The ocular manifestations of methanol poisoning can cause symptoms and sequelae that interfere with the quality of life. This can arise as a decrease in vision to blindness.

The populations at high risk of methanol intoxication are alcoholics, smokers, industrial workers, malnourished patients, and children. Methanol poisoning can result from inhalation or consumption of large quantities of food or beverages containing methanol, whether intentional or not.

Methanol poisoning is an emergency associated with rapid and permanent progressive damage to organs. Abnormalities can range from visual disturbances, metabolic, and neurological dysfunction to death.

The commonly initial symptoms are headache, nausea, vomiting, and pain in the epigastric area. More severe symptoms can occur in advanced conditions in the form of tachycardia, tachypnea, coordination problems, seizures, ataxia, rhabdomyolysis, kidney failure, loss of consciousness, and coma.

In the long term, sequelae such as tremor, rigidity, hypokinesia, and parkinsonism have been reported due to high residual formic acid concentrations in the brain's putamen region dopaminergic pathway the activity of the enzyme dopa-B-hydroxylase.

In particular, methanol poisoning can cause significant and irreversible visual impairment. Some symptoms that accompany are photophobia, eye pain when the eyeball is moved. These symptoms are caused by the optic nerve's demyelination process with clinical manifestations such as hyperemia, edema, and atrophy.

Eye Clinical Manifestations due to Methanol Poisoning
Bilateral mydriasis in the patient intoxicated by methanol

Methanol's Toxic Effects on Eyes

Methanol can cause visual disturbances when the serum level exceeds 20 mg/dl. Ocular disorders' pathophysiology due to methanol poisoning involves the rapid absorption of methanol in the liver's metabolism and gastrointestinal tract.

Breaking down methanol by the alcohol dehydrogenase (ADH) enzyme will produce formaldehyde. Formaldehyde will be metabolized into formic acid. It will lead to systemic metabolic acidosis and intrinsic toxicity.

In the eye, formic acid will accumulate in the optic nerve and interfere with the electron transport chain and mitochondrial function, resulting in a lack of ATP production. The decreased ATP will cause disturbances in the nervous transport system, especially those dependent on ATP, such as the optic nerve. It causes demyelination of the optic nerve.

In general, patients experience initial symptoms 12 to 24 hours after methanol exposure. The ocular complaints include decreased visual acuity, dyschromatopsia, pain with eye movement, and photophobia. The condition of decreased visual acuity occurs rapidly and can cause blindness with a characteristic picture of a central or cecocentral scotoma because peripheral visual acuity is generally good.

Ocular Examination of Methanol Poisoning Effects 

A detailed history and eye examination can confirm the diagnosis of ocular methanol toxicity. Investigations are carried out as indicated, either to evaluate the diagnosis or to rule out differential diagnoses.

a. History

In the history, it is necessary to explore the onset of complaints, the course of the disease, the history of consumption of certain foods or drugs, history of eye diseases and other comorbidities, family history of the disease, and the patient's lifestyle. Methanol can enter the circulation due to accidental or deliberate consumption of traditional alcoholic beverages, cleaning agents, or industrial exposure.

12-24 hours after exposure, the patient may appear normal. This period is called the latent period. After that, methanol toxicity symptoms will appear, such as nausea, vomiting, abdominal pain, followed by central nervous system depression and hyperventilation as metabolic acidosis develops. As mentioned above, eye clinical manifestations include blurred vision, decreased vision, photophobia, and "halo vision."

b. Physical examinations

After evaluating the emergency signs and a general physical examination, the eye examination begins with sharp eyesight. Patients can significantly reduce visual acuity and even sharp vision without light perception (blindness). There may be a pupil defect in the form of a decreased or missing light reflex on the anterior segment. On posterior segment may reveal damage to the optic nerve in the form of hyperemia and edema in acute conditions, which progress to pallor and atrophy in chronic conditions. These findings occur symmetrically and bilaterally. There may be damage to the retina and its surroundings, such as bleeding spots around the optic disc.

c. Supporting Examinations

Performing supporting examinations according to indications include visual field examinations using static (Humphrey) or kinetic (Goldman) instruments, MRI, and Optical Coherence Tomography (OCT) tests.

The visual field examination will obtain the central or cecocentral scotoma's symmetrical characteristics in both eyes. But, no found in examining the peripheral visual field. 

MRI examination is directed specifically at the optic nerve and chiasm to see bilateral putamen necrosis with or without bleeding. MRI is also used to exclude other possible causes, such as tumors or infections.

Electrophysiological tests can be performed repeatedly to see an early decrease in the amplitude of visual contrast sensitivity. Optic nerve-specific examination with OCT will reveal edematous peripapil nerve lining and diffuse thinning of the retina.

The diagnosis of methanol poisoning should be suspected of metabolic acidosis and an osmolar gap in the investigation.

Overview of the Therapy of Ocular Manifestations in Methanol Intoxication

Ocular toxicity of methanol predominantly manifests as toxic ocular neuropathy (TON) requiring rapid therapy. While performing hemodynamic stabilization, give intravenous fomepizole with an initial dose of 15 mg/kg. And then, followed by a 10 mg/kg maintenance dose every 12 hours for four doses or a methanol concentration less than 32 mg/dl. 

Suppose additional doses other than four maintenance doses are required. Fomepizole is used in increments of 15 mg/kg every 12 hours. Give fomepizole every 4 hours for the patient is undergoing hemodialysis because it will also be dialyzed.

Another option is ethanol intravenously, or it can be given orally if injection preparations are not available. However, calculating this drug is more difficult because it is necessary to consider the expected plasma concentration, the volume of ethanol distribution, and the patient's weight. In general, 10% ethanol can be used with an initial dose of 8 ml/kg for 30-60 minutes, followed by a 1-2 ml/kg/hour maintenance dose. Fomepizole or ethanol therapy should be combined with hemodialysis.

Ocular manifestations due to methanol poisoning occur progressively and can cause blindness. Ocular symptoms that can appear are blurred vision, decreased vision, dyschromatopsia, pain with eye movement, and photophobia. 

On physical examination of the eye, it will show a decrease in visual acuity and damage to the optic nerve due to direct destruction by methanol metabolites in formic acid. Treatment that can be given is fomepizole or ethanol, combined with hemodialysis.