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
2 - Analgesics (aspirin, medications
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)
9 - Antimicrobacterial 9 - Pesticides
soaps
10 - Sedatives/hypnotics/ 10 - Household cleaning
antipsychotics supplies
11 - Food poisoning 11 - Anticonvulsant
12 – Alcohol medications
12 - Food, plants, and
 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

 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
 Poisoning
 Suicidal:
 (KCN, HCL, Opium, Barbiturates,
organophosphorus, oxalic acid
oleander etc),

 Homicidal
 (arsenic, aconite, thallium,
organophosphorus, oleander, etc.).
 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,
 Important Definitions:
 Toxicology
 It is the science dealing with

properties,
action,
toxicity,
fatal dose,
detection estimation of,
interpretation of the result of
toxicological analysis
 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.
 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
 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),
 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.
 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.
 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
 Domestic or household sources.
 Agricultural and horticultural
sources.
 Industrial sources
 Commercial sources.
 From uses as drugs and medicines
 Food and drink
 Miscellaneous sources - snakes bite
poisoning,
 Domestic or household sources -
detergents, disinfectants, cleaning agents,
antiseptics, insecticides, rodenticides etc.
 Agricultural and horticultural sources-
different insecticides, pesticides, fungicides
and weedicide.
 Industrial sources- In factories, where
poisons are manufactured or poisons are
produced as by products.
 Commercial sources- From store-houses,
distribution centers and selling shops.
 From uses as drugs and medicines – Due
to wrong medication, overmedication and
abuse of drugs.
 Food and drink – contamination in way of
use of preservatives of food grains or other
 Classification of poisons
 According to the site and mode of action.
 Local Action
 Remote Action
 Combined local and remotes action

 According to motive or nature of use.

 Homicidal:.
 Suicidal:
 Accidental:.
 Abortifacient:.
 Stupefying agent:
 Agents used to cause bodily injury:
 Cattle Poison:
 Used for malingering
 Classification of poisons
 According to the site and mode of
action
b) Local Action
 Corrosive
 Irritant

f) Remote Action
 Neurotics
 Cardiac Poisons
 Classification of poisons
 According to the site and mode of action
b)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
a) Remote Action
 Neurotics
 C.N.S. Poisons
 Somniferous: opium and its alkaloids, Barbiturates.
 Inebriant (Intoxicant): Alcohol, ether, Chloroform.
 Stimulant
 Deliriant: Dhatura, Belladona, Hyocyamus, cannabia
indica.
 Stupefaciant
 Hallucinogens
 Convulsant:

 Spinal (Convulsant)
XIII.Strychnos Nux Vomica

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

i) Combined local and remotes action

 Classification of poisons
 According to motive or nature of use:
 Homicidal: Arsenic, Aconite, Digitalis, Abrus
Precatorius, Strychnos nux-vomica.
 Suicidal: Opium, Barbiturate,
Organophosphorus, carbolic acid, copper
sulphate.
 Accidental: Aspirin, organophosphorus,
copper sulphate, snakes bite, Ergot, CO, CO2,
H2S.
 Abortifacient: Ergot, Quinine, Calotropis,
Plumbago.
 Stupefying agent: Dhatura, cannabis, chloral
hybrate.
 Agents used to cause bodily injury:
Corrosive acids and alkalies.
 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
 Oral (commonest) e.g.: alphos, acids,
 Inhalation: gas poison
 Parenteral (IM, IV, Sub-Cutaneous,
Intra-Dermal)
 Natural Orifices other than mouth
(Nasal, Rectal, Vaginal, Urethral),
 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.
 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
 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.
Factors influencing the actions of
a poison in the body
 Quantity
 Physical form
 Chemical form
 Concentration
 Condition of the stomach
 Route of administration
 Age
 State of body health
 Presence of disease
 Intoxication arid poisoning states
 Sleep
 Exercise
 Cumulative action of poisons
 Tolerance
 Idiosyncracy
 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,
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
 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

 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

 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.
 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

 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
 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
 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, Severe, unexplained
mercury, 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,
odor of peach
 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:
 Sudden vomiting and diarrhoea
 Unexplained coma in children and adults
known to have depressive illness
 Rapid onset of a peripheral neuropathy
 Rapid onset of neurological or
 Diagnosis of poisoning

