Forensic

Toxicology
By
Dr. Houssein Nofal (PhD) MD.
Ass. Professor of Forensic Medicine
College of Medicine – KFU – Dammam
– SA
 Forensic Toxicology
 It is a branch of Forensic Medicine
dealing with Medical and Legal
aspects of the harmful effects of
chemicals on human beings.

 Forensic Toxicology is the study and

practice of application of toxicology
to the purposes of the law.
 Incidence
 The true incidence of poisoning in the
United States is unknown.

 Approximately 2 million cases are

voluntarily reported to poison control
centers each year,

 and officially, a rather steady figure of

about 700 deaths by poisoning is
reported each year.
 Incidence
 Children under age 6 account for
the majority of poisonings
reported,

 but adults account for the majority

of deaths by poisoning,
 most of which is intentional rather
than accidental.
most frequently most frequent deaths
reported poisonings by poisoning
1 - Household cleaning 1 - Antidepressant
supplies medications
2 - Analgesics (aspirin, 2 - Analgesics (aspirin,
acetaminophen) acetaminophen)
3 – Cosmetics 3 - Street drugs
4 - Cough and cold 4 - Cardiovascular drugs
remedies
5 - Plant scrapes and 5 - Alcohol
insect bites
6 – Pesticides 6 - Gases and fumes
7 - Topical creams and 7 - Asthma therapies
lotions
8 - Hydrocarbons (gasoline, 8 - Industrial chemicals
kerosene)
 Paracelsus (1493-1541) once said

 "All substances are poisons; there is none

which is not a poison.
The right dose differentiates a poison and
a remedy.“

 It is not easy to distinguish toxic from non

toxic substances.

 A key principle in toxicology is the

Dose-Response Relationship.
 There is a graded dose-response relationship in
individuals,
and
a quantal dose-response relationship in the
population.

 The quantal dose-response is the more important

one, used to determine the median lethal dose
(LDm)
and judge what percentage of the population is
affected by a dose increase.

 Quantal is a term meaning "all or none",

and comes closest to a classification of
whether something is safe or
toxic.  
 Manner of Death by
poisoning
 Accidental poisoning cases are Most, but a
large number are deliberate.

 Suicidal poisoning is probably the most

common method of self-destruction.
 Corrosive agents (strong acids or alkalis) are
used rarely because less painful substances
are available.

 Homicide by poison is rare nowadays.

 Such weapons of the old fashioned poisoner as

arsenic, strychnine or cyanide are so easily
detected that they are rarely used nowadays.
 Poisoning
 Suicidal:
 (KCN, HCL, Opium, Barbiturates,
organophosphorus, oxalic acid oleander
etc),

 Homicidal
 (arsenic, aconite, thallium,
organophosphorus, oleander, etc.).

 and Accidental poisoning are seen also.

 Poisoning
 Older poisons like opium and arsenic are
replaced by newer poisons.

 Common homicidal poisons are:

Arsenic, Antimony, Oleander, Nux-Vomica,
Madar, powdered glass and aconite.

 Cattle Poisoning is also common, the

poison used are Arsenic, Yellow oleander,
zinc phosphide, nitrates, aconite, Abrus
precatrotius etc.
 Important Definitions:
 Toxicology
 It is the science dealing with

properties,
action,
toxicity,
fatal dose,
detection estimation of,
interpretation of the result of
toxicological analysis
and management of Poisons.
 Important Definitions:
Poison:
A Poison is defined as any substance
which when administered in living body
through any route (Inhalation, Ingestion,
surface absorption etc)
will produce ill-health
or death
by its action which is
due to its physical, chemical or
physiological properties.
E.g.: alphose, sulphuric acid, arsenic etc.
 Important Definitions:
 Drug (WHO 1996):
 “Drug is any substance or product that is
used or intended to be used to modify or
explore physiological systems or
pathological states for the benefit of the
recipient.”

 e.g.: paracetamol, ciprofloxacin, salbutamol,

oestrogen, insulin etc.
 Important Definitions:
 Clinical Toxicology:
 Deals with human diseases caused by, or
associated with abnormal exposure to
chemical substances.

 Toxinology
 refers to toxins produced by living
organism which are dangerous to man,
 e.g.: snake venom, fungal and bacterial toxins
etc.
 Important Definitions:
 Chelating Agents:
 are the substances which act on absorbed
metallic poisons.
 They have greater affinity for metals as
compared to endogenous enzymes.
 The complex of agent and metal is more
water soluble than metal itself, resulting in 
higher renal excretion of the complex.

 E.g.: British anti-lewisite (B.A.L., dimercaprol),

E.D.T.A. (ethylene diamine-acetic acid),
Penicillamine (Cuprimine),
Desferroxamine etc.
 Important Definitions:
 Ecotoxicology:
 It is concerned with the toxic effects of
chemical and physical agents on living
organisms, especially in population and
communities within defined population.
 Important Definitions:
 Acute poisoning
 is caused by an excessive single dose,
or several dose of a poison
taken over a short interval of time.

 Chronic Poisoning
 is caused by smaller doses over a period of
time, resulting in gradual worsening.
e.g.: arsenic, phosphorus, antimony and
opium.
 Important Definitions:

 Subacute poisoning
 shows features of both acute and
chronic poisoning.

 Fulminant poisoning
 is produced by a massive dose. In this
death occur rapidly, sometimes
without preceding symptoms.
 Important Definitions:
 Parasuicide
 (attempted suicide or pseudicide) is a
conscious often impulsive, manipulative
act, undertaken to get rid of an intolerable
situation.

 Culpable Homicide:
 Causing death of a person by an act,

with the intention of causing such bodily

injury and is likely to cause death,
or with the knowledge that he is likely, by such
an act to cause death.
 Important Definitions:
 Antidote:
 Antidotes are substances which
counteract the effect of poison.

 They are divided into Mechanical,

Chemical,
Physiological
and specific receptor antagonists.
 Toxin & Poisons
 A toxin is any material exerting a
life threatening effect upon a
living organism.

 Poisons are a subgroup of toxins

 Toxin & Poisons
 Poisons generally enter the body in a single
massive dose, or accumulate to a massive dose
over time.

 Toxins work in minute quantities or low levels,

requiring sensitive analytical instruments for
detection.

 Some toxins have medicinal value, but many

produce irreparable damage.

 Some toxins have antidotes and others do not.

 Toxin & Poisons
 Poisons can be combated by prompt
treatment, and most organ damage
(except for serious CNS injury) may be
repairable. 

 Whereas poisons are somewhat easily

identifiable by their symptoms, many
toxins tend to disguise or mask
themselves.
 Sources of Poison
1. Domestic or household sources.
2. Agricultural and horticultural sources.
3. Industrial sources
4. Commercial sources.
5. From uses as drugs and medicines
6. Food and drink
7. Miscellaneous sources - snakes bite
poisoning,
city smoke,
sewer gas poisoning
etc.
1. Domestic or household sources - detergents,
disinfectants, cleaning agents, antiseptics,
insecticides, rodenticides etc.
2. Agricultural and horticultural sources- different
insecticides, pesticides, fungicides and weedicide.
3. Industrial sources- In factories, where poisons are
manufactured or poisons are produced as by
products.
4. Commercial sources- From store-houses,
distribution centers and selling shops.
5. From uses as drugs and medicines – Due to wrong
medication, overmedication and abuse of drugs.
6. Food and drink – contamination in way of use of
preservatives of food grains or other food material,
additives like colouring and odouring agents or other
ways of accidental contamination of food and drink.
7. Miscellaneous sources- snakes bite poisoning, city
smoke, sewer gas poisoning etc.
 Classification of poisons
 According to the site and mode of action.
a) Local Action
b) Remote Action
c) Combined local and remotes action

 According to motive or nature of use.

