General Strategies for

Management of Toxic Events

Philip Sasi
Main stay of managing intoxicant is;
1. Intensive Supportive therapy.
Maintaining vital body function by appropriate
drug use and mechanical technique.
2. Additional measures;
- Decontamination
- Elimination enhancement
1. Resuscitation
-Primary survey /Stabilization: Which includes
assessment and A,B,C,D,E approach.
-Secondary survey/Evaluation: Once the patient is
already stable (History and Physical examination).
2. Decontamination
3. Enhancement of Elimination
4. Specific pharmacotherapy(Antidote administration)
 Resuscitation
• Airway- Patency, secured
Secretions,
Positioning, Intubation

• Breathing- Spontaneous,
RR, SpO2
Oxygen therapy

• Circulation- Hemodynamic stability

BP, PR, CPRT,
ECG, IVF, Monitor
 Resuscitation cont..
• Disability- Level of consciousness
-B/Glucose level
Use the “coma cocktail”
D- Dextrose,
O- Oxygen
N- Naloxone,
T- Thiamine
• Exposure- Removal of contaminated clothes.
 Resuscitation cont..
• Evaluation: Focused History on:
- S: Symptoms,
(what, when, how much, what else, why)
- A: Allergies
- M: Medication
- P: Past Medical History. i.e Liver/Kidney disease
- L: Last meal/LNMP
- E: Events
 Physical Examination
• Physical examination with Toxidrome assessment.

-Vital signs: BP, HR, RR, O2, T⁰C

- CNS: Higher centre, Pupils

-R/S: ?Pulmonary Edema

- P/A: Bowel sounds, Bladder dysfunction

- Skin: Dry or Diaphoretic

• Toxidrome; This is a pattern of signs and symptoms
that suggests a specific class of toxicant and allows
one to narrow the differential diagnosis.

• Starting point for management and may suggest the

laboratory tests that follow.
Toxidromes
 Diagnostic Tests
• Blood gases
• Electrolytes
• Liver Function Test
• Ser. Creatinine, BUN
• Drug screen
• Specific drug levels(Plasma concentration
measurement)
 Diagnostic Tests cont.
• Blood gases
-Blood pH, HCO3, PCO2, PO2

• Serum Electrolyte(Na, K, CL, HCO3) and BUN

- Anion Gap: Na⁺ - ( CL⁻+ HCO3⁻), Normal = 12- 16

MUD PILES: ↑
Methanol, Metformin, Uraemia, DKA, Paraldehyde,
Iron, Isoniazid, Lithium, Ethanol, Salicylate.
 Osmolality Gap
• Calculate the expected osmolality.
(2xNa⁺)+ Glucose+ BUN

• Compare with measured osmolality.

Normal value ≤ 10

↑ Alcohol, Ethylene glycol and Methanol

• In some cases of poisonings, there are specific
treatments or antidotes available that
prevent, interrupt, or reverse the toxicity

• In such cases, hazard identification and

knowledge of the toxicodynamics of the
toxicant are critically important for selection
of the appropriate antidote or treatment

• Antidotes or specific treatments may act via a

number of mechanisms including the
following:
• Antibodies
– neutralize toxicants or prevent their distribution to
target organs (e.g., antivenin for snake bites)

• Compounds that sequester the toxicant

– prevent its distribution, and promote its excretion
(e.g., heavy metal chelators)
• Compounds that scavenge the toxicant
– prevent the toxicant interaction with tissues
(e.g., N-acetylcysteine [NAC] in acetaminophen
poisoning)
• Pharmacologic antagonists
– block receptors stimulated by the toxicant
• Pharmacologic agonists
– stimulate receptors blocked by the toxicant
• Treatments that act physiologically to
oppose the actions of the toxicant (e.g.,
pressor agents to reverse hypotension)
• Enzyme inhibitors
– that prevent the formation of toxic intermediates

• Enzyme activators
– that reverse enzymatic inhibition produced by
toxicants
• In addition to specific treatments, a number of
generalized treatment strategies can be used in
poisonings
• These are toxicokinetic treatment strategies
targeted at :
– reducing or preventing the absorption of the
toxicant, at
– reducing the distribution of the toxicant,
– manipulatingbiotransformation to reduce
formation of the toxicant,
– hastening excretion of the toxicant
• Toxicokinetic treatment strategies rely heavily
on the concepts of pharmacokinetics

