TREATMENT OF TOXICITY

ACUTE POISONING

Treatment of toxicity 1
 PRINCIPLES OF NON-SPECIFIC
THERAPY
Maintain respiration and circulation.
Find out what drug was taken and how much.
Stop or retard further absorption of toxic agent
into circulation.
If the drug was ingested and the patient is
conscious induce vomiting by mechanical
gagging or
emetics ( e.g. syrup Ipecacuanha; Mustard
powder ) by mouth or
give injection of Apomorphine. 2
Treatment of toxicity
Vomiting should not be induced if toxic
agent is corrosive ( Lye; Kerosene ) for
it
may cause haemorrhage or perforation
of the oesophagus or stomach.
Gastric lavage should be carried out if
the patient is unconscious and non
corrosive agent was ingested may be
carried out only after inserting a cuffed
endotracheal tube.
Treatment of toxicity 3
Activated charcoal or large
amounts of protein may be given
by mouth to adsorb toxic material.
Apply tourniquets in case drug
was given S.C. or I.M. proximal to
the injection site.
If the toxic substance is being
absorbed through the skin,
thorough washing is indicated.
Treatment of toxicity 4
Haemodialysis (way of cleansing the
blood of toxins thru a dialysis
machine) for drugs like Salicylates;
 long acting Barbiturates;
 Glutethimide bromide and
Menthol.
Peritoneal dialysis may also be an
alternative. Type of dialysis which
uses peritoneum.
Treatment of toxicity 5
Induction of acidosis or alkalosis
may promote the redistribution of
weak acids or bases.
Administration of Bicarbonates
will cause transient alkalosis in
plasma and thus
will promote shift of Barbiturates
out of the brain and other
tissues into plasma.
6
Treatment of toxicity
 PRINCIPLES OF ANTIDOTAL TREATMENT:
MECHANISM –1
Antidote compelexes with poisoning rendering it
inert.
 Chelating agents are used to form tightly bound non-
toxic complexes with heavy metal ions.
 This reduces the concentration of free metal ions
in the body fluids and thus
 promotes the dissociation of bound metal from
tissue enzymes and other functional
macromolecules.
 The metal chelates complexes are water soluble and
can be excreted by the kidney.
Treatment of toxicity
7
• EXAMPLES CHELATING
COMPOUND:
Arsenal mercury Dimercaprol (BAL)
 Lead, Plutonium & Dimercaprol (BAL),
Uranium disodium Edetate
(EDTA)
Diethylene triamine
penta-acetic acid
(DTPA);
Penicillamine
Iron Sodium
ferrocyanide ( by
mouth).
Desferrioxamine by injection or
by mouth Treatment of toxicity 8
 Copper Penicillamine ( for Rx Wilson
disease ) EDTA ( during
poisoning).

 Thallium Dithizone ( Diphenyl-

thiocarbazone) Dithiocarb
( Sodium diethyl-
dithio
Carbamate ).

 Formaldehyde Ammonium ( by mouth ).

 Heparin Protamine
Treatment of toxicity 9
Botulinus toxin Botulinus
antitoxin.

 Various drugs Specific

antibodies
 Digitalis glycosides Steroid binding resin
• (Cholestyramine Colestipol ).

Cholinesterase inhibitors Pralidoxine

Treatment of toxicity 10
Cyanide Methaemoglobin ( formed by
nitrite administration ).

Treatment of toxicity 11
 MECHANISM-2

Antidote accelerates
metabolic conversion of
poison to non-toxic
product.

Treatment of toxicity 12
 CYANIDE
The CN- ion is normally converted to
the innocuous Thiocyanate (CNS-)
By the cyanide thiosulphate sulphur
transferase but the reaction
Is low because sulphur donors e.g.
Thiosulphate are present in the body
in limited amounts.
Treatment of toxicity 13
Administration of Thiosulphate will
accelerate this reaction.
Thiosulphate is a sulphur donor.
The LD 50 is increased 3 fold by
Sodium Thiosulphate alone,
5 fold by Sodium Nitrite alone
and 18 fold by combination of both
antidotes.
Treatment of toxicity 14
Thiosulphate is Sulphur donor
Sodium Nitrite converts normal
Haemoglobin to Meta-HB
Met- Haemoglobin combines with
cyanide to form a complex that will
eventually be excretes thru the
kidneys.
Methylene blue converts Met-HB to
normal Haemoglobin.
Treatment of toxicity 15
Third approach is administration of
oxygen despite the fact that the
Haemoglobin is fully saturated in
cyanide poisoning,
increasing the Physically dissolved
plasma O2 tension by-passes some
of the cyanide Blockade of tissue O2
utilization.

Treatment of toxicity 16
 MECHANISM-3

Antidote blocks
metabolic formation of
poison from less toxic
precursor.
Treatment of toxicity 17
 METHANOL
Methyl alcohol in large doses is a depressant
of CNS but in Methanol Poisoning the cause
of death is not due to CNS depression but to
two
Metabolites FORMALDEHYDE which
selectively damages retinal cells
Causing blindness and FORMIC ACID which
produces acidosis.
Ethanol and Methanol are oxidized by

Treatment of toxicity 18
ALCOHOL DEHYDROGENASE to
acetaldehyde and Formaldehyde
respectively.
Ethanol can competitively inhibit the
metabolism of Methanol because
The affinity of alcohol dehydrogenase is
about 10-fold that of Methanol.
Aldehyde dehydrogenase converts
Acetaldehyde and Formaldehyde to
Acetic acid and Formic acid
respectively.
Catalase also behaves like alcohol
dehydrogenase. Treatment of toxicity
19
 MECHANISM-4

Antidote specifically accelerates excretion of

poison.
BROMIDE
Once used as a sedative and an anti-
epileptic, is handled in the kidney in
The same way as chloride.
The bromide half-life can be reduced from

Treatment of toxicity 20
12 days to 3 to 4 days by Chloride
administration.
Increasing Chloride levels in the
plasma and glomerular filtrate leads to
diminished fraction of Bromide that is
reabsorbed
and thus to an increased bromide
clearance.

Treatment of toxicity 21
 MECHANISM –5

Antidote compete
with poison for
essential receptor.

Treatment of toxicity 22
 CARBON MONOXIDE
Carbon monoxide combines with
Haemoglobin to form
carboxyhaemoglobin.
Administration of pure Oxygen or a
mixture containing 95% Oxygen
And 5% Carbon dioxide will promote
competitive displacement of
carbon monoxide from haemoglobin.
Treatment of toxicity 23
 MECHANISM-6

Antidote blocks receptors that

are responsible for toxic effect.

Treatment of toxicity 24
 CHOLINESTERASE INHIBITORS
Use of Atropine to prevent the toxic
effects of cholinesterase inhibitors.
Atropine is ineffective at neuromuscular
junction hence paralysis
Of respiratory muscle will not be
prevented.
Prompt artificial respiration is called for.
Pralidoxine is also given.
Treatment of toxicity 25
 MECHANISM –7

Antidote restores normal

function by repairing or
by-passing Effects of
poison.

Treatment of toxicity 26
 GUANIDINE HYDROCHLORIDE
Guanidine hydrochloride appears
to act by facilitating the release
Of Acetylcholine by action
potentials arriving at the
cholinergic terminals.

Treatment of toxicity 27
The effect therefore is to bypass
or repair the functional damage
caused
By Botulinus toxin which prevents
both action potential and
spontaneous
Release of Acetylcholine from all
cholinergic axons
Treatment of toxicity 28