Title Layout

Subtitle
Objectives:
 definition
Types
Epidemiology
Clinical diagnosis
Principles of management
Common selected poisoning
Poison:
Poison is a substance ( solid/ liquid or gaseous ),which if
introduced in the living body, or brought into contact with any part
there of, will produce ill health or death, by its constitutional or
local effects or both.”
“Any substance that can harm the body by altering cell structure
or functions.”
Poisoning:
The development of dose related adverse effects
following exposure to chemicals, drugs or other
xenobiotics.”
• Poisoning occurs when any substance interferes with
normal body functions after it is swallowed, inhaled,
injected, or absorbed.
• The branch of medicine that deals with the detection
and treatment of poisons is known as toxicology
Nature of Poisoning
Homicidal – killing of a human being by another human being by
administering poisonous substance deliberately.
Suicidal – when a person administer poison himself to end his/ her
life.
Accidental – E.g. Household poisons nail polish remover , acetone
Occupational – in professional workers. E.g. insecticides, noxious
fumes.
Classification

• Intentional poisoning: A person taking or giving a substance with the

intention of causing harm, e.g. Suicide and Assault

• Unintentional poisoning: If the person taking or giving a substance did

not mean to cause harm, e.g. For recreational such as in an “Overdose”
or Accidentally taken by a toddler

• “Undetermined”: When the distinction between intentional and

unintentional is unclear.a
Types of Exposure:
• Acute: Exposure < 24 hours
Single: a single or continuous exposure (e.g. carbon monoxide)
Repeated: multiple interrupted exposures where there may be
accumulation (e.g. aspirin overdose)
• Chronic: > 24 hours or long-term exposure ,for weeks or months
(e.g. lead poisoning)
• Acute “on chronic”: Acute exposure against a background of
chronic exposure to the same agent (e.g. organophosphorus
pesticide exposure on a chronically exposed child)
• “Hit and run”: Acute exposure leading to delayed effects once the
toxicant is gone (e.g. thalidomide exposure during gestation
leading to phocomelia)
Poisoning Causes:
Cleaning products
Household products, such as nail polish remover and other personal care
products
Pesticides
Metals, such as lead ,Mercury, which can be found in old thermometers and
batteries
Prescription and over-the-counter drugs when combined or taken the wrong
way
Contaminated food
Plants, such as poison ivy and poison oak
Venom from certain snake
› Mechanisms of Toxicity

1.Delivery: Site of Exposure to the Target

2.Reaction of the Ultimate Toxicant with the Target Molecule

› 3.Cellular Dysfunction and Resultant Toxicity

› 4.Repair or Disrepair
Toxic substances have seven common major pathophysiologic
mechanisms that may produce symptom:
Interfere with the transport or tissue utilization of O2 e.g. CO
Depress or stimulate CNS e.g. MDMA
Affect autonomic nervous system e.g. Organophosphate
Affect the lungs by aspiration e.g. Hydrocarbon
Affect the heart and vasculature myocardial dysfunction e.g.
Antidepressant
Produce local damage e.g. Corrosive
Affect on the liver e.g. Acetaminophen
Nature of Poisoning:

› Homicidal– killing of a human by another human being by

administering poisonous substance deliberately.

› Suicidal– when a person administer poison himself to end his/

her life
Accidental-
– E.g. Household poisons nail polish remover , acetone
Occupational– in professional workers. E.g. insecticides, noxious
fumes.
› Inhalational:

Poisons that are breathed in:

Gases: ammonia, chlorine

Vapors: carbon monoxide

Sprays: insecticides

Volatile liquid chemicals: change easily from liquid to gas

› Ingestion
Poisons that are swallowed:
Household and industrial Chemicals
Medications
Improperly prepared food
Plant materials
Petroleum products
› Injection
› Intra venous –
› Benzodiazepines, barbiturates, tricyclic antidepressants etc.
› Intramuscular –Benzodiazepines, opioids etc.
› Subcutaneous – Botulinum Toxin
› Intra- dermal – Local anesthetics, organophosphates
› Absorption:
› Poisons taken in through unbroken skin:
› Corrosives or irritants
› Through bloodstream Insecticides and chemicals
Epidemiology:
1.Poisoning is divided into accidental poisoning and non accidental or self
poisoning.
2. Accessibility of the poisoning agent is the single most important
environmental risk factor.
3. Most drug containers in use in the region are easy to open and do not have
a child lock.
4. Many pediatric drug preparation are sugar coated or sweetened and may be
mistaken for sweets.
5. Seasonal variations in poisoning occur.
6. Illiteracy; unable to follow safety precautions written on the labels of various
drugs and chemicals.
7. Inadequate labeling of drugs and chemicals increase the risk of poisoning.
8. Administration of the wrong drug or the wrong dose.
› Acute Poisoning
› • Pharmaceuticals: sedatives, analgesics,
› contraceptives, cardiovascular drugs
› • Household products: bleaches,
› detergents, solvents, kerosene
› • Cosmetics: perfumes, shampoo, nail
› products
› • Substances of abuse: alcohol, tobacco,
› illicit drugs
› • Pesticides: insecticides, rodenticides,
› herbicides
• Plants and mushrooms: berries, seeds,
leaves
• Seafood Poisoning: paralytic shellfish
poisoning, fish poisoning
• Venomous bites and stings: snake,
scorpions, bees, jellyfishes, spiders
Chronic Poisoning
• Metals
Lead
Mercury
• Pesticides in food or fields
Organophosphates
Carbamates
Warfarins
Organochlorines: Persistent Organic Pollutants (POPs), has
potential developmental neurobehavioral and endocrine
› Ingestion
Poisons that are swallowed:
› Household and industrial chemicals
› Medications
› Improperly prepared food
› Plant materials
› Petroleum products
The effects of poisoning maybe None, Mild or Severe
depending on:
• The amount of poison ingested.
• The nature of the substance.
• The age of the child.
• The nutritional status of the child.
• The state of the stomach-whether empty or full of food.
Approach to the poisoned patient:
• A detailed history and physical examination serves as the
foundation for a thoughtful differential diagnosis and the formation
of an initial prognosis.
• The history and physical examination should not await the
collection of body fluid and the results of a “tox screen.”
• Toxicology laboratory analyses, or “screens,” in fact evaluate for
only a small fraction of common pediatric exposures and rarely
make (vs confirm) the diagnosis.
INITIAL PATIENT EVALUATION
Identification of the patient and toxic agent.
What? Description of the toxin.
How much? Magnitude of the exposure.
When ?Time of exposure.
Progression of symptoms.
Medical history.
PATIENT HISTORY.
Description of Toxins.
• Product names (brand, generic, chemical) and ingredients, along with
their concentrations, may be obtained from labels.
• Several characteristic toxic syndromes, or “toxidromes,” exist for
some of the more common exposures and may assist in identifying the
offending agent.
Example :Increased sympathetic nervous system activity Poison
Syndrome
• Pyrexia
• Flushing
• Tachycardia Hypertension Associated Signs
• Pupillary constriction
• Sweating
Cough and decongestant preparations
Amphetamines
Cocaine Possible Toxins
Ecstasy
Theophylline
 Magnitude of Exposure:
• It is important to attempt to determine as accurately as possible how
much of the substance has been
ingested by counting the remaining tablets or measuring the remaining
volume of liquid.
• It is better to overestimate than to underestimate.
• Estimates can be refined as the patient is assessed over time and initial
laboratory data become available.
• Because the toxicity of most agents is dose-related, knowing the age or
weight of the child aids in assessment.