• They are very useful in situations in which

there are no specific antidotes or the
causative toxicant(s) and/or modes of action
are not sufficiently well defined to allow
application of a specific antidote
Reduction or Prevention of Absorption
• Because the majority of poisonings occur
via ingestion,approaches to limit absorption
via this route are critical for management of
toxic events
• Approaches to limit absorption via other
routes are generally common sense
approaches.
• For example, moving the patient to fresh air if
the exposure route was inhalational or
flushing the skin with water in the case of
dermal exposure
• Several options are available to reduce oral
absorption of toxicant.
• Collectively, these approaches are sometimes
referred to as gastrointestinal (GI)
decontamination.
 GI Decontamination Approaches
• Forced emesis
– can remove toxicants present in the stomach.
– This approach may be useful if there is reason to
believe that there is toxicant remaining in the stomach
(e.g. if the time since exposure is relatively short or if
gastric emptying has been delayed)
– In the past, a number of approaches have been used
to induce emesis.
– However, most have been abandoned.
– The most frequent method in current use is ingestion
of syrup of ipecac.
Ingestion of syrup of ipecac
– Mechanism of action
• Stimulation of sensory receptors in the GI tract
• Stimulation of chemoreceptor zone in the CNS
– Adverse effects
• Aspiration of vomitus into lungs
• Physical damage due to the act of vomiting (e.g., gastric
tears)
• Impairment of other GI decontamination procedures
since patient may continue to vomit for prolonged
period
• Electrolyte imbalance
Ingestion of syrup of ipecac continued
– Contraindications
Ipecac should not be used with toxicants such as:
• Petroleum distillates (e.g., gasoline, furniture polish)
• Corrosives (strong acids, strong bases) (e.g., drain cleaner)
• CNS stimulants, because act of vomiting may trigger
convulsions
Unless a secure (intubated) airway has been established,
ipecac should not be used in the following patients:
• Those who are unconscious
• Those with impaired airway reflexes
• Anticipated use of other GI decontamination procedures,
because emesis would remove the treatments from the GI
tract
• In the past, the use of ipecac to induce forced
emesis was promoted for GI decontamination
in both hospital and home settings

• Recommendations from a number of poison

control organizations now indicate a
much more conservative use of ipecac
because of the potential for harm and the
relative lack of evidence for definitive
benefits.
• Available data suggest that ipecac may be of
use in the following situations:
– In pre-hospital settings when there are no
contraindications for use
– When the ingested toxicant poses substantial risk
– If no alternative means of GI decontamination are
available
– When ipecac can be administered within 30
minutes of toxicant ingestion
– When there will be a substantial delay (>60
minutes) in reaching treatment facilities
• Gastric Lavage
– Gastric lavage involves placing a tube through the
mouth (orogastric) or through the nose
(nasogastric) into the stomach.

– Toxicants are removed by flushing saline solutions

into the stomach, followed by suction of gastric
contents.
• Gastric Lavage continued
– Mechanism of action
• Physical removal of toxicant
– Adverse effects
• Aspiration of lavage into lungs
• Mechanical injury caused by placement of the gastric
tube
• Endotracheal placement (into the trachea and thus into
the lungs) of gastric tube
• Electrolyte imbalance
• Gastric Lavage continued
– Contraindications
Gastric lavage should not be used with toxicants such
as the following:
• Petroleum distillates (e.g., gasoline, furniture polish)
• Corrosives (strong acids, strong bases) (e.g., drain cleaner)
• CNS stimulants, because the act of vomiting may trigger
convulsions
Unless a secure (intubated) airway has been
Established, gastric lavage should not be used in the
Following patients:
• Those who are unconscious
• Those with impaired airway reflexes
• Gastric Lavage continued
– Although in theory gastric lavage would seem to
be the most direct way of removing a toxicant, the
available evidence does not support the routine
use of gastric lavage

– Gastric lavage may be useful in cases in which

there has been very recent ingestion (30 minutes
to 1 hour) of a life-threatening toxicant
• Activated Charcoal
– Activation of charcoal by oxidization increases
its adsorptive surface area

– The large surface area of charcoal is capable of

adsorbing many toxicants, thus sequestering them in
the gut

– Because only free molecules are able to diffuse across

membranes, reduction of the concentration of free
toxicant in the gut by charcoal greatly reduces
absorption into the bloodstream

