Methanol Opticaltoxic Neuropathy in Alcoholic Patient: Case Report
Journal Title: Biomedical Journal of Scientific & Technical Research (BJSTR) - Year 2018, Vol 4, Issue 2
Abstract
The optic neuropathy due to methanol poisoning is a toxic neuropathy most frequently observed in developing countries. It is characterized by acute loss of visual function around 12 to 24 hours after ingestion of methanol. We report a patient with sudden visual loss after deliberate ingestion of methanol seen in a chemical dependency unit of Duque de Caxias, RJ, Brazil. Methanol is a colorless, flammable liquid with a slight alcoholic odor. It is used in automotive fuels, solvents, antifreeze fluid, cleaning products and adulterated alcoholic beverages [1,2]. Methanol has a taste and odor similar to ethanol and it is impossible to differentiate ethanol during ingestion [3]. Signs of methanol intoxication usually begin after 12 to 24 hours after ingestion, with metabolic acidosis associated with increased anion gap and visual disturbances [4]. More rarely there are cases of intoxication by their inhalation in certain branches of professional activity or transdermal intoxication [5]. Methanol itself does not produce toxicity, resulting from its transformation into formic aldehyde and formic acid by the enzymes alcohol dehydrogenase and aldehyde dehydrogenase respectively. This fact explains the delay from its ingestion to the beginning of clinical symptoms. These are characterized by headache, nausea, and vomiting, visual loss and in severe cases coma or death with marked metabolic acidosis [6]. Patient of initials P.R.P, 51 years old, married, a son, with incomplete high school degree, worker in the refrigeration field. He was being treated in the unit due to a history of alcoholism and smoking associated with cocaine abuse and sporadic use of crack. Two years earlier, before starting treatment in the unit, after an episode of alcohol abstinence he deliberately ingested undetermined amount of methanol that was being used in his work, diluted in water. Less than 24 hours later, headache and vomiting were associated with constriction and turbidity of the visual fields followed by bilateral amaurosis. He did not look for an emergency unit after the event, and there was no worsening or subsequent regression of the condition. He then began to complain of complex visual hallucinations, with visions of naked women, skulls and rodents. Due to the limitation imposed by visual loss, he decreased substance abuse with the help of family members. At the time of the neurological evaluation, he had been abstinent from alcohol for more than 90 days. He was under the use ofrisperidone 1mg/ day, diazepam 10mg/day and carbamazepine 200mg/day with control of alterations of sensoperception. Neurological examination demonstrated isocoria, with medium-sized and non-photoreacting pupils, bilateral optic atrophy in the funduscopy, and reduction of the achileu reflex bilaterally associated with decreased pain sensitivity in the lower limbs. The mental state was normal and, despite the visual dysfunction, he kept critical judgment, with self and alopsychic orientation. The remaining clinical examination was normal. During the follow-up period in the unit, the patient was also diagnosed with vitamin B12 deficiency below 200pg/ml currently under replacement. He is also being accompanied by an external ophthalmology service. Therefore, he underwent retinography with fluorescein showing bilateral optic atrophy (Figure 1). Also performed retinal optical coherence tomography with a decrease in the layer of nerve fibers in the right eye, and it was impossible to reliably measure the left retina using such technique (Figure 2).
Authors and Affiliations
Celmir de Oliveira Vilaça, Marco Antônio Araujo Leite, Pietra Moreira Vieira, Fernanda Correa Chaves, Rossano KA Fiorelli, Carlos Eduardo Cardoso, Marco Orsini
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