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Approach to childhood
poisoning
Outline
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 Introduction
 General approach/ Initial evaluation
 Principle of management
 Common poisonings
 prevention
 References
Introduction
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 Poisoning- exposure to a chemical or other agent
that adversely affects functioning of an
organism.
 “ All substances are
poisons, the right dose
separates poisons from
remedy.”
Paracelsus
Epidemiology
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 One of the most common medical emergencies
encountered by young children.
 More than 90% of poisonings occur at home and
most often involve only a single substance
Epi.
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Epi. Cont’d
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 Two peaks 1st under 6 yrs of age and 2nd during
adolescence.
 Most produce minor or no toxicity.
 It could be
 Unintentional(85%) – due to exploratory behavior of under 5
children
 Intentional (15%)- adolescents
Risk factors
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 Complex interplay of host, agent and environmental
factors
 Age
 Gender
 Attractiveness , palatability and toxic potential of a compound
Modes of exposure
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 Ingestion
 Ocular
 Topical
 Envenomation
 Inhalation
 Transplacental
Timing
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 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
Effects of poisons
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 Interfere with the transport or tissue utilization of
O2
 Depress or stimulate CNS
 Effects on the autonomic nervous system
 Effects on the lungs by aspiration
 Effects on the heart and vasculature
 Produce local damage
 Effects on the liver
Initial evaluation
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 Poisoning is a multiple chemical trauma.
1o survey- ABCs + slight additional emphasis on
emergent toxicologic considerations
2o survey- simultaneously initiating generic treatment
while assessing the actual extent of intoxication or
identifying the actual toxicants involved
ABCs
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 In addition to the usual signs of airway obstruction,
attention must be paid to evidence of disturbed
airway reflexes.
 Lesser threshold for intubation
 Cyanosis and apnea- late findings
ABCs
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 Airway obstruction can cause death after poisoning
Flaccid tongue
Aspiration
Respiratory arrest
 Evaluate mental status and gag/cough reflex
ABCs
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 Airway interventions
Sniffing position
Jaw thrust
Head-down, left-sided position
Examine the oropharynx
Clear secretions
Airway devices: e.g. oral airway
ABCs
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 Determine if respirations are adequate
 Give supplemental oxygen
 Assist with bag & mask
 Check oxygen saturation, ABG
 Auscultate lung fields
Bronchospasm: Albuterol nebulizer
Bronchorrhea/ rales: Atropine
Stridor: Determine need for immediate
intubation
ABCs
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 Early IV access
 Shock , hypovolemia- treat accordingly
 Determine RBS/ give 10% d/w – drug/toxicant
induced hypoglycemia does not present uniformly
with coma or seizures
 Continuous ECG monitoring
ABCs
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REASSESS
. . . frequently
History
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 To determine the potential severity of the exposure.
 Amount, type, prior symptoms, time elapsed after
exposure, any treatment given, underlying medical
condition.
HX cont’d
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General historical features suggestive of poisoning
 Acute onset
 Age range
 Hx of known exposure to a toxicant
 Substantial environmental stress
 Multiple organ system involvement
HX cont’d
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 Significant alteration in level of consciousness
 A clinical picture that seems especially puzzling
Focused P/E
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Especially on the
CNS
ANS
Eye findings
Changes in the skin/oral or GI mucous membranes
odors
Laboratory
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 To confirm diagnostic impressions or to demonstrate
toxicant induced metabolic derangements
 Non-emergent
 RBS, LFT, RFT, serum e-s, ECG.