– This treatment is administered as a slurry of the

activated charcoal powder
• Activated Charcoal continued
– Mechanism of action
• Toxicant molecules adsorbed to charcoal are not
absorbed
• May increase elimination by decreasing free
concentration of toxicant in gut
• May interrupt enterohepatic cycling
– Adverse effects
• Vomiting, particularly with premade solutions
containing sorbitol (seen in up to 40% of patients)
• Aspiration; charcoal can cause marked lung damage
• Reduced absorption of other drugs or antidotes
• Constipation
• Activated Charcoal continued
– Contraindications
• Patients at risk for bowel perforation (e.g., ingestion of
corrosives)
• Toxicants with significant potential for aspiration (e.g.,
petroleum distillates)
• Toxicants that are not adsorbed to charcoal
– Alcohols
– Iron
– Highly polar molecules and salts
Unless a secure (intubated) airway has been
Established, activated charcoal should not be used in
the following patients:
• Those who are unconscious
• Those with impaired airway reflexes
• Activated Charcoal continued
– Available data suggest that activated charcoal is
effective at reducing the absorption of many
toxicants

– This treatment may be administered as single-

dose activated charcoal(SDAC) or repeated
as multiple-dose activated charcoal(MDAC)

– However, the efficacy of SDAC charcoal at

preventing drug absorption is very time
dependent and decreases rapidly with time from
ingestion
• Activated Charcoal continued
– SDAC is most effective if administered within 60
minutes of toxicant ingestion

– MDAC is most frequently used in cases of

poisoning with controlled-release substances,
with the goal of binding toxicant as it is released
from its formulation

– In addition, MDAC also may be of benefit in

increasing the elimination of toxicants
• Activated Charcoal continued
– Current recommendations suggest that activated
charcoal should be used in the following
situations:
• When the toxicant is potentially fatal

• When no contraindications to its use are present

• If the toxicant binds to charcoal

• If the time since ingestion suggests toxicant is still

present in the GI tract
• Whole bowel irrigation and Cathartics
– Whole bowel irrigation and cathartics are used to
prevent the absorption of toxicants by increasing
GI motility and passage of the GI contents,
thereby reducing the time available for drug
absorption
– Cathartics use osmotic substances to draw fluid
into the gut and produce diarrhea
– The most commonly used cathartic is sorbitol
– Available recommendations
currently discourage the use of cathartics as sole
therapy for poisonings because of the
associated dehydration and electrolyte
disturbances
• Whole bowel irrigation continued
– Whole bowel irrigation (also called whole gut
lavage) is an evolution of the cathartic concept
– This approach combines oral administration
of high–molecular-weight substances, generally
polyethylene glycol, with iso-osmolar electrolyte
solutions (e.g., Golytely)
– This combination tends to prevent systemic
electrolyte disturbances that complicate the use of
cathartics alone
– Large volumes of these solutions plus water are
administered orally or by gastric tube
• Whole bowel irrigation continued
– Mechanism of action
• Increased volume in GI tract promotes voiding
• Administration is continued until rectal discharge is
clear
– Adverse effects
• Nausea, vomiting
• To date, systemic electrolyte disturbances have not
been reported
– Contraindications
• Patients with impaired bowel function (e.g., ileus) or
perforation
• Patients susceptible to aspiration if vomiting occurs
• Whole bowel irrigation continued
– Whole bowel irrigation has been shown to decrease
the bioavailability of certain toxicants

– Although there are no consensus statements

regarding specific indications for whole bowel
irrigation, this approach may be best suited for
intoxications for which the other methods of GI
decontamination may not be appropriate

– More specifically, whole bowel irrigation may be

particularly useful in cases where there has been
a long time lag between ingestion and treatment and
in cases in which toxicants are released slowly
• Whole bowel irrigation continued
– Current recommendations suggest that whole bowel
irrigation should be used in the following situations:
– For poisonings with controlled-release substances

– When there is an extended time between ingestion

and treatment (2 hours or more)

– For toxicants that are not well adsorbed by activated

charcoal (e.g., iron tablets)

