START WITH THE NAME OF

ALLAH
THE MOST BENEFICIENT,
THE MOST MERCIFUL
 Toxicology

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 Introduction

Paracelsus, the father of toxicology

states; "Everything is poison, there is
poison in everything. Only the dose
makes a thing not a poison"

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 Definition
Toxicology is science of the adverse
effects of chemicals including drugs on
living organisms.
Poisons are substances that can cause
damage, illness, or death to organisms,
usually by chemical reaction or other
activity on the molecular scale, when a
sufficient quantity is absorbed by an
organism.
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 Types

Two specialized areas of toxicology are

particularly important in medicine:
forensic toxicology
clinical toxicology

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 Forensic toxicology
which combine analytical chemistry and
fundamental toxicology is concerned with
medicolegal aspects of chemicals. Forensic
toxicologist assists in postmortem
investigations to establish the cause or
circumstances of death.

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 Clinical toxicology
This branch of toxicology deals with the
harmful effects of chemical substances
on human and animals and examines
poisoning from the lethal point view.

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 Diagnosis
Important variables include
B.P
Pulse Rate
Temperature
Pupil Size
Sweating
Presence or absence of peristaltic
activity
Any clue of poison taken

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 Evaluation

chemical substance being exposed.

Analyzed by the levels of the toxic
substances in biological materials such
as urine, tissue, or organ and dose
response relationship.

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 General Management of
Poisoning and Overdose
Three goals are particularly important in
clinical toxicology.
correct diagnosis
assessment of severity
appropriate initial management

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 Principles of
Management and
Treatment

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 Initial ABC (airway, breathing,
circulation) assessment and
resuscitation if necessary.
A secondary survey for infection or
trauma (of the head and cervical spine if
the patient’s mental status is abnormal.

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 Case specific management such as
preventing further absorption,
administration of antidotes or enhancing
the elimination of toxic agents.

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 Expeditious (speedy ) evaluation of
samples of blood urine vomitus or other
body fluids to identify responsible
compound. In serious cases early
treatment and supportive care should
proceed rapidly prior to the extensive
investigation or apparent diagnosis.

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 Attention must be given providing
immediate treatment of life threatening
conditions such as hypotension,
hypertension, bradycardia, tachycardia,
cardiac arrhythmia, hypo and hyper
thermia and respiratory depression.
Cardiac monitoring and immediate
treatment is needed for arrhythmia.
Metabolic disorders are also identified,
e.g; metabolic acidosis caused by toxic
alcohol like ethylene glycol and
salicylate poisoning.

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 Where it seems possible blood samples
are collected and sent for complete
blood count, hepatic and renal functions
and electrolytes.
In case of suicidal patients the plasma
levels of drug indicated by patient’s
history e.g; iron, lithium, digoxin, are
measured.
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 Toxidrome

Cluster of symptoms and sign in the

same patient known as “toxidrome” may
be of considerable value in helping to
identifying the toxic agent e.g;

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 opioids toxidrome

opioids toxidrome characterized by

pin point pupil, hypotension, respiration
depression and impaired
consciousness.

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 Anticholinergic
syndrome
Anticholinergic syndrome found with
tricyclic antidepressants and
antihistamines. It includes tachycardia,
dilated pupil, dry and warm skin, dry
mucous membrane and urinary
retension.

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 Cholinergic toxidrome

Cholinergic toxidrome found after

exposure to organophosphates
poisoning and carbamate insecticides
includes salivation, lacrimation, urinary
and fecal incontinence emesis,
abdominal pain, diaphoresis and small
pupil.

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 Classification of Toxic
Agents on the Bases of
treatment
Those for which a specific treatment or
antidote exists.
Those for which there is no specific
treatment .

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“Treat the patient and not the poison” is
the most basic and important principle
of clinical toxicology.”

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 Plan of therapy

Decrease absorption of toxins

Enhance elimination of toxins
Chemical inactivation

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 Decrease absorption of
toxin:
Absorption can be reduce by:
inducing emesis with syrup of epicac or
epomorphine
performing a gastric lavage
using chemical adsorbent for example
activated charcoal.

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 Limitations of emesis:
If the patient has ingested corrosive poison
such as strong acid or alkali e.g; drain
cleaner. Here emesis will cause perforation
and further necrosis of esophagus.
If the patient is unconscious. Here the chance
of gastric content aspiration is present.
If the patient has ingested the CNS stimulant.
Here emesis may precipitate convulsions due
to further stimulation of CNS.

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 Gastric Lavage
Procedure:
Insert the nasogastric tube and wash the
stomach with water, normal saline or ½
normal saline solution to remove the
unabsorbed poison.
The procedure can be undertaken within 60
minutes of ingestion of potentially life
threatening amount of poison. It should not
be used routinely.
Care should be taken to avoid mechanical
injury to throat and esophagus.
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 Activated Charcoal
Activated charcoal is a black powder because
the particles are extremely small and contain
many pores, the surface area of one gram of
material may exceed 3,000 meter square. A
compound that is adsorbed to activated
charcoal cannot be absorbed from GIT. Its
elimination is enhanced and systemic toxicity
is minimized.
Dose of activated charcoal is 50 g

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 Systemic antidotes
Systemic antidotes are of two types:
Specific antidotes
Chelating agents

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 Specific antidotes
N-Acetyl cysteine:
It is an antidote for paracetamol. N-acetyl
cysteine acts as sulfhydryl group donor
substituting for the liver’s usuall sulfhydryl
donor, glutathione. It rapidly binds to reactive
metabolites. Reactive metabolite (toxic) is N-
acetyl parabenzoquinonimine (NAQBI).
It is most effective when given within 8-10
hours, but may also be of beneficial in
reducing liver injury when given after 24
hours.

