It is an acute methanol poisoning, with neurological symptoms, metabolic acidosis, amblyopia, etc., and a strong smell of alcohol in the breath. On the one hand, methanol can be slowly oxidized to formaldehyde and formic acid in the body, and on the other hand, the oxidation products of methanol and iron of cytochrome oxidase combine to inhibit the intracellular oxidation process, resulting in the accumulation of organic acids such as lactic acid in the body and causing metabolic acidosis. The patient in this case had lactic acidosis, but the degree was mild and could not explain the severe metabolic acidosis; blood and urine ketone bodies were negative, which did not support diabetic ketoacidosis; osmolality was high, but there was no obvious dehydration manifestation, and the diabetic non-ketotic hyperosmolar state was not very supportive. The clinical manifestations were consistent with methanol toxicology, and acute methanol poisoning was established in combination with toxicological testing. It is lactic acidosis due to tebivudine, etc. This drug is an antiviral drug – a nucleoside reverse transcriptase inhibitor with adverse effects such as severe hepatitis and fatty liver. Long-term use of such drugs by patients causes severe muscle damage and liver damage, resulting in more lactic acid production and impaired utilization, which eventually leads to severe lactic acidosis. There are many causes of lactic acidosis, among which B2 type lactic acidosis due to toxic substances and drugs should be given high clinical attention. Meanwhile, critically ill patients are often accompanied by stress hyperglycemia, which needs to be differentiated from diabetic lactic acidosis and ketoacidosis. CRRT can play an important role in the rescue of severe acidosis.