– For ingestion of transdermal patches or illicit drug

packets
 Manipulation of Distribution
• After absorption, most toxicants must be
distributed to the target tissues to exert
harmful effects
• Accordingly, another strategy for managing
toxicity is to prevent the distribution of toxic
substances
• In general this is accomplished by binding the
toxic substance in the blood and preventing
access to its site of action
• General mechanisms of action of binding
agents
– Antibodies
• Generally highly specific for toxicant
• Eliminated by renal excretion
• Often used as antigen binding fragments (Fab
fragments) resulting from the proteolytic digestion of
the whole antibody
• Use of Fab fragments tends to reduce the incidence of
hypersensitivity reactions
• Antibody fragments also penetrate more readily to the
interstitial spaces to neutralize toxicants that have
already undergone distribution
• General mechanisms of action of binding
agents continued
– Antibodies
• Major adverse effects are hypersensitivity reactions
and delayed serum sickness
• Examples include: Antivenin and Digoxin binding
antibodies
• General mechanisms of action of binding
agents continued
– Chelating agents
• Contain reactive sites such as hydroxyl or sulfhydryl
groups that bind target molecules
• Heavy metal chelators bind to metal ions to form stable
complexes
– Reduces distribution of metal
– Shields metal from reacting with functional groups on cellular
constituents
– Allows excretion of metal chelates in urine or feces (biliary
excretion)
• General mechanisms of action of binding
agents continued
– Edetate calcium disodium (calcium disodium salt
of ethylenediaminetetraacetic acid; EDTA)
• Binds iron, lead, copper, manganese, cobalt, and
calcium

• Primarily used to treat lead intoxication

• Not effective for mercury poisoning

• Highly charged, so has poor oral bioavailability; requires

parenteral administration (intravenous or
intramuscular)
• General mechanisms of action of binding
agents continued
– Edetate calcium disodium (calcium disodium salt of
ethylenediaminetetraacetic acid; EDTA)
• When administered intramuscularly, has the propensity
to cause pain at the injection site, so it is combined with
local anesthetic agents
• Used as the calcium salt to prevent excessive binding of
endogenous calcium and hypocalcemic tetany
• Short half life (<1 hour) necessitates frequent
administration
• EDTA-lead chelates are excreted primarily in the urine
• Main adverse effect is nephrotoxicity
• General mechanisms of action of binding
agents continued
– Dimercaprol (British antilewisite)
• Useful in arsenic, mercury, lead, cadmium intoxication

• Rapidly oxidized in aqueous solutions so given

intramuscularly in peanut oil

• Chelates primarily excreted in urine

• Thiol-metal ion bonds are labile in acidic solutions;

alkalinization of urine is used to prevent release of
metal ions in renal tubule and nephrotoxicity
• General mechanisms of action of binding
agents continued
– Dimercaprol (British antilewisite)
• Main adverse effects include:

– Nausea, vomiting

– Marked hypertension

– Burning sensations
• General mechanisms of action of binding
agents continued
– Penicillamine
• Metabolite of penicillin

• Oral bioavailability sufficient to allow oral therapy

• Useful in intoxication from copper (Wilson’s disease),

mercury, and lead
• General mechanisms of action of binding
agents continued
– Penicillamine continued
• Chelates excreted in urine

• Main adverse effects include the following:

– Dermatologic reactions
– Renal toxicity
– Hematologic toxicity (e.g., leukopenia)

• Patients who become intolerant to penicillamine during

long-term therapy for copper intoxication can be
switched to another copper chelator, trientine
• General mechanisms of action of binding
agents continued
– Succimer
• Mercapto (thiol-containing) analogue of succinic acid

• Oral bioavailability sufficient to allow oral therapy

• Currently used as a chelator in lead toxicity, but may

bind other heavy metals
• General mechanisms of action of binding
agents continued
– Succimer continued
• Water-soluble succimer chelates are excreted in the
urine
• Less toxic than dimercaprol
• Half-life is approximately 2 days
• Main adverse effects include the following:
– GI complaints
– Rash
– Flulike symptoms
• General mechanisms of action of binding
agents continued
– Deferoxamine
• Poor bioavailability necessitates parental
administration via intramuscular, subcutaneous, or
intravenous (least preferred) route

