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Metabolism, elimination and treatment of methanol poisoning

Methanol is an organic compound present in industrial alcohols and alcohols. Methanol poisoning causes serious harm on the nervous system, cardiovascular, digestive.

Harm of methanol

Methanol CH3OH is an industrial alcohol with the chemical formula CH3OH, also known as methyl alcohol, colonial spirit or alcohol solvent. Methanol is a clear, colorless liquid at room temperature, boiling at 650 degrees. Methanol is one of the highly toxic alcohol in humans and primate, widely used in many industries in the form of a solvent and in products containing methyl and formaldehyde compounds.

In the market, methanol is found in products such as paint production solutions, cleaning solutions (such as copy machine cleaning solutions, car window glass cleaners, wood cleaning solvents, etc.), antifreeze, etc.

methanol

Methanol is an organic compound present in industrial alcohols and alcohols. Methanol poisoning causes serious harm on the nervous system, cardiovascular, digestive.

Harm of methanol
Methanol CH3OH is an industrial alcohol with the chemical formula CH3OH, also known as methyl alcohol, colonial spirit or alcohol solvent. Methanol is a clear, colorless liquid at room temperature, boiling at 650 degrees. Methanol is one of the highly toxic alcohol in humans and primate, widely used in many industries in the form of a solvent and in products containing methyl and formaldehyde compounds.

In the market, methanol is found in products such as paint production solutions, cleaning solutions (such as copy machine cleaning solutions, car window glass cleaners, wood cleaning solvents, etc.), antifreeze, etc.

The process of transport, metabolism and elimination of Methanol in the human body (Toxicokinetic) and the effect of toxic substances on the body and primate (Toxicodynamics)

Methanol is an inherent 1 carbon alcohol, when taken, Methanol quickly absorbed from the digestive tract into the bloodstream, not attached to protein. Peak concentrations are reached between 30 and 240 minutes, mainly metabolized in the liver (> 85%) while few are intactly excreted by the kidneys (3%), and breathing (<10%). Methanol has a low molecular weight of 32 daltons, a distribution volume (Vd) of 0.60 to 0.77 l / kg.

  • Methanol is slowly converted, through alcohol dehydgenase to formaldehyde, then formic acid and silent poisoning of anion formate. With the exception of a few primates (monkeys, apes, and humans), the formate is not toxic to Australian animals, so animal studies are not applicable, the reason for this difference may be the amount of folate in the liver. people are too few, not enough for the liver’s tetrahydrofolate enzyme to convert formate into CO2 and H2O, so experimental research limits value in deeper understanding, but more importantly from poisonings In clinical and subclinical areas, it has given important knowledge.
  • In the late stage, fomate inhibits cytocrome oxidase as the last enzyme in the “electron” transport chain in the mitochondria by binding ferric ions of half of this enzyme in Heme

Formate inhibits mitochondrial respiration resulting in highly toxic lactate formaldehyde but half-life is too short (1-2 minutes) is difficult to detect in the blood so it is not important in practice. To increase the metabolism of fomate, folic acid or folimic acid (leucovorin) plays a role in the theory, but has not been clinically proven.

Diagnosis of methanol poisoning

Diagnosis of methanol poisoning is difficult, mainly based on asking questions, assessing specific clinical symptoms, detecting metabolic acidosis, measuring osmotic space (OG) and anions (AG); finally, direct measurement of methanol by gas chrowatography is possible, but this is very difficult in many places, even if it is normally impossible to do it in 24 hours.

The question of the disease plays an important role in the diagnosis of methanol poisoning, but symptoms appear usually late after 12 to 24 hours or longer after drinking and need to make a differential diagnosis, if you drink more ethanol, symptoms. appear later than, for example, drinking a mixture of 20% Methanol and 20% Ethanol 20% clinical symptoms appear late and methanol poisoning is like an alcoholic addict: gastrointestinal contractions, vomiting, nausea, pain of breathing oil Quick, tired, whole body, dilated pupils. If the patient is an alcoholic, it is easy to confuse both the patient and the physician.

Another clinical sign that has a diagnostic value but is difficult to find is pseudopaphillitis characterized by visual disc hemorrhage, translucency, visual disc edema with no refractive effect on the sag. If the eye is visibly dilated, the person may experience visual disturbances, impaired vision, see bright dots of jumping, or see white snow, reflections may disappear.

