GENERAL CONSIDERATIONS ON TOXICOLOGY

DEFINITIONS

TOXICOLOGY

Science dealing with properties, action, toxicity, fatal dose, fatal

period, detection, estimation, interpretation and treatment of poisons.

POISON(a vague definition)

a substance (solid, liquid or gas) which if introduced in the living

body or brought into contact with any part thereof, will produce ill

health or death, by its constitutional or local effects or both.

FORENSIC TOXICOLOGY
Deals with medical and legal aspects of the harmful effects of
chemicals in human beings

Clinical Toxicology
Deals with human diseases caused by or associated with abnormal
exposure to chemical substances

Toxinology
refers to toxins produced by living organisms which are dangerous
to man
 B. Manner /Motives/MLA of Poisoning

I. Human poisons
 Homicidal
Eg: Aconite, As, Morphine
 Suicidal
Eg: Organophosphates, opium, barbiturates,
 Accidental: Household poisons
 Stupefying
Eg: Datura, Cannabis, Chloral hydrate,
 Abortificients:
Eg: Arka, Karaveera, Vatsanabha, Bhallataka,
Pb, As,Hg, , KMnO4, ergot
 B. Manner /Motives/MLA of Poisoning

 Aphrodisiacs:
Eg: Cocaine, Opium, Strychnine, As, cantharides
 Arrow:
Eg: Gunja, Arka, Vatsanabha, Jayapala,
strychnine, curare, snake venom
 Rare:
Eg: Bacteria, insulin

II. CattlePoisons
For destruction of cattle –of enemy/ to obtain hides
Eg: Gunja, Karaveera,, Arka, aconite, strychnine,
Organophosphates, ZnP, nitrates
Methods of Poisoning

For criminal purposes

-Homicidal intent/ Suicidal intent / intent to cause injury
rash or negligent use/for stupefying/ to procure abortion/ to annoy
Accidental:
• Mistakenly swallowing
• Accidental or ignorant inhalation of poisonous vapours
• Accidental intake of large dose of medicine containing poison
• incorrect preparation of medicines containing poison
• Excessive self medication
• Addiction to drugs
• Bites and stings
• Food poisoning
 Ideal Suicidal Poisons

1. Cheap
2. Easily available
3. Highly toxic
4. Tasteless or pleasant taste
5. Capable of being easily taken in food or drink
6. Capable of producing easy/ painless death

Ideal-Opium, Barbiturates
Commonly used-Organophosphorus and endrine
 Ideal Homicidal Poisons
1. Cheap
2. Easily available
3. Colourless, odourless and tasteless
4. Capable of administered in food, drink or
medicine without arousing any obvious change to
prevent suspicion.
5. Highly toxic
6. Signs and symptoms should resemble a natural
disease or serious ill effects delayed sufficiently
long for the accused to escape
 Ideal Homicidal Poisons
7. Should not have any antidote
8. No postmortem changes (detectable)
9. Should not be detected by chemical tests or other
methods
10. Must be rapidly destroyed or made undetectable
in the body

Ideal-Organic compound of Flourine (rodenticides),

Thallium
Commonly used-Arsenic and aconite
D. Classification based on Source
 Synthetic
 Natural
• Vegetable
• Animal
 TYPES OF POISONING
Acute Poisoning: caused by an excessive single dose or
several smaller doses of poison taken over a short period
of time.
Chronic Poisoning: caused by smaller doses over a
period of time,resulting in gradual worsening e.g.
Arsenic, antimony, Phosphorous and opium.
Sub acute Poisoning: :with features of both acute and
chronic poisoning
Fulminant Poisoning: produced by massive dose. Here
death occurs rapidly, sometimes without preceeding
symptoms
 Routes of administration of Poisons
Rapidity increases in ascending order 
•Inhalation>
•Injection into blood vessels (IV)>
•Intramuscular, Subcutaneous, Intradermal>
•Application to wound>
•Application to a serous surface>
•Application to bronchotracheal
mucous membrane>
•Introduction onto stomach>
•Introduction into external orifices>
•Application to unbroken skin
 Routes of elimination of Poisons

Absorbed poisons

Mainly by Kidneys;