• For inhalation, ocular, or dermal exposures, the concentration of the
offending agent and the length of
contact time with the material should be determined, in addition to the
time course for associated symptoms
to occur, their progression, and possible resolution.
 Time of Exposure:
• For some products, toxic manifestations may be delayed for hr. or
days. Knowing the time lapse between exposure
and the onset of symptoms and/or medical evaluation will
markedly influence decisions about obtaining certain
diagnostic testing as well as therapeutic intervention.
Progression of Symptoms:
• Knowing the nature and progression of symptoms is very helpful
for assessing the need for immediate life
support, the prognosis, and the type of intervention that may be
needed.
Medical History
• Underlying diseases may make a child more susceptible to the effects
of a toxin.
• Concurrent drug therapy may also increase susceptibility because
certain drugs may interact
with the toxin.
• Pregnancy is a common precipitating factor in adolescent suicide
attempts and can influence
the patient evaluation and treatment plan.
• At 6 month of age or younger, it is very unlikely that an infant could
become accidentally exposed
to a sufficient quantity of a potentially harmful product in the absence of
other extraneous
factors that require further investigation (social environment).
Signs & Symptoms of Poisoning:
• Lower level, if any of consciousness.
• Altered mood: lethargic, ecstatic,
violent or hostile.
• Differed breathing rate.
• Increased or lowered heart rate.
• Dilated or shrunken pupils
• Change of colour around mouth
• Cramps
• Nausea
• Vomiting
• Diarrhoea
ODOR
Bitter almonds: Cyanide
Acetone: Isopropyl alcohol, Methanol, Paraldehyde, Salicylates
Alcohol: Ethanol
Wintergreen: Methyl Salicylate
Garlic: Arsenic, Thallium, Organophosphates
OCULAR SIGNS
Miosis :Narcotics (except meperidine), Organophosphates,
muscarinic
mushrooms, clonidine, phenothiazine's, chloral hydrate,
barbiturates
(late), PCP
Mydriasis: Atropine, alcohol, cocaine, amphetamines,
antihistamines, cyclic antidepressants, cyanide, carbon monoxide
Nystagmus: Phenytoin, barbiturates, éthanol, carbonmonoxide
Lacrimation: Organophosphates, irritant gas or vapors
Retinal hyperemia :Methanol
Poor vision :Methanol, botulism, carbon monoxide
CUTANEOUS SIGNS
Needle tracks :Heroin, PCP, amphetamines
Bullae: Carbon monoxide, barbiturates
Dry, hot skin: Anticholinergic agents, botulism
Diaphoresis: Organophosphates, nitrates, muscarinic mushrooms,
aspirin, cocaine
Alopecia :Thallium, arsenic, lead, mercury
Erythema :Boric acid, mercury, cyanide, anticholinergics
ORAL SIGNS
Salivation :Organophosphates, salicylates, corrosives, strychnine
Dry mouth: Amphetamines, anticholinergics, antihistamine
Burns :Corrosives, oxalate-containing plants
Gum lines :Lead, mercury, arsenic
Dysphagia: Corrosives, botulism
INTESTINAL SIGNS
Cramps :Arsenic, lead, thallium, Organophosphates
Diarrhea :Antimicrobials, arsenic, iron, boric acid
Constipation: Lead, narcotics, botulism
Hematemesis: Aminophylline, corrosives, iron, salicylates
CARDIAC SIGNS
Tachycardia: Atropine, aspirin, amphetamines, cocaine, cyclic
antidepressants, theophylline
Bradycardia :Digitalis, narcotics, mushrooms, clonidine,
Organophosphates, β blockers, calcium channel blockers
Hypertension: Amphetamines, LSD, cocaine, PCP
Hypotension: Phenothiazines, barbiturates, cyclic antidepressants,
iron, β blockers, calcium channel blockers
RESPIRATORY SIGNS
Depressed respiration: Alcohol, narcotics, barbiturates
Increased respiration: Amphetamines, aspirin, ethylene glycol,
carbon monoxide, cyanide
Pulmonary edema :Hydrocarbons, heroin, Organophosphates,
aspirin
CNS SIGNS
Ataxia: Alcohol, antidepressants, barbiturates, anticholinergics,
phenytoin, narcotics
Coma :Sedatives, narcotics, barbiturates, PCP, Organophosphates,
salicylates, cyanide, carbon monoxide, cyclic antidepressants, lead
Hyperpyrexia: Anticholinergics, quinine, salicylates, LSD,
phenothiazine's, amphetamines, cocaine
Muscle fasciculation :Organophosphates, theophylline
Muscle rigidity :Cyclic antidepressants, PCP, phenothiazines,
haloperidol
Paresthesia :Cocaine, camphor, PCP, MSG
