Presented By:

Maryam Manzoor
M.Phil. Pharmacology
Darsons Institute of Science and Technology

TOXICOLOGY
 INTRODUCTION
• Toxicology is the branch of science that deals with studying
and trea ting poisons.
• Toxicology is defined as study of the
adverse effects of chemicals on living
organism”.
• “Toxicity is the inherent capacity of a
chemical to cause injury”.
 DEFINITIO
N
Toxicology is the branch of science that deals with the study of
poisons, including their mechanism of action, adverse effects on
the body, and treatment of the various conditions produced by the
poisons.

These poisons can be from the environment, industry, home,

or pharmacological substances.
TOXICOLOGY
BRANCHES
1.Experimental
Toxicology 2.Clinical
Toxicology
3.Environmental
Toxicology
BRANCHES
1. Experimental Toxicology:
It is the branch of Toxicology that deals with the study of the
toxic effects of various chemicals on biological systems e.g. pre-
clinical animal studies.
2. Clinical Toxicology:
Clinical Toxicology involves the diagnosis and treatment of
poisoning in human beings.
3. Environmental Toxicology:
This is a new branch of Toxicology and deals with the
identification and elimination of environmental poisons e.g. Lead,
arsenic CO2, etc.
 Occupational toxicology deals with the
chemicals found in the workplace.
 Environmental toxicology deals with the
potentially deleterious impact of chemicals,
present as pollutants of the environment, on living
organisms.
 Ecotoxicology is concerned with the toxic effects
of chemical and physical agents on populations
and communities of living organisms within
defined ecosystems.
 Traditional toxicology is concerned with toxic
effects on individual organisms.
Toxic actions of chemicals
 Routes: Eternal, Parenteral, Topical, Inhalational
 Common target tissues: Lungs, Liver, Brain,
Kidney, Heart. (high blood flow)
 Nonselective actions: Corrosive compounds-
local irritation (alkaline or acidic substances-
denaturation of macromolecules)
 Selective actions: Rodenticide (warfarin)
inhibits vitamin k dependent clotting factors.
 Immediate and delayed actions: Quick
symptoms-organophosphate toxicity , Delayed-
carcinogen asbestos
POISONING AND ITS
MANAGEMENT
 POISON AND PRINCIPLE OF
TREATMENT OF
POISONING
• Poisons are substances that cause disturbances to
organisms, usually by chemical reaction or other
activity at the molecular scale, when a sufficient
quantity is absorbed by an organism. OR
• Poison is a substance that when introduced into the
body in relatively small amounts causes structural
damage and functional disturbances. OR
• Poisons are unwanted substances that produce
harmful effects on the body and sometimes can be
fatal.
 POISONING
Poisoning is injury or death due to swallowing,
inhaling, injecting or touching various drugs,
chemicals, venoms or gases.
• Many substances such as drugs and carbon
monoxide are poisonous only at higher
concentrations or dosages.
 REASON FOR POISONING
1. Accidental
2. Incidental
3. Iatrogenic
4. Intentional
Nearly ~70%-80% of all chemical-related
deaths reported are due to barbiturates,
salicylates, ethanol, or co causes.
 ANTIDOT
E
• Antidotes are substances used to reverse the
harmful effects of a poison.

