GENERAL PRINCIPLES

OF POISOING

 Poisoning is contact with a substance that results in

toxicity. Symptoms vary, but certain common syndromes

may suggest particular classes of poisons.

Treatment is supportive for most poisonings; specific

antidotes are necessary for a few.

1.

Acute poisoning excessive single dose, or several

smaller doses of a poison taken over a short interval of
time.

2.

Chronic poisoning smaller doses over a period of

time, resulting in gradual worsening eg. Arsenic ,
Phosphorus , Antimony etc.

1.

Homicidal killing of a human being by another human

being by administering poisonous substance deliberately.

2.

Suicidal when a person administer poison himself to end

his/ her life.

3.

Accidental Eg. Household poisons- nail polish remover ,

acetone, depilatories- Barium sulphide

4. Occupational in professional workers. Eg. insecticides,

noxious fumes.

Corrosives
a)

Strong acids- H2SO4 , HNO3 , HCl

b)

Strong alkalis- Hydrates & Carbonates of Na+ , K+ & NH3.

c)

Metallic salts Zinc chloride, Ferric chloride, KCN ,

Silver nitrate, Copper sulphate

Irritants
a. Inorganic

i) Nonmetallic Phosphorus, Iodine

Chlorine.
ii) Metallic Arsenic, Antimony, Lead.
iii) Mechanical Powdered glass, hair

b. Organic
Vegetable Abrus precatorius, Castor, Croton,
Calotropis.
Animal Snake & insect venom, Cantharides

Systemic
a) Cerebral
CNS depressants Alcohol, opioids, hypnotics, general anesthetics
CNS stimulants Amphetamines, Caffeine
Deliriant Datura, Cannabis, Cocaine

b) Spinal Nux vomica

c) Peripheral Conium, Curare
d) Cardiovascular - Aconite, Quinine, HCN
e) Asphyxiants CO, CO2 , H2S

4) Miscellaneous Food poisoning, Botulism.

 Following conditions should arouse suspicion of poisoning:

Sudden appearance of symptoms after food or drink in an

otherwise healthy person

Symptoms uniform in character, rapidity
Sudden onset delirium, paralysis, cyanosis, collapse etc.

Fundamentals of poisoning
management
1.

Initial resuscitation and stabilization

2.

Removal of toxin from the body

3.

Prevention of further poison absorption

4.

Enhancement of poison elimination

5.

Administration of antidote

6.

Supportive treatment

7.

Prevention of re - exposure

Fundamentals of poisoning management

Initial resuscitation and stabilization
I/V access I/V fluids
Endo tracheal intubation - to prevent aspiration
Unconscious patients
Respiratory depression/ failure
Convulsions- give anticonvulsants
Removal of toxin from the body

Copious flushing with water or saline of the body including skin

folds, hair
Inhalational exposure
Fresh air or oxygen inhalation

Prevention of poison absorption

1.

Gastric lavage

Useful if done before 3 hr of ingestion of a poison

Done with water ( except infants NS), 1:5000

potassium permangnate , 4% Tannic acid, saturated
lime water or starch solution

Administering & aspirating 5ml/kg through a No. 40 F

orogastric tube ( No. 28 F children) or Ewalds tube

Performed until clear fluid is obtained or a

maximum of 3 L

Complications

a. Aspiration (common)
b. Esophageal / gastric perforation
c. Tube misplacement in the trachea

Contraindications
a.

Corrosive poisoning GE perforation

b.

Petroleum distillate ingestants- Aspiration pneumonia

c.

Compromised unprotected airway

d.

Esophageal / gastric pathology

e.

