2. EPIDEMIOLOGY
More than 90% of toxic exposures occur in the home,
and most involve only a single substance.
Ingestion is the most common route of poisoning
exposure (77% of cases),
Other routes- dermal, inhalation, and ophthalmic routes
Approximately 50% of cases involve nondrug
substances, such as common household products
(cosmetics, cleaning solutions, plants, foreign bodies,
hydrocarbons).
Pharmaceutical preparations comprise the remainder,
with analgesics, cough syrups, antibiotics, and vitamins
the most common categories.
2
3. More than 85% of pediatric poisoning exposures can be
managed without direct medical intervention, because
either not very toxic or take in smaller quantity -not
sufficient to produce clinically relevant toxic effects .
Death due to unintentional poisoning in young children is
uncommon
Common causes of poisoning in our set-up are rat
poisons(intentional in adolescents or unintentional in
children), hydrocarbons s. a. kerosene, improperly
placed drugs , cosmetics etc.
Safety measures like “BABY PROOFING”- placing drugs,
detergents and other household chemicals, health
education are some of the measures in preventing
poisoning
3
4. Counseling parents about potential poisoning
risks, how to “poison-proof” a child's environment
How to diminish the likelihood of serious morbidity
or mortality from an exposure
Poisoning exposures in children 6–12 yr of age are
much less common.
Toxic exposures in adolescents are primarily
intentional (suicide, abuse) or occupational.
should be aware of the signs of drug abuse or
suicidal ideation in this population and should be
aggressively intervened.
4
5. INITIAL PATIENT EVALUATION
Once the patient has arrived in the appropriate
medical care setting- first measure should be
taking care of the ABC of life
- Airway management-remove secretions if
excessive, put in lateral position
- Give oxygen if needed
- Treat shock, arrhythmia , seizure etc
History
Description of Toxins.- ask for container
Product names (brand, generic, chemical) and
ingredients, along with their concentrations, may
be obtained from labels.
5
6. Magnitude of Exposure.
-determine how much of the substance has been
ingested.
-estimate the amount (better to overestimate) by
counting the remaining tablets or measuring the
remaining volume of liquid.
-toxicity is usually dose-related- 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.
Time of Exposure.
For some products, toxic manifestations may be
delayed for hr or days.
6
7. Historical and Physical Findings in Poisoning
ODOR
Acetone- methanol, paraldehyde, salicylates
Alcohol- Ethanol
Wintergreen - Methyl salicylate
Garlic - Arsenic, thallium, organophosphates
OCULAR SIGNS
Miosis-Narcotics, organophosphates, muscarinic
mushrooms, phenothiazines, barbiturates (late), PCP
Mydriasis -Atropine, alcohol, cocaine, amphetamines,
antihistamines, cyclic antidepressants, CO
Nystagmus- Phenytoin, barbiturates, ethanol, CO
Lacrimation -Organophosphates, irritant gas or vapors
7
14. Poisoning and Drug Overdose: Treatment
General Principles
goals include
1. support of vital signs,
2. prevention of further poison absorption,
3. enhancement of poison elimination,
4. administration of specific antidotes, and
5. prevention of reexposure.
Specific treatment depends on
-the identity of the poison,
- the route and amount of exposure,
- the time of presentation relative to the time of
exposure, and
- the severity of poisoning.
*Knowledge of the offending agents' pharmacokinetics
and pharmacodynamics is essential.
14
15. Fundamentals of Poisoning Management
1. Supportive Care
Airway protection
Oxygenation/ventilation
Treatment of arrhythmias
Hemodynamic support
Treatment of seizures
Correction of T℃ abnorm
Correction of metabolic
derangements
Prevention of secondary
complications
15
16. 2. Prevention of Further Poison Absorption
Gastrointestinal
decontamination
Decontamination of other
sites
Syrup of ipecac–induced
emesis
Gastric lavage
Activated charcoal
Whole-bowel irrigation
Catharsis
Dilution
Endoscopic/surgical
removal
Eye decontamination
Skin decontamination
Body cavity evacuation
16
17. 3.Enhancement of Poison Elimination
Multiple-dose activated
charcoal
Diuresis
Alteration of urinary pH
Chelation
Extracorporeal removal
Peritoneal dialysis and
Hemodialysis
Hemoperfusion
Hemofiltration
Plasmapheresis
Exchange transfusion
Hyperbaric oxygenation 17
18. 4. Administration of Antidotes
Neutralization by
antibodies
Neutralization by
chemical binding
Metabolic antagonism
Physiologic antagonism
5. Prevention of Reexposure
Adult education
Child-proofing
Notification of regulatory
agencies
Psychiatric referral
18
19. During the pretoxic phase, decontamination is the
highest priority, and treatment is based solely on the
history.
