Methanol is primarily metabolized in the liver by hepatic alcohol dehydrogenase to formaldehyde. Formaldehyde is then converted by aldehyde dehydrogenase to formic acid. Although both formaldehyde and formic acid are extremely toxic, systemic metabolic acidosis caused by the accumulation of formic acid is thought to be the major toxic effect of methanol. Dyspnoea, coma, convulsion, and blindness may subsequently occur in severe poisoning.
As methanol poisoning is potentially fatal, its prompt diagnosis and treatment is very important. However, in the emergency room, acute methanol poisoning might not be readily diagnosed, especially when we are facing an unconscious patient as in this case.
Moreover, these toxicological facilities are not available in most hospitals. And, the laboratory results of methanol usually take more than 1 day to be complete. Wide serum anionic and osmotic gaps are auxiliary tools for its diagnosis, and fundoscopy might be another useful alternative. The management of acute methanol poisoning is gastric lavage, correction of the metabolic acidosis, competitive inhibition of methanol oxidation by ethanol or 4-methypyrazole, and the removal of both formate and methanol by haemodialysis.
Our patient survived. However, he had permanent visual sequelae, which might be due to severe metabolic acidosis and treatment delay. Once the ocular toxicities occur, the probability of vision recovery after poisoning is poor. Optic atrophy is a common outcome, 4 although according to a recent report high doses of intravenous steroids may protect the vision of patients with methanol-induced optic neuropathy.
In spite of this, benefit to the visual system was not obvious. Therefore, treatments should be given as early as possible, before the irreversible optic neurological damage occurs.
Generally, the prognosis of methanol-induced toxic optic neuropathy is determined by the methanol dose at exposure, the length of any treatment delay, and the pupillary response on presentation. Methanol is particularly toxic to the optic nerve, leading to acute blindness.
Based on a histopathological study, 1 the retrolaminar optic nerve myelin sheath seems to be selectively vulnerable to methanol poisoning due to its anatomical structure. In the acute phase, the hyperaemia and swelling of the optic disc has a papilloedema-like appearance.
Therefore, effective methods to treat the oedema might be important, such as the use of intravenous steroids and diuretics. The bilateral haemorrhagic necrosis of the putamen and oedema in the deep white matter of our patient are the characteristic MRI findings of severe methanol intoxication. The MRI in methanol poisoning not only demonstrates this specific pattern of brain damage but also provides good correlation among brain, visual pathway, and the evolution of the clinical course of the disorder.
In conclusion, methanol poisoning is a rare entity, and historically difficult to treat. Furthermore, it is worthwhile to study the administration of steroids, osmotic diuretics, antioxidants, vitamins, or other methods in protecting the optic nerve in acute or subacute phases of methanol poisoning in the future.
Methanol optic neuropathy: a histopathological study. Neurology ; 32 : — Methanol poisoning in human subjects: role of formic acid accumulation in metabolic acidosis. Am J Med ; 68 : — Smaller doses can cause permanent blindness. Inside the body, methanol is metabolized to formaldehyde, then to formic acid. This can lead to metabolic acidosis, a dangerous buildup of acid in the body that can cause organ damage. Formic acid can also accumulate in the optic nerve , causing severe damage that can lead to permanent blindness.
According to safety documents , symptoms of poisoning by ingestion can manifest as gastrointestinal irritation—with nausea, vomiting, and diarrhea—and central nervous system depression, causing headache, dizziness, drowsiness, nausea, and an intoxicated feeling. It is well-documented that the level of toxicity, which does not correlate with the serum methanol level and hence, is not considered a good indicator of prognosis [ 13 ].
To our knowledge, orbital MRI scan is rarely taken to observe the optic nerves in patients with methanol poisoning. Optic nerve and basal ganglia are the tissues most at risk from methanol intoxication for metabolic or apoptotic sensitivity to methanol metabolites. The typical manifestation on brain MRI scans in patients with ingestion poisoning was hemorrhagic or non-hemorrhagic necrosis in the bilateral putamen, occasionally in frontal and insular cortices and subcortices [ 14 , 15 ].
But manifestation on orbital MRI scan for optic nerve in these patients is rarely reported. In our cases, increased signals of bilateral ONs in the orbit and the canal parts with enhancement were the common features Fig. All these data confirmed that the retrolaminar regions of the optic nerve were vulnerable to damage in methanol poisoning. However, these findings do not fully represent the characteristics of injured optic nerve in methanol poisoning, for most cases of methanol poisoning are caused by oral ingestion, not by inhalation.
In our report, we did not try the treatment protocols of dialysis or detoxification drugs, for the results of blood gas analysis and toxicology tests were normal. Optic nerve MRI showed abnormal signals with enhancement in all patients, indicating the presence of optic nerve inflammatory reaction.