Recent esophageal / gastric surgery

Lavage decreases absorption by an average

of :

52 % - if performed within 5 mins of ingestion

26 % - if performed at 30 mins

16 % - if performed at 60 mins

2. Ipecac Syrup induced emesis

Used for home management of patients with :Accidental ingestions
Reliable history
Mild predicted toxicity
Aministered orally
Dose : 30 ml adults
15 ml children
10 ml small infants

MOA
Ipecac irritates the stomach & stimulates CTZ center.
Vomiting occurs about 20 min after administration
Dose may be repeated if vomiting does not occur

Contraindications
a. Gastric / esophageal tears or perforation
b. Corrosives
c. CNS depression or seizures
d. Rapidly acting CNS poisons ( cyanide, strychnine,

camphor )

3. Activated charcoal
Greater efficacy
Less invasive
Given orally as a suspension ( in water ) or through NG

tube
Dose 1 g/kg body wt.
Charcoal adsorbs ingested poisons within gut lumen

allowing charcoal- toxin complex to be evacuated with

stool or removed by induced emesis / lavage

Barbiturate Poisoning
Barbiturates are a leading cause of acute poisoning

because of their ready availability

The poisoning is characterized by stupor or coma,

areflexia and in late cases, severe respiratory depression

and cardiovascular insufficiency
It is a potentially fatal form of poisoning with overall

mortality of about 7%

 Barbiturates are chemical derivatives of barbituric acid

and depending on their duration of action, they can be

classified as long acting (>6 hours), intermediate acting
(3-6 hours) and short acting (<3 hours).
All barbiturates bind to Gamma amino butyric acid

receptors and prolong the opening of chloride channels,

thus inhibiting excitable cells of the central nervous
system.
Barbiturates are frequently involved in over dosage

 Death occurs from respiratory failure, severe hypotension,

vasomotor failure, non cardiogenic pulmonary oedema,

hypothermia (which aggravates shock) or oliguria with
renal failure

Barbiturate poisoning is characterized by progressive

CNS depression culminating in paralysis of brainstem and

medulla. In early stages, patient is confused and lethargic
with poor coordination, ataxia and dysarthria

Management of barbiturate
poisoning
1. Cardiorespiratory support
2. Measures to prevent absorption:
a. Gastric lavage : If no more than 2-4 hours have passed
since ingestion of the barbiturate, gastric lavage is done.
b. Activated charcoal : Is an inert non toxic adsorbent
which binds high molecular weight compounds due to
intermolecular attractions. 1g/Kg is administered through
nasogastric tube. Cathartic like magnesium sulphate can be
used along with it for further removal of barbiturates but
hypermagnesemia can occur

3. Measures for removal of barbiturates:

Frequent doses of activated charcoal
Forced diuresis with alkalinisation of urine: in long

action barbiturates which are largely excreted by the kidney

Haemodialysis and haemoperfusion
Supportive care

Opioid poisoning
Opioids are a class of drugs that have actions similar to
opium. Opioids act on the brain and produce a number of
effects. The users also experience the following effects:
Drowsiness: due to depressant effect on the brain
Suppression of cough: due to the effect of opioids on the

brain cough centre

Constriction of the pupils in the eyes

Constipation: due to the effect of opioids on the gut system

 Opioid overdose does not happen immediately, it sets in

usually over the course of 1 hour to 90 minutes; as the

person slowly fails to respond and breathing becomes
more difficult.

 Following 3 symptoms/signs confirms that the individual

has overdosed on opioids:

1.Coma
2.Pinpoint pupils: Constriction of the pupils, in which the

pupils become smaller in size than normal

3.Respiratory depression: Difficulty in breathing, in which

the rate of respiration (less than 12/minute) in overdose

Warning Signs of Opioid overdose

Cant be woken up by noise or pain
Blue lips and fingernails due to lack of oxygen
Slow breathing (less than 1 breath every 5 seconds)
Gasping, gurgling, or snoring
Choking sounds
Passing out, Vomiting
Pale face, Tired body

 Naloxone Dose
0.4 2 mg per dose. The dose can be repeated, if

necessary, at 2 3 min intervals.

