ALCOHOL

Dr. Kaschev Shrestha

1
 Objectives

■ Introduction to Ethanol
■ Types
■ Mechanism of action
■ Metabolism
■ Acute and chronic poisoning (Sign and symptoms)
■ Diagnosis
■ Withdrawal symptoms

2
 Introduction to ethanol
■a transparent, colorless, volatile liquid having a
characteristic odor and a burning taste

■specific gravity : 0.79.

■produced by the enzymatic action of yeasts on vegetable

substrate containing sugars.

■Previously, Safe limit: <21 units ( 168-210 g/wk) -men

< 14 units (98-140 g/wk)- women 3
Commercial Preparations of
Alcohol
■Absolute alcohol

■Rectified spirit

■Industrial methylated spirit

■Surgical spirit

4
Various country liquors

5
Proof Spirit

■ It is used to express concentration of alcohol in alcoholic beverages.

■ It referes to that concentration of ethanol which weighs exactly 12/13
of the weight of an equal volume of distilled water at 11* Celsius
■ 100 proof UK= 57.06% ethanol by volume or 48.24% ethanol by
weight

6
Absorption

■ Following absorption, concentration in blood

reaches a maximum in about 45-90 minutes after
ingestion.
■ Blood alcohol concentration ( BAC) is represented
by a graph.

7
 Factors that interfere with absorption
Increased absorption Delayed absorption

Hard drinks (Higher alcohol concentration) Beer, wine (lower alcohol concentration)

Warm drinks (capillary dilation) Cooled drinks

Drinks taken on empty stomach Intake with food (Delayed gastric emptying)

Diluted alcohol (taken with water) Concentrated alcohol (Neat drink)

Drinks taken with carbonated drinks Drinks taken with water or juices when
compared to carbonated drink

Individuals after gastrectomy Achlorhydria

Absorption of alcohol is delayed in concentrated drinks due to gastric mucosal irritation and pyloric
spasm.
Mixing of drinks can cause increased gastric emptying and thus increased absorption from intestine
8
Action

■ Acts mainly on the CNS.

■ Acts as a depressant of specialized and sensitive
cells of cerebral cortex with release of inhibitory
tone, leading to unrestrained behavior.
■ Followed by depression of vital centers of medulla
producing coma and death.
■ Also acts as a hypnotic, diaphoretic, and in small
doses as an appetizer.

9
Metabolism

10
Distribution

■Distributed to all body tissues proportional to their

water content.
■Aqueous compartment:
 Female/Obese>Male

■Attains equilibrium with a constant BAC with other

body fluids, the ratio being:
Blood: Urine = 1:1.33
Blood: Exhaled air (breath) = 2100:1
Blood: Saliva = 1: 12
Blood : CSF = 1: 1.17 11
■ Excretion is mainly by the kidneys, lungs and skin
through urine, breath and sweat resp.

12
Sign and symptoms

13
 Acute alcohol poisoining

■Either in small dose at short intervals, or in one

big dose beyond capacity with BAC exceeding
150mg/100ml

■Causes- deliberately heavy drinking, accidentally

due to continuous inhalation of alcoholic vapors

14
 1. Stage of Excitement
( Blood Level : 50- 150 mg%)

 euphoric (sense of well- being)

 Actions, speech and emotions are less restrained
 Time and space perception is altered.
 Perform dancing, thrilling shows, carelessly and
fearlessly
 Might disclose secrets, show increase in
confidience but lack of self control.
 Lowering of visual acuity, nystagmus is present
 Mental concentration is poor and judgement is
impaired.
 Faculty of attention deteriorates 15
 2. Stage of in-coordination
(Blood level: 150-250 mg%)
■ Further depression of higher centers
– causes person to be morose/ cheerful/ irritable/ ill-
tempered/ excitable/ sleepy/ depending on dominant
impulses
■ Clumsiness, altered speech and fine finger movements.
■ Nausea and vomiting
■ Face: Flushed
■ Pulse: rapid
■ Sense of touch, taste, smell and hearing are diminished.
■ Hypothermia
■ Breath smells of alcohol, Pupils are dilated and react
16
 3. Stage of coma
(blood level > 250 mg%)

■ Thick, slurred speech

■ Coordination is markedly affected- becomes giddy, stagger
and fall.
■ Pulse is rapid.
■ Hypothermia
■ Pupils are contracted, but on stimulation of the person, e.g.
by pinching or slapping causes them to dilate with slow
return ( McEwan’s sign)
■ Patient passes into coma with stertorous breathing.
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Mechanism of toxicity

■ Alcohol crosses the blood brain barrier and causes CNS

depression
■ Frontal lobe depression-Causes mood changes and lack of
judgement
■ Occipital lobe depression-Causes visual disturbance
■ Cerebellar depression-causes motor incoordination,
decreased reaction time
■ RAS depression-loss of consciousness
■ Brain stem depression-CVS and respiratory depression
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 Mellanby effect

■ The physiologic effects of alcohol are more

pronounced when the blood level is rising, as
compared to levels attained at peak or plateau, or
when the level is falling.