Since decontamination is more effective when
accomplished soon after exposure , take focused and
brief Hx.
establish IV access and initiate cardiac monitoring, esp.
in patients with potentially serious ingestions or unclear
Hx.
If you suspect a poison causing delayed toxicity or
irreversible damage is suspected, blood and urine
should be sent for toxicologic screening and, if
indicated, for quantitative analysis.
However, high blood levels of agents whose metabolites
are more toxic than the parent compound
(acetaminophen, ethylene glycol, or methanol) may
indicate the need for additional interventions (antidotes,
dialysis).
19
20. Most patients who remain or become asymptomatic
4–6 h after ingestion will not develop subsequent
toxicity and can be discharged safely.
Longer observation will likely be necessary for
patients who have ingested toxic time-bombs,
agents that are slowly absorbed, slowly distributed
to their sites of action, require metabolic
activation, or disrupt metabolic processes.
During the toxic phase, the time between the onset
of poisoning and the peak effects, management is
based primarily on clinical and laboratory findings.
Effects after an overdose usually begin sooner,
peak later, and last longer than they do after a
therapeutic dose.
20
21. Resuscitation and stabilization are the first priority.
an IV line, oxygen saturation determination, cardiac
monitoring, and continuous observation is needed.
Baseline laboratory, ECG, and x-ray evaluation may also
be appropriate.
Intravenous glucose (unless the serum level is
documented to be normal), naloxone, and thiamine
should be considered in patients with altered mental
status, particularly those with coma or seizures.
Decontamination should also be considered, but is less
likely to be effective during this phase than during the
pretoxic one.
Measures that enhance poison elimination may shorten
the duration of toxicity and lessen its severity. However,
they are not without risk, which must be weighed
against the potential benefit.
21
22. During the resolution phase of poisoning,
supportive care and monitoring should continue
until clinical, laboratory, and ECG abnormalities
have resolved.
Since chemicals are eliminated sooner from the
blood than from tissues, blood levels are usually
lower than tissue levels during this phase and
again may not correlate with toxicity.
This is particularly true when extracorporeal
elimination procedures are used where
redistribution from tissues may cause a rebound
increase in the blood level after termination of
these procedures.
22
23. 1. Supportive Care
The goal is
- to maintain physiologic homeostasis until detoxification
is accomplished and
- to prevent and treat secondary complications such as
aspiration, cerebral/pulmonary edema, rhabdomyolysis,
renal failure, sepsis, coagulopathy, and generalized
organ dysfunction due to hypoxia or shock.
Admission to an intensive care unit is indicated
- for patients with severe poisoning (coma, respiratory
depression, hypotension, cardiac arrhythmias,
hypothermia or hyperthermia, seizures);
- those needing close monitoring, antidotes, or enhanced
elimination therapy; those showing progressive clinical
deterioration; and those with significant underlying
medical problems.
23
24. Respiratory Care
Endotracheal intubation for protection against the
aspiration of GI contents in patients with CNS
depression or seizures.
Mechanical ventilation may be necessary for
patients with respiratory depression or hypoxia.
Cardiovascular Therapy
Maintenance of normal tissue perfusion is critical.
If hypotension is unresponsive to volume
expansion, treatment with norepinephrine,
epinephrine, or high-dose dopamine may be
necessary.
Antibody therapy may be indicated for cardiac
glycoside poisoning
24
25. Supraventricular tachycardia associated with
hypertension and CNS excitation is almost always
due to agents that cause generalized physiologic
excitation
- the etiology could be sympathetic hyperactivity,
RX with a benzodiazepine or Further treatment with a
combined alpha and beta blocker (labetalol), a
calcium channel blocker (verapamil or diltiazem),
or a combination of a beta blocker and a
vasodilator (esmolol and nitroprusside)
- Or high anticholinergic activity
RX with physostigmine
25
26. Central Nervous System Therapies
-Neuromuscular hyperactivity and seizures can lead
to hyperthermia, lactic acidosis & rhabdomyolysis,
with their complications should be treated
aggressively.
-Seizures are best treated with agents that enhance
GABA activity, such as benzodiazepine or
barbiturates.
-Phenytoin is contraindicated in toxicologic seizures:
-For poisons with central dopaminergic effects
(phencyclidine) manifested by psychotic behavior,
use a dopa receptor antagonist like haloperidol.