1. Homicidal:.
2. Suicidal:
3. Accidental:.
4. Abortifacient:.
5. Stupefying agent:
6. Agents used to cause bodily injury:
7. Cattle Poison:
8. Used for malingering
 Classification of poisons
 According to the site and mode of
action
a) Local Action
 Corrosive
 Irritant

b) Remote Action
 Neurotics
 Cardiac Poisons

c) Combined local and remotes action

 Classification of poisons
 According to the site and mode of action
a)Local Action
 Corrosive
 Strong Acid: mineral acid and organic acid
 Strong alkali
 Metallic: Mercuric Chloride
 Irritant
 Mechanical: Glass Powder
 Chemical
 Inorganic: weak acid, weak alkalies,
Inorganic non-metals, Inorganic Metals.
 Organic: Chemical preparations, Animal and
vegetable origin.
 Classification of poisons
b) Remote Action
 Neurotics
 C.N.S. Poisons
I. Somniferous: opium and its alkaloids, Barbiturates.
II. Inebriant (Intoxicant): Alcohol, ether, Chloroform.
III. Stimulant
IV. Deliriant: Dhatura, Belladona, Hyocyamus, cannabia
indica.
V. Stupefaciant
VI. Hallucinogens
VII. Convulsant:

 Spinal (Convulsant)
I. Strychnos Nux Vomica

 Peripheral Nerves
I. Local Anaesthetics: Cocaine, Procaine.
 Classification of poisons
 Remote Action
 Cardiac Poisons
I. KCN, NaCN, Digitalis, Aconite, Nicotine,
Quinine, Oleander
II. Asphyxiants: Carbon Dioxide(CO2), CO,
hydrogen sulphide(H2S)
III. Nephrotoxic: Oxalic Acid, Mercury,
Cantherides
IV. Hepatotoxic: Phosphorus, Carbon
tetrachloride, Chloroform.
V. Miscellaneous: Food Poisons.

c) Combined local and remotes action

 Classification of poisons
 According to motive or nature of use:
1. Homicidal: Arsenic, Aconite, Digitalis, Abrus
Precatorius, Strychnos nux-vomica.
2. Suicidal: Opium, Barbiturate, Organophosphorus,
carbolic acid, copper sulphate.
3. Accidental: Aspirin, organophosphorus, copper
sulphate, snakes bite, Ergot, CO, CO2, H2S.
4. Abortifacient: Ergot, Quinine, Calotropis,
Plumbago.
5. Stupefying agent: Dhatura, cannabis, chloral
hybrate.
6. Agents used to cause bodily injury: Corrosive
acids and alkalies.
7. Cattle Poison: Abrus precatorius, Calotropis,
plumbago.
8. Used for malingering: semicarpus anacardium.
 Ideal Suicidal poison:
 should be easily available,
No bad taste,
cause No pain,
cheap,
highly toxic,
tasteless or pleasant taste,
capable of being taken with
food or drink..
 Ideal Homicidal poison:
 it should be cheap,
easily available,
colourless
tasteless
odourless,
highly toxic,
No residual product lest,
S/S resembles natural diseases,
No antidote,
Shows no post-mortem changes
capable of being administered with food
or drink.
 Route of
Administration/absorption
1. Oral (commonest) e.g.: alphos, acids,
2. Inhalation: gas poison
3. Parenteral (IM, IV, Sub-Cutaneous,
Intra-Dermal)
4. Natural Orifices other than mouth
(Nasal, Rectal, Vaginal, Urethral),
5. Ulcers, wounds and intact skin.
 Fate of poison in body
 A part of the poison taken orally gets
eliminate unabsorbed by means of defecation
and vomiting.

 Before absorption the poison may exert its

effects in the G.I. Tract.

 When absorbed, the poison reaches different

parts of the body and organs through
circulation.

 Some poisons reach some tissues easily. Others

may not cross some tissue barrier.
 Fate of poison in body
 Cumulative poisons get accumulated in some
organs or tissues.
 A part of poison is eliminated as such through
different route of elimination.

 But major part is detoxified or metabolized in

the body and than excreted after exerting its
toxic effects on the body. Liver is the main organ
to detoxify or metabolize most of the poisons.

 Certain poisons like Chloroform, Phosphorus,

Nitrates and Acetic acid disappear by
evaporation or oxidized or destroyed in the
body and no trace of them can be detected in
the body of post-mortem is delayed.
 Excretion of poisons
 Unabsorbed poisons are excreted through
faeces and vomitus.

 Absorbed poisons are excreted mostly by

urine.

 A part of volatile poison is exhaled out.

 Some portion of poison is excreted through

bile, saliva, milk, sweat, tear, hair and nails.
Factors influencing the actions of
a poison in the body
1. Quantity
2. Physical form
3. Chemical form
4. Concentration
5. Condition of the stomach
6. Route of administration
7. Age
8. State of body health
9. Presence of disease
10. Intoxication arid poisoning states
11. Sleep
12. Exercise
13. Cumulative action of poisons
14. Tolerance
 Factors influencing the
actions of a poison in the
body
 1. Quantity:
 A high dose of poison acts quickly and often
resulting in  fatal consequences.

 A moderate dose causes  acute poisoning.

 A low dose may have sub-clinical effects and

causes  chronic poisoning on repeated
exposure.

 Very large dose of Arsenic may produce  death

by shock without dose irritant symptoms,
While smaller dose than lethal dose produces its
 therapeutic effects.
Factors influencing the actions
of a poison in the body
 2. Physical form:
 Gaseous or volatile poisons are very quickly
absorbed and are thus most rapidly effective.

 Liquid poisons are more rapid than solid

poisons.

 Some poisonous vegetable seeds may pass

through the intestinal canal ineffective when
taken intact due to their impermeable pericarp.
 But when taken crushed, they may be rapidly
fatal.
 Factors influencing the
actions of a poison in the
body
 3. Chemical form:
 Chemically pure arsenic and mercury are
not poisonous because these are
insoluble and are not absorbed.

 But white arsenic (arsenic oxide) and

mercuric chloride are deadly poisonous.

 Barium sulphide is deadly toxic

but barium sulphate is
non-toxic.
 Factors influencing the
actions of a poison in the
body
 4. Concentration (or dilution):
 concentrated form of poison
are absorbed more
rapidly
and are also more
fatal
but
there are some exceptions too.
 Factors influencing the
actions of a poison in the
body
 5. Condition of the stomach:
 food content presence of food-stuff acts as
diluent of the poison and hence protects the
stomach wall.
 Dilution also delays absorption of poison.
 Empty stomach absorbs poison most rapidly.

 In cases of achlorohydria, KCN and NaCN is

ineffective due to lack of hydrochloric acid,
which is required for the conversion of KCN
and NaCN to HCN before absorption.
 Factors influencing the
actions of a poison in the
body
 6. Route of administration:
 absorption rate is different for different
routes.