• Extremely high affinity for iron; very effective for iron

intoxication
• General mechanisms of action of binding
agents continued
– Deferoxamine continued
• Eliminated by renal excretion, with a half-life of
approximately 6 hours
• Adverse effects of note include the following:
– Allergic reactions
– Hypotension (especially via intravenous route)
– Reduced compliance with long-term regimens owing to need
for parenteral administration
• General mechanisms of action of binding
agents continued
– Deferiprone
• Orally available iron chelator
• Available in European Union but not in Canada or
United States
• Excreted in urine
• Half-life is less than 1 hour, necessitating frequent
administration
• General mechanisms of action of binding
agents continued
– Deferiprone continued
• Major adverse effects include the following:
– GI disturbances
– Neutropenia
– Agranulocytosis
– Joint pain
• Up to 40% of patients on long-term therapy discontinue
use.
• General mechanisms of action of binding
agents continued
– Deferasirox
• Orally available iron chelator

• Excreted primarily in the feces by biliary excretion

• Half life is 8 to 16 hours, allowing once-a-day

administration
• General mechanisms of action of binding
agents continued
– Deferasirox continued
• Major adverse effects include the following:
– GI disturbances
– Skin rashes
– Mild decrease in glomerular filtration rate

• May be preferred over other iron chelators because

deferasirox has more convenient administration and a
good safety profile
Manipulation of Biotransformation
• Once a substance has been absorbed into the
bloodstream it is subject to biotransformation.
• Biotransformation in most cases causes
inactivation of substances.
• In theory, then, one strategy for reducing
toxicity would be to accelerate inactivation of
the toxicant.
• This could be achieved through metabolic
enzyme induction.
 Manipulation of Biotransformation
Continued
• However, in most cases the time course
of enzyme induction is too slow to be an effective
treatment strategy
• In some cases, the primary toxicants are not
especially harmful but biotransformation results
in the formation of reactive intermediates or
molecules that mediate the toxic effects
• In these situations, an effective strategy for the
management of toxicity is to reduce the
formation of the toxic molecule
• General mechanisms of action of agents used
to manipulate biotransformation
– Inhibition of metabolic enzymes that produce
toxic molecule
– Saturation of an enzyme with substrate that is
converted to non-harmful substance
– Scavenging of reactive metabolites
– Treatments most effective when applied before
formation of the toxic metabolite
– Examples include treatment of acetaminophen
toxicity and treatment of ethylene glycol toxicity
 Enhancement of Toxin Excretion
• Ultimately, the therapeutic goal in treating toxicity is to
remove the toxicant from the body completely or at
least to the point at which plasma concentrations
decline to a nontoxic level

• Several strategies have been used to increase removal

of toxicant from the plasma or, in other words, to
increase clearance

• These involve enhancement of endogenous clearance

mechanisms such as renal excretion and exogenous
mechanisms such as extracorporeal elimination (e.g.,
hemodialysis, hemofiltration).
• Renal Excretion
– In principle, renal excretion could be enhanced
by increasing glomerular filtration and/or tubular
secretion or by decreasing tubular reabsorption of
toxicants

– Forced diuresis

• Forced diuresis involves administration of diuretic agents and

isotonic saline to increase glomerular filtration rate and urine flow

• When combined with bicarbonate infusion, it is referred to

as forced alkaline diuresis

• Fluid overload, pulmonary edema, and electrolyte disturbances

can complicate therapy in compromised patients, especially in the
presence of cardiac, renal, or pulmonary dysfunction.
• Renal Excretion continued
– Forced diuresis continued
• Although it is important to maintain good urine flow
during treatment of toxicities, increasing glomerular
filtration through forced diuresis is not encouraged in
most intoxications

• However, this approach has been used with

nephrotoxic drugs because of the dilutional effect on
nephrotoxic agents in the renal tubules
• Renal Excretion continued
– Urine alkalinization
• Many substances are reabsorbed from the renal
tubules into the bloodstream, limiting the extent of
their urinary excretion
• Tubular reabsorption is dependent on the substance
being in the nonionized form
• The principles of ion trapping (see pharmacokinetics
chapter) can be used to increase urinary excretion
• Urine is generally acidic, and alkalinizing the urine
(generally to above pH 7.5) increases ionization of
acidic substances and thereby prevents their tubular
reabsorption
• Renal Excretion continued
– Urine alkalinization continued
• Because pH is a logarithmic scale, each unit change in
pH results in an approximately tenfold change in
ionization and presumably excretion

• Bicarbonate solution is infused intravenously while

urine pH is monitored, with a goal of reaching a urine
pH of 7.5 to 8.