Principle of management
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Initial life support phase
Specific decontamination
MX cont’d
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Four main wings
1. Decontamination
2. Enhanced elimination
3. Antidotes
4. Supportive care
Decontamination
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 Goal is to prevent absorption of the toxic substance
 Principles of Decontamination
External
Protect yourself and others
Remove exposure
Irrigate copiously with water or normal
saline
Don’t forget your ABC’s
Decontamination
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Skin
Protect yourself and other HC workers
Remove clothing
Flush with water or normal saline
Use soap and water if oily substance
Corrosive agents injure skin and can have
systemic effects
Decontamination
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Eyes
Flush copiously with water or normal
saline
Continue irrigation until pH is normal
Slit lamp exam
Decontamination
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 Inhalation
Give supplemental humidified oxygen
Observe for airway obstruction
Intubate as necessary
GI Decontamination
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 GI decontamination strategies are most likely to be
effective in the first hour after an acute ingestion
 GI absorption may be delayed after ingestion of
agents that slow GI motility (anticholinergic
medications, opioids), massive pill ingestions,
sustained-release preparations, and ingestions of
agents that can form pharmacologic bezoars (e.g.,
enteric-coated salicylates).
GI
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 Syrup of ipecac
Within minutes of ingestion
Contraindicated after the ingestion of
caustics (acids and bases), hydrocarbons,
and agents likely to cause rapid onset of
CNS or cardiovascular symptoms.
GI
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 Gastric lavage
Does not reliably remove pills and pill
fragments
Used 30-60 minutes after ingestion
Not used for sustained release/enteric
coated ingestions
Perforation, nosebleed, vomiting,
aspiration
Lavage and emesis
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 Routine administration no longer recommended
American academy of clinical toxicology and
European association of poisons centers and clinical
toxicologists.
2004, Vol. 42, No. 7 , Pages 933-943
GI
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 Activated charcoal- activated via heating to extreme
temperatures, creating an extensive network of pores
that provides a very large adsorptive surface area.
 Many, but not all, toxins are adsorbed onto its
surface, thus preventing absorption from the GI tract
Activated charcoal
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Limits drug absorption in the GI tract
Within 60 minutes of ingestion
Patient must be awake or intubated
Vomiting, aspiration, bezoar formation
Contraindication: bowel obstruction or
ileus with distention
1 gram/kg PO or NGT
Charcoal
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 Is poorly adsorbed by:
 Lithium
 Iron
 Alcohols
 Lead
 Hydrocarbons
 Caustics
GI
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 Whole bowel irrigation
 WBI involves instilling large volumes (35 ml/kg/hr )
of a polyethylene glycol electrolyte solution to
cleanse the entire GI tract
Large ingestions, SR or EC tablets
Contraindications: obstruction or ileus
Aspiration, nausea, may decrease
effectiveness of charcoal
Enhanced elimination
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 Urinary manipulation
Forced diuresis
Alkalinization
 Multiple dose activated charcoal
 Hemodialysis
 Peritoneal dialysis
Dialysis
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Indications
 Potentially life-threatening toxicity that is caused by
a dialyzable drug and cannot be treated by
conservative means.
 Hypotension threatening renal or hepatic function
that cannot be corrected by adjusting circulating
volume.
Dialysis cont’d
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 Marked hyperosmolality or severe acid–base or
electrolyte disturbances not responding to therapy.
 Marked hypothermia or hyperthermia not
responding to therapy.
Antidotes
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 Acetaminophen N- acetylcysteine
 Organophosphates Atropine, pralidoxime
 Anticholinergic physostigmine
 Benzodiazepines flumazenil
 Beta blockers glucagon
 Calcium channel blockers calcium
 Carboxyhemoglobin 100% O2
 Digoxin digoxin antibodies
Supportive care
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 Excellent supportive care and frequent clinical
assessments are the keys to effective management
and improved outcomes.
 Many poisoned patients arrive to medical care too
late for decontamination
 Goal is to support the vital functions of the patient
until the patient can eliminate the toxin from the
system
Supportive care
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 Supportive care entails careful attention to
airway support,
ventilator management,
blood pressure support, and
appropriate and timely management of
seizures, dysrhythmias, conduction delays,
and electrolyte and metabolic
derangements
Common poisonings
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CONT’D
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 In Zimbabwe, a 10-year retrospective review majority of
the poisonings were in patients aged 0-5 years (35%) and
21-30 years (22.6%).
 The main agents were traditional medicines, household
chemicals, snake and insect envenomation and
insecticides (14.8%, 10% of which is accounted for by
ops).
