Basics of toxicology & it's applications.ppt

guptaasheesh 186 views 58 slides Aug 08, 2024
Slide 1
Slide 1 of 58
Slide 1
1
Slide 2
2
Slide 3
3
Slide 4
4
Slide 5
5
Slide 6
6
Slide 7
7
Slide 8
8
Slide 9
9
Slide 10
10
Slide 11
11
Slide 12
12
Slide 13
13
Slide 14
14
Slide 15
15
Slide 16
16
Slide 17
17
Slide 18
18
Slide 19
19
Slide 20
20
Slide 21
21
Slide 22
22
Slide 23
23
Slide 24
24
Slide 25
25
Slide 26
26
Slide 27
27
Slide 28
28
Slide 29
29
Slide 30
30
Slide 31
31
Slide 32
32
Slide 33
33
Slide 34
34
Slide 35
35
Slide 36
36
Slide 37
37
Slide 38
38
Slide 39
39
Slide 40
40
Slide 41
41
Slide 42
42
Slide 43
43
Slide 44
44
Slide 45
45
Slide 46
46
Slide 47
47
Slide 48
48
Slide 49
49
Slide 50
50
Slide 51
51
Slide 52
52
Slide 53
53
Slide 54
54
Slide 55
55
Slide 56
56
Slide 57
57
Slide 58
58

About This Presentation

Toxicology is a field of science that helps us understand the harmful effects of chemicals, substances, or situations, can have on people, animals, and the environment.
Some refer toxicology as the “Science of Safety” because -evolved from a science focused on studying poisons and adverse effec...


Slide Content

Basics of Toxicology & it’s Basics of Toxicology & it’s
ApplicationsApplications
Dr. Asheesh K. GuptaDr. Asheesh K. Gupta
Professor(Pharmacology)Professor(Pharmacology)
School of Pharmaceutical SciencesSchool of Pharmaceutical Sciences
IFTM University, MoradabadIFTM University, Moradabad

“All The Drugs Are Poison If They
Are Not Used Properly”

What is toxicology?
Toxicology is a field of science that helps us understand the
harmful effects of chemicals, substances, or situations, can have
on people, animals, and the environment.
Some refer toxicology as the “Science of Safety” because -
evolved from a science focused on studying poisons and adverse
effects.
Toxicology uses the power of science to predict what, and how
chemicals may cause harm and then shares that information to
protect public health.

Applications
•Poison - the dose determines the poison
•Drug Poisoning- Excess amounts of drugs in the body
cause toxicity
•Toxicology Screening- Screened using either blood,
urine, or saliva samples.
•Drug safety- finding safe dose and Lethal Dose(LD)
•Public health safety- Awareness & information provided
to regulatory agencies, to put programs and policies to limit our
exposures to these substances, thereby preventing or reducing
the likelihood.

DEFINITIONDEFINITION

Poisoning can be defined as a Poisoning can be defined as a
chemical injury to body organs or chemical injury to body organs or
a chemically induced disturbance a chemically induced disturbance
of the functions in biological of the functions in biological
systems. Such toxic effects may systems. Such toxic effects may
follow the exposure to exogenous follow the exposure to exogenous
(environmental) substances. (environmental) substances.

Accidental?

  
                                                                             
Deliberate?Suicidal?
‘Poison implies a high level of toxicity’

INTRODUCTIONINTRODUCTION
By tradition an agent has been considered as a By tradition an agent has been considered as a
poison if it may damage the organism in a very poison if it may damage the organism in a very
small dose.small dose.
The toxic properties of a certain poison are often The toxic properties of a certain poison are often
specific, and hence the clinical symptoms after specific, and hence the clinical symptoms after
exposure to a poison may be quite exposure to a poison may be quite
characteristic. characteristic.
Substances that normally are considered as Substances that normally are considered as
harmless may also, if the dose is big enough, harmless may also, if the dose is big enough,
cause deleterious effects and thereby act as cause deleterious effects and thereby act as
poisons. Examples of this are sodium chloride, poisons. Examples of this are sodium chloride,
oxygen and water. oxygen and water.