To some extent by skin

Bile, milk, saliva, mucous and serous secretions

Unabsorbed poisons – faeces and vomit

 Fate of ingested poison in the body

Poison

Greater part –expelled

via vomiting, purging local action Absorbed

liver

unmetabolised partially metabolised completely metabolised

bioactivation stored in tissues harmless

action on destroyed
target organ/ by evaporation
body /oxidation---

retained for long time excreted

via urine
Action of Poisons
1. Local
2. Remote
3. Combined
4. General

# Local: on the part with which contact occurs

Corrosives: corrosion of affected part by corrosives

Irritants: Inflammation/ congestion by irritants

Effect on motor & sensory nerves :tingling of skin

and tongue by aconite, mydriasis by belladona or Datura

Action of Poisons

# Remote: away from area of direct contact

Shock-reflexly through pain by corrosives (Non-specific)

Exerting action on a target organ(specific) or remote part

after absorption (remote local)

eg: Cantharides- nephritis, Nux vomica- tetanic

convulsions

# Combined (Local and Remote):Local & Systemic action

eg: Carbolic acid, Oxalic acid, Phosphorous

# General: More than one system

eg: Barbiturates, Hg, As, Pb

 FACTORS AFFECTING ACTION OF POISONS

Substance Related Condition of the Body

1. Quantity 1. Age
2. Form
2. Idiosyncrasy
• Physical state
• Chemical composition 3. Habit

• Mechanical Composition 4. State of Health

5. Sleep and intoxication

3. Mode of Administration
6. Cumulative Action
 DIAGNOSIS OF POISONING

In the Living

In the dead

Not many toxidromes or single symptom characteristic of

poisoning.

Symptoms of toxicity may simulate a disease or vice versa

 DIAGNOSIS OF POISONING

Points to be considered

 History

 Clinical Manifestations /Post mortem findings

 Investigations, Toxicological Analysis

 Moral and circumstantial evidence

 Experimentation in animals
 DIAGNOSIS IN THE LIVING
Acute Poisoning
 Clinical History
• Time of onset: Sudden onset in a healthy person
• Relation with food: Initial symptoms within short
period of intake / exposure (if not oral almost
immediate)
• Progress: Rapidly increase in severity
• Status of other persons taking same food or
drink:Several exposed-at same time – all have
similar symptoms
 Clinical History
• Possible source of poison
• HPI: Note time and duration of PC& associated
complaints, Aggravating factors ; if any external
contact, its source
• Any relation to food/drink/ drug intake; how
related-
Personal History: Type and manner of food intake
• H/o previous poisoning
• Family/ Occupational/ Social History-H/o
depression or quarrel….
• Finding the poison in vomit, urine or excreta
 Clinical manifestations suggestive of poisoning
1. Nausea, Vomiting, Abdominal pain, Diarrhoea,
Collapse
2. Coma with constriction of pupils
3. Convulsions
4. Delirium with dilated pupils
5. Paralysis esp. Of LMN type
6. Jaundice & Hepatocellular failure
7. Oliguria with proteinuria and haematuria
8. Persistant cyanosis
9. Rapid onset of neurological or GIT disease in persons
with known occupational exposure to chemicals
 Chronic Poisoning

1. Aggravation of symptoms following administration of

a suspected food, drink or medicine

2. Malaise, cachexia, depression and gradual

deterioration of general condition

3. Repeated attacks of diarrhoea, vomiting

4. Symptoms disappear when removed from his usual

surroundings

5. Traces of poison in vomit, urine or stool

 History from relatives

•Quantity and Quality of poison/ suspected material

administered (In c/c cases duration)
•Character of symptoms with reference to their onset
•Time between administration and development of signs
and symptoms
•Duration of illness; (Remissions and relapses in c/c cases)
•Treatment given, if any
•If death occurred, time of Death
Materials to be collected for Analysis

Stomach wash (entire quantity)

Blood 10 ml

Urine as much as possible

Vomit, faeces, saliva or other secretions/ body fluid

Preservative: Sodium fluoride100g for 10ml of blood

(also as anticoagulant)

Suspected material if any

Note(vomit, urine, faeces, any suspected material)

•Colour

•Smell

•Consistency

&

•taste

•quantity of possible poisonous substance

Experimentation on animals:
Cats and dogs are affected by poison as man.
Some animals are in susceptible to certain poisons
A.H Su 7/1-29
C.S.Chi 23
Circumstantial evidence
Any motive
Evidence regarding recent purchase, recent activities of
suspect
Behaviour of suspect/witness before & after commission
(Vishadata lakshanam)
H/o previous poisoning
H/o depression or quarrel
Recovery of poison from suspect/accused
 Ayurvedic Aspect