 There was 15% mortality
Nhachi etal J Appl Toxicol. 1992 Dec;12(6):435-8.
CONT’D
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 A retrospective study in a university teaching
hospital in Nigeria showed 0.52% of the total
pediatric admissions over a 10-year period.
 Poisoning was more common among the lower
socioeconomic classes and in males than females.
CONT’D
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 Of the children involved, 80.3% were below the age
of five years and poisoning was unintentional in
98.4%. Kerosene was the most common agent,
40.9%, followed by caustic soda, 20.4%, and
traditional mixtures 11.9%.
Lamireau et al. Eur J Emerg Med, 2002; 9:9–14.
Paracetamol (Acetaminophen )
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 Most common cause of acute liver failure in the
United States.
 Results from the formation of a highly reactive
intermediate metabolite, N-acetyl-p-benzoquinone
imine (NAPQI).
 single acute toxic dose >200 mg/kg in children and
>7.5-10 g in adolescents and adults
PCM
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 Repeated administration of acetaminophen at
supratherapeutic doses (>75 mg/kg/day for
consecutive days) can lead to hepatic injury or failure
in some children.
 Four classical clinical stages
STAGE
TIME AFTER
INGESTION
CHARACTERISTICS
I 0.5-24 hr
Anorexia, nausea, vomiting,
malaise, pallor, diaphoresis
Labs typically normal, except for
acetaminophen level
II 24-48 hr
Resolution of earlier symptoms;
right upper quadrant abdominal
pain and tenderness; elevated
bilirubin, prothrombin time, and
hepatic enzymes; oliguria
III 72-96 hr
Peak liver function abnormalities;
fulminant hepatic failure;
multisystem organ failure and
potential death
IV 4 days-2 wk
Resolution of liver function
abnormalities
Clinical recovery precedes
histologic recovery
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Mx
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 Initial treatment should focus on the ABCs and
consideration of decontamination with activated
charcoal in patients who present within 1-2 hr of
ingestion.
 The antidote for acetaminophen poisoning is NAC,
which works primarily via replenishing hepatic
glutathione stores. NAC therapy is most effective
when initiated within 8 hr of ingestion.
Salicylates (aspirin)
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 The incidence of salicylate poisoning in young
children has declined dramatically since
acetaminophen and ibuprofen replaced aspirin as
the most commonly used analgesics and antipyretics
in pediatrics.
 Acute toxic dose >150 mg/kg. More significant
toxicity >300 mg/kg, and severe, potentially fatal,
toxicity >500 mg/kg.
C/F
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 Classified as acute or chronic, and acute toxicity is
far more common in pediatric patients.
 Early signs of acute salicylism include nausea,
vomiting, diaphoresis, and tinnitus.
 Moderate salicylate toxicity can manifest as
tachypnea and hyperpnoea, tachycardia, and altered
mental status.
c/f
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 Signs of severe salicylate toxicity include
hyperthermia, coma, and seizures.
 Chronic salicylism can have a more insidious
presentation, and patients can show marked toxicity
at significantly lower salicylate levels than in acute
toxicity.
Mx
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 Initial therapy focuses on aggressive volume
resuscitation and prompt initiation of sodium
bicarbonate therapy in the symptomatic patient
 For the patient who presents soon after an acute
ingestion, initial treatment should include gastric
decontamination with activated charcoal
 Urinary alkalinization.
Hydrocarbons
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 Hydrocarbons are organic substances that contain
carbon and hydrogen.
 Specific characteristics of each product determine
whether exposure will produce systemic toxicity,
local toxicity, both, or neither
Hydrocarbons
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 Classes of hydrocarbons
 Aromatic hydrocarbons
 Aliphatic hydrocarbons
 Halogenated hydrocarbons
 Terpene hydrocarbons
Hydrocarbons
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 Potential for toxicity
 Low toxicity- asphalt, tars, mineral oil, petroleum
jelly, motor oil, and axle grease.
 Aspiration hazard – Clinical effects are typically
limited to direct pulmonary damage and subsequent
inflammation. Gasoline, kerosene, mineral seal oil
(furniture polish), mineral spirits, or outdoor torch
and cigarette lighter fluids.
