The document discusses various types of poisoning including iron toxicity, organophosphate poisoning, drug toxicity, hydrocarbon poisoning, and prevention of poisoning. It provides details on the clinical presentation, management, and common causes of poisoning in children, such as accidental ingestion of household chemicals, medications, or plants. Factors that contribute to childhood poisoning include developmental stage, accessibility of toxic substances, and improper storage of drugs and chemicals.
2. Outline
• Introduction
• Iron Toxicity
• Organophosphate Poisoning
• Drugs Toxicity
• Hydrocarbon Poisoning
• Principles of Management
• Prevention of Poisoning
3. What is a poisoning?
• A 2 year old eats
Chewable vitamins; A watch battery;
A jade plant; The dog’s medicine….
• A 4 year old with anemia has a father who is a
welder.
• 16 year old girl takes mom’s Elavil(Antidepressant)
after a fight with her boyfriend.
• Your patient on albuterol syrup gets a 10x dosing
error.
• Mom is worried about toxic mold, mercury fillings,
vaccination risks, arsenic in the water….
4. Poison
• Any substance (Liquid, Solid or Gas) that is harmful to the body
when Ingested, Inhaled, Injected, or Absorbed through the
skin.
• Does not include adverse reactions to medications taken
correctly.
• 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.
5. • Poisoning is the fourth most common cause of accidents in
children.
• Ages less than 5…accidental.
• Ages adolescents…intentional, experimental.
• More than 90% of toxic exposures in children occur in the home.
• Ingestion is the most common route of poisoning exposure (77%
of cases), with the dermal, inhalation, and ophthalmic routes
accounting for approximately 7.5%, 6%, and 5% of cases,
respectively.
• Approximately 50% of cases involve nondrug substances, such as
common household products (cosmetics, personal care items,
cleaning solutions, plants, foreign bodies, hydrocarbons).
6. Which is Candy??? Pharmaceutical
preparations comprise
the remainder; These are
products that are familiar
to young children; in
addition, they are usually
manufactured in visually
appealing and great-
tasting formulations.
7. • Acute exposure
Is a single contact that lasts for seconds, minutes
or hours, or several exposures over about a day
or less.
• Chronic exposure
Is contact that lasts for many days ,months or
years.
8. How
Poison Ivy
Drug overdose
Poisoning
• Overdosing on medicine or • Inhaling poisonous gases such
using medicine that doesn’t as carbon monoxide, or fumes
belong to you. from strong cleaning products.
• Being bitten or stung by
May • Pesticides.
venomous animals. • Petrochemical products
• Swallowing or sniffing Paints. e.g. Vasoline
• Coming in contact with Occur, & • Illegal drugs.
poisonous chemicals. • Household cleaning products.
• Touching poisonous plants.
Poisonous
Cleaning Products Products!!! Venomous Bites
9. FACTORS THAT CONTRIBUTE TO THE OCCURRENCE OF POISONING IN CHILDREN
1. Developmental stage
2. Gender
3. Child-caring practices
4. Poverty
5. Children with special needs
10. 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.
11. 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.
12. 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
13. Common Substances Causing Poisoning in Children
Household Agents:- Organophosphates, pesticides, malathion,
Rat poison,
Désinfectants and bleach.
Médicaments:- Aspirin, Paracétamol,
Anti-convulsant drugs (cabarmazepine, phenobarbitone),
Haematinics (iron and vitamins),
Major tranquilizers (phénothiazines),
Some herbal therapies.
14. One year study done in Tikur Anbessa (2007/2008)
• Acute poisoning with in one year was 116.
• 75 male and 41 female.
• Mean age 21 years.
• 96.5% intentional.
• Cause of poisoning
- 43.1% House hold cleaning agents
- 20.7% Organophosphate
- 10.3% Phenobarbital
• Mortality 8.6%,death occur by organophosphate and
Phenobarbital poisoning.
15. Recognition
It may be easily observable that someone has been poisoned if:
• Chemical products are evident at the victims scene.
• Drugs are on or around the victim (medical or illegal).
Example of
• A syringe is in or next to victim. poisonous chemical
• Warning signs of gases and chemicals are at/around the location.
• Victim is conscious and tells first aider they have been poisoned.
If none of these points are apparent in a possible poisoning case, there
are numerous signs and symptoms to look for in the victim, that will
enable you to establish if they have been poisoned.
Sign indicating presence of
Syringe
hazardous chemicals
16. 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.
17. 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.