Peeta visha (S.S.K 3)

Savatam gradhoomabham pureesham yoƒtisaryate

Aadhmatoƒtyarthamushnaasro vivarna: saadapeedita:
Udwamatyatha phenam cha vishapeetam tamaadiset

Visha in Amasaya and Pakwasaya (A.H.Su 9)

 DIAGNOSIS IN THE DEAD

 History
 Post-mortem appearance
 Chemical &Toxicological Analysis with
Histopathological investigation
 Experimentation in animals
 Moral and Circumstantial Evidence
HISTORY

• From the inquest report & from relatives of the

deceased

• How long he survived after appearance of initial

symptoms

• Treatment taken
 DIAGNOSIS OF POISONING IN THE DEAD

Autopsy

invariably preceded by Inquest

Chemical Analysis

Histopathological Examination
 TREATMENT OF POISONING

GENERAL PRINCIPLES OF TREATMENT

• Removal from exposure
• Assessment of general condition & Resuscitation
• Removal of unabsorbed Poisons
• Administration of Antidotes
• Elimination of absorbed poisons
• Treatment of signs and symptoms
• Maintenance of General condition
• General nursing care
• Psychiatric care
• Proper Follow ups
Treatment-Ayurvedic Aspects
Treatment Principle
Ato anyatha to twarayaa pradeeptaagaravadbhishak
Rakshan kanthagataan pranan vishamaasu samam nayet
A.H.U 36/37
Iti prakriti satmya ritu sthanavega balabalam
Alochya nipunam buddhya karmanantharamacharet
A.H.U 35/65

Treatment modalities
Chaturvimsatyupakrama

Mantraarishta………
(C.S.Chi.23 (35 – 37)
REMOVAL FROM EXPOSURE

• Inhaled poisons:

Removed from surroundings to fresh air or O2

inhalation(mask/ nasal catheter) or artificial respiration

• Contact poisons:

Skin/Eyes/mocous membranes : remove contaminated

clothing & wash

ASSESSMENT OF GENERAL CONDITION &
RESUSCITATION
Conscious/ not; Stable/not, Oriented/not
Comatose pts—vitals-ABCD of Resuscitation
Airway: Opening up& cleaning up of airway;
endotracheal intubation
Breathing: ABG maintenance; O2 supplementation
Circulation: eg. I.V. Fluids
Depression of CNS: Recovery Position, Assessment of
Coma, reflexes; resuscitation,
REMOVAL OF UNABSORBED POISONS

Inhaled Poisons

Removed from surroundings to fresh air or O2

inhalation(mask/ nasal catheter) or artificial

respiration

Free airway-by postural drainage or aspiration

Management of bronchospasm, pulmonary oedema

REMOVAL OF UNABSORBED POISONS

Contact poisons:

Skin/Eyes/mocous membranes : remove contaminated

clothing, jewellery, contact lenses

Wash with copius amount of water/ neutralising

solution for 30 mts (or normal saline for eyes -15mts

Acid burns :flooded with water for 5 minutes

Alkali burns: flooded with water for 20 minutes

 REMOVAL OF UNABSORBED POISONS

Injected poisons to limb(injection/bite)

• Ligature above wound- loosened for 1mt every10mts

• Excision and sucking out of poison

• Neutralisation by suitable chemicals

• Local vaso constriction and retardation of blood flow

• In snake poison--Do it R.I.GH.T

REMOVAL OF UNABSORBED POISONS

Ingested Poisons

Gastric Lavage (Stomach wash)

Emesis
Gastric Lavage-

To wash out the contents of stomach

Within 3 hours of ingestion (upto 12-18 hrs in c/o salicylates,

phenothiazines, anti-histamines, tricyclic anti-depressants)

Equipment used- Stomach tube(Ewald’s/ Boas tube)

-ordinary, soft, non-collapsible

rubber tube- 1cm diameter & 1.5 m

long

- in children-No.10-12 French
 Stomach tube

• soft, non-collapsible rubber tube

• 1cm diameter & 1.5 m long; a funnel on one end &

• a mark at 50cm (25 cm in case of children) from other

• Other end is rounded with lateral openings.