Hydrocarbons
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Systemic toxicity – Halogenated and aromatic
hydrocarbons are absorbed readily through the
gastrointestinal and/or respiratory systems.
Determinants of pulmonary aspiration
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 Volatility – The ability to vaporize or to exist in a
gaseous form.
 Surface tension – The adherence of molecules along
a liquid surface. Lower surface tension allows
compounds to spread over a larger area.
 Viscosity – The resistance to flow through an orifice.
Lower viscosity facilitates deeper penetration into
the tracheobronchial tree.
c/f
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 Clinical manifestations of hydrocarbon ingestion
depend largely on the specific profile of toxicity of
the ingested substances.
 The aspiration hazard of hydrocarbons is inversely
related to viscosity and surface tension and directly
related to volatility
c/f
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 Fever (30-60%), persistence beyond 48hr suggests
super infection
 tachypnea, dyspnea, cyanosis, wheezing, diminished
resonance on percussion, rales, nasal flaring, and/or
grunting respirations
 asphyxia, necrotizing chemical pneumonitis,
hemorrhagic pulmonary edema, which quickly
progresses to shock and respiratory arrest
c/f
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 somnolence, headache, ataxia, dizziness, blurred
vision, weakness, fatigue, lethargy, stupor, seizures,
and coma
 Cardiac dysrhythmias and myocardial dysfunction
 Leukocytosis occurs early in the clinical course of
hydrocarbon aspiration unrelated to pneumonitis
and may last as long as one week
Workup
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 CXR – immediately and within 4-6 hrs after
exposure
 Blood gas
 Complete blood count
 Serum glucose
 Serum electrolytes
 Urinalysis
Mx
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 Successful management of hydrocarbon aspiration
requires recognition of pulmonary toxicity and rapid
initiation of appropriate supportive care
 Stabilization
 External decontamination
 Treatment of hydrocarbon pneumonitis is supportive
and includes oxygen and close monitoring of
respiratory status.
Indication for abcs
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 Recurrence of fever after the first 48 hours
 Increasing infiltrate in chest radiograph
 Leukocytosis after the first 48 hours
 Sputum or tracheal aspirate positive for bacteria
Organophosphates
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 Inhibitors of cholinesterase enzymes (acetyl
cholinesterase, pseudo cholinesterase, and
erythrocyte acetyl cholinesterase).
 Most pediatric poisonings occur as the result of
unintentional exposure to insecticides in and around
the home or farm.
Organophosphates
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 Organophosphates and carbamates produce toxicity
by binding to and inhibiting acetyl cholinesterase,
preventing the degradation of acetylcholine and
resulting in its accumulation at nerve synapses.
 Diagnosis of poisoning is based primarily on history
and physical exam findings
c/f
4/3/2024
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Intermediate syndrome
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 Ten to 40 percent of patients poisoned with
organophosphates develop a distinct neurologic
disorder 24 to 96 hours after exposure.
 neck flexion weakness, decreased deep tendon
reflexes, cranial nerve abnormalities, proximal
muscle weakness, and respiratory insufficiency
Delayed neurotoxicity
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 Organophosphorus agent induced delayed
neuropathy (OPIDN) typically occurs one to three
weeks
 transient, painful "stocking-glove" paresthesias
followed by a symmetrical motor polyneuropathy
characterized by flaccid weakness of the lower
extremities, which ascends to involve the upper
extremities.
Mx
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 Basic decontamination should be performed,
including washing all exposed skin with soap and
water and immediately removing all exposed
clothing.
 Basic supportive care should be provided, including
fluid and electrolyte replacement and intubation and
ventilation if necessary.
Mx
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 Antidotes
Atropine, which antagonizes the muscarinic
acetylcholine receptor, is useful for both
organophosphate and carbamate intoxication.
(0.05mg/kg)
Pralidoxime breaks the bond between the
organophosphate and the enzyme, reactivating acetyl
cholinesterase.