The science devoted to the study of the The science devoted to the study of the
structures, effects and fate of poisonous structures, effects and fate of poisonous
substances is called toxicology. substances is called toxicology.
This is nowadays a wide, heterogeneous This is nowadays a wide, heterogeneous
and rapidly expanding discipline. Clinical and rapidly expanding discipline. Clinical
toxicology is a subentity that deals with toxicology is a subentity that deals with
problems related to poisonings in humans problems related to poisonings in humans
and their treatment. and their treatment.

Poisoning may be-Poisoning may be-
 ACUTE POISONING;- ACUTE POISONING;-
In acute poisoning the body is exposed to the In acute poisoning the body is exposed to the
toxic substance in a high dose on one occasion toxic substance in a high dose on one occasion
and during a short period of time. and during a short period of time.
Symptoms of poisoning develop in close relation Symptoms of poisoning develop in close relation
to the exposure. to the exposure.
E.g- massive drug overdoses, poisonings after E.g- massive drug overdoses, poisonings after
mushroom meals, alcohol poisonings, and mushroom meals, alcohol poisonings, and
venomous bites or stings.venomous bites or stings.

CHRONIC POISONING:- CHRONIC POISONING:-
•In chronic poisoning the organism is on the contrary
exposed repeatedly to toxic agents during a long period, but
every exposure means that just a low dose of the poison is
entering the body.

• Normally no symptoms develop in relation to each
exposure, although that may happen (e.g. in chronic
exposure to solvents). Instead the patient gradually becomes
ill after a period of months or years.

•In chronic poisoning the toxic substance may
accumulate in body tissues or cause a small
irreversible damage at each exposure. After a
long time, enough poison has been
accumulated in the body, or the damage has
become significant enough, to cause clinical
symptoms.
E.g- long-term exposure to heavy metals like
lead, mercury or cadmium, inhalation of
organic solvents in the occupational context,
and exposure to pesticides

Incidence in IndiaIncidence in India
The exact incidence of this problem in The exact incidence of this problem in
our country remains uncertain but it is our country remains uncertain but it is
estimated that about 10-15 million estimated that about 10-15 million
cases of poisoning are reported every cases of poisoning are reported every
year, of which, more than 50,000 die.year, of which, more than 50,000 die.

Suicides in the India
•~6,300 suicides pa
–50% of deaths in young
people
•~140,000 attempted suicides
(parasuicides)
–Most common 15-19 year
old females
–Most common method is
poisoning
•50% paracetamol

Acute Poisoning in the Emergency Acute Poisoning in the Emergency
DepartmentDepartment
Common - 3-5% of ED attendancesCommon - 3-5% of ED attendances
2000 Deaths per year2000 Deaths per year
Some of the highest rates of deliberate Some of the highest rates of deliberate
poisoning in Europepoisoning in Europe
Often multiple drugsOften multiple drugs
DON’T FORGET ALCOHOL !!DON’T FORGET ALCOHOL !!

Summary of LectureSummary of Lecture
General Principles in the Management General Principles in the Management
of ANY Poisoningof ANY Poisoning
Specific management options with Specific management options with
certain substancescertain substances
ParacetamolParacetamol
Opiates (Heroin, Methadone, Morphine)Opiates (Heroin, Methadone, Morphine)
Salicylates (Aspirin)Salicylates (Aspirin)
Tricyclic Antidepressants (e.g Dothiepin)Tricyclic Antidepressants (e.g Dothiepin)

General Management -HistoryGeneral Management -History
Applies to ANY episode of PoisoningApplies to ANY episode of Poisoning
WHATWHAT
HOW MUCH (Ideally mg/Kg)HOW MUCH (Ideally mg/Kg)
WHENWHEN
WHAT ELSE (Including Alcohol)WHAT ELSE (Including Alcohol)
WHYWHY
Use Paramedics, friends, relatives, Use Paramedics, friends, relatives,
anyone!!anyone!!