• At mid part a suction bulb (to pump stomach contents)

&

A wooden mouth-gag with a pointed end and a hole to

let the tube through

 Gastric Lavage

Patient laid on left lateral/ prone position

with head at lower level- mouth lower than larynx

Dentures removed
 Gastric Lavage

Mouth end lubricated and inserted into stomach by

depressing tongue and mouth gag ( sp. care in non-

cooperative pts) kept in place.

Inserted till mark at 50cm/ distance between bridge of

nose and tip of xiphoid process is reached

 Gastric Lavage contd.

Confirm that tube has not entered trachea

240ml of warm water (35o C) passed through funnel

Funnel held high above patients head

When empty, tube compressed below funnel

Funnel end lowered below level of stomach

Stomach contents emptied by siphon action on

releasing the pressure /on pumping is collected and

send for chemical analysis

 Gastric Lavage

Gastric lavage continued with 500ml 0f suitable

solutions- 1:5000 KMnO4,1% Na or K iodide, saturated

lime water or starch solution, 1-3% calcium lactate or

0-9% saline. (Process stopped if bleeding occurs)

Repeated till clear, odourless fluid comes out

A small quantity of antidote solution or activated

charcoal suspension is left behind

 Gastric Lavage- Contra indications

Absolute CI- Corrosives-except Carbolic acid-perforation

After taking proper precautions only in-

-Convulsant poisons (after controlling convulsions

-Comatose patients (seal airway with endo-tracheal

tube)

-Volatile poisons

-Oesophagal varices/other upper GIT Disease

-Haemorrhagic diathesis
 Gastric Lavage- Complications

Laryngeal spasm

Aspiration pneumonitis

Perforation of stomach

Sinus bradycardia

Trauma due to insertion

 Emesis

In absence of stomach wash tube .

Only if medullary centres are responsive. Hence only

in conscious patient

With Ipecacuanha powder (2g) or Ipecac syrup(30ml)

Followed by several glasses of water

Dose repeated if no vomiting in 30mts.

Action: local activation of peripheral sensory receptors

in GIT and stimulation of vomiting centre

Emesis-Contra indications
Corrosive poisoning: [Absolute CI- Corrosives-except Carbolic acid-due to
danger of perforation; coma- aspiration, volatile- inhalation]

Unconscious patients
Convulsant poisons
Volatile poisons
Oesophagal varices/other upper GIT Disease
Haemorrhagic diathesis
Marked hypothermia
Severe heart and lung disease
Advanced pregnancy
After ingestion of CNS stimulants
Administration of Antidotes
Antidotes: Substances which help to prevent the
absorption or neutralise or counteract the effects of
poisons.
Types
Mechanical/Physical

Chemical

Physiological

Chelating agents

Serological
Mechanical/Physical Antidote
Prevent absorption of poisons /neutralise by mechanical
action
Types
i. Adsorbant-Activated charcoal
ii. Demulscents
iii. Bulky food
Activated charcoal

fine odourless, tasteless powder –

small particles with large surface area

Mechanical action- adsorption and retention of

organic & also mineral poisons delay absorption

Initial dose-60-100g (adult); 15-30g in (child)

Useful in opiates, quinine, strychnine, digitalis,

barbiturates, atropine, anti-histamines, AlP etc.

Disadvantages: May release chemical as Ph

changes during passage through GIT
Demulscents
Substances which form a protective coating on mucous
membrane of stomach-protection and prevention of
absorption
Eg. Milk, starch, egg-white, milk of magnesia,
aluminium hydroxide gel, mineral oil etc.
Caution: Fats and oils in fat soluble poisons is
hazardous
Bulky food:
mechanical action- by locking poisons within its mesh
Eg. Glass powder –particles detained in the meshes –
protection from harm to mucosa
 Chemical Antidote

• Neutralise action of poisons by oxidising or forming

insoluble /harmless compounds via chemical

reaction
Eg. a) NaCl +AgNO3 AgCl + NaNO3

b) Albumen precipitates HgCl2

c)CuSO4 precipitates P
d)KMnO4 oxidises opium, strychnine, HCN, etc.
• Acids neutralise alkalis & vice versa (exothermic –
may cause additional injury. Weak alkalis &
 Physiological/Pharmacological Antidote
• Act on tissues of body and produce signs and symptoms
which are opposite to those produced by poison.
• Used after some of the poison is absorbed
• Act on principle of antagonism-by interfering with each
other’s action on tissues, enzymes or opposing nervous
systems.
• Action is limited , partial and not without danger
Eg: atropine and physostigmine, strychnine and
barbiturates, barbiturates and amphetamine
Chelating Agents (Metal Complexing Agents)

