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 reported most frequent deaths by
poisonings poisoning
1 - Household cleaning supplies 1 - Antidepressant medications
2 - Analgesics (aspirin, acetaminophen) 2 - Analgesics (aspirin, acetaminophen)
3 – Cosmetics 3 - Street drugs
4 - Cough and cold remedies 4 - Cardiovascular drugs
5 - Plant scrapes and insect bites 5 - Alcohol
6 – Pesticides 6 - Gases and fumes
7 - Topical creams and lotions 7 - Asthma therapies
8 - Hydrocarbons (gasoline, kerosene) 8 - Industrial chemicals
9 - Antimicrobacterial soaps 9 - Pesticides
10 - Sedatives/hypnotics/ 10 - Household cleaning supplies
antipsychotics
11 - Food poisoning 11 - Anticonvulsant medications
12 – Alcohol 12 - Food, plants, and insects
 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
 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.
II. Relaxants (curare).
 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
15. 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,
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, hydrochloric, Burns around mouth, lips, nose

sulphuric)
Aniline (hypnotics, nitrobenzene) Skin of face and neck quite dark
Arsenic (metals, mercury, copper, Severe, unexplained diarrhea
etc.)
Atropine (Belladonna), Pupil of eye dilated
Scopolamine
Bases (lye, potash, hydroxides) Burns around mouth, lips, nose

Carbon monoxide (CO) Skin is bright cherry red.

Carbolic acid (or other phenol) Odor of disinfectant
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 (phosphorous) Odor of garlic

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
 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 acid
 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. 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:
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. Urinary bladder – 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 immediately
removed to fresh air.
 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 poisoning.
 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 Poisons
1. 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 are unlikely to be poisonous
nowadays.
 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.
 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 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