If there is no response after a total of 10 mg of Naloxone

has been given, consider the possibility that the person

may be suffering from conditions other than opioid
overdose.

Organophosphorus poisoning
Organophosphorous

(OP) compounds have been

employed as pesticides, petroleum additives and chemical
warfare nerve agents.

Organophosphates work by inhibiting acetylcholinesterse

thereby leading to an accumulation of acetylcholine and

over stimulation of muscarinic and nicotinic receptors.

Common organophosphate pesticides include malathion,

dichlorvos, trichlorfon, and fenitrothion/malathion.

Clinical Findings
Signs and symptoms can be divided into muscarinic,

nicotinic and central nervous system effects

Muscarinic

effects (over stimulation acetylcholine

receptors
of
the
parasympathetic
system):
Bronchospasm, bronchorrhoea, salivation, urination,
diarrhoea, hypotension, bradycardia and vomiting

Nicotinic

effects (over stimulation acetylcholine

receptors of the sympathetic system): Hypertension,
mydriais, tachycardia and sweating.

Clinical Findings
Nicotinic effects at neuromuscular junction: Confusion,

agitation, coma, respiratory failure

Central

nervous system effects: Muscle weakness,

fasciculations and paralysis (seizures may occur
secondary to hypoxia or due to nerve agents)

Signs

Symptoms

Mild

Dizziness, anxiety, headache, Rhinorrhea, sweating, salivation,

tightness of breath
nausea, weakness, coughing,
lacrimation, mild bradycardia and
hypotension

Moderate

Restlessness,
confusion,
dyspnoea,
disorientation,
abdominal
pain,
vomiting,
diarrhoea, drowsiness

Pallor,
miosis/mydriasis,
bradycardia/tachycardia,
hypotension/hypertension,
muscle twitching, fasciculation,
respiratory
depression,
bronchorrhea,
bronchospasm,
loss of consciousness

Symptoms
Severe

Convulsions,
respiratory
failure,
pulmonary edema, flaccid paralysis,
involuntary
micturation/defecation
cyanosis, deep coma

Fatal

Coma, convulsions, hypersecretions

and apnea within a few minute after
exposure

Management
Ensure adequate airways protection
Ensure adequate oxygenation give high flow oxygen via a

face mask
Ensure adequate circulation insert cannula and give i. v fluids
Give atropine until patient is fully atropinised. Start with

0.05mg/Kg of atropine i. v
Repeat every 15 mins until full atropinisation. Aim for pulse rate

>80 beats per minute and systolic blood pressure >80mm/Hg.

Management
Monitor patient over 15 minutes. If the dose of atropine is

too low cholinergic features will reoccur. If the dose of

atropine is too high agitation, pyrexia, reduced bowel
sounds and urinary retention will occur then reduce
atropine infusion
If patient presents within 24 hours of exposure and has

signs of moderate to severe organophosphate poisoning

give obidoxime 250mg ivi repeat after 2 hours.

Management
Monitor patient for secretions, pulse rate (use cardiac

monitor), pupil size, blood pressure, oxygen saturation

and pulse
The aim of treatment is to excessive oral and respiratory

secretions and prevent respiratory failure. Adequate

atropinisation is indicated by reduction of secretions
Control fits with boluses of diazepam give 10mg i. v

Diazepam is also useful for delirium and agitation in these

patients.

Atropine Poisoning
Clinical manifestations are caused by CNS effects,

peripheral nervous system effects, or both:

Flushing
Dry skin and mucous membranes
Dilated pupil with loss of accommodation
Altered mental status (AMS)
Fever, dryness of mouth,

Additional manifestations include the

following
Sinus tachycardia
Decreased bowel sounds
Functional ileus
Urinary retention
Hypertension
Tremulousness, Myoclonic jerking

 The antidote for anticholinergic toxicity is physostigmine

If marked excitement present give diazepam
Artificial respiration

Heavy Metals
large amounts of any of heavy metals cause acute or

chronic toxicity (poisoning).