-Neuromuscular paralysis is indicated in refractory
seizures
26
27. 2. Prevention of Poison Absorption
Gastrointestinal Decontamination
Effectiveness and which procedure to use, depends on
a. the time since ingestion;
b. the existing and predicted toxicity of the ingestant;
c. the availability, efficacy, and contraindications of the
procedure;
d. and the nature, severity, and risk of complications.
The efficacy of activated charcoal, gastric lavage, and
syrup of ipecac decreases with time, esp. when they
are used >1 h after ingestion.
-GI decontamination should be performed selectively, not
routinely.
27
28. a. Activated charcoal
-Activated charcoal suspension (in water) is given
orally via a cup, straw, or small-bore nasogastric
tube.
-The recommended dose is 1 g/kg body weight.
Palatability may be increased by adding a
sweetener (sorbitol) or a flavoring agent
- Charcoal adsorbs ingested poisons within the gut
lumen, allowing the charcoal-toxin complex to be
evacuated with stool.
Advantages
-comparable or greater efficacy,
-fewer contraindications and complications
- is less aversive and invasive
28
29. Disadvantages
-ionized chemicals such as mineral acids, alkalis,
and highly dissociated salts of cyanide, fluoride,
iron, lithium, and other inorganic compounds are
not well adsorbed by charcoal.
-prevent the absorption of orally administered
therapeutic agents
=Complications include mechanical obstruction of
the airway, aspiration, vomiting, and bowel
obstruction and infarction caused by inspissated
charcoal.
Contraindication-in patients who have ingested
corrosives because it obscures endoscopy.
29
30. b. Gastric lavage
-is performed by sequentially administering and
aspirating ~5 mL/kg water or N/S (in infants)
-Place the patient in Trendelenburg and left lateral
decubitus positions to prevent aspiration.
-Lavage decreases ingestant absorption by 50% if
performed within 5 min of ingestion , 25% if performed
at 30 min, and 15% if performed at 60 min. Its efficacy
is similar to that of ipecac.
Complications- aspiration in 10% of patients
- Esophageal ,gastric perforation, misplacement
Containdications
- hydrocarbon, petrolium distilates,corrosive ingestion
- Those with bleeding risks
- Combative, uncooperative patients(absolute)
30
31. c. Syrup of ipecac, now no role in the hospital setting.
-it can still be considered for the home management of
patients with unintentional ingestions, reliable histories,
and mild predicted toxicity when transport to a hospital
site is prolonged.
-Ipecac irritates the stomach and stimulates the central
chemoreceptor trigger zone. Vomiting usually occurs
about 20 min after administration.
Advantage- except for aspiration,serious complications
(e.g., gastric or esophageal tears and perforations) are
rare.
contraindication - patients with recent GI surgery, CNS
depression, or seizures, and in those who have ingested
corrosives or rapidly acting CNS poisons (camphor,
cyanide, tricyclic antidepressants, propoxyphene,
strychnine).
31
34. Whole-bowel irrigation is performed by administering a
bowel-cleansing solution containing electrolytes and
polyethylene glycol (Golytely, Colyte) orally or by gastric
tube at a rate of 2.0 L/h (0.5 L/h in children) until rectal
effluent is clear. The patient must be in a sitting
position.
-appears to be as effective as other decontamination
procedures.
Indication
-for those who have ingested foreign bodies, packets of
illicit drugs, slow-release or enteric-coated
medications, and agents that are poorly adsorbed by
charcoal (e.g., heavy metals).
Contraindications- bowel obstruction, ileus,
hemodynamic instability
34
35. Cathartics are salts (disodium phosphate, magnesium
citrate and sulfate, sodium sulfate) or saccharides
(mannitol, sorbitol) that promote the rectal evacuation
of GI contents.
The most effective cathartic is sorbitol in a dose of 1–2
g/kg of body weight.
Adv- to prevent constipation following a single dose of
charcoal.
Disadv- do not prevent ingestant absorption and should
not be used alone as a method of gut decontamination.
S/E-Abdominal cramps, nausea, and occasional vomiting.
- repeated dosing causes hypermagnesemia and
excessive diarrhea.
Contraindication- in patients who have ingested
corrosives and in those with preexisting diarrhea.
Magnesium-containing cathartics should not be used in
patients with renal failure.
35
36. Dilution (i.e., drinking 5 mL/kg of body weight of water
or another clear liquid) is recommended only after the
ingestion of corrosives (acids, alkali).
Contraindication- increases the dissolution rate (and
hence absorption) of capsules, tablets, and other solid
ingestants and should not be used in these cases.