• They act either by preventing absorption or

by inactivating or antagonizing the actions
of poisons.
 GENERAL
PRINCIPLES
EMPLOYED FOR
THE MANAGEMENT
OF POISONING
 GENERAL PRINCIPLES EMPLOYED
FOR THE MANAGEMENT OF
POISONING
• Poisoning symptoms vary for different agents,
but certain common syndromes may suggest
particular classes of poisons.
• Diagnosis is primarily clinical, but blood and
urine tests can help for some poisonings.
• Treatment is supportive for most poisonings;
specific antidotes are necessary for a few.
• Prevention includes labeling drug containers
clearly and keeping poisons out of the reach of
children.
 IDENTIFY THE CAUSE OF
POISONS
• The first step of the management/treatment is to
identify the poisons.
• The cause of poison can be known by the
relative of the patient or by the patient himself if
he/she is conscious.
• This step helps in deciding the specific
treatment for the poisoning.
 SPECIFIC STRATEGIES
1. PREVENTING
ABSORPTION
2. HASTENING
ELIMINATION
3. USE OF ANTIDOTES
 PREVENTING ABSORPTION OF THE POISON
• 1. Induction of vomiting
• A syrup of ipecac is the preferred emetic for
Inducing vomiting.
• The dose of ipecac syrup is 15 ml for
children less than 6 months and 30 ml for
adults.
• Emesis is contraindicated in
• In comatose patients,
• In caustic poisoning,
• In petroleum distillate poisoning.
• Where is a risk of convulsions in the patient.
 Preventing absorption of the poison
• 2. Gastric lavage:
 It is animportant
measure
To control poisoning when
it occurs due to some
aromatic substances
Such as perfumes.
 It is also helpful
when is
Emesis
contraindicated.
 PREVENTING ABSORPTION OF THE POISON
• 3. Use of activated charcoal:
 Activated charcoal adsorbs
the poisons and delays the
gastrointestinal absorption
of the poison.
 It is helpful in the treatment
of poisoning fro aromatic
and alkaloid compounds
 HASTENING ELIMINATION OF THE
POISON
• 1. Altering the ph of urine
In case of poisoning from basic substances such
as amphetamine or quinine urine of the patient
should be made acidic to hasten the elimination
of these substances.
In case of acidic substances poisoning such as
salicylates or phenobarbitone, urine should be
made alkaline to speed the elimination of the
poison.
 HASTENING ELIMINATION OF THE
POISON
2. Dialysis
Peritoneal dialysis is used in the treatment of alcohol
poisoning and snake bites.
Hemodialysis is more superior technique but requires a
highly sophisticated unit for care. These have limited use
in the treatment of intoxication with chemicals.
3. Cathartics:
Cathartics are used to hasten the removal of a toxic
substance and are useful in the ingestion of
hydrocarbons and enteric-coated tablets.
Sodium sulphate is a frequently used cathartic.
USE OF SPECIFIC ANTIDOTES:
 There are certain specific antidotes for
treating specific cases of poisoning.
SUPPORTIVE MEASURES FOR
IMPROVING THE
CONDITION OF THE
PATIENT
 Supportive measures
 Use of oxygen therapy when there is hypoxia
or
Probability of the same in the patient.
 Correction of the blood pressure by fluid therapy.
If there is cardiac arrhythmia in the patient then safety
measures should be taken under the supervision of the
expert.
 Correction of plasma biochemistry like, acidosis
or
Alkalosis in the blood.
Airways should be cleared with the help of
suction apparatus.
 Monitoring of the patient
• After a patient is recovered from the adverse
effects it is important to monitor the patient for
some time.
• This step is necessary and performed to ensure
that there are no other complications in the
case.
• After ensuring that the patient is fully recovered
he/she shall be allowed to go home.
SPECIFIC POISONING AND
THEIR TREATMENT
Occupational And Environmental
Toxicology
 A- Halogenated hydrocarbons: volatile lipid soluble can
pass through the blood-brain barrier.
 Acute exposures: CNS depression through inhalation or
ingestion.
 1. Carbon tetrachloride: contaminated drinking water.
 Low-level inhalation :irritation of the eyes and respiratory
system
 Higher levels: nausea, vomiting, stupor, convulsions, coma,
and death from CNS depression
 M.O.A: cytochrome P450–mediated metabolic activation to
produce free radicals that cause lipid peroxidation and
membrane breakdown.
 At nonlethal acute exposure: centrilobular hepatonecrosis and
 2. Chloroform: Ingestion or inhalation
resulting in nausea, vomiting, dizziness,
headaches, and stupor. Chloroform can
also sensitize the heart to
catecholamine-induced arrhythmias.
 Chloroform is hepatotoxic and
nephrotoxic due to its metabolic
activation.
 B. Aromatic hydrocarbons: volatile,
through inhalation and ingestion.
 Large acute exposures: CNS depression,
and cardiac arrhythmias through
sensitization of heart cells to
catecholamines.
 1. Benzene: Tobacco smoke.
 Chronic benzene exposure: hematopoietic
toxicities, of which the most serious are
agranulocytosis and leukemia, particularly
acute myelogenous leukemia.
 2. Toluene: Automobile emissions
 Indoors exposure occurs from the use of
household products containing toluene-like
degreasers, certain paints and primers, and
furniture polish.
 Acute and chronic exposure: CNS depression,
with symptoms including drowsiness; ataxia;
tremors; and impaired speech, hearing, and
vision.
 Chronic exposure: Hepatotoxicity , Renal
toxicity and death.
HYDROCARBON
POISONING
Hydrocarbons Include:
 Petrol
 Kerosene
 Lighter Fluid
 Mineral Turpentine
 Paraffin Oil
 Lubricating Oil
 Furniture Polishes
 2 Stroke Fuel
 Diesel Fuel

 White
Spirit
HYDROCARBON POISONING
Assessment

 Main complication is Aspiration Pneumonitis

 C.N.S. toxicity can be evident (either depression or
excitement)
HYDROCARBON POISONING

 Symptoms
: Coughing,
 choking, respiratory distress
ataxia, drowsiness, coma, convulsions
persistent burping (particularly
seen after petrol ingestion
MANAGEMENT

orally charcoal is contraindicated.

