Bilateral Methanol Optic Neuropathy After Intravenous Administration

Medications Damaging Ganglion Cell Layer or Optic Nerve: Pathogenesis, Diagnosis, and Treatment; (Quinine sulfate, Methanol, Carbon monoxide, Ritonavir, Fludarabine, Ethambutol, Methotrexate, Tamoxifen)

“…[37][38][39] Fundus muayenesinde genellikle intoksikasyondan 6-24 saat sonra iki taraflı optik diskte hiperemi ve ödem ortaya çıkar. [34,40,41] Geç dönemde (10-60. gün) ise genellikle majör retinal vasküler arklar boyunca retinal ödem gözlenir. [33,37] Resim 1' de metanol intoksikasyonunun geç döneminde bilateral optik atrofi gelişmiş bir hastanın OCT görüntüleri gösterilmiştir.…”

Methanol-induced optic neuropathy: a still-present problem

“…Analysis of the results of an ophthalmological examination after the outbreak of mass methanol poisoning in Atlanta showed the presence of fundus lesions in 87% of patients with initial vision loss and in nearly 100% of patients in whom continued follow-up examination showed a persistent decrease in visual acuity (Benton and Calhoun 1953 ). A fundus examination usually reveals bilateral hyperemia and edema of the optic disc, manifesting 6–24 h after methanol intoxication, with or without accompanying edema of the peripapillary RNFL, which may precede the onset of visual disturbances (Sharma et al 2012 ; Yang et al 2005 ; Yieh and Chou 2002 ). It is known that retinal edema is frequently observed along the major retinal vascular arches and may persist for 10–60 days (Benton and Calhoun 1953 ; Ingemansson 1984 ), then, after the resolution, transforms into retinal atrophy (Ingemansson 1984 ).…”

“…Hemodialysis allows for the rapid removal of methanol and formic acid from the body (Kraut 2016 ), while the increase in pH secondary to the use of bicarbonates reduces the entry of formic acid into the cells by increasing the ionization of methanol, and thus alleviating tissue damage (Garner et al 1995 ; Tasli et al 2018 ). The oxidation of methanol by alcohol dehydrogenase (ADH) is a key stage leading to the formation of its toxic metabolites in the body—hence, the first-line antidotes used in methanol poisoning are the competitive inhibitors of alcohol dehydrogenase—ethanol and fomepizole, also known as 4-methylpyrazole, preventing methanol metabolism to its toxic metabolites (Noor et al 2020 ); their use allows to increase the ratio of unchanged methanol excreted from the body to metabolized methanol (Rasheed et al 2017 ; Yieh and Chou 2002 ). Fomepizole has 500–1000 times stronger affinity for alcohol dehydrogenase compared to ethanol (Kraut 2016 ; Sharma et al 2012 ); however, due to the much higher cost of fomepizole therapy, as well as a similar side effect profile and mortality rate, ethanol is a much more widely used antidote, especially in developing countries (Kraut 2016 ; Noor et al 2020 ).…”

“…Usually, severe nervous system dysfunction is noticed 12–24 h after exposure to methanol (Seme et al 2001 ), while visual symptoms usually appear within 12–48 h and occur in about 50% of cases (Grzybowski et al 2015 ; Klein et al 2017 ; Seme et al 2001 ). In severe poisoning, disturbances of consciousness, memory loss, parkinsonism, severe cardiovascular symptoms, renal failure, rhabdomyolysis, coma, convulsions, and, consequently, death may occur (Choi et al 2017 ; Klein et al 2017 ; Yieh and Chou 2002 ). Lethal dose of methanol after oral ingestion is estimated to be 1.2 mL/kg (Noor et al 2020 ); however, it has been shown that if the appropriate management is implemented promptly, poisoning with a much higher dose of nearly 7 mL/kg (920 mg/dL) can be successively treated (Martens et al 1982 ).…”