Endoscopic or surgical removal of poisons may be
useful in
-ingestion of a potentially toxic foreign body that fails to
transit the gastrointestinal tract,
-a potentially lethal amount of a heavy metal (arsenic,
iron, mercury, thallium), or
-agents that have coalesced into gastric concretions or
bezoars (barbiturates, glutethimide, heavy metals,
lithium, salicylates, sustained-release preparations).
36
37. Decontamination of Other Sites
Immediate, copious flushing with water, saline, or
another available clear, drinkable liquid is the initial
treatment for topical exposures (exceptions include
alkali metals, calcium oxide, phosphorus).
Saline is preferred for eye irrigation.
A triple wash (water, soap, water) may be best for
dermal decontamination.
Inhalational exposures should be treated initially with
fresh air or oxygen.
The removal of liquids from body cavities such as the
vagina or rectum is best accomplished by irrigation.
Solids (drug packets, pills) should be removed manually,
preferably under direct visualization.
37
38. Enhancement of Poison Elimination
Multiple-Dose Activated Charcoal
-can enhance the elimination of previously absorbed
substances by binding them within the gut as they
are excreted in the bile, secreted by GI cells, or
passively diffuse into the gut lumen. Doses of 0.5–
1 g/kg body weight every 2–4 h, tapering.
-considered only for selected agents (theophylline,
phenobarbital, carbamazepine, dapsone, quinine)
-Complications include intestinal obstruction,
pseudoobstruction, and nonocclusive intestinal
infarction in patients with decreased gut motility.
-cathartics are absolutely contraindicated when
administering multiple doses of activated charcoal.
38
39. Urinary Alkalinization
Ion trapping via alteration of urine pH may prevent the renal
reabsorption of poisons that undergo excretion by glomerular
filtration and active tubular secretion.
acidic (low-pKa) poisons are ionized and trapped in alkaline
urine, whereas basic ones become trapped in acid urine.
Urinary alkalinization (producing a urine pH 7.5 and a urine
output of 3–6 mL/kg body weight per hour by adding sodium
bicarbonate to an IV solution) enhances the excretion of some
herbicides, phenobarbital, sulfonamides, and salicylates.
Contraindications - CHF, renal failure, and cerebral edema.
Extracorporeal Removal
Peritoneal or hemodialysis, charcoal or resin hemoperfusion,
hemofiltration, plasmapheresis, and exchange transfusion are
capable of removing toxins from bloodstream
39
40. Administration of Antidotes
Antidotes counteract the effects of poisons by
-neutralizing them (e.g., antibody-antigen reactions,
chelation, chemical binding) or
-by antagonizing their physiologic effects (e.g.,
activation of opposing nervous system activity,
provision of competitive metabolic or receptor
substrate).
Some Poisons or conditions have specific antidotes.
Antidotes can significantly reduce morbidity and
mortality but are potentially toxic if used for
inappropriate reasons.
40
41. COMPOUNDS COMMONLY INVOLVED IN PEDIATRIC
POISONINGS
HYDROCARBONS.
Hydrocarbons include a wide array of chemical
substances found in thousands of commercial
products.
produce systemic toxicity, local toxicity, or both.
Nevertheless, aspiration of hydrocarbons into the
lung can lead to serious, even life-threatening
toxicity.
Pathophysiology.
The most important adverse effect of hydrocarbons
is aspiration pneumonitis.
41
42. Aspiration usually occurs at the time of ingestion, when
coughing and gagging are common, but can also be
secondary to vomiting.
The propensity of a hydrocarbon to cause aspiration
pneumonitis is inversely proportional to its viscosity.
Compounds with low viscosity, such as mineral spirits,
naphtha, kerosene, gasoline, and lamp oil, spread
rapidly across surfaces and cover large areas of the
lungs when aspirated.
Only small quantities (<1 mL) of low-viscosity
hydrocarbons need be aspirated to produce significant
injury.
Gasoline and kerosene often cause considerable
gastrointestinal mucosal irritation as they pass through
the intestines.
42
43. absorbed after ingestion, inhalation, or dermal
contact.
have anesthetic properties and can cause transient
CNS depression.
chlorinated solvents s.a. carbon tetrachloride, can
produce hepatic toxicity.
also been associated with renal and bone marrow
toxicity. Benzene is known to cause cancer (AML)in
humans after long-term exposure.
Methylene chloride, found in some paint removers,
is metabolized to carbon monoxide. Some produce
methemoglobinemia.
Most volatile hydrocarbons are being abused.