 Asymptomatic

 Observe 6 hours
 Discharge if remains asymptomatic
MANAGEMENT
(CONT.)
 Symptomatic
 If develops respiratory symptoms
(aspiration), do Chest X Ray & O2
saturation
 Give O2 to maintain saturation > 94%
 If stable, admit to general medical ward
 If increasing O2 requirements or increased
respiratory distress contact I.C.U.
 If altered conscious state at any time
contact I.C.U.
 C. Alcohols
 1. Methanol (wood alcohol) and ethylene
glycol:
 Methanol and ethylene glycol are oxidized to
toxic products: formic acid in the case of
methanol, and glycolic, glyoxylic, and oxalic acids
in the case of ethylene glycol.
 Coma, seizures, hyperpnea, and hypotension
 2. Isopropanol:
 This secondary alcohol is metabolized to acetone
via alcohol dehydrogenase. Acetone cannot be
further oxidized to carboxylic acids and, therefore,
shows only limited acidemia and toxicity.
 D. Pesticides
 1. Organophosphosphate and carbamate insecticides:
 Toxicity through inhibition of acetylcholinesterase, with subsequent
accumulation of excess acetylcholine.
 2. Pyrethroids:
 Toxicity by extending the open time of sodium channels throughout the
central and peripheral nervous systems.
 Symptoms of toxicity: loss of coordination, tremors, convulsions,
burning and itching sensations, and contact dermatitis or asthma-like
symptoms and Death.
 3. Rotenone:
 It acts by inhibiting the oxidation of the reduced form of nicotinamide-
adenine dinucleotide
 Symptoms: nausea, vomiting, convulsions and death at very high
dose.
 E. Rodenticides
 The most commonly used rodenticides are the anticoagulants such as
warfarin.
ORGANOPHOSPHATES AND
CARBAMATES
 These insecticides exert their toxicity through inhibition
of acetylcholinesterase, with subsequent accumulation
of excess acetylcholine producing nicotinic (mydriasis,
fasciculations, muscle weakness, hypertension) and
muscarinic (diarrhea, urination, miosis, bradycardia,
bronchorrhea, emesis, lacrimation, salivation) effects.
 Carbamates reversibly bind to acetylcholinesterase,
whereas organophosphates undergo an aging process to
ultimately irreversibly inactivate the enzyme.
ORGANOPHOSPHATES AND
CARBAMATES
 Organophosphate nerve agents, such as sarin, soman,
and tabun, have the same mechanism of action, but
the aging process is much more rapid compared to
insecticides.
 Atropine, a muscarinic receptor antagonist, and
pralidoxime, an oxime to reactivate cholinesterase,
should be administered intravenously or
intramuscularly to treat the muscarinic and nicotinic
effects, respectively.
Heavy Metals
 Lead:
 Source: old paint, drinking water, industrial pollution, food, and
contaminated dust.
 Absorption :Age-dependent
 Adults: about 10 percent of an ingested dose
 Children: about 40 percent.
 Distribution:
 Inorganic forms of lead distributed to the soft tissues and more
slowly redistribute to bone, teeth, and hair. Lead has an apparent
blood half-life of about 1 to 2 months, whereas its half-life from bone
is 20 to 30 years.
 Detection: by x-ray examination.
 M.O.A: Oxidative stress
 a. Central nervous system: Encephalopathy.
 Symptoms: headaches, confusion,
clumsiness, insomnia, fatigue, and impaired
concentration, convulsions, coma.
 Children are more susceptible than adults to
the CNS effects of lead. Furthermore, blood
levels of 5 to 20 μg/dL in children have been
shown to lower IQ in the absence of other
symptoms.
 b. Gastrointestinal system:
 Early symptoms : discomfort, constipation (and,
occasionally, diarrhea)
 Higher exposures: Painful intestinal spasms
 Calcium gluconate infusion is effective for relief of pain.
 c. Blood: Hypochromic, Microcytic anemia
 Lead inhibits several enzymes involved in the synthesis
of heme
 Elevated blood and urinary levels of these intermediates
can be used diagnostically for determining lead
intoxication, provided that blood lead levels are greater
than about 25 μg/dL.
Mercury
a. Elemental mercury:
 Occupational through inhalation
 Symptoms: Tremors, depression, memory loss, decreased verbal skills,
and inflammation of the kidneys.
 High concentrations : nonselective pulmonary toxicity

b. Inorganic mercury salts:

 Inorganic salts of mercury (mercuric chloride)-occupational in nature,
corrosive and can destroy the mucosa of the mouth, Renal damage
c. Organic mercury:
 one covalent bond to a carbon atom, more lipid soluble
 Contaminated food, particularly fish, contaminated with methylmercury.
 Symptoms: neurologic in nature-visual disturbances, paresthesias, ataxia,
hearing loss, mental deterioration, muscle tremors, movement disorders,
paralysis and death (Parkinson disease or Alzheimer disease). Although all
forms of mercury are toxic to the fetus, organic mercury is the most
dangerous, because its lipid solubility allows passage through the
Cadmium:
 Ingestion or inhalation through contaminated food ,
fertilizers, atmospheric deposition.
 Occupational in nature, although low-level
exposure occurs from the burning of fossil fuels.
 Cigarette smoking, industries and environmental
contamination.
 Absorption: poor absorption with about 5 percent
bioavailability. Upon inhalation, about 10 to 40
percent of the dose is absorbed.
 Distribution: Liver and kidney, t1/2 life= 10-30
years.
 Pulmonary and Renal toxicity
ARSENIC POSIONING
Vomiting, bloody stools, pain in throat, inflamed
conjunctiva , hematemesis
Air Pollutants (Gases and inhaled particles)
 Five major substances: 98% of air pollution-carbon monoxide
(CO=52%), sulfur oxides (14%), hydrocarbons (14%), nitrogen
oxides (14%), and particulate matter (about 4%).
 1. Carbon monoxide: Colorless, odorless, tasteless (difficult to
detect).
 Sources: combustion of carbonaceous materials, automobiles,
poorly vented furnaces, fireplaces, wood-burning stoves, kerosene
space heaters, and charcoal grills.
 M.O.A: Following inhalation, CO rapidly binds to hemoglobin to
produce carboxyhemoglobin. The binding affinity of carbon
monoxide to hemoglobin is 230 to 270 times greater than that of
oxygen.
 This high-affinity binding of oxygen prevents the unloading of
oxygen at the tissues, further reducing oxygen delivery.
 Symptoms: Hypoxia, with the brain and
heart showing the greatest sensitivity.
headache, dyspnea, lethargy, confusion,
and drowsiness, seizures, coma, and
death.
 Treatment: removal from the source of
carbon monoxide and institution of 100-
percent oxygen by non rebreathing face-
mask or endotracheal tube.
Sulfur Dioxide
 Sulfur dioxide (SO 2 ): colorless, irritant gas generated by
combustion of sulfur-containing fossil fuels.
 M.O.A: On contact with moist membranes, SO 2 forms
sulfurous acid, which is responsible for its severe irritant
effects on the eyes, mucous membranes, and skin.
 90% of inhaled SO 2 is absorbed in the upper respiratory
tract, the site of its principal effect.
 Complications: Bronchial constriction; parasympathetic
reflexes and altered smooth muscle tone appear to be
involved. Asthmatic individuals are especially sensitive to
SO 2.
 Symptoms: eyes, nose, throat irritation, reflex
bronchoconstriction, pulmonary edema
Nitrogen dioxide (NO 2 )
 Brownish irritant gas associated with fires. It is
formed also from fresh silage
 Exposure of farmers to NO 2 in the confines of
a silo can lead to silo-filler’s disease
 M.O.A: NO 2 is a relatively insoluble deep lung
irritant capable of producing pulmonary edema.
The type I cells of the alveoli appear to be the
cells chiefly affected on acute exposure.
 Symptoms: Irritation of the eyes and nose,
cough, mucoid or frothy sputum production,
dyspnea, and chest pain.
Ozone (O 3 )
 is a bluish irritant gas-earth’s
atmosphere-absorbent of ultraviolet
light.
 Symptoms: Respiratory Irritation,
Bronchoconstriction, Dryness of throat,
Pulmonary Edema
2. Cyanide:
 Once absorbed into the body, cyanide quickly
binds to metalloenzymes-the inactivation of the
enzyme cytochrome oxidase (cytochrome a3),
leading to the inhibition of cellular respiration.
Therefore, even in the presence of oxygen,
those tissues, such as the brain and heart,
which require a high oxygen demand, are
adversely affected.
 Death can occur quickly due to respiratory
arrest of oxidative phosphorylation and
production of adenosine triphosphate.
3. Silica(Silicosis):
 Source: Workers in mines, foundries,
construction sites, stone cutters
 Silicosis is a progressive lung disease
that results in fibrosis and, often,
emphysema.
 Silicosis is currently incurable, and the
prognosis is often poor.
4. Asbestos:
 Pulmonary toxicity due to inhalation of fibers
 Complications: Asbestosis, Mesothelioma, lung cancer.
 Symptoms: (up to 15 to 30 years ) interstitial fibrosis in the
lungs and pleural fibrosis or calcification, shortness of breath,
severe cough, chest pains.
 Asbestosis is a lung disease resulting from the inhalation of
asbestos particles, marked by severe fibrosis and a high risk
of mesothelioma (cancer of the pleura).
 Mesothelioma is a rare cancer, usually in the chest wall (or
peritoneum, mesothelium), which seems to be caused only
by asbestos. The first noticeable symptom is usually pain in
the vicinity of the lesion, with dyspnea and cough developing
with pleural mesothelioma. Patients usually survive no longer
than 2 years after diagnosis.
 Barbiturates
• Barbiturates are sedative-hypnotic Agents,
non-selective in effects.
• At low doses, the barbiturates Produce
Sedation (calming effect, reduced excitement).
• At higher doses, the drugs cause hypnosis,
followed by anesthesia, and finally coma, and
death.
 SYMPTOMS
 Neurological or CNS manifestation
• Lethargy/drowsiness
• Hypothermia (reduced temperature)
• Vertigo, slurred speech, and ataxia
• Coma
• Psychiatric manifestation
• Memory disturbances
• Poor judgment, delirium, and
irritability,
 Symptoms
• Respiratory depression
• Apnea or hypoxia
• Acute respiratory distress syndrome (low oxygen)
• Tachycardia or bradycardia
• Hypotension
• Shock
• Gastrointestinal (reduced bowel sounds)
• Skin (barbiturate blisters)
• Barbiturates cause fetal craniofacial deformities and
contribute to mental retardation
 Treatment
• Cardio respiratory support
• Cleaning of the airways by thorough suction
and insertion of oral airways
• Correction of serum electrolytes. (Fluid therapy)
• Gastric lavage
• Activated charcoal is administrated orally or
by nasogastric tube.
 Antidote
• Flumezinil
• Hydrocortisone sodium
succinate as a rescue agent
has provenvitalto
Improve symptoms.
Breathing, intestinal, blood
problems and skin conditions
 Digitalis
Cardio active glycoside, is obtained from the dried leaves
of the common foxglove (digitalis purpurea) and used as
medicine to strengthen contractions of the heart muscle.

Toxicity symptoms include

• Confusion
• Irregular pulse
• Loss of appetite
• Nausea, vomiting, Foxglove
diarrhea
• Palpitations
• Visual changes (unusual)
 Treatment
• GI decontamination and/or enhanced elimination
• Electrolyte balance because hypokalemia
increases
Digoxin cardiac sensitivity and should be corrected.
• Anti-arrhythmic (lidocaine)
• Anti-seizure (phenytoin)
 Antidote
• Digoxin immune fab (antibody) act as an antidote.
• Note: most often it is not needed, just stopping digitalis,
treating the arrhythmias, and supplementing potassium
if needed is enough
Acetaminophen
 Acetaminophen produces toxicity when its usual metabolic

pathways become saturated.

 Usually, acetaminophen undergoes metabolism by sulfation,

glucuronidation, and N-hydroxylation by the cytochrome P450

system.

 When a toxic amount of acetaminophen is ingested, the first

two processes are overwhelmed and more acetaminophen is

metabolized by the cytochrome P450 system to a hepatotoxic

metabolite (N-acetyl-p-benzoquinoneimine, NAPQI).