 7. Age:
 some poisons are better tolerated in some
age groups.

 Opium and its alkaloids are tolerated better by

elderly subjects but badly by children and infants.
 Belladonna group of drugs are better tolerated by
children than by adults.
 Factors influencing the
actions of a poison in the
body
 8. State of body health:
 A well built person with good health can
tolerate the action of poison better than a
weak person.

 9. Presence of disease:
 In certain diseased conditions some drugs
are tolerated exceptionally well
 e.g.: sedatives and tranquilizers are tolerated in
very high dose by manic and deliriant patients.
 Factors influencing the
actions of a poison in the
body
 10. Intoxication arid poisoning states
 In certain poisoning cases some drugs
are well tolerated, like, in case of
strychnine poisoning, barbiturates
and sedatives are better tolerated.

 Whereas in case of barbiturate

poisoning any sedative or tranquilizer
will accentuate the process of death.
 Factors influencing the
actions of a poison in the
body
 11. Sleep
 Due to slow metabolic process and depression of
other body functions during sleep, usually the
absorption and action of the poison is also slow.
 But depressant drugs may cause, more harm
during the state of sleep.

 12. Exercise
 Action of alcohol on C.N.S. is slowed during
exercise because more blood is drawn to the
muscles during exercise.
 Factors influencing the
actions of a poison in the
body
 13. Cumulative action of poisons:
 Preparations of cumulative poisons
(poisons which are not readily excreted from the
body and are retained in different organs of the
body for a long time) like lead may not cause
any toxic effect when enters the body in
low dose.

 But when such poisons enter over a long

period of time, may cause harm when their
concentration in different tissue reaches
high level due to their cumulative property.
 Factors influencing the
actions of a poison in the
body
 14. Tolerance
 may develop by individuals on long
term exposure to a particular poison.

 15. Idiosyncracy:
 some persons may react adversely to a
particular drug though the general
population tolerates the drug well.
 Symptoms and Signs
 The symptoms and signs may be
different for different poisons and
is responsible on the nature and
action of the poison.

 They can be local, remote or

combined and are will be taught
in the individual poisons.
 Poisons their Symptoms
Acids (nitric, Burns around mouth,
hydrochloric, sulphuric) lips, nose
Aniline (hypnotics, Skin of face and neck
nitrobenzene) quite dark
Arsenic (metals, mercury, Severe, unexplained
copper, etc.) diarrhea
Atropine (Belladonna), Pupil of eye dilated
Scopolamine
Bases (lye, potash, Burns around mouth,
hydroxides) lips, nose
Carbon monoxide (CO) Skin is bright cherry red.
Carbolic acid (or other Odor of disinfectant
phenol)
Cyanide Quick death, red skin,
 Poisons their Symptoms
Food poisoning Vomiting, abdominal
pain
Metallic compounds Diarrhea, vomiting,
abdominal pain
Nicotine Convulsion
Opiates Pupil of eye
contracted
Oxalic acid Odor of garlic
(phosphorous)
Sodium fluoride Convulsion
Strychnine Convulsion, dark face
and neck
 Symptoms and Signs
 Sometimes poisoning is difficult to recognise
but there are signs and symptoms that may
cause a doctor to think about poisoning.

 They are:
1. Sudden vomiting and diarrhoea
2. Unexplained coma in children and adults
known to have depressive illness
3. Rapid onset of a peripheral neuropathy
4. Rapid onset of neurological or
gastrointestinal illness in persons
occupationally exposed to chemical
 Diagnosis of poisoning

 In the Living
 In the Dead
 Diagnosis of poisoning
 In the Living
1. History of the case as stated by the patient himself and
his/her relatives or friend.
Full information about time of onset of the present
illness, Initial symptoms, progress, relation with food,
condition of other persons taking same food or drink,
possible source, any previous history of poisoning, H/o
depression, quarrel.
Also note down the colour, smell, consistency, taste
and quantity of the possible poisonous substance.
2. Symptoms and Signs.
3. Details of examination.
4. Preservation and laboratory investigation of vomitus,
excreta, stomach wash, scraps from any stains area on
the body, blood, stained part of the clothes, contents of a
doubtful container, left over ant part of food or drink.
 Diagnosis of poisoning
 In the Dead:
1. History of the case as stated by police or
relatives. H/o 2 or more vital points (1 how
long the victim survived after initial symptoms.
2. any treatment).
2. Post-mortem Examination (external and
internal)
3. Chemical Analysis: detection of poison
in the body fluids.
4. Preservation of viscera and other
material for lab. Examination.
 Postmortem Findings in Case
Of Death Due To Suspected
Poisoning
 External Examination
1. Postmortem Staining:
Deep blue - In case of asphyxiant poisons and aniline.
Bright red or cherry red - In case of CO and HCN
poisoning.
2. Deep Cyanosis - With opium and cardiac poisons.
3. Early Rigor mortis - With strychnine.
4. Early appearance of the sign of Decomposition -
With H2S gas.
5. Detectable Smell - In case of volatile poisons, opium
and HCN, KCN or NaCN.
 Postmortem Findings:
External Examination
6. Haemorrhagic spots under the skin
and mucus membrane: Phosphorus. .
7. Ulceration on lips and near the angles
of mouth - Corrosive poisons.
8. Stain near mouth and on hands -
Nitric acid and copper sulphate.
9. White froth from mouth and nose –
Opium and its alkaloids. .
10. Blood tinged froth from mouth and
nose Organophosphorus compounds.
 Postmortem Findings
External Examination
11. Alopecia, hyper pigmentation and
hyperkeratosis - Arsenic poisoning over
a long period.
12. Staining, erosion and ulceration near
the female external genitalia - Use of
abortifacient agents or torturing agents.
13. Injection marks - Injection of poisons
(snake bite or otherwise), sign of
treatment.
 Postmortem Findings in Case
Of Death Due To Suspected
Poisoning
 Internal findings:

 The G.I.T. should be examined very carefully

since signs of corrosive or irritant poisons are
likely to be find therein.

 These signs are Hyperemia,

Softening,
Ulceration
and Perforation.

 Apart from this below given is a brief note of

internal finding in cases of poisoning.
 Postmortem Findings
Internal findings:
1. Corrosion, ulceration and desquamation
of inner aspects of lips, mucus membrane
of mouth and tongue - Corrosive agents.