Peripheral neuropathy: Lead, arsenic, mercury, organophosphates
Altered behaviour: LSD, PCP, amphetamines, cocaine, alcohol,
anticholinergics, camphor
Fundamentals of poisoning management:
1. Initial resuscitation and stabilization
2. Removal of toxin from the body
3. Prevention of further poison absorption
4. Enhancement of poison elimination
5. Administration of antidote
6. Supportive treatment
7. Prevention of re - exposure
1. Initial resuscitation & stabilization:
First priorities are ABC’s
I/V access – I/V fluids
Endo tracheal intubation - to prevent aspiration
Unconscious patients
Respiratory depression/ failure
Convulsions- give anticonvulsants
Toxicological Diagnosis
History
Need to obtain as much information as possible about exposure
i.e. number of exposed persons, type of exposure, amount or
dose, route
Patients intent must be determined
Examination
Undress patient completely for thorough examination
Check clothing for objects or substances
Assess general appearance of patient
Examine skin for bruising, cyanosis, flushing
Assess ABCDE (Airways, Breathing, Circulation, Disability,
Exposure)
Removal of toxin:
Copious flushing with water or saline of the body including skin
folds, hair
Inhalational exposure
Fresh air or oxygen inhalation
Prevention of poison absorption:
Gastric Lavage:
Done with water ,1:5000 potassium permanganate , 4% Tannic
acid, saturated lime water or starch solution with orogastric or
Ewald’s tube.
Performed until clear fluid is obtained or a maximum of 3 L .
Lavage decreases ingestant absorption by an average of :-
52 % - if performed within 5 min. of ingestion
26 % - if performed at 30 min.
16 % - if performed at 60 min.
Contraindications:
o Corrosive poisoning
o Recent esophageal / gastric surgery
o Unconscious patient
3.Prevention of poison absorption
Ipecac Syrup induced emesis
Administered orally
Dose :-
› 30 ml – adults
› 15 ml – children
› 10 ml – small infants
› Contraindications:
› Corrosives
› CNS depression or seizures
› Rapidly acting CNS poisons ( cyanide, strychnine, camphor )
Activated Charcoal:
o Charcoal adsorbs ingested poisons within gut lumen allowing
charcoal- toxin complex to be evacuated with stool or removed by
induced emesis / lavage
o Dose – 1 g/kg body wt.
o Given orally as a suspension ( in water ) or through NG tube
Contraindications:
o Mineral acids, alkalis, cyanide, fluoride ,iron
Whole bowel irrigation
Administration of bowel cleansing solution containing
electrolytes & polyethylene glycol
Orally or through gastric tube
Rate – 2 L/hr. ( 0.5 L /hr. in children)
End point- rectal fluid is clear
Position – sitting
Contraindications :
a. Bowel obstruction
b. Ileus
c. Unprotected airway
Enhancement of Elimination of Poison:
Infusion of large amount of NS+NAHCO3
Used to eliminate acidic drug that mainly excreted by the kidney
eg: salicylates
Serious fluid and electrolytes disturbance may occur
Need expert monitoring
Acidification of urine:
o Enhance elimination of weak bases such as Phencyclidine &
Amphetamine
Alkalanization :
Beneficial in certain ingestions: 2-4-D
(herbicide), phenobarbital, chlorpropamide,
salicylates, methanol
Alkalinization achieved by IV dose of
bicarbonate at 1-2 mEq/kg, followed by
intermittent boluses or continuous
bicarbonate drip for urine pH 7.5-8.0
Profound hypokalemia may result, must
aggressively replace
Enhancement of Elimination of Poison
Extracorporeal Removal:
Dialysis:
Acetone, Barbiturates, Bromide, Ethanol, Ethylene glycol,
Salicylates, Lithium
Less effective when toxin has large volume of distribution (>1
L/kg), has large molecular weight, or highly protein bound.
Peritoneal Dialysis:
Alcohols , long acting salicylates, Lithium
Chelation:
Heavy metal poisoning
Complex of agent & metal is water soluble & excreted by
kidneys
Eg. BAL, EDTA,
BAL – Arsenic, Lead, Copper, Mercury
EDTA- Cobalt, Iron, Cadmium
Administration of Antidote:
• Not all poisons have antidotes
Prevention:
By following these guidelines you will be able to prevent most
poisoning emergencies:
Keep the household products and medications out of the reach of
children.
Use childproof safety caps on containers of medications and other
potentially dangerous substances.