Acetaminophen
 In therapeutic acetaminophen ingestions, the liver
generates glutathione, which detoxifies NAPQI. However,
in overdose, the glutathione is depleted, leaving the
metabolite to produce toxicity.
 The antidote for acetaminophen toxicity, N-acetylcysteine
(NAC), initially works as a glutathione precursor and
glutathione substitute and assists with sulfation. Later on,
NAC may function as an antioxidant to aid in recovery.
NAC is the most effective when initiated 8 to 10 hours post
ingestion.
 SALICYLATES POISONING
Assessment
Symptoms

Tinnitus Seizures
Vomiting Hyperthermia
Hyperventilation
Hypoglycemia
Dehydration
Lethargy Non cardiogenic pulmonary
Coma edema
 SALICYLATES POISONING
Cont.
• Initial respiratory alkalosis (may be
transient), followed by paradoxical
aciduria (pH <6), then metabolic
acidosis & Hypokalemia (± ongoing
respiratory alkalosis).
SALICYLATES
POISONING
Patients Requiring Treatment
 Acute ingestion ≥ 150mg/kg
 All symptomatic patients
 Ingestion of unknown
quantity
 SALICYLATES
POISONING
 Investigations

 Serum salicylate level at presentation (on

patients requiring treatment), and 2 hrly if
symptomatic or enteric coated preparation.
Urea & electrolytes, creatinine, acid-base,
glucose
SALICYLATES
POISONING
SALICYLATES
POISONING
 SALICYLATES POISONING
Symptomatic
(Cont.)
 I.V. bicarbonate infusion 1mmol/kg/hr, after initial slow

bolus of 2mmol/kg, (keep urine pH >7.5)

 Potassium replacement as required
 Worsening symptoms, convulsion, coma, contact I.C.U.
for respiratory support and hemodialysis
 Salicylate level >7mmol/l following an acute poisoning
contact I.C.U. for consideration of hemodialysis.
 IRON POISONING
Background

 Iron is found in several different forms in

different medicines.
 The important ingestion is the amount of
elemental iron not the iron salt.
IRON POISONING
Percentage elemental iron:
• Ferrous fumarate 33%
• Ferrous chloride 28%
• Ferrous sulfate 20%
• Ferrous chloride 28%
• Ferrous gluconate 12%
Iron is also found in plant fertilizers
(e.g. sulphate of iron -20% elemental
iron).
 ASSESSMENT
Patients Requiring Assessment
1. Ingestion of > 40 mg/kg elemental iron.
(approximately > ½ tablet/kg or 6.5 ml
syrup/kg)
2. Ingestion of an unknown quantity.
3. Any symptomatic patients
HISTORY AND EXAMINATION
Initial symptoms:

 Usually occur within 20 minutes

 Nausea, vomiting, diarrhea, abdominal
pain, hypotension, Hematemesis, fever
 Gastrointestinal symptoms related to the corrosive
nature of iron may occur without systemic
toxicity, however any symptoms require
iron levels.
 Lack of symptoms within the first 6 hours makes
significant toxicity unlikely.
 HISTORY AND EXAMINATION
Latent period:
 There is often 6-24 hour latent period when
initial symptoms resolve, before overt
systemic toxicity
 Thus improvement over this time may be
a result of improvement or
deterioration
 HISTORY AND EXAMINATION
Other symptoms:
 Usually appear at 6-24 hours and lasts
for 12-24
 Tachycardia, vasoconstriction,
hypotension and shock
 Metabolic acidosis can occur due to
fluid shifts from intravascular to
extravascular compartments and cellular
hypoxia
HISTORY AND EXAMINATION

Multiple organ failure:

 Occurs 12-48 hours after ingestion
 Particularly hepatic failure
 IRON POISONING
Management
 ABC
 Supportive therapy to maintain adequate
blood pressure and electrolyte balance is
essential
 I.V. fluid resuscitation 20 ml/kg
 Potassium and glucose administration as
necessary.
 IRON POISONING
Investigations
Asymptomatic patients:
 Ifunknown amount or >60mg/kg
ingested need serum iron levels 4
hourly until falling
IRON POISONING

 All symptomatic patients should have

the following investigations:
 AXR if tablet ingestion

 ABG (acidosis)

 Glucose (hyperglycaemia)
 IRON POISONING
Cont.
 Serum iron
 Peak levels are usually seen at 4 hours.
 Levels taken after four hours may
underestimate toxicity because the subject iron
may have either been distributed into tissues or be
bound to ferritin.
 In the case of slow release or enteric coated
tablets, levels should be repeated at six to eight
hours as absorption may be erratic.
 Once desferroxamine is commenced, iron
levels are not accurate at most labs using
automated methods
IRON POISONING
Cont.
 FBE (full blood examination)
 Clotting (reversible early coagulopathy and
late coagulopathy secondary to hepatic injury)
 LFTs
 AXR may be helpful in evaluating
gastrointestinal decontamination after
treatment if tablets have been ingested.
 IRON POISONING
Cont.
 Decontamination
 Charcoal is of no benefit.
 Decontamination of choice is whole bowel irrigation
(WBI) with naso-gastric colonic lavage solution
30ml/kg/hr until rectal effluent clear (contraindicated if
there are signs of bowel obstruction or haemorrhage).
 WBI is indicated:

 If AXR reveals tablets, or capsules ingested

 In symptomatic patients
IRON POISONING

Antidote:
 Desferroxamine is a chelating agent
which forms a water soluble
desferroxamine-iron complex.
 IRON POISONING
 Dose: Desferroxamine 15 mg/kg/hr I.V. The rate
is reduced after four to six hours so that the total
intravenous dose in general does not exceed 80
mg/kg/24 hours.
 Desferroxamine -iron complex is renally
excreted.
 If oliguria or anuria develop, peritoneal dialysis
or hemodialysis may become necessary to remove
ferrioxamine.
 IRON POISONING
Cont.
It is recommended to continue
desferroxamine until
 Patient is asymptomatic.
 decontamination complete
 acidosis resolved
 Iron level (if measurable) is <54
micromol/L
 Desferroxamine has been associated with
pulmonary toxicity and should be used with
caution if indications persist >24 hours.
ALKALIS POISONING

Alkalis include:
 Drain cleaners, Oven cleaners
 Automatic dish washing liquids &
powders
 Laundry detergents, Ammonia
• cement
 ALKALIS POISONING
 pH of >11.5 is likely to cause
significant GI ulceration
 Attempt to obtain container to
check contents and strength of substance.
 ALKALIS POISONING(CONT.)
 Corrosive potential varies with concentration of
specific ingredients and preparations, i.e liquid
preparations are more likely to cause esophageal
burns than powders.
ASSESSMENT
 Toxicity
Exposure may lead to severe burns of
GIT, especially esophagus Absence of mouth
or pharyngeal ulcers does not preclude gastro-
oesophageal lesions

 Symptoms: May be minimal Pain, Nausea

& vomiting, drooling or refusing to eat and
drink , respiratory distress.
 MANAGEMENT
 Activated charcoal is contraindicated
 If asymptomatic treat with fluid dilution:

10ml/kg of water (max 250ml)

 If asymptomatic after 4 hours and able
to eat and drink the patient can be safely
discharged , If symptoms persist then
refer for oesophagoscopy.
ANTICONVULSANT POISONING
 CARBAMAZEPINE, PHENYTOIN, SODIUM VALPROATE,
PHENOBARBITONE

Assessment
 CNS
 Ataxia, drowsiness, coma, convulsions
 GIT
 Nausea & Vomiting
 CVS
 Hypotension, Arrhythmias
PATIENTS REQUIRING
TREATMENT
 All symptomatic patients
 Acute ingestion of unknown quantity.
• ingestion of >20mg/kg (for patients
not on maintenance treatment) or the
greater of more than twice the daily
dose or 20mg/kg for patients on
maintenance treatment
MANAGEMENT
 Charcoal 1g/kg unless altered conscious state
(protect airway).
 Mild symptoms (e.g. ataxia, blurred vision),
observe 4 hours, discharge if symptom free
 Moderate or persistent symptoms (after 4 hours of
observation)
 Admit for observation
 Severe symptoms
 Depressed . conscious state or cardiac
arrhythmias, shift to ICU
TRICYCLIC OVERDOSE
Assessment
Symptoms
 Anticholinergic
 vomiting, blurred vision, ataxia, tachycardia,
urinary retention

 Sodium Channel blockade

 QT prolongation
 reduced cardiac contractility &
hypotension
 CNS Depression
 drowsiness, coma, convulsions
 Symptomatic patients require urgent medical
assessment
 MANAGEMENT
 Charcoal 1g/kg unless altered conscious state (protect
airway first)
 Require ECG, cardiac monitoring
 Asymptomatic: observe for 6 hours post ingestion and
discharge if have a normal ECG just prior to discharge
 All symptomatic patients should be admitted

If widened QRS on ECG commence Sodium

Bicarbonate infusion 1mmol/kg/hr, after initial slow
bolus of 2mmol/kg
 If altered conscious state, widened QRS or arrhythmia
contact I.C.U. & protect airway
STRYCHNINE
 MOA: An antagonist of glycine, a major
inhibitory neurotransmitter in the
mammalian nervous system
 Effects: Increased reflex action
Increased rate of respiration
Enlargement of the capacity of the lungs
Increased force, rate, and volume of the pulse
Raised arterial pressure
Increased sharpness to sight, hearing, and
smell, and general irritation .
STRYCHNINE
Toxic effects: Extremely poisonous (100 mg is
fatal )
 Suffocation
 Tremors
 Convulsions
 Eariness
 Death usually taking place after three
or four convulsions
 Death may occur during the interval
from exhaustion, or paralytic asphyxia or
respiratory or heart muscles paralysis.
STRYCHNINE
 The main targets of the treatment of
strychnine poisoning are:
Prevention of convulsion and Support of
respiration.
Diazepam may be used as it is the most
useful agent for this purpose because it
antagonizes convulsion without causing
respiratory depression.
Adequate respiratory ventilation is
necessary for support of respiration.
Nicotine
 Nicotine is a compound found
abundantly in tobacco leaves.
 Nicotine is addictive and acts as a
stimulant when consumed
 Nicotine Poisoning is caused by the
intake of nicotine compounds
 This intake could be accidental, or in
some cases intentional, to bring self-
harm
Nicotine
 The signs and symptoms of Nicotine Poisoning may include:
 Headaches
 Burning and associated pain in the mouth and throat; drooling
from the mouth
 Breathing difficulties, include absence of breathing
 Vomiting
 Stomach pain and cramps
 Seizures
 Neurological symptoms that include confusion, restlessness,
depression, anxiety, and nervousness
 Twitching of muscles
 Rapid heartbeat (palpitations), which is followed by decreased
heartbeats
 Unconsciousness, coma
Nicotine
 Treatment:
 Activated charcoal – if the patient is conscious and able to take

it by mouth. Also, this treatment is more effective if the time of

Nicotine overdose has not gone beyond a few hours. This may
help to reduce its absorption inside the digestive tract.
 Benzodiazipines to control seizures

