This document discusses alcohol poisoning and the effects of ethanol. It covers the categories of alcohols, ethanol uses including as a beverage and in medicine, toxicokinetics of ethanol absorption and metabolism, mechanisms of action on the body, acute and chronic poisoning symptoms, and treatment approaches for alcohol poisoning and chronic alcoholism.

1. Prepared by B.Muni Sai Gagan
ALCOHOL POISONING
Presented by M.DIWAKAR
PharmD IVth YEAR

2. ALCOHOLS
• Alcohols are actually (hydroxyl) derivatives of (aliphatic)
hydrocarbons. There are 3 categories of alcohols—
1. Mono hydroxy alcohols : They have only one hydroxyl (OH) group,
e.g. ethanol, methanol, isopropanol, etc.
2. Di hydroxy alcohols : They possess two hydroxyl groups and are
referred to as glycols, e.g. ethylene glycol, propylene glycol, etc.
3. Tri hydroxy alcohols : They are not really alcohols, but only
derivatives, e.g. propane derivative glycerol or glycerine.

3. ETHANOL
Synonyms
Ethyl alcohol; Grain alcohol.
Physical Appearance
Clear, colourless liquid with a faint fruity odour, and sweetish
burning taste. It is both water soluble and lipid soluble

4. ETHANOL USES
Beverage—Popular alcoholic beverages include beer, wine, whisky, gin, brandy, rum,
and vodka
• In addition there are several
indigenous preparations
peculiar to particular regions,
e.g. arrack, toddy,
and feni in India, tequila in
Mexico, sake in Japan, eau de
vie or fruit brandy in France,
etc.
■ Solvent for after-shaves,
colognes, mouthwashes, and
perfumes. The alcohol content
Beverage
Light Beer (Lager and Pilsener)
Heavy Beer (Ale and Stout)
Natural Wine (Cider)
Fortified Wine (Sherry and
Port)
Whisky, Gin, and Brandy
Rum
Liqueurs (e.g. Cognac, Crème
de menthe, Schnapps, etc.)
Ethanol Content
(percentage by
volume)
4 to 6
6 to 8
2 to 3
10 to 20
40 to 45
40 to 50
17 to 50
Ethanol Content in Alcoholic Beverages

5. MEDICINAL USES
• Several antihistaminic, decongestant, multivitamin, and cough syrups contain
varying percentage of alcohol (2 to 25 %).
• Ethanol has been popular in the past as an antiseptic. Surgical spirit used even
today is mostly ethanol with a small quantity of methanol (90 to 95% and 5 to
10 % respectively), along with traces of castor oil and methyl salicylate.
• Ethanol sponging is an effective remedy for hyperthermia.
• Injection of dehydrated alcohol (absolute alcohol) in close proximity of nerves
or sympathetic ganglia is said to be effective for the relief of long lasting pain in
conditions such as trigeminal neuralgia.
• Antidote for methanol and ethylene glycol.

7. OTHER USES
Preservative— Rectified spirit (90 to 95 % ethanol) is used as
a preservative for viscera, for chemical analysis.
■ Fuel.
■ Ethanol is used to extract nucleic acids from whole tissue or
tissue culture in virtually all biotechnology processes.

8. UsualFatalDose
• One pint (approximately 550 ml) or quart (two pints or
approximately 1100 ml) of a strong distilled spirit such as whisky
taken in a short span of time can be lethal.
• The usual fatal dose corresponds to approximately 6 grams of
ethanol/Kg body weight (adult); 3 gm/Kg (child).
• In terms of blood alcohol, a level in excess of 400 to 500 mg/100
ml is usually considered to be lethal. However there is a great deal
of controversy regarding this since there are case reports of
individuals succumbing to much lower blood alcohol
concentration (BAC), while there have been reports of survival
even with a BAC of over 1000 mg.

