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Editor,—Methanol intoxication is a severe and often blinding disease. Irreversible visual loss may occur within hours to days after ingestion. Treatment regimens are aimed at controlling acid-base balance, removing the toxic agent by haemodialysis, or using ethanol solution as a competitive drug. If treatment is delayed beyond the first hours after ingestion, permanent damage to the optic pathways may occur. We report on successful treatment of methanol (methyl alcohol) induced blindness with late steroids and vitamin B-1.
A 40-year-old man was admitted to our eye department with sudden bilateral visual loss. He was generally healthy except that he was a heavy smoker and consumed alcohol regularly. During a period of 4–10 days before admission, the patient consumed pure methanol used for cleaning metal electrical wires. One day before admission, the patient complained of vomiting, nausea, and abdominal pain; however, a complete medical examination in the emergency room was inconclusive and his vision was not affected. On admission, physical and neurological examination were normal. Ophthalmic examination revealed visual acuity of hand movements in the right eye and 50 cm counting fingers in the left eye. Ocular examination was normal except for mild dilatation of the pupils which reacted sluggishly to light. No funduscopic abnormalities were observed. One day after admission, visual acuity deteriorated to no light perception in the right eye and remained as counting fingers in the left eye, with a large central scotoma. Relative afferent papillary defect was detected in the right eye. Visual evoked response (VER) was undetectable in the right eye and prolong latency was detected in the left eye (Fig 1A). Computed tomography of the brain and an electroencephalogram were normal. Blood laboratory tests were normal with no evidence of metabolic acidaemia. Nine to 15 days after methanol ingestion, no significant recovery was evident. The conventional treatment with bicarbonate was longer not appropriate because the patient’s acid-base balance was normal. Furthermore, the treatments with ethanol or haemodialysis were too late to be effective. Medical therapy was initiated including prednisone 60 mg/day by mouth and an intramuscular injection of vitamin B-1 100 mg/day. Three days after initiating the treatment, visual acuity, visual field analysis, and VER showed evidence of significant improvement in both eyes (Fig 1B). The patient was treated with vitamin B-1 injections for 20 days and with oral prednisone for 1 month with gradual tapering off. Seven weeks later the visual acuity had fully recovered in both eyes to the 20/20 level. Visual fields of both eyes showed only slight concentric constriction with no scotoma; VER demonstrated normal patterns on both eyes (Fig 1C).
Methanol intoxication may be associated with severe damage to the visual pathways, potentially leading to permanent blindness. In an outbreak of methanol intoxication involving 320 people, Benton et al stated that in cases of visual impairment or blindness, if vision did not return to normal within 6 days, recovery was not complete and the vision deteriorated.1 Other reported cases of methanol intoxication also demonstrated the guarded prognosis of visual loss.2 Thus, prolonged visual malfunction is considered an unfavourable prognostic sign, and vision almost never fully recovers. Delayed recovery is rare, and usually not complete. Scrimgeour et al 3 reported a patient who, after 12 days of blindness, regained vision and after 12 weeks his vision was hand movements in one eye and 10/20 in the other eye. One case, reported by Buzna et al, finally recovered to 10/20 in one eye and 2/20 in the other after treatment with ethanol and various vitamins including vitamin B-1.4 The present case is an extreme exception since the patient experienced almost absolute blindness (NLP and CF) for at least 4 days, as late as 15 days after methanol was first ingested, and yet recovered to almost perfect vision of 20/20 in both eyes. An interval between methanol consumption and deterioration of vision is typical. Therefore, severe visual loss in a young and apparently healthy individual should raise a suspicion of methanol intoxication, even if it was consumed several days before presentation of symptoms. During hospitalisation our patient was under close supervision, he was practically blind and totally dependent, therefore we assume that he did not consume alcohol during this period—that is, ethylism did not play a role in his clinical symptoms.
The rationale for using steroids in methanol toxic neuropathy was based on the clinical experience with this drug being effective in other forms of optic neuropathies. The potential therapeutic effect of steroids on methanol optic neuropathy might be a reduction in the oedema of the nerve sheaths caused by the histotoxic anoxia as suggested by Sharpe et al.5 Steroids are usually not used to treat ill effects of ethylism. Vitamin B-1 is given for treatment of Wernike–Korsakoff syndrome, following prolonged ethanol consumption. We assumed that since vitamin B-1 is highly effective in ethanol intoxication, it might well be effective in methanol intoxication. Other ocular associated pathologies in which thiamine may be effective are nutritional amblyopia, and Leigh’s disease (infantile necrotising encephalomyopathy), both irrelevant in this case.
In conclusion, the combination of steroids and vitamin B-1 was highly effective in treating severe methanol optic neuropathy. We do not know whether using only one of the drugs might be sufficient but, since the risk of permanent blindness is high, we recommend using this combination in the event of methanol intoxication.
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