 In the Living
 In the Dead
 Diagnosis of poisoning
 In the Living
 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.
 Symptoms and Signs.
 Details of examination.
 Preservation and laboratory investigation of
vomitus, excreta, stomach wash, scraps from any
 Diagnosis of poisoning
 In the Dead:
 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).
 Post-mortem Examination (external
and internal)
 Chemical Analysis: detection of
poison in the body fluids.
 Preservation of viscera and other
 Postmortem Findings in Case
Of Death Due To Suspected
Poisoning
 External Examination
 Postmortem Staining:
Deep blue - In case of asphyxiant poisons and
aniline.
Bright red or cherry red - In case of CO and
HCN poisoning.
 Deep Cyanosis - With opium and cardiac
poisons.
 Early Rigor mortis - With strychnine.
 Early appearance of the sign of
 Postmortem Findings:
External Examination
 Haemorrhagic spots under the skin
and mucus membrane: Phosphorus. .
 Ulceration on lips and near the
angles of mouth - Corrosive poisons.
 Stain near mouth and on hands -
Nitric acid and copper sulphate.
 White froth from mouth and nose –
Opium and its alkaloids. .
 Blood tinged froth from mouth and
nose Organophosphorus compounds.
 Postmortem Findings
External Examination
 Alopecia, hyper pigmentation and
hyperkeratosis - Arsenic poisoning
over a long period.
 Staining, erosion and ulceration
near the female external genitalia - Use
of abortifacient agents or torturing
agents.
 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:
 Corrosion, ulceration and
desquamation of inner aspects of lips,
mucus membrane of mouth and
tongue - Corrosive agents.

 Soft, swollen, sodden, translucent,

bleached tongue and mucus
membrane of mouth- Corrosive alkali

 Hardening of mucus membrane -

 Postmortem Findings
Internal findings:
 Bluish discolouration - Copper
sulphate

 Carbonization and charring- Conc.

Sulphuric acid

 Chalky appearance and consistency of

teeth - Sulphuric acid

 Blue lining in the gum - Chronic lead

 Postmortem Findings
Internal findings:
 Swollen gum, loose teeth, foetid smell -
Acute mercuric chloride poisoning; chronic
phosphorus poisoning
 Corrosion, irritation, desquamation and
haemorrhage in the inner wall of the
esophagus - Corrosive and irritant
poisons
 Hardening and whitish discolouration –
Carbolic acid poisoning
 Discoloration and staining of inner aspects
of mouth - With coloured poisons
 Postmortem Findings
Internal findings:
1. Stomach
 Thickening and softening of the wall -
Corrosive and irritant poisons
 Hard wall- Carbolic acid
 Hard and leathery wall- Formaldehyde
 Hyperemia haemorrhage and
desquamation of mucus membrane.-
Irritant poison
 Laceration and sloughing – Corrosive
poison
 Perforation - H2SO4 and HN3
 Yellowish discolouration of mucus
membrane - HNO3; Bluish - CuSO4;
 Postmortem Findings
Internal findings:
1. Stomach
 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:
 Small intestine –
May show irruption, sometimes may
show presence of poisonous remains.

 Large intestine - 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:
 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
 Postmortem Findings
Internal findings:
1. 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
 Postmortem Findings
Internal findings:
 Urinary bladder – Haemorrhage in
cases of abrus precatorius, viper snake
bite, cantharide poisoning.

 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
 Postmortem Findings
Internal findings:
 Chest cavity -Smell of volatile poisons
cyanogen, opium etc. can be detected.

 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.

 Heart- Presence of subendocardial

haemorrhagic spots in cases of arsenic,
 Postmortem Findings
Internal findings:
 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.

 Uterus and vagina –

 Staining, congestion haemorrhage,
Preservation of viscera and
other materials
 In all cases of poisoning
 Stomach with its full contents.
 Half of Liver or 500 gms
whichever is more.
 A loop of Small Intestine.
 Half of Each kidney.
 Some portion of Spleen.
 In some particular poisons
 Blood 100ml: in cases of absorbed poisons.
 Urine 100ml in all cases where blood is
preserved.
 Part of both lungs in cases of Volatile
poisons.
 Heart in case of cardiac poisons.
 Brain in cerebral poisons.
 Spinal in spinal poisons.
 Bones in arsenic and lead.
 Hair in arsenic and copper.
 Nails in arsenic.
 Skin-scrap from areas stained with a
suspected poison.
 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.
 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.