• Urine alkalinization will be most effective for toxicants

that are:
– Weak acids with a low pKa value
– Cleared primarily by the kidney
• Renal Excretion continued
– Urine alkalinization continued
• Examples of toxicants whose clearance is increased by
urine alkalinization include:
– Salicylates
– Chlorophenoxy herbicides (e.g., 2,4-D)
– Barbiturates
– Methotrexate
• Main adverse effect of urine alkalinization is:
– Hypokalemia (potassium shifts to intracellular space as a
result of alkalemia)
• Renal Excretion continued
– Urine acidification
• Acidification of urine could theoretically assist in renal
excretion of toxicants that are weak bases

• Urine is usually acidic, so it not clear how much

additional benefit can be achieved by acidifying urine

• Acidification of urine also carries the risk of inducing

systemic acidosis

• Acidification of urine is not encouraged but can be

accomplished with administration of ammonium
chloride or ascorbic acid
• Gastrointestinal Excretion
– Although the majority of toxins are excreted in the urine, a
number may be excreted in the feces

– Biliary secretion is an important route of movement of

conjugated toxicants from the plasma into the lumen of
the GI tract

– However, in many cases these conjugates are cleaved in

the gut and the toxicants can be reabsorbed
(enterohepatic cycling)

– Interruption of enterohepatic cycling can increase fecal

excretion of toxicants.

– In addition, strategies to hold toxicants in the GI

tract until they can be passed in the feces can be an
effective means of detoxification.
• Gastrointestinal Excretion Continued
– Interruption of Enterohepatic Cycling

• Treatments bind toxicants in the GI tract and prevent

their reabsorption after cleavage of toxicant conjugates

• Activated charcoal, particularly MDAC, may increase

toxicant elimination in part by interrupting
enterohepatic cycling
• Gastrointestinal Excretion Continued
– Interruption of Enterohepatic Cycling

• Special binding substances can be ingested to bind

toxicants in the GI tract, interrupt enterohepatic
cycling, and increase toxicant elimination in the feces.

• Bile acid binding resins increase fecal elimination of

digoxin.

• Thiol-containing resins can be used to interrupt

enterohepatic cycling of mercury
• Enterocapillary Exsorption (Gastrointestinal
Dialysis)
– Refers to the removal of toxicants that
have already been absorbed into the
bloodstream by increasing their transport into
the lumen of the GI tract

– Binding of toxicant in gut lumen decreases the

free concentration of drug in the gut

– The very low concentration of free toxicant in the

gut lumen means that free toxicant
concentrations in the plasma are higher than
those in the gut
• Enterocapillary Exsorption (Gastrointestinal
Dialysis) Continued
– This blood-to-gut concentration gradient favors
diffusion of toxicant from the blood into the gut
lumen where the toxicant binds to the charcoal

– The charcoal-bound toxicant is eventually

excreted in the feces

– As this cycle repeats itself, the blood is cleared of

toxicant.
• Enterocapillary Exsorption (Gastrointestinal
Dialysis) Continued
– Enterocapillary exsorption may contribute to the
ability of MDAC to increase the elimination of
drugs such as:
• Amitriptyline

• Carbamazepine

• Nadolol

• Piroxicam
 Manipulate
Decrease or prevent absorption biotransformation
•Emesis Decrease distribution •Inhibition of
•Gastric lavage •Antibodies production of toxic
•Whole bowel irrigation •Chelating agents metabolites
•Activated charcoal •Scavenging of reactive
intermediates

General Strategies in
Management of Toxic Events

Enhance renal excretion Enhance gastrointestinal excretion

•Forced diuresis •Interruption of enterohepatic cycling
•Urine alikalinization or acidification •Enterocapillary exsorption
 Summary
• Toxicants may include synthetic(drug) or natural
from living organism(Toxin).
• Ingestion is the commonest mode of acquisition of
toxicant.
• Clinical presentation will depend on Dose,
Interaction and individual body state.
 Summary
Intoxicated Patient

RESUSCITATION/TREATMENT DIAGNOSIS

Airway
Breathing
History
Circulation Physical examination
Decontamination Toxidrome recognition
Enhanced Elimination Diagnostic Test
Focused Therapy
 Take Home Message
• Specific antidotal therapy is available for relatively
few toxicants, hence main stay of management is
Intensive Supportive therapy.

• Majority of intoxicated patients recover with

measures to ensure adequate gas exchange in the
lungs, ensure Cardiac output and when necessary
control of complications e.g convulsion, arrhythmias.