S5499 Not Just Jaundice: Furosemide-Induced Yellow-Tinted Vision in Decompensated Liver Cirrhosis

Introduction: Xanthopsia—a yellow-tinted visual disturbance—is a rare, FDA-listed adverse effect of furosemide that has not yet been described in patients with cirrhosis. It is believed to result from dysfunction in retinal cone photoreceptors or optic nerve signaling. While furosemide is a widely prescribed loop diuretic, it is not a benign medication. This case describes the presentation of furosemide-associated yellow vision disturbance in advanced liver disease. Case Description/Methods: A 45-year-old man with alcohol-related cirrhosis presented for management of decompensated liver disease. Laboratory evaluation revealed thrombocytopenia and elevated aspartate aminotransferase, ALP, and direct bilirubin, with otherwise normal electrolytes, creatinine, international normalized ratio, and alpha-fetoprotein. Within 2 months of initiating furosemide 20 mg and spironolactone 50 mg daily for ascites, the patient reported persistent green-yellow visual changes. Upon reporting these symptoms, he was advised to stop furosemide and his vision returned to normal within 7 days of stopping the medication. Subsequent ophthalmologic evaluation, including fundoscopy, revealed mild acute angle glaucoma. He was later started on vitamin A supplementation. Other medications, including carvedilol and amlodipine, had been used previously without this reported symptom. At a 3-month follow-up, the patient remained at baseline, and his volume status was clinically stable on spironolactone monotherapy. Discussion: The temporal relationship between furosemide initiation and the onset of symptoms, followed by resolution after discontinuation, strongly implicates furosemide as the likely cause of this reversible visual disturbance. The absence of pre-existing ocular or neurologic disease and normal serum electrolytes increases the likelihood of a drug-induced etiology. Although furosemide is known for its central nervous system side effects—such as ototoxicity and paresthesia—this is the first reported case of furosemide-induced xanthopsia. A potential mechanism may involve impaired hepatic metabolism in cirrhosis, leading to increased drug accumulation in retinal tissues and subsequent disruption of visual signal processing. We highlight this rare but reversible adverse effect of furosemide and close monitoring, especially among patients with hepatic or renal dysfunction.

Publication Details

Journal
The American Journal of Gastroenterology
Published
2025-10-01
DOI
https://doi.org/10.14309/01.ajg.0001149456.30911.a8
Primary Topic
Drug-Induced Ocular Toxicity
Type
article
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article

S5499 Not Just Jaundice: Furosemide-Induced Yellow-Tinted Vision in Decompensated Liver Cirrhosis

The American Journal of Gastroenterology
Drug-Induced Ocular Toxicity
article

S5499 Not Just Jaundice: Furosemide-Induced Yellow-Tinted Vision in Decompensated Liver Cirrhosis

article en

Abstract

Introduction: Xanthopsia—a yellow-tinted visual disturbance—is a rare, FDA-listed adverse effect of furosemide that has not yet been described in patients with cirrhosis. It is believed to result from dysfunction in retinal cone photoreceptors or optic nerve signaling. While furosemide is a widely prescribed loop diuretic, it is not a benign medication. This case describes the presentation of furosemide-associated yellow vision disturbance in advanced liver disease. Case Description/Methods: A 45-year-old man with alcohol-related cirrhosis presented for management of decompensated liver disease. Laboratory evaluation revealed thrombocytopenia and elevated aspartate aminotransferase, ALP, and direct bilirubin, with otherwise normal electrolytes, creatinine, international normalized ratio, and alpha-fetoprotein. Within 2 months of initiating furosemide 20 mg and spironolactone 50 mg daily for ascites, the patient reported persistent green-yellow visual changes. Upon reporting these symptoms, he was advised to stop furosemide and his vision returned to normal within 7 days of stopping the medication. Subsequent ophthalmologic evaluation, including fundoscopy, revealed mild acute angle glaucoma. He was later started on vitamin A supplementation. Other medications, including carvedilol and amlodipine, had been used previously without this reported symptom. At a 3-month follow-up, the patient remained at baseline, and his volume status was clinically stable on spironolactone monotherapy. Discussion: The temporal relationship between furosemide initiation and the onset of symptoms, followed by resolution after discontinuation, strongly implicates furosemide as the likely cause of this reversible visual disturbance. The absence of pre-existing ocular or neurologic disease and normal serum electrolytes increases the likelihood of a drug-induced etiology. Although furosemide is known for its central nervous system side effects—such as ototoxicity and paresthesia—this is the first reported case of furosemide-induced xanthopsia. A potential mechanism may involve impaired hepatic metabolism in cirrhosis, leading to increased drug accumulation in retinal tissues and subsequent disruption of visual signal processing. We highlight this rare but reversible adverse effect of furosemide and close monitoring, especially among patients with hepatic or renal dysfunction.

The American Journal of GastroenterologyVol. 120(10S2)
Good health and well-being
Openalex Percentile: Top 32%
Drug-Induced Ocular Toxicity
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