Prognosis
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 Without treatment, symptoms can persist for weeks,
requiring continuous supportive care.
 Even with treatment, some patients develop a
delayed polyneuropathy and a range of chronic
neuropsychiatric symptoms
Phenobarbitone
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 Classified as long acting barbiturate
 Cause depression of the brainstem RAS
with resultant generalized depression of the
CNS
 Onset of effects in 20-60min.
 Slowly metabolized by liver microsomal
enzymes & are eliminated, half lives of
2-6days
c/f
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 Respiratory depression and coma
 Shock can occur secondary to myocardial
depression and venodilation
 Nausea ,vomiting nystagmus ataxia ,steven-
johnson syndrome and hematologic
abnormalities
Mx
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General measure
 Intubations and ventilatory support
 Gastric lavage
 Charcoal
Toxic specific measures
 Alklinization of the urine with NAHCO3
 Hemodialysis
 Multiple dose charcoal
Carbon monoxide
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 The most common gas involved in pediatric
exposures
 CO binds to Hg with an affinity >200 times that of
oxygen, forming carboxyhemoglobin. In doing so,
CO displaces oxygen and creates a conformational
change in hemoglobin that impairs the delivery of
oxygen to the tissues, leading to tissue hypoxia.
Co
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 Early symptoms are nonspecific and include
headache, malaise, nausea, and vomiting.
 At higher exposure levels, patients can develop
mental status changes, confusion, ataxia, syncope,
tachycardia, and tachypnea.
 Severe poisoning is manifested by coma, seizures,
myocardial ischemia, acidosis, cardiovascular
collapse, and potentially death.
Mx
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 General supportive care, move pt to fresh air
 Administration of 100% oxygen to enhance
elimination of CO.
 The average half-life of COHb is 4-6 hr, reduced to
60-90 min by providing 100% oxygen at normal
atmospheric pressures via a non- re breather
facemask.
 Hyperbaric oxygen decreases the half-life of COHb to
20-30 minutes.
Caustics
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 Caustics include acids and alkalis
 Strong acids and alkalis can produce severe injury
even in small-volume ingestions.
 Alkalis produce a liquefaction necrosis, allowing
further tissue penetration of the toxin and setting the
stage for possible perforation.
 Acids produce a coagulative necrosis, which limits
further tissue penetration, though perforation can
still occur
Caustics
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 The severity of the corrosive injury depends on the
pH and concentration of the product as well as the
length of contact time with the product.
 Agents with a pH of <2 or >12 are most likely to
produce significant injury.
C/f
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 pain, drooling, vomiting, abdominal pain, and
difficulty swallowing or refusal to swallow. Laryngeal
injury can manifest as stridor and respiratory
distress, necessitating intubation.
 In the most severe cases, patients can present in
shock after perforation of a hollow viscus.
 Esophageal stricture.
 Caustics on the skin or in the eye can cause
significant tissue damage.
ENDOSCOPIC APPEARANCE OF
ESOPHAGEAL MUCOSA
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Grade 0 Normal mucosa
Grade 1 Erythema
Grade 2 Erythema, sloughing, ulceration, and exudates
(not circumferential)
Grade 3 Deep mucosal sloughing and ulceration
(circumferential)
Grade 4 Eschar, full thickness injury and perforation
Mx
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 Initial treatment of caustic exposures includes
thorough removal of the product from the skin or eye
by flushing with water.
 Dilution by water or milk is recommended as acute
treatment(15ml/kg, max 250ml.)
 Emesis and lavage are contraindicated.
 Endoscopic evaluation
Prevention
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 Use packages with safety closures and learn how to
use them properly.
 Keep household cleaning supplies, medicines, and
insecticides out of the reach and sight of children.
Lock them up whenever possible.
 Never store food and cleaning products together.
Store medicine and chemicals in original containers
and never in food or beverage containers.
Prevention cont’d
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86
 Avoid taking medicine in children's presence. Never
suggest that medicine is candy.
 Read the label on all products, warnings and
cautions. Never use medicine from an unlabeled or
unreadable container.
 If interrupted while using a product, take it with
you—it takes only a few seconds for a child to get into
it.