2. Soft, swollen, sodden, translucent,

bleached tongue and mucus membrane of
mouth- Corrosive alkali

3. Hardening of mucus membrane - Phenol

4. Phenol Yellowish discoloration - Nitric
 Postmortem Findings
Internal findings:
5. Bluish discolouration - Copper sulphate

6. Carbonization and charring- Conc.

Sulphuric acid

7. Chalky appearance and consistency of

teeth - Sulphuric acid

8. Blue lining in the gum - Chronic lead

poisoning
 Postmortem Findings
Internal findings:
9. Swollen gum, loose teeth, foetid smell -
Acute mercuric chloride poisoning; chronic
phosphorus poisoning
10. Corrosion, irritation, desquamation and
haemorrhage in the inner wall of the
esophagus - Corrosive and irritant poisons
11. Hardening and whitish discolouration –
Carbolic acid poisoning
12. Discoloration and staining of inner aspects of
mouth - With coloured poisons
13. Oesophageal stricture - A complication of
sulphuric acid ingestion
 Postmortem Findings
Internal findings:
14. Stomach
a) Thickening and softening of the wall -
Corrosive and irritant poisons
b) Hard wall- Carbolic acid
c) Hard and leathery wall- Formaldehyde
d) Hyperemia haemorrhage and desquamation
of mucus membrane.- Irritant poison
e) Laceration and sloughing – Corrosive poison
f) Perforation - H2SO4 and HN3
g) Yellowish discolouration of mucus membrane
- HNO3; Bluish - CuSO4;
Slaty grey – HgCl3
 Postmortem Findings
Internal findings:
14. Stomach
h) Stomach content –
Blood - Corrosive and irritant;
Yellowish – HNO3
Bluish - CuSO4
Luminous in dark - Phosphorus;
Detectable tablet - soneryl; Powder oxalic
acid, white arsenic;
Detectable smell - kerosene, alcohol,
chloroform, organophosphorus compounds,
chlorinated hydrocarbons, opium, cyanogen,
formaldehyde, phosphorus;
Detectable liquid - kerosene.
 Postmortem Findings
Internal findings:
15. Small
intestine –
May show irruption, sometimes may
show presence of poisonous remains.

16. Largeintestine - May show

ulcerations, as in case of HgCI3 similar
in appearance of ulcers of bacillary
dysentery. It particularly involves the
ascending and transverse colons.
 Postmortem Findings
Internal findings:
17. Liver –
 Different degenerative changes occur in
cases of poisoning with poisons like
phosphorus, carbon tetra-chloride,
chloroform, tetrachlorethylene and
many other poisons.
 The type and extent of the degenerative
changes occur depending on the type of
poison, dose, duration of the exposure
and physical condition of the patient.
 Postmortem Findings
Internal findings:
18. Kidneys –
 Swollen, reddish, soft, sometime greasy in
touch with haemorrhage in calyces and
other degenerative changes - cases of
poisoning with mercury, oxalic and carbolic
acid, phosphorus, cantharides, viper snake
venom and many others.

 In case oxalic acid poisoning, white powder

of oxalate crystals are present in the
tubules and the calyces .
 Postmortem Findings
Internal findings:
19. Urinarybladder – Haemorrhage in cases of
abrus precatorius, viper snake bite, cantharide
poisoning.

20. Larynx and trachea – Hyperaemic, inflamed

-In cases of inhalation of irritating gases leaking
of corrosive agents while ingestion vomiting;
froth in the lumen of trachea and larynx in case
of opium and organophosphorus poisoning.
 Postmortem Findings
Internal findings:
21. Chest
cavity -Smell of volatile poisons cyanogen,
opium etc. can be detected.

22. Lungs - Voluminous, congested, presence of

Tardieu's spots - In case of asphyxiants and
inhaled poisons.
Cut section gives blood stained frothy-fluid in
case of opium and other asphyxiants.

23. Heart-
Presence of subendocardial
haemorrhagic spots in cases of arsenic,
phosphorus, mercuric chloride etc.
 Postmortem Findings
Internal findings:
24. Brain and spinal cord –
 Congestion and edema of brain and spinal
cord in cases of cerebral and spinal poison (e.g.
strychnine)
 Brain – may be congested.
 oedematous with occasional haemorrhagic
points at places in cases of asphyxiant poisons.

25. Uterus and vagina –

 Staining, congestion haemorrhage,
ulceration in cases of attempted abortion by use
of local abortifacient agents.
Preservation of viscera and
other materials
 In all cases of poisoning
1. Stomach with its full contents.
2. Half of Liver or 500 gms
whichever is more.
3. A loop of Small Intestine.
4. Half of Each kidney.
5. Some portion of Spleen.
 In some particular poisons
1. Blood 100ml: in cases of absorbed poisons.
2. Urine 100ml in all cases where blood is preserved.
3. Part of both lungs in cases of Volatile poisons.
4. Heart in case of cardiac poisons.
5. Brain in cerebral poisons.
6. Spinal in spinal poisons.
7. Bones in arsenic and lead.
8. Hair in arsenic and copper.
9. Nails in arsenic.
10.Skin-scrap from areas stained with a suspected
poison.
11.Stained areas of dress, suspected packet of
poison, strips of tablets recovered from pocket.
 Preservative used
 For Viscera: absolute alcohol or rectified
spirit. Exception: alcohol, chloroform, chloral
hydrate, formaldehyde, ether, phosphorus
(alcohol prevents the luminosity of
phosphorus in dark) etc.

 Blood should be preserved in fluoride,

oxalate, E.D.T.A., gold chloride or citrate.

 Urine and clothes: without any

preservative.
 Management of a case of
poisoning
 Immediate resuscitative (Basic Management)
measures in comatose patient should be adopted
to stabilize respiration, circulation and the
correct CNS depression.

A. Airway: Opening Up and Cleaning the Airways

(oral cavity, Nostrils) of secretions, vomit or any
foreign body. Pull Tongue forward
B. Breathing: Supplemental Oxygen Therapy
should be administered
C. Circulation: I.V. Fluid administration
D. Depression of CNS should be corrected.
 Specific Management
1. Removal of patient from source
of exposure.
2. Removal of the unabsorbed
poison.
3. Diluting the poison
4. Elimination of absorbed poison
5. Use of specific antidote
6. Symptomatic treatment.
 Specific Management
1. Removal of patient from source of exposure: as
quickly as possible.
2. Removal of the unabsorbed poison.
In case of contact poison washing of affected
area with soap water with gentle rubbing will be
helpful.
In cases of ingested poisons Gastric lavage is
useful within 3 hours of ingestion and is done
by stomach tube (Ewald or Boas tube) or by
Ryle’s tube followed by emesis (physical or by
drugs like Ipecacuanha 1-2 gm, mustard oil 1 Tsf
in a glass of water, concentrated salt solution
6%, Zinc Sulfate 1-2gm in water, apomorphine
hcl 1-2ml o 3 mg /ml). In case of injected
poison ligature is applied above the wound.
In cases of inhaled poison the patient should be
 Specific Management
3. Diluting the poison and delaying the
absorption by water or food.
4. Elimination of absorbed poison
by increases urination (diuresis),
increased perspiration
(diaphoresis),
Dialysis, use of chelating
agents.
5. Use of specific antidote
6. Symptomatic treatment including
safeguarding respiration and maintenance of
circulation
 Counterindications of
gastric lavage with stomach
tube:

1. In corrosive poisons.
2. Convulsant poisons.
3. Unconscious or semi-conscious
patients
4. In infants and children: Ryle’s
tube or infant feeding tube is
used.
 Antidote
 Antidotes are substances which
counteract the effect of poison.

 They are divided into

Mechanical (physical),
Chemical,
Physiological
and specific receptor antagonists.
 Physical or Mechanical
Antidote
 It prevents the action of poison mechanically,
without
destroying or inactivating the damaging
actions of the poisons.

 E.g.: Adsorbents like activated charcoal,

Demulcents like egg albumin, starch or
milk,
Diluents like water or milk, bulky food like
boiled rice or
vegetables.
 Chemical Antidotes
 They are Substances which disintegrate
and
inactivate poisons
by
undergoing chemical reaction with
them.