9. TOXICOKINETIC
S
OF ETHANOL
Ethanol is toxic by oral, inhalation, subcutaneous, intravenous,
intra-arterial, intraperitoneal, and dermal routes.
Following oral administration, ethanol is rapidly absorbed from
the stomach (20%) and small intestine (80%). MAC in blood is
reached in 30 to 90 minutes following the last drink.
Following an equivalent dose of ethanol, women achieve a
higher blood alcohol level than do men as a result of decreased
gastric alcohol dehydrogenase activity
MAC=Maximum or peak alcohol concentration

10. TOXICOKINET
ICS
OF ETHANOL
More than 90% of ethanol ingested is
metabolised in the body, and only 5 to 10% is
excreted unchanged by the kidneys, lungs, and
sweat.
Excretion of ethanol by the lungs obeys
Henry’s Law

11. HENRY’S LAW
It is the ratio between the concentration of ethanol in the
alveolar air and the blood is constant. This alveolar
air/blood constant (1 : 2100) forms the basis for reliably
estimating blood alcohol concentration by breath analysis

12. ALCOHOL METABOLISM
Metabolism of alcohol is accomplished through 3
pathways in the liver:
1.Alcohol dehydrogenase pathway
2.Microsomal ethanol oxidising system (MEOS, located on the
endoplasmic reticulum)
3.Peroxidase-catalase system (in the hepatic
peroxisomes).

13. ALCOHOLIC DEHYDROGENASE
PATHWAY

14. MICROSOMAL ETHANOL
OXIDISING SYSTEM

15. PEROXIDASE-CATALASE SYSTEM

16. REACTIONS

17. In adults, the average rate of ethanol metabolism is 100 to 125 mg/kg/hr
in occasional drinkers, and upto 175 mg/kg/hr in habitual drinkers. The
blood alcohol level generally falls at a rate of 15 to 20 mg/100 ml/hr. This
may be higher ( upto 30 mg/100 ml/hr) in chronic alcoholics.
ETHANOL METABOLISM RATE
One standard drink contains
14g of pure alcohol

18. MECHANISM OF ACTION
Ethanol acts by enhancing gamma aminobutyric acid (GABA)-
nergic function through interaction with GABA A receptors and
associated chloride ion channels. However some investigators
are not convinced by this theory.
The second theory which appears to be more convincing has to
do with N-methyl-d-aspartate (NMDA) ligand gated, glutamate
receptors. NMDA receptors mediate neurotoxicity by increasing
permeability to calcium and regulate neuronal long-term
potentiation. Studies demonstrate that in the acute form of
ethanol use, NMDA receptor function is inhibited, while chronic
ethanol use results in up-regulation of NMDA receptors.

19. PHARMACOLOGICAL EFFECTS
Inhibitory control mechanisms in the brain, person becomes expansive, garrulous
and may demonstrate emotional lability with mood swings, sensory and motor
disturbances general impairment of CNS function, and finally coma supervenes.
Tachycardia and vasodilation of cutaneous vessels with resultant warm and
flushed skin. No beneficial increase in coronary blood flow occurs; in fact there
may be appreciable vasoconstriction which can aggravate existing angina. recent
studies have indicated that regular use of moderate amounts of ethanol is
associated with reduced risk for coronary heart disease
Ethanol normally stimulates salivary and gastric secretion but if the concentration
is too high (> 40%) they are inhibited, and the GI mucosa becomes congested and
inflamed leading to erosive gastritis. Regular intake of excessive amounts of
ethanol leads to chronic gastritis, pancreatitis, and cirrhosis of liver.
Ethanol is an aphrodisiac induces diuresis by inhibition of antidiuretic hormone.
Chronic ethanol consumption can lead to impotence, sterility, testicular atrophy,
and gynaecomastia (because of hyper-estrogenisation, and reduced production
as well as enhanced metabolic inactivation of testosterone)
CNS
CVS
GIT
GENITO-
URINARY
SYSTEM

20. ACUTE ETHANOL POISONING
Blood Alcohol
Concentration
(mg/100 ml)
0 – 50
50 – 100
100 – 150
150 – 200
200 – 300
300 – 500
> 500
Stage of
Intoxication
Sobriety
Euphoria
Excitement
Confusion
Stupor
Coma
Death
Clinical Features
Near normal behaviour
Feeling of well being, sociability, talkativeness, increased self confidence, decreased
inhibitions, fine movements affected.
Emotional instability, impairment of memory and comprehension, increased reaction
time, mild ataxia
Disorientation, confusion, vertigo, diplopia, ataxia, slurred speech, staggering gait
General inertia, diminished response to stimuli, inability to stand or walk, vomiting
Unconsciousness, abolished reflexes, subnormal temperature, incontinence of urine and
faeces, respiratory compromise
Death due to respiratory failure