Prevention cont’d
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87
 Know what a child can do physically.
 Non accidental poisoning is a psychiatric emergency
that can be prevented by developing good
communication and a supportive environment for
the adolescents within the family
 Poison control centers.
4/3/2024
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4/3/2024
89
What can be done in our
setup?
References
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90
 Nelson 19th ed.
 Text book of pediatric emergency 6th ed.
 5 minute pediatric consult
 Current diagnosis and management in pediatrics
 Casarett and Dohul’s toxicology
 Katzung pharmacology
 Up to date 21.2
THANK YOU
4/3/2024
91

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Approach to Childhood Poisoning......pptx

  • 2. Outline 4/3/2024 2  Introduction  General approach/ Initial evaluation  Principle of management  Common poisonings  prevention  References
  • 3. Introduction 4/3/2024 3  Poisoning- exposure to a chemical or other agent that adversely affects functioning of an organism.  “ All substances are poisons, the right dose separates poisons from remedy.” Paracelsus
  • 4. Epidemiology 4/3/2024 4  One of the most common medical emergencies encountered by young children.  More than 90% of poisonings occur at home and most often involve only a single substance
  • 6. Epi. Cont’d 4/3/2024 6  Two peaks 1st under 6 yrs of age and 2nd during adolescence.  Most produce minor or no toxicity.  It could be  Unintentional(85%) – due to exploratory behavior of under 5 children  Intentional (15%)- adolescents
  • 7. Risk factors 4/3/2024 7  Complex interplay of host, agent and environmental factors  Age  Gender  Attractiveness , palatability and toxic potential of a compound
  • 8. Modes of exposure 4/3/2024 8  Ingestion  Ocular  Topical  Envenomation  Inhalation  Transplacental
  • 9. Timing 4/3/2024 9  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
  • 10. Effects of poisons 4/3/2024 10  Interfere with the transport or tissue utilization of O2  Depress or stimulate CNS  Effects on the autonomic nervous system  Effects on the lungs by aspiration  Effects on the heart and vasculature  Produce local damage  Effects on the liver
  • 11. Initial evaluation 4/3/2024 11  Poisoning is a multiple chemical trauma. 1o survey- ABCs + slight additional emphasis on emergent toxicologic considerations 2o survey- simultaneously initiating generic treatment while assessing the actual extent of intoxication or identifying the actual toxicants involved
  • 12. ABCs 4/3/2024 12  In addition to the usual signs of airway obstruction, attention must be paid to evidence of disturbed airway reflexes.  Lesser threshold for intubation  Cyanosis and apnea- late findings
  • 13. ABCs 4/3/2024 13  Airway obstruction can cause death after poisoning Flaccid tongue Aspiration Respiratory arrest  Evaluate mental status and gag/cough reflex
  • 14. ABCs 4/3/2024 14  Airway interventions Sniffing position Jaw thrust Head-down, left-sided position Examine the oropharynx Clear secretions Airway devices: e.g. oral airway
  • 15. ABCs 4/3/2024 15  Determine if respirations are adequate  Give supplemental oxygen  Assist with bag & mask  Check oxygen saturation, ABG  Auscultate lung fields Bronchospasm: Albuterol nebulizer Bronchorrhea/ rales: Atropine Stridor: Determine need for immediate intubation
  • 16. ABCs 4/3/2024 16  Early IV access  Shock , hypovolemia- treat accordingly  Determine RBS/ give 10% d/w – drug/toxicant induced hypoglycemia does not present uniformly with coma or seizures  Continuous ECG monitoring
  • 18. History 4/3/2024 18  To determine the potential severity of the exposure.  Amount, type, prior symptoms, time elapsed after exposure, any treatment given, underlying medical condition.