■ Results from an acute intolerance to alcohol that

develops during intoxication.

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 Recovery
■ unless large quantity of alcohol is consumed in a
short time, recovery is rule
■ Alcoholic blackout
■ Micturition syncope-Alcohol induced postural
hypotension
■ pathological intoxication
■ With recovery, coma lightens into deep sleep.
■ wake up in 8-10 hrs with acute depression of mood,
nausea and headache ( alcohol hangover)

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 Fatal dose

■Depends upon age and habits of individual

and strength of alcohol ingested
■150-250 ml of absolute alcohol consumed
in 1 hr
■BAC>300mg/dl  risk of death
■BAC >400-500 mg % death

■Fatal period: 12-24 hours 21

 DEATH

If doesn’t recover from coma within 5 hr,

due to

 Shock

 depression of respiratory center

 aspiration of vomit

22
 Diagnosis

■The distinctive aroma

■Altered mental status (AMS)
■Confirmation by: analysis of blood ( serum
glucose level is done along with it)
■Possibility of intoxication with other drugs
should be considered.
■Blood/ urine sample indicated to screen for
opioid and other CNS depressants,
Benzodiazepines and barbiturates. 23
Diagnostic and statistical manual of
mental disorders (DSM-IV)
■ Recent ingestion of alcohol
■ Clinically significant maladaptive behavior or psychological
changes that developed during or shortly after alcohol ingestion
■ One or more of :
– Slurred speech - Unsteady gait
– Incoordination - Impairment in attention and
memory
– Nystagmus - Stupor or coma
■ Symptoms not due to general medical condition and are not
accounted for by another mental disorder

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Treatment

25
1. Stabilization of patient

26
2. Patients sedation (if necessary)
3. Acceleration of ethanol elimination-single
dose of Metadoxine (300-900 mg IV)

27
 Complications
■Holiday heart syndrome: Cardiac
arrhythmias (atrial fibrillation and ventricular
arrhythmias)
■Hypoglycemia, gastritis, pancreatitis, and toxic
psychosis
■Anemia, macrocytosis, elevated enzymes,
bilirubin and uric acid
■Zieve syndrome-a triad of jaundice, hemolytic
anemia, and hyperlipidemia that develops
secondary to alcohol-induced liver injury 28
Postmortem findings:

■ Odor of alcohol around the mouth and nose.

■ Congestion of conjunctiva
■ Rigor mortis is prolonged and decomposition is
retarded
■ Acute inflammation of the stomach with coating of
mucus.
■ All viscera are congested and smells of alcohol
■ Blood is fluid and dark
■ Brain is edematous and congested
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 Medico- legal aspects:
■ Medical and drug related conditions must be excluded
before diagnosis, to avoid medical negligence
■ Strong association between binge drinking and violent
crimes; homicide, robbery, assault and sexual offences
■ Increased risk of injury and accidents
■ A patient with altered mental status is simply considered
intoxicated without consideration of other possible causes.
Hypoglycemia should always be sought in such cases.

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 Chronic alcoholism

■ A Chronic, progressive disease characterized by

tolerance and physical dependence to ethanol and
pathological organ changes.

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It is characterized by a gradual physical, mental and moral
deterioration
■ Alcohol hepatitis and cirrhosis ( leading to liver failure),
Alcohol hallucination
■ B1 deficiency (Wernicke’s Korsakoff’s psychosis)
■ Chronic gastritis and peptic ulceration (leading to
absorption defects), Cardiomyopathies, Chronic
pancreatitis
■ Dependence
■ Encephalopathy
■ Fetal alcohol syndrome (teratogenic effects-mental
retardation, microcephaly, facial abnormalities and growth
deficiency) 32
■ Mallory Weiss syndrome (Lower esophageal mucosal tear
and hemorrhage)
■ Munich beer heart (cardiac dilation and hypertrophy in
heavy beer drinkers)
■ Marchiafava Bignami Syndrome (Degeneration of corpus
callosum-Dementia)