Used in Heavy metal poisoning

Form stable, soluble complexes with Ca and certain

heavy metals

Have greater affinity for metals than the enzymes

Form inert complexes with metals and the complex is

more water soluble than metal higher renal excretion

Eg. BAL, EDTA,DMSA, DMPS, Penicillamine

BAL –(British anti-Lewisite, Dimercaprol,
Dimercaptopropanol)

Has two unsaturated -SH radicals  have more affinity

towards metal than respiratory enzymes & thus
prevent union of metal with SH radical of enzymes
Used in treatment of As,Pb, Bi, Cu, Hg, Au, Th, Sb
The complex formed – stable, carried into tissue fluids,
and excreted in urine
not used in liver damage, causes haemolysis in 6-PGD
(6-phospho gluconate dehydrogenase) deficient
persons.
 EDTA- Ethylene Diamine Tetra Acetic acid

[Calcium disodium versenate,edathemil edetic acid, versene]

Effective in Pb, Co, Hg, Cu, Cd, Fe and Ni poisoning

Superior to BAL in treatment of As and Hg poisoning

Treatment of choice in Pb poisoning- forms water-soluble,

non-toxic, non-ionised, non-metabolised chelates

with Pb which are excreted in urine

DMSA- Meso-2,3, Dimercapto Succinic Acid, Succimer
Used in Pb, Hg, As poisoning
Superior to EDTA in Pb poisoning as it does not cause
redistribution of Pb to brain
Less toxic to kidneys
Can be given in 6-PGD deficient individuals
DMPS-2,3, Dimercapto Propane1-Sulfonate
Effective in Pb, Hg, As poisoning
Both DMSA & DMPS possess same -SH chelating
grouping as BAL and molecules are more hydrophilic
Have better therapeutic index
Penicillamine
Hydrolysis product of penicilline
Has a stable -SH group
Chelating agent of max. efficiency for Cu, Pb & Hg
Desferrioxamine
•Useful in Fe poisoning
•Has a trivalent iron as chelate
•given orally to absorb iron in the stomach
•Also used to promote removalof radioactive heavy metals

Serological Antidote
eg. Antivenom
Antidotes-Modes of action

• Reduced toxic conversion: eg. ethanol for methanol

• Receptor site blockade: eg. Naloxone for opiates

• Accelerated de-toxification: eg. Thiosulphate for

cyanide

• Toxic effect bypass: eg. 100% O2 in cyanide poisoning

• Inert complex formation: eg. chelating agents for

heavy metals
ELIMINATION OF ABSORBED POISONS
Indications
1. Severe poisoning
2. Progressive deterioration in spite of supportive
care
3. High risk of serious morbidity or mortality
4. Poison produces delayed but serious toxic effects
5. Cardiovascular, respiratory or other diseases that
increase the hazards
6. When normal route of excretion of toxic
compounds is impaired
ELIMINATION OF ABSORBED POISONS
Renal Excretion-Diuresis
Forced diuresis and alteration of urinary pH
Purging
Whole Bowel Irrigation
Diaphoresis
Extracorporeal Removal
• Peritoneal Dialysis
• Haemodialysis
• Charcoal/ Resin Haemoperfusion
• Haemofiltration
• Plasmapheresis
• Exchange transfusion
Treatment of signs and symptoms:
as indications arise
Eg: Pain- morphine
Respiratory failure- O2/ artificial respiration
Convulsions- diazepam, barbiturates
Acidosis- NaHCO3
Hypoglycaemia- glucose infusion
 Maintenance of General condition
 Patient kept warm and comfortable
 General nursing care: Especially in paralysis or
bedridden (long term) patients
 Prevent bedsores
 Prevent UTI esp. In paralysis
 Prophylactic antibiotics
 Physiotherapy
• Psychiatric care: Depression follows usually
necessary in suicidal cases
• Follow up: to treat complications or long term sequelae