Treatment steps
For effective management of an acutely poisoned
victim, six complementary steps are required.
These are :
1.Termination of exposure
2. Resuscitation and initial stabilization
3. Diagnosis of type of poison
4. Nonspecific therapy
5. Specific therapy
6. Supportive care

General Management -1General Management -1
A (Airway)A (Airway)
B (Breathing)B (Breathing)
C (Circulation)C (Circulation)
D (Disability-AVPU/ Glasgow Coma Scale) D (Disability-AVPU/ Glasgow Coma Scale)

DEFG ( Don’t ever forget the Glucose)DEFG ( Don’t ever forget the Glucose)
GET A SET OF BASIC OBSERVATIONSGET A SET OF BASIC OBSERVATIONS

General Management -2General Management -2
Use all your senses, search for the cluesUse all your senses, search for the clues
LOOKLOOK
Track MarksTrack Marks
Pupil SizePupil Size
FEELFEEL
Temperature, SweatingTemperature, Sweating
SMELLSMELL
AlcoholAlcohol

Table I : Clinical Features and Associated Poisons-
Clinical features Poisons
Odour of Breath Chloroform, Ethanol, Cyanide, Arsenic, Organophosphates,
Phosphorus, Kerosene
Hypertension with
Tachycardia
Amphetamines, Cocaine, LSD, MAO inhibitors, Marijuana,
Phencyclidine, Alcohol withdrawal, Nicotine, Antihistamines,
Antipsychotic agents,
Hypotension with
bradycardia
Antidepressants (severe cases), Barbiturates, Narcotics,
Benzodiazepines, Cyanide, Nicotine, Organophosphates
Hypotension with
tachycardia
Aluminium phosphide, Antipsychotics, Caffeine, Cyanide,
Disulfiram-ethanol interaction, Tricyclic antidepressants
Hyperthermia Amoxapine, Amphetamines, Antidepressants, Cocaine, Lithium,
LSD, MAO inhibitors, Phencyclidine, Anticholinergic agents,
Salicylates, Antihistamine
Hypothermia Antidepressants, Ethanol, Benzodiazepine, Narcotics,
Barbiturates, Phenothiazines
Tachypnoea Amphetamines, Atropine, Cocaine, Salicylates, Carbon
monoxide, Cyanide, Hepatic Encephalopathy (paracetamol,
amatoxin mushrooms), Metabolic acidosis

Bradypnoea Antidepressants, Antipsychotic agents, Barbiturates,
Ethanol, Benzodiazepines, Chlorinated hydrocarbons,
Narcotics, Nicotine, Organophosphates, Cobra bites
Altered sensoriumAntidepressants, Antihistamines, Antipsychotics,Atropine,
Organophosphates, Barbiturates,Lithium, Cyanide,
Benzodiazepines, Ethanol,Narcotics, Carbon monoxide
Seizures Antidepressants (amoxapine and maprotiline),Antipsychotic,
Antihistamines, Chlorinated hydrocarbons, Organophosphates,
Cyanide,
Lead and other heavy metals, Lithium,
Narcotics,Sympathomimetics (amphetamines, cocaine,
phencyclidine)
Miosis Barbiturates, Phenothiazines, Ethanol, Narcotics,Nicotine,
Organophosphates
Mydriasis Amphetamines, Caffeine, Cocaine, LSD, MAO inhibitors,
Nicotine, Antidepressants,Antihistamines, Atropine
Cyanosis Methaemoglobinaemia-inducing agents, Terminal stages of all
poisonings

Specific Management Options-1Specific Management Options-1
DECREASING DRUG ABSORPTIONDECREASING DRUG ABSORPTION
Gastric Lavage ( Unpopular - need to protect the Gastric Lavage ( Unpopular - need to protect the
airway, may push drug through pylorus into small airway, may push drug through pylorus into small
bowel.) bowel.)
NEVER Ipecacuanha.NEVER Ipecacuanha.
Absorbants - Activated Charcoal , usually within 1 Absorbants - Activated Charcoal , usually within 1
hour of ingestion, hour of ingestion, 50 g single or repeated dose (50 g single or repeated dose (
elimination) elimination)
Doesn’t bind heavy metals, ethanol, acids,etc..Doesn’t bind heavy metals, ethanol, acids,etc..
longer repeated doses in drugs that delay gastric longer repeated doses in drugs that delay gastric
emptying (e.g. Aspirin)emptying (e.g. Aspirin)