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Wernicke’s encephalopathy and
Korsakoff’s Psychosis
■ Vitamin B1 (thiamine)deficiency

■ Lesion in mammillary bodies, thalamic nuclei, hippocampi

■ Classical triad of ataxia, encephalopathy and
ophthalmoplegia

■ Amnesia, confabulation and polyneuropathy

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 Postmortem Appearance
 Gastric mucosa is deep reddish-brown with
patches of congestion or effusion, hypertrophied
 Liver is congested and shows fatty infiltration,
enlarged or cirrhotic or contracted
 The kidneys show granular degeneration
 The heart is dilated and shows fatty degeneration
 Brain with shrinkage of cerebral cortex (grey
matter) is common in chronic alcoholics

35
 Treatment

Consists of medicinal therapy, condition reflex therapy and

psychotherapy

Medicinal therapy
■ Antabuse (Disulfiram) -given as aversion technique
■ Aldehyde dehydrogenase inhibitor which causes
accumulation of acetaldehyde resulting in unpleasant
effects
Symptoms: Flushing, palpitation, nausea, vomiting, anxiety,
tightness of chest, hypotension, sweating, throbbing
headache, giddiness, sense of impending doom and
abdominal cramps appear due to which patient dislikes 36
■ Contraindications: Coronary artery
disease, liver failure, chronic renal failure,
peripheral neuropathy, muscular disease,
history of psychosis and pregnancy (1st
trimester).

37
■ Condition reflex therapy-Alcoholic drinks given
with drugs that casues nausea and vomiting for a
week
■ Supportive therapy- (alcohol anonymous)
■ Nutrients, vitamins and gradual return to a normal
balanced diet.
■ Symptomatic treatment

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Withdrawal symptoms

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Common Alcohol Seizures Delerium Tremens
abstinence hallucinations
Syndrome

6-8 hours 24-36 hours 48 hours 3-5 days

Nausea, headache, Auditory and visual Clonic tonic , Fever, confusion,

irritability, insomnia, hallucinations Unconsciousness hallucinations and
tremors, anxiety death

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■ Withdraw
■ Insomnia
■ Tremors, Tachycardia
■ Hallucinations
■ Hypertension
■ Diaphoresis, Delirium tremens, Delusion
■ Rum fits
■ Anxiety, agitations
■ Withdraw 41
Clinical syndromes associated
with chronic alcoholism
■ Delirium tremens
■ Alcoholic hallucinosis
■ Korsakoff’s psychosis
■ Wernicke’s encephalopathy
■ Marchiafava- Bignami syndrome
■ Alcoholic paranoia
■ Alcoholic seizures

42
 Delirium Tremens

■This is an acute organic brain syndrome,

usually seen within 2–4 days of complete
absence from heavy alcohol drinking in
chronic alcoholics, and most severe alcohol
withdrawal syndrome

43
 Causes

■ Sudden excess or sudden withdrawal of alcohol

■ Long continual ingestion of alcohol
■ Shock due to severe trauma, e.g. fracture in a
chronic alcoholic
■ Acute infections, like pneumonia or influenza in a
chronic alcoholic

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 Signs and symptoms
There is an acute attack of insanity in which there is:
■Clouding of consciousness with disorientation in time
and space, loss of memory
■Coarse muscular tremors of face, tongue and hands
■Insomnia with reversal of sleep-wake cycle, and loss
of memory
■Psychomotor agitation, ataxia, uncontrollable fear,
and tendency to commit suicide/homicide/violent
assault or cause damage to property

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■ Marked autonomic disturbances with tachycardia,
fever, sweating, hypertension and pupillary dilatation
■ Peculiar type of delirium of horrors due to
hallucinations of sight and hearing
■ Tactile hallucinations of insects and ants crawling
under the skin or on the beds may occur

46
 Treatment

■ Diazepam (40–80 mg/day in divided doses) is used

■ Oral multi-B vitamins, including thiamine 50–100mg
is given daily for a week or more.

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■ In some, only restoration of alcoholic drinks helps.
■ Symptomatic treatment.

48
 Medico-legal aspects

■ It is a medical emergency and should be treated

on an inpatient basis
■ When a person in delirium tremens commits any
illegal act, he is not held responsible by the
reason that he/she is considered to be mentally
unsound during this state

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 Alcoholic Hallucinosis
■ It is a state of hallucination, mainly auditory with
systematized delusions of persecution lasting from weeks
to months
■ Occurs during abstinence in 2% of patients who have
been on regular alcohol till then.
■ Psychiatric emergency, requiring hospitalization, sedation
and close monitoring.
■ recovery occurs in a month.
■ may become homicidal or suicidal in response to his
hallucination.
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■Alcoholic peripheral neuropathy:
Symptoms of alcoholic polyneuritis are
weakness, pain in extremities, wrist and foot
drop, unsteady gait, loss of deep reflexes and
tenderness of muscles of arms and legs.

