoglobinemia Revisited: A Case of Chronic Tylenol Ingestion Leading to Methemoglobinemia
Document Type
Conference Proceeding
Publication Date
10-2024
Publication Title
Journal of the American Society of Nephrology
Abstract
INTRODUCTION: Methemoglobinemia is a rare disorder in which there is oxidation of divalent iron molecule in hemoglobin to its trivalent form. Oxygen cannot bind to the trivalent form (ferric) which is responsible for difficult to correct hypoxemia in these patients, despite supplemental oxygen (1). Herein we present one such interesting case of methemoglobinemia from chronic acetaminophen use in setting of glucose-6-phosphate dehydrogenase (G6PD) deficiency.
CASE PRESENTATION: 41-year-old African American male with recent history of retinal detachment repair presented to the hospital with symptoms of ongoing abdominal pain, nausea, vomiting, and loose stools for 2 weeks. He had been using 3-4 gm of Tylenol daily after his procedure and last Tylenol use was 2 days prior to presentation. On arrival he had acute elevation in his liver enzymes with AST 3,257 U/L and ALT 2, 467 U/L. An extensive acute liver failure work-up was initiated including a RUQ ultrasound with doppler which was unremarkable. tylenol and ethanol levels were within normal limits. An initial infectious work-up with Hep A, B, C, E, HIV, EBV and CMV was also unremarkable. Due to unclear etiology, he was put on N-acetylcysteine treatment per toxicology recommendations. In a span of a day his LFTs rose to greater than 7000 U/L, bilirubin (1.4 to 14.9 mg/dl), INR (1.3 to 3.2 sec), creatinine (1.13 to 3.79 mg/dl) were increasing rapidly. Due to his deteriorating condition, it was decided that he should be transferred to liver transplant center. An arterial line was placed, and it was noted to have dark "chocolate” color. The methemoglobin level was elevated to 11.5%. Hematology was consulted who recommended starting methylene blue (MB) and vitamin C and to send out testing for G6PD deficiency. No significant improvement in methemoglobinemia levels was seen following MB administration. At this time, he was transferred to a liver transplant center for further management. Of note his G6PD level came back significantly low (1.1 U/g Hb). Review of records from outside hospital indicated that he passed due to worsening multi-organ failure.
DISCUSSION: The presence of refractory hypoxemia, cyanosis and dark brown blood are cues to the rare diagnosis of methemoglobinemia. Drugs including local anesthetics, nitrates, antibiotics, and toxins can lead to oxidative stress resulting in methemoglobinemia (2). Typically, when a patient is symptomatic or methemoglobin level is above 30%, methylene blue (MB) is the treatment of choice. It acts by getting converted to leukomethylene blue after accepting electron from NADPH, which further reduces ferric to ferrous state. However, when G6PD deficiency is suspected, caution is advised with MB administration. As these patients already lack NADPH and its further reduction will lead to more oxidative stress causing hemolysis (3). This is usually managed with ascorbic acid and exchange transfusion (4). There are case reports of massive acetaminophen ingestion and its metabolite being the oxidative stress leading to methemoglobinemia. However, there is paucity of literature from long-acting oxidant stress of chronic acetaminophen.
CONCLUSIONS: This case highlights the unique setting in which chronic acetaminophen use can lead methemoglobinemia in presence of G6PD deficiency.
Volume
166
Issue
4
First Page
A2522
Last Page
A2523
Recommended Citation
Buddharaju S, Gulati S, Cret N, Akbar S, Fitzgerald KE, Kukhon FR. Methemoglobinemia revisited: a case of chronic tylenol ingestion leading to methemoglobinemia. JASN. 2025;166(4)A2522-A2523. doi: 10.1016/j.chest.2024.06.1536
DOI
10.1016/j.chest.2024.06.1536
Comments
CHEST Annual Meeting 2024, October 6-9, 2024, Boston, MA.