Specific Management Options- 2Specific Management Options- 2
INCREASING DRUG ELIMINATIONINCREASING DRUG ELIMINATION
Multiple dose activated charcoalMultiple dose activated charcoal
Quinine, phenobarbitoneQuinine, phenobarbitone
Charcoal haemoperfusionCharcoal haemoperfusion
Barbiturates, theophyllineBarbiturates, theophylline
Alkaline Diuresis (Aspirin)Alkaline Diuresis (Aspirin)
Haemodialysis (Aspirin)Haemodialysis (Aspirin)

Induce vomiting
•Syrup of Ipecac?
•Soapy water?
•Don’t use:
–Finger gag
–Salt water
–Copper sulfate

Specific Management Options - 3Specific Management Options - 3
ANTAGONISING THE EFFECTS OF ANTAGONISING THE EFFECTS OF
THE POISONTHE POISON
Desferrioxamine (IRON)Desferrioxamine (IRON)
Naloxone (OPIATES)Naloxone (OPIATES)
N Acetylcysteine (PARACETAMOL)N Acetylcysteine (PARACETAMOL)

Specific Poisons- ParacetamolSpecific Poisons- Paracetamol
Commonest drug used Commonest drug used
As little as 12g can be fatalAs little as 12g can be fatal
50% of all Self Poisoning Episodes50% of all Self Poisoning Episodes
100- 200 deaths per year100- 200 deaths per year
DANGEROUS AND PEOPLE DON’T DANGEROUS AND PEOPLE DON’T
KNOW IT. YOU FEEL WELL AND THEN KNOW IT. YOU FEEL WELL AND THEN
THE LIVER FAILURE SETS IN..THE LIVER FAILURE SETS IN..

Paracetamol Metabolism

Paracetamol-Normal MetabolismParacetamol-Normal Metabolism
Paracetamol converted to: Paracetamol converted to:
N-Acetyl-p-benzoquinonamine (TOXIC)N-Acetyl-p-benzoquinonamine (TOXIC)
This is conjugated with Glutathione This is conjugated with Glutathione
Glutathione stored in the bodyGlutathione stored in the body
Produces a NON TOXIC metaboliteProduces a NON TOXIC metabolite

Paracetamol Metabolism in Paracetamol Metabolism in
OverdoseOverdose
Glutathione stores are used up by the Glutathione stores are used up by the
excess Paracetamolexcess Paracetamol
Toxic Metabolite build upToxic Metabolite build up
Binds IRREVERSIBLY to Hepatic Cell Binds IRREVERSIBLY to Hepatic Cell
membranesmembranes
Resulting in LIVER NECROSISResulting in LIVER NECROSIS

Paracetamol Overdose-Paracetamol Overdose-
managementmanagement
Initial ABC ( usually well systemically)Initial ABC ( usually well systemically)
Get a good historyGet a good history
TIME TAKEN, AMOUNTTIME TAKEN, AMOUNT
Any other medicationAny other medication
History of Liver diseaseHistory of Liver disease
N-Acetylcysteine. Shown to be N-Acetylcysteine. Shown to be
advantageous if given in the first 10 hoursadvantageous if given in the first 10 hours

Treatment Graph

N - AcetylcysteineN - Acetylcysteine
 Specific antidote used for Specific antidote used for
Paracetamol,provides the Sulphydryl groups Paracetamol,provides the Sulphydryl groups
needed to increase the availability of needed to increase the availability of
Glutathione so that body can turn the Glutathione so that body can turn the
TOXIC metabolite into the non toxic form TOXIC metabolite into the non toxic form
and prevent liver cell damage and and prevent liver cell damage and
NECROSIS problem: Not shown to be NECROSIS problem: Not shown to be
effective after 15 hours.effective after 15 hours.