Heavy metal toxicity can result in damaged or reduced

mental and central nervous function, lower energy levels,

and damage to blood composition, lungs, kidneys, liver,
and other vital organs.

 Long-term exposure may result in slowly progressing

physical, muscular, and neurological degenerative

processes that mimic Alzheimer's disease,Parkinson's
disease, muscular dystrophy, and multiple sclerosis

 Acute Toxicity:

cramping, nausea, and vomiting; pain;

sweating; headaches; difficulty breathing; impaired
cognitive, motor, and language skills; mania; and
convulsions.

Chronic Toxicity: (impaired cognitive, motor, and language

skills; learning difficulties; nervousness and emotional

instability; and insomnia, nausea, lethargy, and feeling ill

Chelators
Chelation is the formation of a metal ion complex in which

the metal ion is associated with a charged or uncharged

electron donor referred to as a ligand. It usually attaches
or coordinates using one, two or more electron pair donor
atoms (oxygen, nitrogen and sulfur).

Requirements for the ideal chelating agent

The compound should be soluble in aqueous medium

The chelating agent should be stable in the circulation

If it is given orally, it should be absorbed by the GI tract

and it should be cleared by the kidney

The compound should be active at physiological pH

Requirements for the ideal chelating agent

The compounds should chelate only the specific metals
The chelator itself should not be toxic
The chelator-metal complex should be less toxic than the

metal alone

METALS AND DRUGS (CHELATORS)

TO CONSIDER
Lead

Ethylenediamine-tetraacetic acid (EDTA)

2,3-dimercaptosuccinic Acid (Succimer)
2,3-dimercaptopropanol (BAL, Dimercaprol)
Penicillamine

Cadmium

Ethylenediamine-tetraacetic Acid (EDTA)

Mercury

N-acetyl-penicillamine (NAP)
Penicillamine
2,3-dimercaptopropanol (BAL, Dimercaprol)
2,3-dimercaptosuccinic Acid (Succimer)

Arsenic

N-acetyl-penicillamine (NAP)

Iron

Deferoxamine

Arsenic
Acute arsenic poisoning symptoms are sore throat from

breathing, red skin at contact point, or severe abdominal

pain, vomiting, and diarrheal, often within 1 hour after
ingestion.

Other symptoms are anorexia, fever, mucosal irritation,

and arrhythmia.

Cardiovascular changes are often subtle in the early

stages but can progress to cardiovascular collapse.

Arsenic
Progressive peripheral and central nervous changes, such

as sensory changes, numbness and tingling, and muscle

tenderness

Burning sensation ("needles and pins") in hands and

feet

Mechanisms of toxicity
Membranes: protein damage of capillary endothelium

increased vascular permeability leading to vasodilation

and vascular collapse
Inhibition of sulfhydryl group containing enzymes
Inhibition of anaerobic and oxidative phosphorylation

(substitutes for inorganic phosphate in synthesis of highenergy phosphates)

Symptoms
Acute - damage to mucosa, sloughing, hypovolemic

shock, fever, GI discomfort/pain, anorexia

Chronic - weakness, GI, hepatomegaly (jaundice >

cirrhosis), melanises, arrhythmias, peripheral neuropathy,

peripheral vascular disease (black foot disease)
Carcinogenicity

epidemiologic
angiosarcoma, skin and lung cancer

evidence;

liver

Treatment
Dimercaprol (2, 3 dimercaptopropanol, also known as

British anti Lewisite or BAL) earlier used

2-3-dimercapto-1-propanesulfonate (DMPS) or meso 2, 3-

dimer-captosuccinic acid (DMSA). These are more water

soluble than BAL, and can be administered orally with
lower toxicity

Acute: supportive therapy: fluid, electrolyte replacement,

blood pressure support (dopamine)

Chronic: Penicillamine w/o dialysis