18. Cont.
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
19. 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.
20. 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 mo 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).
21. 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
• Vomiting
• Diarrhoea
26. Iron Toxicity
• The most common cause of death in toddlers.
• Classically taught as having five clinical stages.
• Remember prenatal vitamins, supplements, and
“natural products”.
• Toxic doses occur at 10-20mg/Kg of elemental iron.
• Prenatal vitamins typically contain about 65 mg of
elemental iron.
• Children's vitamins contain about 10-18 mg of
elemental iron.
27. The Five Stages
• Stage 1
• Nausea, vomiting, abdominal pain and diarrhea.
• Stage 2
• This is the latent phase often between 6-24 hours as the patient resolves GI symptoms.
• Stage 3
• Shock stage involving multiple organs including coagulopathy, poor cardiac output,
hypovolemia, lethargy and seizures.
• Stage 4
• Continuing of hepatic failure and ongoing oxidative damage by the iron in the
reticuloendothelial system.
• Stage 5
• Gastric outlet obstruction secondary to scarring and strictures.
28. • If possible, determining the number of pills ingested, how much iron was in
each pill, and the formulation of iron in the supplement is important.
Different formulations of iron contain varying amounts of elemental iron:
Ferrous sulfate - 20% elemental iron
Ferrous gluconate- 12% elemental iron
Ferrous fumarate - 33% elemental iron
Ferrous lactate - 19% elemental iron
Ferrous chloride - 28% elemental iron
• The following is a formula used to calculate the amount of ingested iron
for a 10-kg child who consumed ten 320-mg tablets of ferrous gluconate
(12% elemental iron per tablet):
10 tablets X 38.4 mg elemental iron per tablet = 384 mg/10 kg = 38.4 mg/kg
29. Laboratory Studies
• A serum iron level should be determined (during peak levels) at 2 -4
hours after ingestion:
> 300 mg/dL indicates mild intoxication,
> 500 mg/dL indicates serious intoxication, but a serum iron level in
excess of the total iron-binding capacity does not serve as a useful
predictor of iron poisoning.
• Laboratory data may reveal leukocytosis, hyperglycemia& radiopaque
tablets on a flat plate of the abdomen.
30. 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
31. 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.
34. Signs of overexposure
(within the first few hours)
1. Parasympathetic 2. Sympathetic nervous system 3. CNS
(muscarinic) (nicotinic) Giddiness
Sweating Hypertension Anxiety
Salivation Muscle fasciculation's Drowsiness
Lacrimation Motor weakness
Convulsions
Bradycardia Tachycardia
35. 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.
36. Cont.
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.
37. Cont.
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.
38. Cont.
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
39. 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.
40. Nicotinic Symptoms
• Remember the days of the week!!!!!
• Mydriasis
• Tachypnea
• Weakness
• Tachycardia
• Fasciculation's
• Pediatric patients tend to present with a predominance of nicotinic symptoms!!!
42. Laboratory Studies
• Obtain a CBC count to rule out infectious causes.
• Chemistry tests may be useful in ruling out electrolyte disturbances.
• Hypokalemia, hyperglycemia ,leukocytosis, proteinuria, glycosuria
• ECG sinus tachycardia.
• RBC cholinesterase tests may reveal decreased activity, which confirms
the diagnosis.
43. Legislation
• The Poison Prevention Packaging Act of 1970. (PPPA)
• Requires child protective packaging of hazardous household
products.
• Over the last 30 years the list of substances regulated by the
PPPA have expanded to include medicines, solvents, and oils.
• Data shows reduction of 45% mortality of pediatric patients
since the introduction and expansion of PPPA.
45. THANK YOU
“Everything is poisonous, there is nothing that is nonpoisonous.
Solely the dose separates a poison from a remedy.”
Paracelsus, Father of Toxicology
Notas del editor
Accidental Causes are Usually due to exploration of their environmentPrevention We need to know the normal development to anticipate when the child is restless so we advice parents to keep a watch outLock up Cabinets, plug up outlets, medicine shuld be kept out of reach from the child geared to make it difficult for the child to access thereby frustrating the kid in to giving up!!! Get rid of expired medications; don’t take medicine infront of a child Don’t refer to drugs as candy!!!
Yersinia requires iron as a growth factor. Deferoxamine acts to solubilize iron and aid in intracellular entry for Yersinia.Suspect Yersinia infection in patients who develop abdominal pain, fever, and diarrhea following resolution of iron toxicity.