Paracetamol ManagementParacetamol Management
Able to measure levels of Paracetamol Able to measure levels of Paracetamol
in the blood.in the blood.
Helps to guide whether amount taken is Helps to guide whether amount taken is
enough to be Hepatotoxic.enough to be Hepatotoxic.
IF IN DOUBT start treatment before the IF IN DOUBT start treatment before the
Paracetamol levels get back to save Paracetamol levels get back to save
time.time.

Paracetamol Management-PitfallsParacetamol Management-Pitfalls
Patients with Liver Disease/ AlcoholicsPatients with Liver Disease/ Alcoholics
Depleted stores of Glutathione will start to Depleted stores of Glutathione will start to
get toxic build up sooner than healthy get toxic build up sooner than healthy
people.people.
Staggered OverdosesStaggered Overdoses
Levels unreliableLevels unreliable
After 15 hours- what do you do??After 15 hours- what do you do??

Paracetamol ManagementParacetamol Management
Timebomb waiting to happen.Timebomb waiting to happen.
If have late presentation have to monitor If have late presentation have to monitor
for impending liver failure.for impending liver failure.
Refer to specialist liver unit.Refer to specialist liver unit.
People die from this.People die from this.

Opiate Poisoning- FeaturesOpiate Poisoning- Features
Common (particularly in BRI)Common (particularly in BRI)
Heroin, Methadone, Analgaesics in ElderlyHeroin, Methadone, Analgaesics in Elderly
Action on the mu receptors giving the effects Action on the mu receptors giving the effects
in overdose.in overdose.
1. PINPOINT PUPILS1. PINPOINT PUPILS
2. RESPIRATORY DEPRESSION2. RESPIRATORY DEPRESSION
3.COMA3.COMA

Opiate Overdose-ManagementOpiate Overdose-Management
INITIAL MANAGEMENTINITIAL MANAGEMENT
AA
BB
CC
DD

Opiate Overdose-Management- 2Opiate Overdose-Management- 2
NALOXONENALOXONE
Opioid antagonistOpioid antagonist
High Affinity for the opiate receptorsHigh Affinity for the opiate receptors
Little other effectsLittle other effects
Rapid onsetRapid onset
Effects last 2-4 hrs, may need repeated Effects last 2-4 hrs, may need repeated
dosesdoses
Give I-M or I-VGive I-M or I-V

Salicylate (Aspirin) PoisoningSalicylate (Aspirin) Poisoning
Toxicity occurs due to disturbance in Toxicity occurs due to disturbance in
Acid-Base BalanceAcid-Base Balance
1. Respiratory Alkalosis1. Respiratory Alkalosis
2. Metabolic Acidosis2. Metabolic Acidosis

Aspirin Poisoning- mechanism- 1Aspirin Poisoning- mechanism- 1
1.Direct stimulation of the respiratory 1.Direct stimulation of the respiratory
centre makes you overbreathe. centre makes you overbreathe.
Hyperventilation and Respiratory Hyperventilation and Respiratory
Alkalosis.Alkalosis.
2. Kidney attempts to compensate for 2. Kidney attempts to compensate for
the alkalosis by excreting alkali to give the alkalosis by excreting alkali to give
you a metabolic Acidosis.you a metabolic Acidosis.
3. Aspirin inhibits the normal metabolic 3. Aspirin inhibits the normal metabolic
pathways. pathways.

Aspirin poisoning- mechanism- 2Aspirin poisoning- mechanism- 2
3. Aspirin inhibits the normal metabolic 3. Aspirin inhibits the normal metabolic
pathways, so you get failure of the pathways, so you get failure of the
normal metabolism of CHO, Fats and normal metabolism of CHO, Fats and
Protein.Protein.
Build up of Organic AcidsBuild up of Organic Acids
KETONES, LACTATE AND PYRUVATEKETONES, LACTATE AND PYRUVATE
CAUSES MORE METABOLIC ACIDOSISCAUSES MORE METABOLIC ACIDOSIS
METABOLIC ACIDOSIS, BAD NEWSMETABOLIC ACIDOSIS, BAD NEWS