■Alcoholic paranoia:
In this, there is a fixed delusion, but no
hallucinations. Patient becomes suspicious of
the motives and actions of those he meets and
of his family members.
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■Alcoholic seizures (‘rum fits’):
In alcohol dependence persons, generalized tonic
clonic seizure may occur after 12–48 h of heavy
bout of drinking alcohol. Multiple seizures are more
common than single seizure. Sometimes, status
epilepticus and delirium tremens may be
precipitated

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54
Methanol poisoning
■ Methyl alcohol/ wood spirit/ wood naptha/ carbinol/ wood alcohol

■ three ingredients-
 90 per cent by volume ethyl alcohol
 9.5 per cent wood naphtha
 0.5 per cent crude pyridine

■ PHYSICAL PROPERTY: colorless, volatile liquid with odor to ethyl

alcohol and a burning taste

■ USES: in industries as solvent, in laboratories with ethanol as an

antiseptic spirit
 ABSORPTION AND EXCRETION

 rapidly absorbed from stomach, SI, lungs and skin

 achieves 30-90 min after ingestion

 oxidation is slow, 15% of ethyl alcohol

 Methanol -> formaldehyde -> formic acid -> folic acid -> CO2 and
water

 80% is excreted unchanged from lungs and 3-5% in urine

 ACTION

■ CNS depressant and increased serum osmolality

- formic acid causes high anion gap metabolic acidosis and retinal
toxicity.
 SIGNS AND SYMPTOMS

Within 12-24 hours

 GIT - nausea, vomiting, cramps spirit like odor - mouth, dehydration
 RS - dyspnea, cyanosis, respiratory depression
 CNS - headache, dizziness, vertigo, restlessness, muscular weakness,
hypothermia, delirium, amnesia, convulsion, coma
 Renal - acidic and scant urine, acidosis
 Pancreas – pancreatitis

 Ocular - pupils: fixed and dilated,

-visual disturbances like photophobia, snowfield vision, scotoma,
decreased light perception, decreased visual fields causing temporary or
permanent blindness due to atrophy and optic neuritis due to
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61
 DOSE

■ > 20mg/dl is considered toxic

■ Fatal dose : range is 30-240

■ Fatal period: 24-36 hours

■ Lab – Blood MeOH levels

 TREATMENT
• Gastric lavage- 5% NaHCO3 is used and 500 ml is kept in stomach
• Oral NaHCO3, 2g in 250 ml water 4 hourly
• Folate therapy- folinic acid (50-75mg every 6 hourly)

• Administration of ethanol as competitive antagonist

• Antidote : 4-methylpyrazole

• Hemodialysis
• Protect eye from sunlight
 POSTMORTEM FINDINGS
■ External - cyanosis, postmortem staining, frothing, purple skin due to
pyridine
■ Internal :
 GIT - congestion and inflammation of mucus membranes with small
hemorrhages
 Lungs - congested and oedematous
 Liver - necrosis and fatty changes
 Kidney - tubular degeneration
 Brain - oedematous and focal hemorrhage
 Eyes - may show retinal oedema or optic atrophy.
 MEDICO-LEGAL ASPECTS
■ Accidental consumption of cheap alcohol

■ Intoxicating beverage when ethanol is not available

■ Accidental poisoning in children

 ETHYLENE GLYCOL

■ major constituent of antifreeze solutions

■ clear, colorless, odorless, non-volatile liquid

■ bitter-sweet taste

■ Absorbed through the skin

■ Ethylene glycol itself is not toxic, but the toxicity is due to
metabolites glycolic and oxalic acids which inhibits oxidative
phosphorylation.

 Oxalic acid combines with calcium to form calcium oxalate

crystals which accumulates in the proximal convoluted
tubules causing renal failure.

 Metabolic acidosis occurs from glycolic acid.