Retrobulbar optic neuritis or neuro-retinitis is the well-reported mode of presentation in cases of acute methanol poisoning [ 16 , 17 , 18 ]. The routine treatment regimens include the use of ethanol, fomepizole, folinic acid, sodium bicarbonate, and hemodialysis, etc.
These treatments mainly prevent the formation of formic acid and further toxicity, but do not have any effect on established ocular inflammation [ 18 ]. There are some studies reporting the use of intravenous methylprednisolone, resulting in good visual outcomes [ 11 , 18 , 19 ].
In a report, Shukla et al. But compared to the visual functions before treatment, the improved visual function was not satisfactory, which is inconsistent with the results of foreign studies. Additionally, except for ethnicity effect, we speculated that chronic optic nerve injury caused by chronic methanol-inhaled poisoning was also an important reason for the poor prognosis.
The inhalation of methanol to the poisoned dose might be a chronic process of accumulation of methanol and its metabolites in body before acute onset. It should be noted that the prominent visual symptoms may compel patients to consult an ophthalmologist or neuro-ophthalmologist time and again. Without typical intoxication history, after differential diagnosis including NMOSD, various optic neuritis and optic neuropathy were all excluded in outpatients, these patients had missed the best treatment timing.
Although proper treatments were given, the severe vision symptoms of these patients did not get well-relieved. However, we believed that the medical treatment might prevent further damage to the optic nerves according to the treatment effect.
By comparison, cases of methanol poisoning caused by oral ingestion experienced an acute attack following just once intake or misusing of methanol, with obvious systemic symptoms such as mental changes, extrapyramidal symptoms and convulsions.
Most of the patients would typically seek medical attention, and they might be cured or partially improved after given appropriate treatment timely. Recently, more and more attention has been paid to inhalation methanol poisoning.
These cases in our report presented severe vision loss and transient systemic symptoms resulting from this distinctive intoxication. Methanol poisoning via non-oral exposure can also cause severe neurologic complications especially dramatic loss of vision, and might be in a chronic process. It is suggested that emergency physicians, ophthalmologists and neuro-ophthalmologists should be aware of inhalation methanol poisoning and raise their vigilance against the disease.
Accurate and fast diagnosis and effective treatments guarantee the better prognosis. Methanol Toxicity. Am Fam Physician. Google Scholar. Methanol poisoning as a result of inhalational solvent abuse. Ann Emerg Med. Methanol inhalation toxicity. Comparison of methanol exposure routes reported to Texas poison control centers. J Emerg Med. Outcomes following abuse of methanol-containing carburetor cleaners. Hum Exp Toxicol. Neurological complications resulting from non-Oral occupational methanol poisoning.
J Korean Med Sci. Bilateral total optic atrophy due to transdermal methanol intoxication. Middle East Afr J Ophthalmol. Article Google Scholar. Transdermal Spirit methanol poisoning: a case report. Iran Red Crescent Med J. Acta Derm Venereol. Sharma P, Sharma R. Toxic optic neuropathy. Indian J Ophthalmol. Methanol-induced optic neuropathy: treatment with intravenous high dose steroids. Int J Clin Prac. CAS Google Scholar.
The distributions of mitochondria and sodium channels reflect the specific energy requirements and conduction properties of the human optic nerve head. Our distillation equipment is designed for legal uses only and the information in this article is for educational purposes only. Please read our complete legal summary for more information on the legalities of distillation.
Methyl alcohol methanol is the bad stuff that could be found in moonshine or any distilled spirit for that matter. Pure methanol is very dangerous and it is definitely able to cause blindness and even kill people. As little as 10 ml of pure methanol could blind someone and as little as 30 ml could kill someone.
Methanol is found naturally in certain fruits and vegetables. It may also be produced as an unintended byproduct during the fermentation process. Spirits distilled from fruits, such as apples, oranges, and grapes, are more likely to contain methanol. Both beer and wine generally contain methanol.
This makes distilled wine grappa, brandy, etc. If wine contains methanol but doesn't pose a risk of methanol poisoning then why is it potentially dangerous to drink once distilled? The difference is that the methanol concentration in, say, 5 gallons of wine, is evenly distributed among the 5 gallons.
For someone to ingest a potentially dangerous amount they would need to ingest more than 5 gallons During the distillation process methanol is concentrated at the start of the production run because it has a lower boiling point than ethanol and water. The boiling point of methanol is approximately degrees farenheit, which is quite a bit lower than ethanol the good stuff.
This means that methanol F boiling temp will start to boil before the ethanol F boiling temp.
0コメント