  • 19. HX cont’d 4/3/2024 19 General historical features suggestive of poisoning  Acute onset  Age range  Hx of known exposure to a toxicant  Substantial environmental stress  Multiple organ system involvement
  • 20. HX cont’d 4/3/2024 20  Significant alteration in level of consciousness  A clinical picture that seems especially puzzling
  • 21. Focused P/E 4/3/2024 21 Especially on the CNS ANS Eye findings Changes in the skin/oral or GI mucous membranes odors
  • 22. Laboratory 4/3/2024 22  To confirm diagnostic impressions or to demonstrate toxicant induced metabolic derangements  Non-emergent  RBS, LFT, RFT, serum e-s, ECG.
  • 23. Principle of management 4/3/2024 23 Initial life support phase Specific decontamination
  • 24. MX cont’d 4/3/2024 24 Four main wings 1. Decontamination 2. Enhanced elimination 3. Antidotes 4. Supportive care
  • 25. Decontamination 4/3/2024 25  Goal is to prevent absorption of the toxic substance  Principles of Decontamination External Protect yourself and others Remove exposure Irrigate copiously with water or normal saline Don’t forget your ABC’s
  • 26. Decontamination 4/3/2024 26 Skin Protect yourself and other HC workers Remove clothing Flush with water or normal saline Use soap and water if oily substance Corrosive agents injure skin and can have systemic effects
  • 27. Decontamination 4/3/2024 27 Eyes Flush copiously with water or normal saline Continue irrigation until pH is normal Slit lamp exam
  • 28. Decontamination 4/3/2024 28  Inhalation Give supplemental humidified oxygen Observe for airway obstruction Intubate as necessary
  • 29. GI Decontamination 4/3/2024 29  GI decontamination strategies are most likely to be effective in the first hour after an acute ingestion  GI absorption may be delayed after ingestion of agents that slow GI motility (anticholinergic medications, opioids), massive pill ingestions, sustained-release preparations, and ingestions of agents that can form pharmacologic bezoars (e.g., enteric-coated salicylates).
  • 30. GI 4/3/2024 30  Syrup of ipecac Within minutes of ingestion Contraindicated after the ingestion of caustics (acids and bases), hydrocarbons, and agents likely to cause rapid onset of CNS or cardiovascular symptoms.
  • 31. GI 4/3/2024 31  Gastric lavage Does not reliably remove pills and pill fragments Used 30-60 minutes after ingestion Not used for sustained release/enteric coated ingestions Perforation, nosebleed, vomiting, aspiration
  • 32. Lavage and emesis 4/3/2024 32  Routine administration no longer recommended American academy of clinical toxicology and European association of poisons centers and clinical toxicologists. 2004, Vol. 42, No. 7 , Pages 933-943
  • 33. GI 4/3/2024 33  Activated charcoal- activated via heating to extreme temperatures, creating an extensive network of pores that provides a very large adsorptive surface area.  Many, but not all, toxins are adsorbed onto its surface, thus preventing absorption from the GI tract
  • 34. Activated charcoal 4/3/2024 34 Limits drug absorption in the GI tract Within 60 minutes of ingestion Patient must be awake or intubated Vomiting, aspiration, bezoar formation Contraindication: bowel obstruction or ileus with distention 1 gram/kg PO or NGT
  • 35. Charcoal 4/3/2024 35  Is poorly adsorbed by:  Lithium  Iron  Alcohols  Lead  Hydrocarbons  Caustics
  • 36. GI 4/3/2024 36  Whole bowel irrigation  WBI involves instilling large volumes (35 ml/kg/hr ) of a polyethylene glycol electrolyte solution to cleanse the entire GI tract Large ingestions, SR or EC tablets Contraindications: obstruction or ileus Aspiration, nausea, may decrease effectiveness of charcoal
  • 37. Enhanced elimination 4/3/2024 37  Urinary manipulation Forced diuresis Alkalinization  Multiple dose activated charcoal  Hemodialysis  Peritoneal dialysis
  • 38. Dialysis 4/3/2024 38 Indications  Potentially life-threatening toxicity that is caused by a dialyzable drug and cannot be treated by conservative means.  Hypotension threatening renal or hepatic function that cannot be corrected by adjusting circulating volume.
  • 39. Dialysis cont’d 4/3/2024 39  Marked hyperosmolality or severe acid–base or electrolyte disturbances not responding to therapy.  Marked hypothermia or hyperthermia not responding to therapy.