 E.g.: Weak acids and alkali,

 common salt,
egg albumin,
KMNO4.
 Physiological Antidote
 They have their own action producing
signs and symptoms opposite to that
produced by the poison.

 E.g.: Naloxone for morphine,

Neostigmine for datura or
hyoscin group,
Barbiturate for strychnine.
 Serological Antidote
 Anti-snake venom serum for
snake bites poisoning.
 Universal Antidote
 It is a combination of physical and chemical
antidotes.
When the exact nature of poison is not known
then universal antidote is used which acts
against a wide range of poisons.

 Constituents Activated charcoal 2 parts

 Magnesium oxide 1 part
 Tannic acid 1 part
 Dose 1TSF (15gms) in a glass water (can
be repeated)

 Activated charcoal  for its adsorbent action,

Magnesium oxide  neutralizes acids poisons,
Tannic acid  precipitates alkaloids.
 Household Antidotes
1. Strong liquid tea (contains tannic acid)
precipitate alkaloid and metallic poisons.
2. Starch for iodine.
3. Milk and raw egg for mercury, arsenic,
heavy metal.
4. Flour suspension and mashed potatoes
can be used in place of activated charcoal.
5. Milk of magnesia or soap solution for acid
poisoning.
6. Orange, lemon juice or vinegar for alkali
poisoning.
 Chelating Agents
 They are the substances which act on
absorbed metallic poisons.
 They have greater affinity for metals as
compared to endogenous enzymes.
 The complex of agent and metal is more
water soluble than metal itself, resulting in
 higher renal excretion of the complex.

 E.g.: British anti-lewisite (B.A.L.,

dimercaprol),
E.D.T.A. (ethylene diamine acetic acid),
Penicillamine (Cuprimine),
Desferroxamine etc.
 B.A.L. (British Anti-
Lewisite)
 It is (2-3 dimercaptopropanol) has 2
unsaturated SH radicals which combines
with metal in circulation , thus tissue
enzymes are spared.

 It’s Useful in cases of Arsenic, mercury,

copper, bismuth, gold etc

 Dose: 3-4 mg/kg BW as a preparation of 10% with

20% Benzyl benzoate in arachis oil given deep intra-
muscular (may cause embolism on I.V. inj.)4 hourly
for first 2 days followed by twice daily for 10 days.
 E.D.T.A.
(Ethylene diamine tetra-acetic
acid)
 It combines with (Na+) sodium to form  sodium salt
and then
with (Ca++) calcium to form disodium calcium
edentate
which
combines with free metal and  inactivates it
biologically.

 It is best chelate for lead.

 Dose : for adults 1gm twice daily at 12 hour interval slow I.V.
Injection mixed with 5% glucose saline.
 Penicillamine
 It has stable SH radical which
combines with free metal.

 Dose:
30mg/Kg BW/Day in 4 divide doses
for 7 days.
 Desferroxamine
 It is specific antidote for iron.

 Dose: 8-12 gm orally.

For absorbed iron 2gm I.V. with
50% laevulose solution.
 Duties of a Registered Medical
Practitioner
in connection with poisoning cases
1) Try to save the life of the patient and give
emergency necessary treatment.

2) If necessary, the patient should be sent to a better

hospital, if possible a government hospital, if the
condition of the patients demands and permits the
shift.

3) Take a detailed history of the case as to when and

how the symptoms started,
what is the progress;
whether related to taking of any food or drink ;
whether the number of sufferer is more than one,
whether any treatment was already given,
and whether there is any history of previous
 Duties of a Registered Medical
Practitioner
4) The doctor should himself record full
history of the case, the signs and
symptoms and progress.

5) The doctor should collect and preserve the

vomitus, stool, urine, clothes stained with
poison or vomitus, doubtful container with
remaining part of the poison, if any, and if
necessary blood, for laboratory
investigations.

6) The doctor should arrange for a reliable

attendant of his own choice, for the patient.
 Duties of a Registered Medical
Practitioner
7) The doctor should inform the police station of the
area about the case irrespective of whether the
patient survives or dies and whether it appears to
be a case of suicide or homicide or accident..

8) If death is apprehended then arrangement for

recording dying declaration should be made.

9) In case of death, death certificate should mention

about the poisoning or suspected poisoning with
recommendation for post-mortem examination.
 COMMON POISONS AND
DRUGS
1. Corrosive poisons
2. Irritant poisons
3. Analgesic, Hypnotic, Tranquilliser, and
Narcotic poisons.
4. Stimulants, Excitants, and Convulsants
poisons.
5. Paralytic, Anticholinesterase and
Antihistamine poisons.
6. Gaseous and Volatile poisons.
7. Industrial gaseous and Volatile poisons
8. Poisons by Plants, flora, and fungi.
 Corrosive Poisons
 Inorganic Acids and alkalis.

 Organic Acids.

 Oxalic, Carbolic and Chromic

Acids.

 Metallic Salt Corrosives.

 Irritant Poisons
 Metallic ( Arsenic, Antimony,
Mercury, Lead, Copper, Zinc,
etc.).

 Non-Metallic (phosphorus, etc.)

 Insecticides and Herbicides.

 Analgesic, Hypnotic,
Tranquilliser, and
Narcotic Poisons.
 Analgesic (Aspirin, Antipyrin, Chloral,
Paracetamol, etc.).

 Barbiturates.

 Glutethmides and Ureides,

 Tranquillisers.

 Opium, Morphine, Cannabis, and Synthetic

narcotics.
 Stimulants, Excitants, and
Convulsants Poisons.
 Amphetamines.
 Atropine .
 Hyoscine .
 Camphor
 Cocaine
 Strychnine
 Aconite
 Veratrine, Picrotoxin, etc
 Paralytic,
Anticholinesterase and
Antihistamine poisons
 Coniine
 Curare
 Nicotine
 Anticholinesterases
 Antihistamines
 Gaseous and Volatile
poisons
 Domestic.
 Ammonia fumes.
 Hydrocyanic acid.
 Carbon dioxide.
 Carbon monoxide.
 Alcohols.
 Glycols.
 Industrial gaseous and
Volatile poisons
 Sulphuric gases.
 Carbon bisulphide.
 Petroleum distillates.
 Aromatic compounds.
 Chlorinated hydrocarbons.
 ‘Glue-sniffing’
Poisons by Plants, flora, and
fungi
 Waterside
 Country
 Town
 Food Poisoning
 The bacterial food poisoning should be clearly
distinguished from toxic reaction due to:

1) Contaminant Metals such as Arsenic, Lead, or

Tin.
2) Toxic Vegetable and Substances such as
Muscarine or Amanitin from Fungi or
Myelotoxin from Mussels.
3) Allergic Reaction to food.

 Bacterial food poisoning by Staphylococci or

the Salmonella group of organisms.
 Corrosive Poisons
 Acids
 Acids-mineral, such as Hcl, HNO3, H2SO4 or HF
and flourides;
 or organic, such as Oxalic, Acetic and Carbolic
Acid (phenol), Cresols such as a Lysol.

 Alkalis-caustics such as NaOH (lye), KOH, CaOH

(lime), Amonia, the alkaline or chlorinated
household bleashes and detergents.

 Heavy metal salts-chlorides of Sb, Zn, or Hg,

and Zn or ferrous sulphate.
 Corrosive Poisons
 Caustic substances (strong acids and alkalies),
when swallowed,  can burn the tongue, mouth,
esophagus, and stomach.

