Methyl alcohol
Pure methyl alcohol (wood alcohol o; methanol)
is a colourless, volatile liquid, with an odour similar to
ethyl alcohol, and has a burning taste. Mineralised
methylated spirit consists of 90% by volume of ethyl
alcohol, 9.5% of wood naphtha, and 0.5% of crude
pyridine. It is present in certain homemade beverages,
antifreeze, paint removers, dyes, resins, adhesives and
varnish.
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Methyl alcohol poisoning Signs and Symptom : Can you drink methyl alcohol?
Methyl alcohol produces symptoms of drunkenness in the same way as ethyl
alcohol, but inebriation is not prominent, and the
effects are more prolonged. Toxicity can result
following its absorption through skin or respiratory
tract. Symptoms may appear within an hour, or may
not appear for 24 hours. They consist of nausea,
vomiting and pain or severe cramps in the abdomen,
headache, dizziness, neck stiffness, confusion, vertigo.
There is marked muscular weakness, and depressed
cardiac action and hypothermia. There may be
dyspnoea and cyanosis. The odour is usually present
in the breath. The effect on the central nervous system
is more intense and persistent than with ethyl alcohol.
There may be delirium and coma which may last for
two or three days. There is a toxic effect on the liver
and kidneys (acute tubular necrosis) and on highly
specialised nerve elements. Urine is strongly acid and
may contain acetone and a trace of albumin. Acidosis
is caused by the inhibitory effect on oxidative enzyme
systems produced by methanol with the resultant
accumulation of lactic and other unidentified acids.
Severe non-diabetic anion metabolic acidosis in
unconscious person is suggestive of methyl alcohol
poisoning. Anion gap acidosis is also seen in diabetic
ketoacidosis and lactic acidosis. The pupils are dilated
and fixed. Visual disturbances like photophobia and
blurred or misty vision (snowfield vision), seeing
spots, central and peripheral scotomata, decreased
light perception, concentric diminution of visual fields
for colour and form, followed by fairly sudden failure
of vision or complete blindness occur due to optic
neuritis and atrophy from the effects of formic acid
on the optic nerve. 10 to 20 ml. of methanol can cause
blindness. Fundoscopy shows hyperaemia of optic
disc followed by retinal oedema. The retinal ganglion
cells and optic disc show degenerative changes. In
fatal cases, convulsions are usual as a terminal event.
An increased osmolal gap accompanied by visual
symptoms suggest methanol poisoning. An anion
metabolic acidosis is characteristic of methanol,
ethylene glycol and salicylate intoxication.
Fatal Dose : 60 to 200 ml.
Fatal Period : 24 to 36 hours; may be delayed for
2 to 4 days.
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Absorption of methyl alcohol : What is methyl alcohol used for?
It is rapidly absorbed through the
stomach and intestines, and also through the lungs
and the skin. Though its action resembles that of
ethyl alcohol to a great extent, its rate of oxidation
is one-fifth that of ethanol and with repeated small
doses tends to accumulate in the blood. 80 mg/100
ml. of blood is a dangerous level. It does not completely
disappear from the blood for 3 or 4 days. Methanol
is oxidised by the liver to formaldehyde, (which is
33 times more toxic than methanol), which in tum
is oxidised to formic acid, which is six times more
toxic than methanol, which is responsible for the
associated metabolic acidosis and the retinal toxicity.
Formate may inhibit the cytochrome oxidase chain,
increasing lactate production and metabolic acidosis.
It is distributed in the tissues according to their water
content, and a high concentration is found in the vitreous
body and optic nerve.
Elimination of methyl alcohol : What products contain methyl alcohol?
The liver slowly metabolises
methanol. 3 to 5% is excreted through the lungs and
up to 12% through kidneys.
Cause of Death: Death is mainly due to acidosis
from production of organic acids, and CNS depression
is a minor factor.
Treatment of methyl alcohol poisoning:
(1) Gastric lavage using
5%bicarbonate solution should be done, and 500
ml. of this may be left in the stomach. (2) Activated
charcoal reduces mortality significantly. It acts by
reducing the absorption of alcohol from the digestive
tract, and by creating a concentration gradient in
favour of movement of alcohol and its metabolites
back into the gut. (3) Ethanol is the antidote. It is
given i.v. as a 10% solution, starting with 500 ml.
as an infusion and repeated as required, until blood
level falls below 25 mg%. Serum ethanol levels
must be checked frequently to assure that a level of
100 to 150 mg.% is being maintained at all times.
The i.v. the route is preferred to avoid gastritis. Methyl
alcohol is oxidised to formaldehyde by the enzyme
catalase. This catalase can also oxidise ethyl alcohol
to acetaldehyde. In methyl alcohol poisoning, ethyl
alcohol by competition for catalase blocks the
formation of formaldehyde and allows the Jess toxic
methyl alcohol to be excreted unmetabolised. (4)
Alternatively, 60 ml of ethyl alcohol in 200 ml fruit
juice can be given orally over a period of 30 minutes.
For maintenance, give 15 ml of 50% ethyl alcohol
every hour. (5) Haemodialysis is the treatment of
choice in severe poisoning. It reduces the half-life of
methanol from 40 hours to about one hour. There is
no role for peritoneal dialysis or haemoperfusion. (6)
4 methyl pyrazole (4MP, or fomepizole). The usual
dose is 15 mg/kg of 4 MP, followed 12 hours later by
I 0 mg/kg 12th hourly for 4 doses, and then increased
to 15 mg/kg 12th hourly for as long as necessary. It is
a competitive inhibitor of alcohol dehydrogenase. It
blocks the formation of formaldehyde and formic acid and
can be used instead of ethanol. (7) Folinic or folic acid
50 to 75 mg. every four hours is useful to increase the
elimination of formic acid, decreasing the metabolic
acidosis, and reducing symptoms. (8) Blood sugar
should be measured frequently while ethanol is being
given, as it may cause hypoglycaemia, especially
in children. (9) The basic treatment for alcoholic
ketoacidosis is crystalloid therapy, dextrose, thiamine,
and phosphate. Correct potassium and magnesium
defects. (1 0) Soda bicarbonate i. v. to correct metabolic
acidosis. (11) Place patient in a left lateral decubitus
position with head down to avoid aspiration of vomit.
(12) Eyes should be kept covered to protect them from
light. (13) Keep the airway clear.
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What happens after death by methyl alcohol
Postmortem Appearances : Cyanosis is marked,
and there is an absence of postmortem clotting of
the blood. The pyridine may give the skin a purple
colour. The mucous membrane of the stomach and
the duodenum is congested and inflamed with small
h~morrhages. The small or large intestine or both are
CNS Depressanant
contracted resembling a thick pipe of a very narrow
lumen. The lungs are congested and oedematous . The
brain is oedematous and shows a local haemorrhage.
The mucosa of the bladder is often congested. The
liver shows fatty change and sometimes early necrosis
and there is tubular degeneration of the kidneys.
ANALYSIS: Methyl alcohol and formic acid are
found in all organs, blood and urine. Formaldehyde
cannot be demonstrated probably because of the rapidity
with which it combines with protein and its speedy
oxidation to formic acid.
Anticoagulants such as EDTA, heparin ,
methanarnine and formalin give a positive test for
methanol.
The Circumstances of Poisoning : Poisoning
is mostly accidental. Sometimes it is used as an
intoxicating beverage, when ethyl alcohol is not
available.
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