 Fluid and salt injection to treat low blood pressure

 Atropine – It acts against the activities of ACh to treat slowed

pulse
 If breathing is very slow, recommend artificial ventilation.
OPIOIDS/ NARCOTICS
 Signs and Symptoms:
 Mild sedation
 Nausea
 Vomiting
 Constipation / dry mouth / urine retention
 Visual / tactile hallucinations
 Confusion / delirium / dizziness
 Hyperalgesia / tolerance
 Drug seeking behavior
 Impotence, menopausal symptoms
 Pruritus
 Pin point pupil
OPIOIDS
 Opioid Bowel syndrome: GI activity slowed down,
constipation, dehydration
 Treatment:
○ Increase fluid
○ Laxatives (Bulk agents, osmotic laxatives)
○ Anthraquinones (Increase peristalsis)
○ Diphenylmethanes (Bisacodyl)
○ Opioid antagonists:
 Naloxone
 Naltrexone

 Nausea and Vomiting: Antiemetics

 Cutaneous pruritis: Antihistamine
 Respiratory depression: Naloxone, IV fluids, Breathing
support.
ANTIDOTES
 1. Antagonizing the toxicants: Atropine
against organophosphates
 2. Neutralization of oxidative stress:
 Acetaminophen (high doses): Liver
necrosis- result of its metabolic activation
by cytochrome P450.
 N-acetylcysteine: antidote of
acetaminophen serves-substitute for
glutathione by removing reactive
metabolites produced from acetaminophen.
Chelating agent

 These are the drugs used to prevent heavy

metal poisoning.

 Chelation : The process by which these

organic compounds combine with the
metals to form relatively stable nonionised
ring complexes (chele-clow).
 Drug + Metallic ions

Non toxic , water soluble complex

eliminated by the kidney

 These compounds are usually flexible
organic molecules which can incorporate
metal ions into their molecular structure by
means of chemical groups called ligands
 Chele =crab’s claw
 Ligare =to bind
 Have two or more electronegative groups
that form stable coordinate covalent bonds
with the cationic metal atom
 Chelator –metal complex is stable,
biologically inert and excreted in urine
 Thus appropriate chelating agent can be
effectively used in cases of heavy metal
poisoning
 Chelating agents useful as drugs are:

Dimercaprol (BAL)

Dimercaptosuccinic acid (DMSA)

Dimercaptopropane sulfonic acid (DMPS)

Disodium edetate

Calcium disodium edetate

Pencillamine

Desferrioxamine

Deferiprone
 Drug Used against
EDTA ----------------  Lead
Dimercaprol ---------------  Arsenic,copper,mer.
Succimer ---------------  Lead,arsenic,mercury
Penicillamine -------------  Copper,mercury,lead
Trientine -------------  Copper
Deferrioxamine -----------  Iron
Deferiprone -----------  Iron
 It was synthesized during the world war II by
Britishers as an antidote to arsenic war gas
lewisite
 Oily, pungent smelling, viscous fluid
 It is administered i.m in oil (arachis oil)
 -SH ligands of dimercaprol compete with –SH
groups of enzymes for heavy metal
 Dimercaprol –metal complex is stable and
excreted in urine
Uses:
 For the treatment of arsenic and mercury

poisoning
 As adjuvant to Cal. disod. Edetate in lead

poisoning
 As an adjuvant to pencillamine in copper

poisoning and in Wilson’s disease

Contraindicated in iron and cadmium poisoning
Adverse effects:
 Frequent, dose related, but generally not

damaging
 Rise in BP, tachycardia, tingling and burning

sensations, inflammation of mucous

membranes, sweating, cramps, headache
and anxiety
 Dose 5mg/kg followed by 2-3mg/kg

4hr/2days
DMSA (Succimer):
 Dimercaprol analogue
 Water soluble, less toxic and orally effective
 Marketed in USA and some other countries, not
in India for the treatment of lead intoxication
 Side effects are nausea, anorexia and loose
motions
 Dose-10mg/kg 8hrly/5days
COOH
|
CHSH
|
CHSH
|
COOH
DMPS (unithiol):
 Dimercaprol analogue
 Water soluble, less toxic
 Can be administered orally as well as IV
 Used for severe acute poisoning by mercury and arsenic
 Also effective in the treatment of lead poisoning
 Dose-3-5mg/kg 4hrly by i.v in 20min
Adverse effects are low, except for mild self-limited
urticaria
 It is a disodium salt of EDTA
 Potent chelator of calcium
 Causes tetany on i.v. injection (but not on
slow infusion)
 Can be used for emergency control of
hypercalcaemia (rare) 50mg/kg i.v. over 2-
4hours
 Calcium chelator of Na2 EDTA
 Has a high affinity for lead
 Most important use is lead poisoning
 Poorly absorbed from GI –given i.m or i.v.
 i.m is very painful –i.v. preferred
 Not metabolized
 Excreted by glomerular filtration and
tubular secretion
Adverse reactions:
 Does not produce tetany –relatively safe