 These burns  may cause perforation (piercing)

of the esophagus or stomach.

 Food and saliva leaking from a perforation 

cause severe, sometimes deadly infection
within the chest (mediastinitis or empyema) or
abdomen (peritonitis).

 Burns that do not perforate can  result in

scarring of the esophagus and stomach.
 Corrosive Poisons
 Industrial products are usually the most
damaging because they are highly
concentrated.

 However, some common household products,

including drain and toilet bowl cleaners and some
dishwasher detergents, contain damaging caustic
substances, such as sodium hydroxide and sulfuric
acid.

 Caustic substances are available as solids and

liquids.
 Symptoms of Corrosive
1.
Poisons
Pain in the mouth and throat develops rapidly,
usually within minutes, and can be severe, particularly
with swallowing.
2. Coughing,
3. drooling,
4. an inability to swallow,
5. and shortness of breath may occur.
6. In severe cases involving strong caustic substances , a
person may develop very low blood pressure (shock),
7. difficulty breathing,
8. or chest pain,
9. possibly leading to death.
 Perforation of the esophagus or stomach may occur
during the first week after ingestion, often after
vomiting or severe coughing.
 Symptoms of Corrosive
Poisons
 The esophagus may perforate into the area between the
lungs (the mediastinum) or into the area surrounding the
lungs (the pleural cavity).
1. Either circumstance causes chest pain,
2. fever,
3. rapid heart rate,
4. very low blood pressure,
 and the development of an abscess that requires
surgery.
 Peritonitis results in  severe abdominal pain.
 Scarring of the esophagus results in narrowing 
(stricture),
which causes difficulty in swallowing.
 Strictures usually develop weeks after the burn, sometimes
in burns that initially caused only mild symptoms .
 Diagnosis and Treatment of
Corrosive Poisons
 an endoscope down the esophagus to look for burns,
 The extent of damage determines treatment.
 People with severe burns sometimes need
immediate surgery .
 Corticosteroids and antibiotics are used to try to
prevent strictures and infections.
 a person who has swallowed a caustic substance should
not be made to vomit.
 If burns are mild, the person may be encouraged to begin
drinking fluids fairly soon during recovery.
 Otherwise, fluids are given intravenously until
drinking is possible.
 If strictures develop, a bypass tube may be placed in the
narrowed portion of the esophagus to prevent esophageal closure and to
allow for future widening (dilation).
 Irritant Poisons
 Metallic Irritant

 Arsenic
 as the metal itself is not poisonous but its
salts, called arsenites, are. Arsenic gas (AsH3)
is poisonous also.

 White arsenic powder is highly soluble in hot

liquids;
 it is almost tasteless, colourless and odourless
in solution.
 Arsenic is still used in agriculture (sheep-
dips) and industry but weed-killers and flypapers
that used to contain enormous amounts of arsenic
 Arsenical poisoning
 The principal effects of poisoning are
produced by combination of the
poison with sulphhydryl (SH)
enzymes.

 There are differences in acute

and chronic
arsenical poisoning.
Acute Arsenic poisoning
 Acute poisoning mimics cholera;
there are signs of gastro-enteritis
1. with abdominal pain,
2. vomiting
3. and diarrhoea,
4. Dehydration and electrolyte
imbalance lead to  cardiovascular
failure
5. and death.
 chronic Arsenic

poisoning
The victim of chronic Arsenic poisoning may be
suspected of suffering from some wasting systemic
illness.
 The symptoms are
1. the loss of appetite and weight,
2. anaemia,
3. mild nausea
4. and skin changes, which are probably, more
specific.
 Chronic arsenical poisoning causes a
hyperkeratosis of the palms of hands,
 "raindrop" skin pigmentation,
 brittle nails
 and loss of hair.
 Postmortem finding Arsenic
poisoning
 At autopsy,
 in acute deaths only haemorrhagic gastritis can be
found.
 The stomach mucosa is oedematous with bleeding
along the top ridges of the folds ('red velvet' mucosa).

 In chronic poisoning there are degenerative

changes in the liver, myocardium and the kidneys,
stomach may show the signs of a chronic gastritis
with excess mucus and patchy erosion.
 Arsenical poisoning could be detected even long
time after death because arsenic would remain in the
hair and nails for a considerable period
 Treatment of Arsenic
poisoning
 In acute:
 gastric lavage
 Ferric hydroxide (precipitate any poison
remaining in stomach)
 Antidote is BAL (greater affinity with
sulphhydryl enzymes), as early as possible.

 In chronic ;
 Removed from the source
 BAL
 Hospital admitted.
 Mercury poisoning
 is an industrial poison but previously it was used in the
treatment of syphilis, as a protection from rheumatism
(quicksilver was carried in the pocket) and as a diuretic.

 The symptoms and signs of acute poisoning are

 gastrointestinal,
 excess salivation
 and renal failure.

 Chronic poisoning leads to

 black gums,
 salivation,
 mandibular necrosis
 and encephalopathy.

 Antidote is Sodium Fomaldehyde Sulphoxylate.

 Iron poisoning
 is best known for cases of acute poisoning in
children who eat ferrous sulphate (attractive-
looking tablets prescribed for anaemia).
 Gastrointestinal symptoms occur soon after
ingestion, even 3-5 tablets may be sufficient for
death to occur.
 This happens due to the liver damage and acidosis
from release of free iron into the circulation, because
the trasferrin system that binds iron to protein is
overloaded.
 Antidote is desferrioxamine (deferoxamine)
 Lead Poisoning
 Although it is far less common since paint containing
lead pigment was banned in 1977 and lead was
eliminated from most gasoline ,
 lead poisoning (plumbism) is still a major public health
problem in U.S. cities on the East Coast.
 Workers in industries that handle lead are at risk of lead
poisoning, as are children who live in older houses that
contain peeling lead paint or lead pipes. Young children may
eat enough paint chips to develop symptoms of lead poisoning .

 Lead affects many parts of the body, including the brain,

nerves, kidneys, liver, blood, digestive tract, and sex
organs.

 Children are particularly susceptible because lead

produces the most damage in nervous systems that are
still developing.
 Symptoms and Diagnosis of Lead
Poisoning
 Symptoms that do occur usually develop over
several weeks or longer.
 Typical symptoms of lead poisoning include
 personality changes,
 headaches,
 loss of sensation,
 weakness,
 a metallic taste in the mouth,
 uncoordinated walking,
 poor appetite,
 vomiting,
 constipation,
 crampy abdominal pain,
 bone or joint pains,
 and anemia.

 Symptoms and Diagnosis of Lead
Poisoning
 Young children may become cranky and play less
frequently .

 Encephalopathy can then begin suddenly and worsen over

the next several days, resulting in persistent, forceful
vomiting; confusion; sleepiness; and, finally, seizures
and coma.

 Adults often develop loss of sex drive, infertility, and,

in men, impotence.
 Encephalopathy rarely develops in adults.

 Lead poisoning is diagnosed with a blood test.

 In children, bone and abdominal x-rays often show
evidence of lead poisoning.
 Treatment of Lead
Poisoning
 People with more serious lead poisoning are
treated in the hospital with injections of chelating
drugs,
 such as BAL,
 Penicillamine ,
 and edetate calcium disodium .