 Airway: Opening Up and Cleaning the

Airways (oral cavity, Nostrils) of secretions,
vomit or any foreign body. Pull Tongue
forward
 Breathing: Supplemental Oxygen Therapy
 Specific Management
 Removal of patient from source
of exposure.
 Removal of the unabsorbed
poison.
 Diluting the poison
 Elimination of absorbed poison
 Use of specific antidote
 Symptomatic treatment.
 Specific Management
 Removal of patient from source of exposure:
as quickly as possible.
 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
 Specific Management
 Diluting the poison and delaying the
absorption by water or food.
 Elimination of absorbed poison
by increases urination
(diuresis),
increased perspiration
(diaphoresis),
Dialysis, use of
chelating agents.
 Use of specific antidote
 Counterindications of
gastric lavage with
stomach tube:

 In corrosive poisons.
 Convulsant poisons.
 Unconscious or semi-conscious
patients
 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
 Chemical Antidotes
 They are Substances which
disintegrate
and
inactivate
poisons
by
undergoing chemical reaction
with them.

 E.g.: Weak acids and alkali,


 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)
 Household Antidotes
 Strong liquid tea (contains tannic
acid) precipitate alkaloid and metallic
poisons.
 Starch for iodine.
 Milk and raw egg for mercury,
arsenic, heavy metal.
 Flour suspension and mashed
potatoes can be used in place of
activated charcoal.
 Milk of magnesia or soap solution for
 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
 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.

 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
 Try to save the life of the patient and give
emergency necessary treatment.

 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.

 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
 Duties of a Registered Medical
Practitioner
 The doctor should himself record full
history of the case, the signs and
symptoms and progress.

 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.
 Duties of a Registered Medical
Practitioner
 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..

 If death is apprehended then arrangement

for recording dying declaration should be
made.
 COMMON POISONS AND
DRUGS
 Corrosive poisons
 Irritant poisons
 Analgesic, Hypnotic, Tranquilliser, and
Narcotic poisons.
 Stimulants, Excitants, and Convulsants
poisons.
 Paralytic, Anticholinesterase and
Antihistamine poisons.
 Gaseous and Volatile poisons.
 Industrial gaseous and Volatile poisons
 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

 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:

 Contaminant Metals such as Arsenic,

Lead, or Tin.
 Toxic Vegetable and Substances such as
Muscarine or Amanitin from Fungi or
Myelotoxin from Mussels.
 Allergic Reaction to food.
 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

 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

 Symptoms of Corrosive

Poisons
Pain in the mouth and throat develops rapidly,
usually within minutes, and can be severe, particularly
with swallowing.
 Coughing,
 drooling,
 an inability to swallow,
 and shortness of breath may occur.
 In severe cases involving strong caustic substances, a
person may develop very low blood pressure
(shock),
 difficulty breathing,
 or chest pain,
 possibly leading to death.
 Perforation of the esophagus or stomach may
 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).
  Either circumstance causes chest pain,
 fever,
 rapid heart rate,
 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.

 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
 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
 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
 with abdominal pain,
 vomiting
 and diarrhoea,
 Dehydration and electrolyte
imbalance lead to 
cardiovascular failure
 and death.
 chronic Arsenic

poisoning
The victim of chronic Arsenic poisoning
may be suspected of suffering from some
wasting systemic illness.
 The symptoms are
 the loss of appetite and weight,
 anaemia,
 mild nausea
 and skin changes, which are probably, more
specific.
 Chronic arsenical poisoning causes a
hyperkeratosis of the palms of hands,
 "raindrop" skin pigmentation,
 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.
 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
 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.
 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.
 Kidney damage often develops without symptoms.
 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
 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,
 the smell of cyanide - bitter almonds -
may be obvious (but ~ 40% of people can
not smell it);
 the organs will be dark red and
congested.
 The oesophagus, in a case of swallowed
cyanide, will be black due to erosion and
haemorrhage.
 The skin in the areas of hypostasis will
be of a purplish-pink colour due to
 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
 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
 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
:

 Opiates (morphine, heroin, methadone,

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

3. Dizziness,
4. sedation,
5. Incoordination
6. Sexual dysfunction,
7. weight gain
8. Hypotension
9. & coma with high dose
 BENZODIAZEPINES
 Chronic effects:
 Tolerance Physical & psychological
dependence
A state of chronic intoxication
 with slurred speech,
 poor concentration,
 impaired comprehension,
 impaired memory,
 emotional liability,
 Irritability
 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
 Euphoria,
 self-confidence and self-esteem
 Feeling of calm, peace and friendliness towards
strangers (the 'hug drug'),
 Heightened sense of awareness & concentration
 Increased energy,
 desire and ability to dance for long periods
 Irritability & restlessness
Irrational behaviour,
 confusion
 Hallucinations
 Delusions, paranoia, psychosis
 Psychological dependence
 AMPHETAMINES
 Acute intoxication
 Physical:
3. Tachycardia (fast pulse),
4. hypertension (high blood pressure),
5. Tachypnea (breathing)
6. Loss of appetite
7. Dilated pupils
8. Brisk reflexes
9. Dry mouth, sweating,
10. blurred vision, dizziness, flushing or
pallor
11. Teeth grinding (bruxism), repetitive
actions (stereotypy)
 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
 AMPHETAMINES
 Chronic adverse effects
2. Chest pains
3. & muscle spasms
4. Anorexia,
5. malnutrition
6. & weight loss
7. Diarrhoea & vomiting
8. Damage to the heart muscle (cardiomyopathy)
9. Aggression, fatigue & insomnia
10. Depression
11. 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:
 Tachycardia,
 hypertension,
 Tachypnea
 Dilated pupils,
 Increased mental excitement
 Hyperpyrexia,
 COCAINE
 Psychological:
2. Euphoria & well-being
3. Irritability & confusion
4. Hallucinations,
5. formication (sensation of
insects crawling under the skin)
6. Depression,
7. paranoia as effects wear off
 COCAINE
 Chronic effects & External signs of
cocaine abuse:
 Intense psychological dependence
 Chest pains, muscle spasms
 Weight loss
 Male impotence & female orgasm
problems
 Nasal septum may become ulcerated and
perforated due to ischaemia and blood
vessel spasm.
 Eyes may exhibit "crack keratitis" due to
the local anaesthetic effect allows
excessive rubbing of the eyes.
 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
 reduces blood flow.
 Premature hardening and narrowing
 (atherosclerosis).
 (myocardial infarction)
 Increased incidence of coronary artery
thrombosis & myocardial infarction).
 COCAINE
 The heart muscle
 myocarditis.
 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
 Causes of Cocaine-Induced
Death
 causes of cocaine-induced death are:
2. convulsions,
3. respiratory arrest,
4. cardiac arrhythmia
5. and coronary artery spasm
6. 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:
 Morphine
 Heroin (Diamorphine)
 Methadone
 Dipipanone (Diaconal ), Pethidine,
Pentazocine (Foetal ),
 Buprenorphine (Temgesic)

 Medical uses are

 pain relief (analgesia),
 cough suppressants
 & 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):
 Craving for the drug,
 Anxiety, restlessness,
irritability, insomnia
 Alternate sweating and
shivering
 Generalised aches
 Pains and cramps in the back,
 OPIATE ABUSE
 withdrawal syndrome
 Physical signs:
 Dilated pupils
 Watering of the eyes (lacrimation),
 Yawning,
 Tachycardia, hypertension
 Cold clammy skin with goose flesh
 Loudly audible bowel sounds
(borborygmy)
 Diarrhoea.

 Treatment with regular Diazepam &

Lomotil (Diphenoxylate & Atropine) is often
 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
 Skin abscesses and ulceration
 Skin scarring and the needle track
marks
 Fat necrosis due to injection beneath
the skin
 Myositis (inflammation of the
muscle)
 Thrombosis following repeated
injection into veins
 Lymph channels become blocked and
 OPIATE ABUSE
 General complications of injecting

 Pulmonary granulomas (foreign body

granulomas).
 Liver granulomas.
 Blood vessel
 and nerve cell damage in the brain.
 Infections
 Hepatitis B infection and HIV
Thanks for
attention