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 Loading dose: given 140 mg per KG, 10% or
20% solution diluted to 5% in juice.
Maintenance dose: 70 mg /kg every four
hours for 17 doses or until acetaminophen
level is zero.
Parenteral route: initial dose is 150 mg /kg
body given in 200 ml o0f 5% dextrose by slow
I/V infusion over 15 minutes following 50
mg /kg in 500 ml of 5% dextrose is
administered. Finally 100mg/kg in 1 L of 5%
dextrose is given over 16 hours.

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 Naloxone :

It is indicated in patients with opiate

poisoning such as morphine, heroin,
codeine and methadone usually
associated with respiratory depression.

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 It is indicated in patients with opiate poisoning such
as morphine, heroin, codeine and methadone usually
associated with respiratory depression.
Mechanism of action
It acts as a competitive antagonist.
Adult dose: 0.4 to 2 mg I/V bolus, repeat after every
2-3 minutes interval until desired response is
achieved. Naloxone is usually diluted in sufficient 5%
dextrose or normal saline to provide adequate fluid
maintenance for patient.
Child dose: 0.01-0.1 mg /kg
Formulation: naloxone HCl
1, 2ml, 10ml ampule or vial . maximum stock level
required for treatment is 30 mg. (1mg/ml)
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 Flumazenil
It is an antidote for BZP, which are
commonly taken inself harm attempts. It
is licensed for the complete or partial
reversal of sedative effect of
benzodiazipines following anesthesia or
in intensive care. It is generally sager to
provide supportive care including airway
or ventilating support if required, until
the BZP toxicity has reversal.

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 Titrate the dose until desired response is
achieved.
Administer 0.2 mg I/V over 30 seconds. If no
response occur, give 0.3 mg, if no response,
give 0.5 mg and repeat every 30 seconds, if
needed to a total max. dose or 3mg. reversal
occur within 1-2 min, peaks at 6-10 min and
last for 1-5 hrs depending on the dose and
the degree of pre existing BZP effects.
If multiple repeated doses are needed, give
continues infusion at rate of 0.2-1mg per
hour.
The formulation
0.1 mg/ml of 5 ml or 10 ml of vials.
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 Sodium nitrite and
Sodium thiosulfate
These antidotes are indicated in
cyanide poisoning. Cyanide poisoning
may occur in workplace accidents or as
a products of combustion along with
CO, in household fires. Cyanide
poisoning may also be encounter as
side effect of sodium nitropruside
infusion.

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 Dose

Sodium nitrite = 10 ml of 3 % solution

(300mg ) given I/V over 5-20 minutes,
usually followed by sodium thiosulfate.
The dose of sodium thiosulfate is 50 ml
of 25% solution i.e; 12.5 g given I/V
over ten minutes.

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 Glucagon
It is recommended antidote for over doses of
B-Blockers such as propranolol and atenolo,
causing hypotension and bradycardia.
Mechanism of action
It exerts the positive inotropic effect by
stimulating adenylate cyclase independently
of B- receptors.
Dose
A bolus dose of 10 mg is recommended given
I/V over 5-10 min. the dose can be repeated
depending on the response.
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 Pralidoxime
It is an antidote of rganophosphate poisoning.
Atropine can also be used as antidote if pralidoxime
is not available. Organophosphate poisoning occur
due to enhance acetyl choline activity.
Mechanism of action
Pralidoxime reactivate inhibited acetyl choline
estrases. Presence of a charged group allows it
approach an anionic site on the enzyme where it
essentially displaces the organophosphate and
regenerate the enzyme.

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 Dose

Adult dose: 1 g I/V bolus over 5-10

min( rate not to exceed 200mg per min)
Child dose: 20-40 mg/kg I/V over 5-10
min ( rate not to exceed 4mg /kg per
min)

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 Chelating Agents
The agent that posses ability to form complex with
heavy metals and there by prevent or reverse the
binding of metallic cations to body ligands are known
as chelating agents
Mechanism of action
Chelating agents are large anionic molecules that
reversibly bind with high affinity to di and trivalent
metal cations to form a metal complex. This complex
is eliminated from body using the body’s natural
mechanism of waste product removal.

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 chelating agent
Name of chelating agent
Dimercaptol ( BAL)
Penicillamine
Desferrioxamine mesilate or
deferoxamine mesilate
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Heavy metal
Lead, mercury, gold, arsenic
Copper (Wilson’s disease), also
used in the treatment of
nephrolithiasis and rheumatoid
arthritis.
Iron toxicity
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 Questions

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 Thankyou
Have a nice day.

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