 Because chelating drugs also can remove

beneficial minerals, such as zinc, copper, and iron,
from the body, the person often is given
supplements of these minerals.
 NON-METALLIC
IRRITANTS
Cyanides
 Cyanides are extremely poisonous.
 Potassium and sodium cyanides need to
be mixed with water or gastric acid
before releasing free cyanide that acts
as a cytochrome oxidase inhibitor.
 Cyanides are used as a wasp killer and in
some laboratory techniques.
 Death is usually rapid but some victims
have known to survive.  
 NON-METALLIC
IRRITANTS
Cyanides
 At autopsy,
1. the smell of cyanide - bitter almonds - may be
obvious (but ~ 40% of people can not smell it);
2. the organs will be dark red and congested.
3. The oesophagus, in a case of swallowed
cyanide, will be black due to erosion and
haemorrhage.
4. The skin in the areas of hypostasis will be of a
purplish-pink colour due to
cyanmethaemoglobin.
 Alcohol
 Alcohols:
 a group of organic liquids which have a
particular chemical grouping (OH).
Named according to the length of the
carbon backbone

 Methanol (methyl alcohol)

Ethanol (ethyl alcohol) = "alcohol" !
Propanol (propyl alcohol)
Butanol (butyl alcohol)
 ABSORPTION OF

ALCOHOL
Blood Alcohol Concentration (BAC);
 Urinary Alcohol Concentration (UAC);
 Vitreous Humour Alcohol Concentration (VHAC);
 Breath Alcohol Concentration (Br AC).

 20% of ingested alcohol absorbed in the stomach

80% absorbed in the upper small intestine.

 Absorption is most rapid when the stomach is

empty

 Absorption is generally complete in one to three

hours.
 ALCOHOL
 The Widmark equation gives a rough
estimate of peak BAC expected following
ingestion of a known amount of alcohol.

 Peak BAC = Weight of alcohol

ingested (g) x 100, divided by Body
Weight (kg) x Widmark Factor
 ELIMINATION OF
ALCOHOL
 Alcohol is eliminated through all bodily routes of
excretion.
 5% is excreted in the breath;
 5% in the urine
 90% broken down in the body, mostly in the
liver, by liver enzymes including hepatic alcohol
dehydrogenase (Alc DH).
Oxidation of the products (acetaldehyde and
acetic acid) finally yields carbon dioxide
(CO2) and water H2O.
Clinical Features of Alcohol
Intake:
1. Acute alcohol intoxication
2. Pathological intoxication
3. Alcohol abuse
4. Alcohol dependence
5. Alcohol withdrawal:
a) uncomplicated
b) alcohol withdrawal fits
c) alcohol withdrawal delerium
d) Wernicke's encephalopathy
e) Korsakoff syndrome
f) alcoholic hallucinosis
 1. Acute alcohol
intoxication
 Alcohol is a nervous system
depressant.

 Stages of Intoxication

 1. Excitement (<100)
 2. Confusion (100-200)
 3. Stupor (>200)
 Recovery
 Recovery is in three phases

1) Drying out period of 1-10 days

2) Physical rehabilitation over 10
days to 2 months
3) Personality recovery takes months
or years
 COMPLICATIONS OF
EXCESSIVE ALCOHOL
INTAKE
 Physical,
 Psychological
 and Social complications
 are not confined to alcoholics, they can
affect any individual who drinks heavily
for a prolonged period
 COMPLICATIONS OF
EXCESSIVE ALCOHOL
INTAKE
 a) Physical
 1. Gastro-intestinal tract:
 oesophagitis, gastritis, duodenitis, peptic ulcer,
small bowel malabsorption acute and chronic
pancreatitis
 2. Liver:
 fatty liver; alcoholic heptatitis; alcoholic
cirrhosis.
 3. Cardiovascular System:
 hypertension; cardiomyopathy and wet beri-
beri (thiamine deficiency
 COMPLICATIONS OF
EXCESSIVE ALCOHOL
INTAKE
 a) Physical
 4. Central Nervous System:
 cerebral atrophy (alcoholic dementia); Wernicke-
Korsakoff Syndrome due to thiamine (vitamin B
deficiency); cerebellar degeneration, central pontine
myelinosis, and peripheral neuropathy.
 5. Metabolic Effects: imbalance of metabolism of
many bodily compounds including glucose, uric acid,
phosphate, magnesium, potassium, fats and proteins.
 6. Endocrine Effects: male impotence; female
infertility.
 7. Others: Severe bruising of various ages due to
frequent, unprotected clumsy falls
 COMPLICATIONS OF
EXCESSIVE ALCOHOL
INTAKE
 b) Psychological
Anxiety, depression, high suicide risk,
dementia, pathological jealousy, alcoholic
hallucinosis, sexual dysfunction.

 c) Social
 Marital & family problems, including
domestic violence ,Work problems,
unemploymentRoad accidents and crime.
 CAUSES OF DEATH IN
CHRONIC ALCOHOLICS
(Clark, 1988)
 1. Trauma.
 The largest group (26%).
Fire deaths were the most common.
Drunken falls were frequently followed by
fatal head injury.
Murder,
Road traffic accidents (pedestrians),
Drowning,
Railway line accidents,
Accidental poisonings, and
Accidental hangings
 CAUSES OF DEATH IN
CHRONIC ALCOHOLICS
 Hypothermia
 2. Incidental Natural Disease (25%).
Ischaemic heart disease, cerebral
haemorrhage, chronic obstructive
airways disease and malignancy.
 3. Alcohol Related Disease (22%).
Bronchopneumonia and lobar
pneumonia are the commonest.
Cirrhosis of the liver due to ruptured
varices or hepatic failure
 CAUSES OF DEATH IN
CHRONIC ALCOHOLICS
 4. Acute Intoxication (24%).
Simple intoxication causing
respiratory depression

 5.'Obscure' cause of Death

 DRUG RELATED DEATHS &
DRUG ABUSE
 There is a spectrum of drug use, mis-use and
abuse.
 The 6 main classes of misused drugs are :

1. Opiates (morphine, heroin, methadone,

dihydrocodeine)
2. Depressants (barbiturates)
3. Minor tranquilisers (benzodiazepines, e.g.
Diazepam (Valium), Temazepam)
4. Stimulants (cocaine, amphetamines, Ecstasy,
ADAM, EVE, ICE)
5. Hallucinogens (LSD, magic mushrooms,
mescaline)
6. Others (cannabis, nicotine, volatile solvents)
 BENZODIAZEPINES
 Acute intoxication
 Psychological:
1. Relief of anxiety,
2. Relaxation
3. Impaired memory
4. Paradoxical aggression
5. Uncharacteristic criminal behaviour (shoplifting &
indecent exposure)
6. Uncontrollable emotions (giggling & weeping)
7. 'Hangover' with drowsiness,
8. inability to concentrate
9. & impairment of skilled tasks
Effects are potentiated by alcohol
 BENZODIAZEPINES
 Acute intoxication
 Physical:

1. Dizziness,
2. sedation,
3. Incoordination
4. Sexual dysfunction,
5. weight gain
6. Hypotension
7. & coma with high dose
 BENZODIAZEPINES
 Chronic effects:
1. Tolerance Physical & psychological
dependence
A state of chronic intoxication
2. with slurred speech,
3. poor concentration,
4. impaired comprehension,
5. impaired memory,
6. emotional liability,
7. Irritability
8. and depressed mood.
 AMPHETAMINES
 Amphetamines are synthetic
stimulants.
 Their use is popular in rave culture.