43
44. Clinical and Laboratory Manifestations.
Transient, mild CNS depression.
Cough usually begins immediately or within 2–5 min of
the aspiration, and persists.
CXR is often will be positive after 6 hr or longer from
the time of exposure.
Respiratory symptoms may remain mild or may
progress rapidly to respiratory failure.
need close clinical monitoring of the patient's
respiratory status.
Fever occurs and may persist for as long as 10 days
Accompanying leukocytosis may be misleading because,
in most cases of aspiration pneumonitis, no bacteria are
present in the lungs.
CXR may remain abnormal long after the patient is
clinically normal, and they should not be used to guide
acute treatment.
44
45. Treatment.
Emesis gastric lavage are contraindicated because
of the risk of aspiration.
If gastric lavage(only in case of highly toxic HCs
s.a. CCl4) is to be performed, the patient should be
intubated with a cuffed tube to protect the airway
from further aspiration.
Activated charcoal also is not useful.
If hydrocarbon-induced pneumonitis develops,
respiratory treatment is supportive .
Corticosteroids and Prophylactic antibiotics should
not be given because bacterial pneumonia occurs
in only a very small percentage of cases.
45
46. CHOLINESTERASE-INHIBITING INSECTICIDES.
The most commonly used insecticides are organophosphates
and carbamates; both are inhibitors of cholinesterase
enzymes.
poisonings occur as the result of accidental exposure to
insecticides in and around the home or farm.
Pathophysiology. –bond to cholinesterase preventing the
degradation of acetylcholine, resulting in its accumulation at
nerve synapses.
Enzymes affected include acetylcholinesterase or red blood cell
cholinesterase, pseudocholinesterase (found in plasma), and
neurotoxic esterase (nervous system).
If left untreated, organophosphates form a permanent bond to
these enzymes, inactivating them.
This process, called aging, may occur as soon as 18 hr to 2–3
days after exposure. A period of weeks to months is required
to regenerate inactivated enzymes.
carbamates form a temporary bond to the enzymes, allowing
regeneration of the enzymes over several hours.
46
47. Clinical and Laboratory Manifestations.
Clinical manifestations relate to the accumulation of
acetylcholine at peripheral nicotinic and muscarinic
synapses and in the CNS.
Muscarinic signs and symptoms include diaphoresis,
emesis, urinary and fecal incontinence, tearing,
salivation, bronchorrhea and bronchospasm, miosis,
hypotension, and bradycardia.
Nicotinic signs and symptoms include muscle weakness,
fasciculations, tremors, hypoventilation (diaphragm
paralysis), hypertension, tachycardia, and dysrhythmias.
CNS effects include confusion, delirium, seizures, and
coma.
Symptoms caused by carbamate toxicity are usually less
severe than those seen with organophosphates.
A commonly used mnemonic for the most common
symptoms-DUMB BELS.
47
48. Treatment.
- A B C of life
-washing all exposed skin with soap and water and immediate
removal of all exposed clothing.
-Activated charcoal can be used for gastric decontamination,
but for insecticides, it is of limited value because these highly
lipid-soluble agents are rapidly absorbed.
-Basic supportive care -including fluid and electrolyte
replacement and intubation, with artificial ventilation,
-if necessary. Two “antidotes” are useful to treat poisoning with
cholinesterase inhibitors: atropine and pralidoxime .
-Atropine, which antagonizes the muscarinic acetylcholine
receptor, is useful for both organophosphate and carbamate
intoxication.
-Pralidoxime chemically breaks the bond thus enhancing the
insecticide's body clearance( only for organophosphate)
48
49. Atropinization
Atropine in sufficient dosage effectively antagonizes
the actions at muscarinic receptor sites, including
increased tracheobronchial and salivary secretion,
bronchoconstriction, bradycardia, and to a
moderate extent, peripheral ganglionic and central
actions.
Larger doses are required to get appreciable
concentrations of atropine into the CNS.
Atropine has no effect against the peripheral
neuromuscular compromise, which can be reversed
by pralidoxime (2-PAM), a cholinesterase
reactivator.
49
50. As an antidote to organophosphate poisoning.
Give atropine 0.02–0.05 mg/kg
every 10–20 min until atropine effect (tachycardia,
mydriasis, fever)etc is seen or features of
muscarinic receptor stimulation symptoms
dissaprear s.a. bronchospasm ,excessive
salivation,myosis etc
then q 1–4 hr for at least 24 hr.
Read on acetaminophen, salysylate, NSAIDs , CO and
caustics poisoning
50