Aspirin Poisoning -Aspirin Poisoning -
Clinical FeaturesClinical Features
COMMON FEATURES:COMMON FEATURES:
Vomiting, Dehydration, Tinnitus, VertigoVomiting, Dehydration, Tinnitus, Vertigo
Sweating, Bounding pulses, HyperventilationSweating, Bounding pulses, Hyperventilation
UNCOMMON FEATURES:UNCOMMON FEATURES:
Confusion, Disorientation, Coma, ConvulsionsConfusion, Disorientation, Coma, Convulsions
Haematemesis, Hyperpyrexia, clotting Haematemesis, Hyperpyrexia, clotting
abnormalities, renal failureabnormalities, renal failure

Aspirin Overdose-ManagementAspirin Overdose-Management
Initial Supportive therapy. If small Initial Supportive therapy. If small
amounts and asymptomatic may need amounts and asymptomatic may need
no treatment.no treatment.
Management tailored according to the Management tailored according to the
amount taken.amount taken.
Able to take Salicylate levels to help Able to take Salicylate levels to help
guide treatment options.guide treatment options.

Aspirin Management - GeneralAspirin Management - General
AA
BB
CC
DD
(EFG)(EFG)

Aspirin Management - SpecificAspirin Management - Specific
When extremely high levels of Aspirin When extremely high levels of Aspirin
have been ingested and the patients are have been ingested and the patients are
symptomatic steps may be taken to-symptomatic steps may be taken to-
1. DECREASE ABSORPTION1. DECREASE ABSORPTION
2. INCREASE DRUG ELIMINATION2. INCREASE DRUG ELIMINATION

Aspirin- Decreasing absorptionAspirin- Decreasing absorption
Activated CharcoalActivated Charcoal
Given in those who have taken more than Given in those who have taken more than
250mg/Kg body weight less than 1 hour ago.250mg/Kg body weight less than 1 hour ago.
Gastric LavageGastric Lavage
May be considered in those who have taken May be considered in those who have taken
more than 500mg/kg body less than 1 hour more than 500mg/kg body less than 1 hour
ago. Steps must be taken to protect the airway.ago. Steps must be taken to protect the airway.

Aspirin-Increasing Drug Aspirin-Increasing Drug
EliminationElimination
Urinary AlkalinisationUrinary Alkalinisation
If you increase urinary pH from 5 to 8 there is a If you increase urinary pH from 5 to 8 there is a
10-20 fold increase in the renal salicylate 10-20 fold increase in the renal salicylate
clearanceclearance
This is done by giving an infusion of Sodium This is done by giving an infusion of Sodium
Bicarbonate. Care must be taken because this Bicarbonate. Care must be taken because this
in itself is dangerous and can cause severe in itself is dangerous and can cause severe
Acid Base DisturbancesAcid Base Disturbances

Aspirin- Increasing Drug Aspirin- Increasing Drug
EliminationElimination
HAEMODIALYSISHAEMODIALYSIS
Used in severe life threatening overdose.Used in severe life threatening overdose.
Aims to correct the Acid Base disturbances Aims to correct the Acid Base disturbances
while removing the Salicylate.while removing the Salicylate.

Tricyclic AntidepressantsTricyclic Antidepressants
Seen relatively frequentlySeen relatively frequently
Can be fatalCan be fatal
Can be very symptomatic, effects made Can be very symptomatic, effects made
worse by alcohol.worse by alcohol.
Main effects are on the Heart and Brain.Main effects are on the Heart and Brain.
Effects areEffects are
1. Anticholinergic1. Anticholinergic
2. Quinidine like2. Quinidine like

TCA Overdose- Clinical TCA Overdose- Clinical
features features
ANTICHOLINERGIC EFFECTSANTICHOLINERGIC EFFECTS
Dry Mouth, Dry Eyes, Dilated Pupils, Dry Mouth, Dry Eyes, Dilated Pupils,
Urinary Retention, Blurred Vision, Urinary Retention, Blurred Vision,
Dizziness, Palpitations, Pyrexia without Dizziness, Palpitations, Pyrexia without
sweating.sweating.
CNS Effects- Confusion, Delerium, Coma, CNS Effects- Confusion, Delerium, Coma,
Convulsions, Myoclonus and Respiratory Convulsions, Myoclonus and Respiratory
Depression.Depression.