Subclinical tests also suggest that an important diagnostic suggestion is that hyperventilation is associated with an initial reduction in PaCO2, and particularly a very large BD deficiency of> 20 mmol / l. The more severe the prognosis, the worse the prognosis (pH 10 mosmol / kg H2O) while the anion gap is still within the normal range in the intermediate stage, both gaps appear to increase (at this stage most patients are newly hospitalized. ) and in the late stage (≤ 30 hours), when all methanol is metabolized, the lower osmotic gap is high or returns to normal, while the anion gap is very high due to the accumulation of acid. formic and lactate.

Late stages can be prolonged if the victim drinks methanol with ethanol. Where there is a special condition for testing blood levels of Methanol will see higher than 20 mg / dl, if high> 40 mg / dl is very serious poisoning, patients may appear blind, convulsions, coma and In the case of death in decompensated acidosis, the measurement of formate in the blood is a definite diagnosis but is not yet feasible in many places. Cranial tomography (CT scan) and magnetic resonance imaging (MRI) can detect edema and necrosis of basal ganglia, characterized by the gray duckweed (Putamen). These signs may explain a complication of life-saving methanol poisoning: Parkinson-like extrapyramidal syndrome manifests itself: stiffness, mild muscle twitching, slow movement, dullness, or slight insanity.

Treatment of methanol poisoning

The initial measures to eliminate methanol from the digestive tract are not necessarily as ineffective as: gastric lavage for activated charcoal, because when methanol is absorbed very quickly, most patients are late. Control of living function is necessary first; promptly resolve metabolic acidosis with sodium bicarbonate (500 – 800 mEq) infusion over the first few hours to reduce the amount of undissociated formic acid. Reducing the amount of formate into the central nervous system and reducing toxicity to the eyes. To inhibit the conversion of methanol to formic acid, two antidote (antidote) drugs are used:

Formepizole (Antizol) is very effective in treating Methanol poisoning and Ethylenglycol poisoning. Fomepizole is effective with symptoms of methanol poisoning, does not cause easy to use CNS, has few side effects (does not cause pancreatitis) and reduces the need for dialysis. But the price is very expensive, also difficult to implement.

Ethanol is an alcohol that inhibits the competition of alcohol dehdrogenase 10 times more vein than Methanol, but much weaker than Fomepizol. Ethanol can be administered intravenously with a 10% solution and given orally with a 20% solution. A blood Ethanol level of 22 mmol / L (100 mg / dl) may be sufficient to stop methanol metabolism (Ethanol / Methanol concentration is at least 1/4). Many authors recommend giving ethanol ethanol bolus of 0.6 g / kg (13 mmol / kg), followed by 66 – 154 mg / kg / hour (1.4 – 3.3 mmol / kg / hour) intravenously or to drink. However, blood Ethanol must be monitored every 1.2 hours as blood sugar can drop.

Hemodialysis is a measure that is indicated even when the patient has vision disorders, kidney failure, metabolic acidosis. Dialysis increases the elimination of methanol and metabolites. However, if dialysis is used, the dose of Ethanol must be doubled because dialysis also removes Ethanol. Dialysis should be continuous for at least 4 to 8 hours so that blood methanol is less than 20 mg / dl (<6mmol / l) and the acidosis is adjusted. Peritoneal dialysis is less effective, while dialysis adsorption is most effective. However, the effect has not been proven in practice.

Conclude

Despite the improvement in methanol poisoning, Vietnam has a very serious medical condition and high mortality. Delayed diagnosis is a major problem because the characteristic clinical symptoms are often masked and lost for many other reasons.Treatment is difficult, so consultations with the Poison Control Center are particularly difficult. difficulty in dealing with medications especially when in front of a patient who is comatose with metabolic acidosis of unknown origin or who has a history of suspected disease requiring blood gas analysis, OG and AG measurements, fundoscopy, Methanol and blood formate measurement (if available). Early treatment is critical for success, for alkaline acidosis is normal, if fomepizol is excellent, ethanol should also be used before a definite diagnosis, if both gaps are increased and OG> 20mosm / kg H2O, dialysis should be concerned as soon as possible if any visual disorders and metabolic acidosis are observed. The length of treatment is based on OG and pH.

Bad prognosis if patient is comatose, pH 25 mmol / l and respiratory decompensation.

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