21. CHRONIC POISONING
GIT— Gastritis, periodic diarrhoea, increased incidence of oropharyngeal and oesophageal
cancer.
Liver— Fatty liver with portal hypertension, hepatitis, cirrhosis, increased incidence of hepatic
carcinoma.
Pancreas— Acute or chronic pancreatitis, pancreatic cancer.
CVS— Cardiomyopathy, dysrhythmias, hypertension.
CNS— Polyneuropathy, cerebellar degeneration, demyelination of corpus callosum
(MarchiafavaBignami disease), amblyopia, stroke.
RS— Aspiration pneumonia, alcohol-induced asthma.
Endocrine— Hypogonadism and feminisation in males, amenorrhoea, menorrhagia, and
infertility in females, pseudo-Cushing syndrome.
Blood— Anaemia, thrombocytopenia.
Skeletal muscle— Myopathy.
Neuropsychiatric— Memory disturbances (amnesia, blackout), delusions, delirium tremens,
Wernicke’s encephalopathy, Korsakoff’s psychosis, dementia, alcoholic hallucinosis.
Teratogenecity— Foetal Alcohol Syndrome (FAS)

25. ACUTE POISONING TREATMENT
a. Airway protection- ventilatory support.
b. Activated charcoal is NOT useful.
c. Stomach wash.
d. Thiamine 100 mg IV 30
e. Dextrose
1. Indications—If rapidly determined bedside glucose level is less
than 60 mg/100ml, or if rapid determination is not available.
2. Adult—25 grams (50 ml of 50% dextrose solution)
intravenously; may repeat as needed.
3. Paediatric—0.5 to 1 gram dextrose per kg as 25% dextrose
solution or 10% dextrose solution (2 to 4 ml/kg).
4. Precautions—Glucose administration should necessarily be
preceded by 100 mg of thiamine IV or IM if chronic alcoholism or
malnutrition is suspected, to prevent development of Wernicke’s
encephalopathy.

26. f. Intravenous fluids.
g. A variety of drugs have been tried to hasten the elimination of ethanol or
reverse its intoxicating effects, including naloxone, physostigmine, and caffeine.
None of them have been proved to be truly effective. Recently, flumazenil (3 mg
IV) has been shown to be effective (in experimental studies) in reversing the
respiratory depression associated with ethanol ingestion
h. Haemodialysis can eliminate ethanol 3 to 4 times more rapidly than liver
metabolism. May be useful in patients with excessive blood levels, impaired
hepatic function and in those whose condition deteriorates in spite of maximal
supportive measures. However, it is unusual for dialysis to be necessary to treat
even severe ethanol intoxication.

27. CHRONIC POISONING
Carbamazepine— It has been shown to be effective in treating alcohol
withdrawal, including delirium tremens.
Chlormethiazole— It is one of the most popular drugs used for alcohol
withdrawal abroad, and is administered in a rapidly reducing dosage over 6 to 7
days. However it is itself associated with a strong abuse potential.
Clonidine and gamma-hydroxybutyric acid have also shown promising results in
the treatment of withdrawal symptoms. The former is given at a dose of 60 to
180 mcg/hr IV, and the latter 50 mg/ kg, orally.
most recent entrants is tiapride, an atypical neuroleptic agent which is a
selective dopamine D2-receptor antagonist. the recommended dose is 400 to
1200 mg/day 6th hourly, while the maintenance dose subsequently to help
abstain from alcohol should not exceed 300 mg/day.

28. Aversion therapy
The main aim in the treatment of alcoholism is to
gradually wean away the patient from the clutches of
ethanol, once the acute manifestations of withdrawal
have been taken care of. This process referred to quit
loosely as de-addiction or detoxification, should be
undertaken only after admission to a hospital over a
period of several days, under close medical
supervision. The insatiable craving for alcohol that is
often present must be tackled effectively, and usually
requires strongly deterrent measures one of the more
successful ways is to administer a drug called
disulfiram. It is a disulfide molecule (tetra ethyl
thiuram)

29. PRINCIPLES OF DISULFIRAM
THERAPY
• Ensure that the patient is off alcohol
for a minimum period of 12 hours
before starting therapy.
• The usual dose of disulfiram is 250
mg/day which may have to be taken
for an indefinite period of time. Such
chronic use unfortunately often
produces side effects like halitosis,
pruritis, headache, drowsiness,
impotence, peripheral neuropathies,
depression, mania, psychosis, and
hepatotoxicity.

30. THANK YOU