Keep products in their original containers.
Use poison symbols to identify dangerous substances.
Dispose of outdated medications and household products.
Use chemicals only in well-ventilated areas.
Wear proper clothing.
Food Poisoning:
signs and symptoms:
Nausea, vomiting, abdominal cramps, chills, diarrhea, and fever
Home Remedies:
Take enough amount of fluids
Drink oral rehydration mixtures to replace fluids and minerals lost through vomiting and
diarrhea
Get plenty of rest
In case of severity;
In the hospital, the treatment is designed to rehydrate the pt. This is usually done with
intravenous (IV)
fluids. The doctor may prescribe antibiotics if your food poisoning is bacterial.
Prevention:
-Wash your hands, utensils and food surfaces often –
Keep raw foods separate from ready-to-eat foods.
-Cook foods to a safe temperature
Inhaled Poisoning::
Eye tearing, nose and throat irritation , Sneezing, Excess salivation,
Vomiting.
TREATMENT:
Nebulized lidocaine analgesia & cough.
Nebulized sodium bicarbonate
Saline irrigation for skin or eye exposures
Organophosphate Poisoning (Pesticides):
Insecticides (worldwide).
Nerve gas (sarin, tabun).
• Chlorpyrifos, parathion, diazinon, famphur, phorate, terbufos, and malathion
are examples of
organophosphates while
• Carbofuran, aldicarb, and carbaryl, are carbamates.
• They work by inhibiting acetyl cholinesterase resulting
in an overabundance of acetylcholine at synapses &
the myoneural junction.
• Present with cholinergic symptoms
• Cutaneous exposure
• Inhalation
• Ingestion
MECHANISM OF ACTION
Organophosphorous compounds contain carbon and
phosphorous acid derivatives.
They bind to acetyl cholinesterase (AChE), also known as red
blood cell (RBC) acetyl cholinesterase or neural acetyl
cholinesterase, and render this enzyme non-functional.
Incapable of degrading the neurotransmitter acetylcholine.
Acetylcholine accumulate at neuromuscular junctions and
synapses.
Stimulate the muscarinic and nicotinic receptors.
Signs of overexposure:(within the first few hours)
1. Parasympathetic(muscarinic)
Sweating
Salivation
Lacrimation
Bradycardia
2. Sympathetic nervous system (nicotinic)
Hypertension
Muscle fasciculation's
Motor weakness
Tachycardia
3. CNS
Giddiness
Anxiety
Drowsiness
Convulsions
CLINICAL FEATURES
Onset and duration of AChE inhibition varies depending:-
- On the Organophosphorous agent's rate of AChE inhibition
- The route of absorption
For most agents, oral or respiratory exposures generally result in
signs
or symptoms within three hours.
While symptoms of toxicity from dermal absorption may be
delayed
up to 12 hours.
 Primary toxic effects involve the autonomic nervous system,
neuromuscular junction, and central nervous system (CNS).
The parasympathetic nervous system is particularly dependent on
acetylcholine regulation.
Both the autonomic ganglia and the parasympathetic nervous
system are regulated by nicotinic and muscarinic cholinergic
receptor subtypes, respectively.
 The muscarinic signs can be remembered by use of one of two mnemonics:
SLUDGEBB (Salivation, Lacrimation, Urination, Defecation, Gastric
Emesis,
Bronchospasm, Bradycardia)
DUMBELS (Defecation, Urination, Miosis, Bradycardia, Emesis,
Lacrimation,
Salivation)
Stimulation of nicotinic receptors
Release of epinephrine and nor epinephrine ,muscle weakness, fasciculation
hypertension, central respiratory depression, lethargy convulsion and coma
 Depends on the balance between stimulation of muscarinic and
nicotinic receptor.
The balance depend on the:
- Type of organophosphate
- Dose
- Route and rate of absorption
- Individual factor
DIAGNOSIS
• The diagnosis of organophosphate poisoning is made on clinical
grounds.
• If doubt exists as to whether an organophosphate has been ingested,a trial of
atropine 0.01 to 0.02 mg/kg may be employed.
• The absence of signs or symptoms of anticholinergic effects following
atropine challenge strongly supports the diagnosis of poisoning.
› https.//www.emedicine.medscape.com
› https.//www.medicinenet.com
› Hinkle, J. L., Brunner, L. S., Cheever, K. H., &Suddarth, D.
S. (2014). Brunner &Suddarth's textbook of medical-
surgical nursing. Philadelphia: Lippincott Williams &
Wilkins.