 Kidney damage with proximal tubular

necrosis –but dose related

 An acute febrile reaction with chills, body

ache, malaise, tiredness occurs in some

individuals
 Dose- 50-75mg/kg /day i.v
 Dimethylcysteine
 Water soluble degradation product of penicillin
 D –isomer is used-relatively non toxic compared to l –isomer
(optic neuritis)
 Easily absorbed from GIT
 Little metabolized, excreted in urine and faeces
 It has strong copper chelating property and was used in 1956
for Wilson’s disease
 It selectively chelates Cu, Hg, Pb and Zn
Uses:
 Wilson’s disease (hepatolenticular degeneration)
 Copper/ mercury (alternate to BAL & DMSA) poisoning
 Adjuvant to cal. disod. Edetate in lead poisoning but DMSA is
preferred
 Cystinuria and cystine stones
 Scleroderma –benefits by increasing the soluble collagen
 It was used as a disease modifying drug in rheumatoid arthritis,
but now replaced by safer drugs
Adverse effects:
 Short term administration –does not cause
much problem (cutaneous reactions)
 Long term use –produces pronounced toxicity
 Dermatological, renal, hematological and collagen
tissue toxicities

Dose-0.5-1g daily in divided doses

 Chelates copper and is used in Wilson’s
disease
 May be less toxic than pencillamine
 However, in animal studies it has been
found to be teratogenic
 Ferrioxamine Obtained from actinomycete, long chain iron containing

complex

 Chemical removal of iron from it yields desferrioxamine

 1gm is capable of chelating 85mg of elemental iron

 Low affinity for calcium

 Little of orally administered desferrioxamine is absorbed

 Parenterally –partly metabolized, rapidly excreted in urine

Uses:
 Acute iron poisoning: mostly in children,
important and life saving
 Transfusion siderosis
Adverse effects:
 Hypotensive shock due to histamine release
 Abdominal pain, muscle cramps, fever and
dysuria
 Dose- i.v ,10-15mg/kg/hr infusion
 Orally active
 Used in transfusion siderosis
 Somewhat less effective, alternate to injected
desferrioxamine
 Side effects and cost of treatment are reduced
 Also indicated in iron poisoning (less effective than
desferrioxamine) and iron load in liver cirrhosis
Side effects are:
 Anorexia, vomiting, altered taste, joint pain,
reversible neutropenia, rarely
agranulocytosis
 Long term safety is not yet known
 Dose-50-100mg/kg
Primary goals of chelation therapy:
 To reduce metal retention

 To decrease morbidity and mortality

 To prevent complications

Many efficient chelators exist today

Administer less toxic chelator when possible
Unsolved issues:
 Chelation of cadmium, chromium, platinum…

 Chelation therapy in infants, children and during

pregnancy
 Combined chelation therapy (chelators, vitamins,
minerals…)
POLLUTION AND ITS TYPES
 Pollutions
Types of pollution are :
• Air pollution
• Water pollution
• Noise pollution
• Land pollution

AIR POLLUTION:
Air pollution is the human introduction into the atmosphere of chemicals ,
particulate matter
Or biological materials that cause harm or other living organisms or damage
the environment.
Examples of air pollution:
• Acid rain
• Smog
• Indoor air pollution
• Dust particles.

Causes of Air Pollution

• Smoke from chimneys or factories
• Smoke from vehicles
• Smoke from burning or fire
 P revention of air pollution:-
1. We should share vehicles for going to office.
2. We should get a regular pollut io n check of our vehicle.
3. We should use a bicycle for going to near by places.
4. Chimneys of factories should be fitted with proper filters to prevent
smokes from coming out and effect atmosphere.

Water Pollution:-
Water pollut io n is the introduction into fresh or ocean waters of chemical,
physical, or biological material that degrades the quality of the water and
affects the organisms living in it.
Examples of Water pollution:-
Industrial afflue nt
Mining and Agricultural Wastes
Sewage Disposal and Domestic Wastes
 Causes of water pollution:-
1. Factories throw their waste in water bodies.
2. People bath and wash clothes in water bodies.
3. Some oil ships drown in water which hardly affects the aquatic life
4.Smoke from vehicles lets the river to dry.

P revention of water pollution:-

1. Factories should not throw their waste in water bodies.
2. People should not bath and wash clothes in rivers or lakes.
3. People should not take their animals to take bath in rivers or lakes.
Noise Pollution:-
Noise pollution is unwanted human-created sound that disrupts the
environment. The dominant form of noise pollution is from
transportation sources, principally motor vehicles, referred to as
environmental noise.
Examples of Noise P ollution:-
• Loudspeakers
• Aircrafts
Causes of noise pollution:-
1. Jet planes.
2. Loud speakers and other loud speaking things.
3. Cinema halls.
4. Factories
5. Road traffic
P revention of noise pollution:-
1. We should not use loud speakers.
2. Factories should be made out of the city.
3. There should be not more noise making vehicles on the roads.
Land Pollution:-
Land pollution is the degradation of the Earth's land surface through misuse of
the soil by poor agricultural practices, mineral exploitation, industrial waste
dumping, and indiscriminate disposal of urban wastes.
Examples of Land pollution:-
Soil Pollut io n
Waste Disposal
Causes of land pollution:-
1. People Cut forest for furniture.
2. Plastic is the main source of land pollutio n.
3. People throw house garbage on roads.
4. Some industr ie s throw their waste on land.
 P revention of land pollution:-
1. People should not cut trees for making furniture.
2. People should not throw garbage on land.
3. Plastic bags should be avoided for preventio n of land pollutio n.
4. Industries should not throw their waste on land.
THANK YOU