Pathogenesis Methanol is absorbed through the respiratory and digestive tracts and partially through the skin. It is mainly distributed in cerebrospinal fluid, blood, bile and urine and is present at very high levels, with the lowest levels in bone marrow and adipose tissue. Methanol is slowly oxidized and excreted in the body, so it has a significant accumulation effect. The main toxicity mechanism of methanol is: ① anesthetic effect on the nervous system; ② methanol by dehydrogenase, metabolic transformation into formaldehyde, formic acid, inhibit certain oxidative enzyme system, resulting in impaired aerobic metabolism, the accumulation of lactic acid and other organic acids in the body, causing acidosis; ③ because methanol and its metabolites formaldehyde, formic acid in the atrial fluid and eye tissue content is high, resulting in retinal metabolic disorders, easy to cause retinal cells, retinal nerve damage and optic nerve damage, (3) Because of the high content of methanol and its metabolites formaldehyde and formic acid in the atrial fluid and eye tissue, it causes retinal metabolism disorder, and is likely to cause retinal cell and optic nerve damage and optic nerve demyelination. Clinical manifestations Acute poisoning is mainly seen when methanol vapor is inhaled in large quantities or mistakenly consumed as ethanol. Acute methanol poisoning is mainly manifested by damage to the central nervous system, eye damage and metabolic acidosis. 1.Incubation period: There is a clear clinical incubation period for acute methanol poisoning, regardless of the route of absorption, the incubation period is generally l2h～24h, and a few patients can reach 2d～3d. For those who are poisoned through oral route, the incubation period is related to the intake dose, and there are reports of clinical symptoms appearing 40min after oral intake of pure methanol; simultaneous intake of ethanol can prolong the incubation period. 2. Central nervous system symptoms: The milder ones show symptoms such as headache, dizziness, weakness, drowsiness, and confusion, and rarely show euphoria in ethanol poisoning. In severe cases, coma and epileptic-like convulsions appear. 3. Eye symptoms: Visual impairment appears earlier and can appear 1h or several days after oral administration. Initially, it manifests as black shadows in front of the eyes, flashing sensation, blurred vision, or in severe cases, a rapid decrease in vision, or even complete blindness. There are often changes in the visual field, and the peripheral visual field shrinks centripetally mostly in the late stage of poisoning, and the simple peripheral visual field shrinks centripetally in the early stage is less common. 4. Metabolic acidosis: Those with milder degrees often have no obvious symptoms and are usually detected when relevant laboratory tests are performed. Patients with severe metabolic acidosis may present with headache, drowsiness, impaired consciousness, and changes in respiratory rhythm and amplitude. 5. Others: In severe cases, multi-organ system damage such as liver, kidney and cardiovascular system can occur. Some patients have a combination of bradycardia, pre-term contraction and electrocardiographic changes.