 Amphetamines act by stimulating

the release of catecholamines,
particularly adrenaline within the
body.
 AMPHETAMINES
 Acute intoxication:
 Psychological
1. Euphoria,
2. self-confidence and self-esteem
3. Feeling of calm, peace and friendliness towards
strangers (the 'hug drug'),
4. Heightened sense of awareness & concentration
5. Increased energy,
6. desire and ability to dance for long periods
7. Irritability & restlessness
Irrational behaviour,
8. confusion
9. Hallucinations
10. Delusions, paranoia, psychosis
11. Psychological dependence
 AMPHETAMINES
 Acute intoxication
 Physical:
1. Tachycardia (fast pulse),
2. hypertension (high blood pressure),
3. Tachypnea (breathing)
4. Loss of appetite
5. Dilated pupils
6. Brisk reflexes
7. Dry mouth, sweating,
8. blurred vision, dizziness, flushing or
pallor
9. Teeth grinding (bruxism), repetitive
actions (stereotypy)
10. Pyrexia
 AMPHETAMINES
 Acute adverse affects

 Disturbances in the electrical rhythm of the heart (cardiac

arrhythmias)

 Stroke due to elevated blood pressure bursting a blood

vessel
within the brain itself (intracerebral haemorrhage)
on the surface of the brain (subarachnoid haemorrhage ).
Severe disturbance in the blood clotting mechanisms ( DIC)
Acute paranoid psychosis
Hyperpyrexia): heat production by amphetamines and
reduced heat loss by the skin result in a dangerous rise in
body temperature This is particularly dangerous when
dehydration and heavy sweating coexist following
prolonged dancing
 AMPHETAMINES
 Chronic adverse effects
1. Chest pains
2. & muscle spasms
3. Anorexia,
4. malnutrition
5. & weight loss
6. Diarrhoea & vomiting
7. Damage to the heart muscle (cardiomyopathy)
8. Aggression, fatigue & insomnia
9. Depression
10. Chronic paranoid psychosis, schizophrenia

 Psychological dependence
leads to anxiety, depression, disturbed sleep and
irritability on cessation
 COCAINE
 Acute intoxication:
 Short acting & dose dependent.
 It causes the body to secrete
adrenaline in a similar fashion to
amphetamines
 but the detrimental and
pleasurable effects are more
florid.
 COCAINE
 Physical:
1. Tachycardia,
2. hypertension,
3. Tachypnea
4. Dilated pupils,
5. Increased mental excitement
6. Hyperpyrexia,
 COCAINE
 Psychological:
1. Euphoria & well-being
2. Irritability & confusion
3. Hallucinations,
4. formication (sensation of
insects crawling under the skin)
5. Depression,
6. paranoia as effects wear off
 COCAINE
 Chronic effects & External signs of cocaine abuse:
1. Intense psychological dependence
2. Chest pains, muscle spasms
3. Weight loss
4. Male impotence & female orgasm problems
5. Nasal septum may become ulcerated and perforated
due to ischaemia and blood vessel spasm.
6. Eyes may exhibit "crack keratitis" due to the local
anaesthetic effect allows excessive rubbing of the
eyes.
7. Teeth may show acid erosion of the surface enamel
8. Hands may show 'crack callus' of the fingers due to
repeated use of lighter.
 COCAINE
 Cocaine has serious detrimental effects
both acutely and chronically
 on the coronary arteries,
 heart muscle
 and central nervous system
 COCAINE
 The coronary arteries
Proliferation and thickening of the inner
lining
1. reduces blood flow.
2. Premature hardening and narrowing
3. (atherosclerosis).
4. (myocardial infarction)
5. Increased incidence of coronary artery
thrombosis & myocardial infarction).
 COCAINE
 The heart muscle
1. myocarditis.
2. cardiomyopathy.
 As a result of this myocardial damage
there is a risk of sudden death due to
cardiac arrhythmia which is most
likely to occur during acute
intoxication
 COCAINE
 Brain:
 Stroke, due to hypertensive blood vessel
rupture
 within the brain (intracerebral
haemorrhage) or on the surface of the brain
(subarachnoid haemorrhage).

 In addition blood vessels may undergo

spasm, causing ischaemic infarction of the
brain
 Causes of Cocaine-Induced
Death
 causes of cocaine-induced death are:
1. convulsions,
2. respiratory arrest,
3. cardiac arrhythmia
4. and coronary artery spasm
5. and stroke.

 Although cocaine itself is quite short lived in

the body it can be detected in the brain and
blood within a short time of a hit and its
metabolites are detectable for longer periods
in nasal swabs, urine, hair and saliva.
 OPIATE ABUSE
 Main drugs:
1. Morphine
2. Heroin (Diamorphine)
3. Methadone
4. Dipipanone (Diaconal ), Pethidine, Pentazocine
(Foetal ),
5. Buprenorphine (Temgesic)

 Medical uses are

1. pain relief (analgesia),
2. cough suppressants
3. & antidiarrhoeal agents.
 OPIATE ABUSE
 Acute intoxication:
Psychological:
Rush of euphoria & contentment
Relief of anxiety, inability to concentrate

 Physical:
 Constricted pupils
 Suppression of cough reflex
 Nausea & vomiting
 Decreased heart & breathing rate
 Unconsciousness,
 respiratory arrest
 and death
 Fatal reaction to impurities
 OPIATE ABUSE
 Chronic effects:
Tolerance
Physical & psychological
dependence
Constipation
Loss of libido
Complications of intravenous
injection
 OPIATE ABUSE
 withdrawal syndrome
 Symptoms (easily fabricated by the
addict wanting more drugs):
1. Craving for the drug,
2. Anxiety, restlessness, irritability,
insomnia
3. Alternate sweating and shivering
4. Generalised aches
5. Pains and cramps in the back, legs
and abdomen
6. Nausea & vomiting
 OPIATE ABUSE
 withdrawal syndrome
 Physical signs:
1. Dilated pupils
2. Watering of the eyes (lacrimation),
3. Yawning,
4. Tachycardia, hypertension
5. Cold clammy skin with goose flesh
6. Loudly audible bowel sounds (borborygmy)
7. Diarrhoea.

 Treatment with regular Diazepam & Lomotil

(Diphenoxylate & Atropine) is often necessary.
 OPIATE ABUSE
 A similar withdrawal syndrome is seen
on stopping benzodiazapines.

 Methadone treatment programs are

aimed at reducing intravenous opiate
abuse
 OPIATE ABUSE
 Local complications of injecting
1. Skin abscesses and ulceration
2. Skin scarring and the needle track marks
3. Fat necrosis due to injection beneath the skin
4. Myositis (inflammation of the muscle)
5. Thrombosis following repeated injection into
veins
6. Lymph channels become blocked and
lymph nodes enlarged resulting in swelling
or oedema of the limb.
 OPIATE ABUSE
 General complications of injecting

1. Pulmonary granulomas (foreign body

granulomas).
2. Liver granulomas.
3. Blood vessel
4. and nerve cell damage in the brain.
5. Infections
6. Hepatitis B infection and HIV
Thanks for
attention