VOLATILE POISONS

Ethyl alcohol (Ethanol)

• It is colorless liquid with characteristic odor. It

is obtained from fermentation of food
• Ethanol is the most common ingested toxin
throughout the world, thousands of deaths
occur due to overdose, suicide and accidental
intake of alcohol.
 Alcoholic beverage:

• The alcoholic content of different beverages

are:
• Beer: 2-8%.
• Light wines: 5-10%.
• Heavy wines: 10-20%.
• Brandy, Rhum (rum), Vodka and Wisky: 40-
50%.
 Pharmacokinetics
• Absorption
• 80% from small intestine
• 20% from stomach and large intestine
• Distribution
• To all tissues and body fluids
• Passes the blood brain barrier
• Passes placenta
 Pharmacokinetics
• Metabolism
• Ethanol is oxidized to acetaldehyde by alcohol
dehydrogenase and then to acetic acid ,then it
metabolized into C02 and water,
 Pharmacokinetics
• Excretion
• Urine
• Breath
• Sweat ,tears bile
 Condition of poisoning
• Accidental
• Addicts
• Children
• Workers
• Homicidal
• To facilitate rape & robbery
• suicidal
 Mechanism of action
• CNS
– Depression
• Peripheral
– Vasodilatation lead to false sensation of heat
• Metabolism
– Hypoglycemia
– Accumulation of fat in liver(hepatotoxic poison)
– Accumulation of lactic acid and ketone
Fatal dose: 150 – 200 mls of absolute ethyl alcohol.

Barbiturates and Tranquilizers enhance [synergism], the fatal effect of

alcohol.
Fatal period: 1 – 10 hours after intake of fatal dose.
 Clinical presentation
• Mild toxicity (stage excitation )
• blood concentration 0.05-0.15%
• There is inhibitions of centers which control
judgment & behaviours .
• Euphoria
• Talkativeness &behavioral changes .
 Clinical presentation
Moderate toxicity (stage of incoordination )
blood concentration 0.15-0.3%

Motor incoordination
• Drunked (staggering)gait
• Tremors of hands
• Slurred speech
• Decreased motor skills.
• Diaphrag – sudden
contraction – hiccough.
• Eyes – diplopia
• GIT – vomiting
• Skin – flushed
 Clinical presentation
• Severe toxicity (stages of seizures &coma)
• blood concentration more than 0.5%(Blackout)
• Severe depression
• Seizures
• Shock
• Breath alcohol smell
• Pupil (miosis that dilated on pinching of the skin
of face or neck ) [McEwen's sign]
• coma with respiratory depression
 Investigation
• Rapid tests
• Finger to nose test
• To walk along a straight line
• Chemical analysis
• The concentration of alcohol in the blood can be
indirectly estimated by measuring its
concentration in alveolar air by Alco meter.
 Treatment:

• a. Aspiration of stomach contents, and wash

by sodium bicarbonate, then leave strong
coffee in the stomach (stimulates respiratory
center).
• b. Clear air passages.
• c. inhalation.
• d. Respiratory stimulants.
(Rate of elimination of ethanol is (15 - 20mg/dl/hour))
 Antidote
• No specific antidote but Vit.B6 may accerelate
ethanol metabolism through stimulation of
alcohol dehydrogenase enzyme.
• Administration of thiamine: Chronic alcohol
use can lead to thiamine deficiency, which can
cause a serious condition called Wernicke-
Korsakoff syndrome. Thiamine
supplementation is often given to prevent or
treat this deficiency.
METHYL ALCOHOL (Methanol)
 METHYL ALCOHOL (Methanol)

• Methyl alcohol is widely used in industry

and laboratories and hospitals as a solvent.
• Many cases of poisoning occurs due to
adulteration of ethyl alcohol by adding
methyl alcohol, or methyl alcohol is taken
as a substitute for ethyl alcohol.
 Metabolism:

• Methyl alcohol is metabolized mainly in the liver by

alcohol dehydrogenase to formaldehyde and formic acid,
both are more toxic than methanol, leading to blindness
and acidosis.
Fatal dose; 60-150 mls
15 mls is enough to cause visual effect.

Fatal period: variable. There is a latent period 12 hours between ingestion and
onset of symptoms, this period might extend to 72 hours and is due to the slow rate
of production of formaldehyde and formic acid
 Action
• CNS depression, cyanosis, metabolic acidosis,
retinal edema, optic neuritis, optic atrophy
and blindness.
 Clinical picture:

• Headache.
• Visual symptoms: Blurred vision and flushing
lights (visual acuity may diminish to
perception of light or blindness)
• Violent attacks of abdominal pain due to
pancreatitis.
• Vomiting.
• Drowsiness leading to coma.
 Treatment:

• 1.Stomach wash, if more than 20 ml has been

ingested.
• 2.I.V sodium bicarbonate to correct metabolic
acidosis.
 Antidotal therapy
• Ethanol
Ethanol is agonist for methanol and competes with it for
metabolism by alcohol dehydrogenase and aldehyde dehydrogenase,
thus minimizes the formation of toxic metabolites of methanol,
formaldehyde and formic acid.
• Fomepizole (4-methyl pyrazole):
Strong inhibitors of alcohol dehydrogenase
• Folinic acid (leucovorin) for conversion of
formic acid to Co2&H2O