 SIGNS AND SYMPTOMS
■ CNS symptoms
 usually develop within half hour to 12 h after ingestion.
 nausea, vomiting, slurred speech, tipsy sensation, severe headache, delusions,
dizziness, feeling of breathlessness, convulsions and coma.
■ Cardiorespiratory symptoms
 usually appear 12– 24 h after ingestion
 Tachycardia, tachypnea and congestive heart failure are present.
■ Renal: Acute tubular necrosis.
 usually is seen 24–72 h after ingestion.
 Oxalate crystals are seen in the urine.
 Death occurs from renal failure or heart attack.
■ FATAL DOSE: 100-200 ml.

■ FATAL PERIOD: Few hours to 3 days.

■ TREATMENT:
 Gastric lavage is done. Charcoal is not very effective.

 Treatment is similar as for methanol.

■ POSTMORTEM FINDINGS - Non-specific findings.
 Organs are congested.
 Mucous membrane of the GIT is congested and inflamed.
 Cerebral edema, chemical meningoencephalitis, liver and kidney
damage may be seen.
 Oxalate crystals are seen in the brain, spinal cord and kidneys.

■ MEDICO-LEGAL ASPECTS:
 Extensively used as industrial solvent, coolant and antifreeze,
agent for motor engine
 Poisoning is accidental or suicidal in nature.
CHLOROFORM
■ inebriant cerebral poison.

PROPERTIES
■ Heavy, colourless, volatile liquid
■ Strong odour
■ Burning sweet taste

ACTION
■ acts as an anaesthetic and respiratory depressant.
 SIGNS AND SYMPTOMS

• Oral ingestion - symptoms are similar to alcohol.

■ burning pain in the mouth, throat and stomach and vomiting.
■ Within ten minutes, unconsciousness and coma with slow
stertorous breathing occurs
■ Pupils are dilated and pulse feeble, rapid and irregular.
• Nasal inhalation - produces four stages:
Analgesia, excitement, anaesthesia and paralysis.
■ All the muscles are relaxed, pupils dilated and reflexes are lost
completely.
■ Body temperature is subnormal.
■ Death is due to cardiac or respiratory failure.
 Fatal dose: 30 ml by mouth (>0.04% in blood).
Fatal period: 30 minutes.

TREATMENT
• Orally ingested cases -
gastric lavage, demulcent drinks, and stimulants and symptomatic
measures.

• Nasally inhaled cases –

give artificial respiration, oxygen and cardiac stimulants.

• Maintain body warmth.

 POSTMORTEM APPEARANCES

■ They are not characteristic except marked congestion and chloroform

odour.

■ Internal examinations reveal:

• Irritation of the gastrointestinal and respiratory mucosa
• Chloroform odour for contents of the stomach, in the serous cavities,
lungs and brain
• Findings of asphyxia predominate when death is due to Inhalation
poisoning.
 MEDICOLEGAL IMPORTANCE

■ Chloroform was the first general anaesthetic used, but presently is

being used as an industrial solvent

■ Poisoning is usually accidental when liquid chloroform is swallowed

accidentally

■ Delayed chloroform poisoning was common even after 2-4 days of

recovery from general anaesthesia.
ETHER
 inebriant cerebral poison

PROPERTIES
■ colourless, volatile, highly inflammable liquid
■ penetrating ethereal odour and sweetish pungent taste

ACTION
■ Ether acts as an anaesthetic and respiratory depressant.
 SIGNS AND SYMPTOMS

• ORAL INGESTION - burning of throat, oesophagus and stomach,

nausea, vomiting, followed by inebriation as with alcohol
• NASAL INHALATION - same as chloroform.

■ FATAL DOSE: 30 ml by mouth.

■ FATAL PERIOD: May be immediate due to syncope during
anaesthesia - rarely.

■ TREATMENT: Gastric lavage, demulcents, stimulants and

anticonvulsants. Maintain blood pressure.
 POSTMORTEM APPEARANCES

• Smell of ether on opening the body

• Congestion of proximal gastrointestinal tract when taken

orally

• Findings of asphyxia, oedematous lungs and brain.

Abundant mucus in the respiratory tract.

 MEDICOLEGAL IMPORTANCE

•Accidental deaths are common while administering

anaesthesia (if dies due to anaesthesia - report to the police
immediately).

• An alcoholic addict may consume this when he or she is

deprived of alcohol.

• Presently, it is not used as anaesthetic, but as an industrial

solvent.
THANK YOU
 REFERENCES :

■ Textbook of Forensic Medicine and Toxicology, 2nd Ed - Nageshkumar

G Rao
■ Review of Forensic Medicine and Toxicology, 3rd Ed - Gautam Biswas
■ The Essentials of Forensic Medicine And Toxicology, 33rd Ed - K.S.
Reddy