TCA Overdose Clinical TCA Overdose Clinical
FeaturesFeatures
Cardiac Toxicity (quinidine effects)Cardiac Toxicity (quinidine effects)
Heart Block, Asystole, Bradycardia, Heart Block, Asystole, Bradycardia,
Tachycardia, Ventricular DysrythmiasTachycardia, Ventricular Dysrythmias
ECG Changes - broadening of QRS ECG Changes - broadening of QRS
complex, Widened QT Intervalcomplex, Widened QT Interval

TCA Overdose- Management 1TCA Overdose- Management 1
Mainstay of initial management is Mainstay of initial management is
Supportive. Try not to give other drugs Supportive. Try not to give other drugs
ontop with a few specific exceptions.ontop with a few specific exceptions.
A- May need intubatingA- May need intubating
BB
C- Give IV fluids if low BPC- Give IV fluids if low BP
D -Control convulsions with DiazepamD -Control convulsions with Diazepam

TCA Overdose Management 2TCA Overdose Management 2
Activated Charcoal if more than 4 Activated Charcoal if more than 4
mg/Kg within 1 hour.mg/Kg within 1 hour.
N.B WATCH OUT FOR THE AIRWAYN.B WATCH OUT FOR THE AIRWAY
Correct Hypoxia with OxygenCorrect Hypoxia with Oxygen
Correct Acidosis with Na BicCorrect Acidosis with Na Bic
Correct any arrythmias with Na Bic (i.e Correct any arrythmias with Na Bic (i.e
start by controlling the acid base start by controlling the acid base
disturbance). disturbance).

Benzodiazepine Overdose
•Deaths from poisoning with benzodiazepines alone are
rare, but may be lethal in combination with other CNS
depressants
•Treatment is supportive and aimed at maintaining adequate
ventilation whilst supporting cardiovascular depression
•Flumazenil (specific benzodiazepine antidote) is not
licensed (in the UK) for routine use in benzodiazepine
overdoses
•Flumazenil may induce seizures; particularly dangerous
where tricyclic antidepressants have been taken
•Flumazenil, may however, be used in the differential
diagnosis of unclear cases of multiple overdoses but expert
advice is ESSENTIAL.

Poison/Drug Antidote
• Paracetamol (acetaminophen) N-acetylcysteine
• Vitamin K anticoagulants, e.g.
warfarin
Vitamin K
• Opioids Naloxone
• Iron (and other heavy metals)
Desferrioxamine, Deferasirox or
Deferiprone
• Benzodiazepines Flumazenil
• Ethylene glycol Ethanol or fomepizole, and thiamine
• Methanol Ethanol or fomepizole, and folinic acid
• Cyanide
Amyl nitrite, sodium nitrite and sodium
thiosulfate
• Organophosphates Atropine and Pralidoxime
• Magnesium Calcium Gluconate
o Antidotes :- Some poisons have specific antidotes:

• Calcium Channel Blockers (Verapamil,
Diltiazem)
Calcium Gluconate
• Beta-Blockers (Propranolol, Sotalol) Calcium Gluconate and/or Glucagon
• Isoniazid Pyridoxine
• Atropine Physostigmine
• Thallium Prussian blue
•Hydrofluoric acid Calcium Gluconate
• Anticholinergics Cholinergics (and vice-versa)
Poison/drug Poison/drug AntidotesAntidotes

QUESTIONS QUESTIONS
??

SUMMARYSUMMARY
Get as much history as you can, know your Get as much history as you can, know your
enemy.enemy.
Mainstay of any poisoning is Supportive.Mainstay of any poisoning is Supportive.
Don’t Forget the ABCDon’t Forget the ABC
For specific substances there maybe For specific substances there maybe
antidotes.antidotes.
For Specific circumstances consider For Specific circumstances consider
decreasing the absorption or increasing decreasing the absorption or increasing
the elimination of the drug.the elimination of the drug.