  • 40. Antidotes 4/3/2024 40  Acetaminophen N- acetylcysteine  Organophosphates Atropine, pralidoxime  Anticholinergic physostigmine  Benzodiazepines flumazenil  Beta blockers glucagon  Calcium channel blockers calcium  Carboxyhemoglobin 100% O2  Digoxin digoxin antibodies
  • 41. Supportive care 4/3/2024 41  Excellent supportive care and frequent clinical assessments are the keys to effective management and improved outcomes.  Many poisoned patients arrive to medical care too late for decontamination  Goal is to support the vital functions of the patient until the patient can eliminate the toxin from the system
  • 42. Supportive care 4/3/2024 42  Supportive care entails careful attention to airway support, ventilator management, blood pressure support, and appropriate and timely management of seizures, dysrhythmias, conduction delays, and electrolyte and metabolic derangements
  • 44. CONT’D 4/3/2024 44  In Zimbabwe, a 10-year retrospective review majority of the poisonings were in patients aged 0-5 years (35%) and 21-30 years (22.6%).  The main agents were traditional medicines, household chemicals, snake and insect envenomation and insecticides (14.8%, 10% of which is accounted for by ops).  There was 15% mortality Nhachi etal J Appl Toxicol. 1992 Dec;12(6):435-8.
  • 45. CONT’D 4/3/2024 45  A retrospective study in a university teaching hospital in Nigeria showed 0.52% of the total pediatric admissions over a 10-year period.  Poisoning was more common among the lower socioeconomic classes and in males than females.
  • 46. CONT’D 4/3/2024 46  Of the children involved, 80.3% were below the age of five years and poisoning was unintentional in 98.4%. Kerosene was the most common agent, 40.9%, followed by caustic soda, 20.4%, and traditional mixtures 11.9%. Lamireau et al. Eur J Emerg Med, 2002; 9:9–14.
  • 47. Paracetamol (Acetaminophen ) 4/3/2024 47  Most common cause of acute liver failure in the United States.  Results from the formation of a highly reactive intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI).  single acute toxic dose >200 mg/kg in children and >7.5-10 g in adolescents and adults
  • 48. PCM 4/3/2024 48  Repeated administration of acetaminophen at supratherapeutic doses (>75 mg/kg/day for consecutive days) can lead to hepatic injury or failure in some children.  Four classical clinical stages
  • 49. STAGE TIME AFTER INGESTION CHARACTERISTICS I 0.5-24 hr Anorexia, nausea, vomiting, malaise, pallor, diaphoresis Labs typically normal, except for acetaminophen level II 24-48 hr Resolution of earlier symptoms; right upper quadrant abdominal pain and tenderness; elevated bilirubin, prothrombin time, and hepatic enzymes; oliguria III 72-96 hr Peak liver function abnormalities; fulminant hepatic failure; multisystem organ failure and potential death IV 4 days-2 wk Resolution of liver function abnormalities Clinical recovery precedes histologic recovery 4/3/2024 49
  • 50. Mx 4/3/2024 50  Initial treatment should focus on the ABCs and consideration of decontamination with activated charcoal in patients who present within 1-2 hr of ingestion.  The antidote for acetaminophen poisoning is NAC, which works primarily via replenishing hepatic glutathione stores. NAC therapy is most effective when initiated within 8 hr of ingestion.
  • 51. Salicylates (aspirin) 4/3/2024 51  The incidence of salicylate poisoning in young children has declined dramatically since acetaminophen and ibuprofen replaced aspirin as the most commonly used analgesics and antipyretics in pediatrics.  Acute toxic dose >150 mg/kg. More significant toxicity >300 mg/kg, and severe, potentially fatal, toxicity >500 mg/kg.
  • 52. C/F 4/3/2024 52  Classified as acute or chronic, and acute toxicity is far more common in pediatric patients.  Early signs of acute salicylism include nausea, vomiting, diaphoresis, and tinnitus.  Moderate salicylate toxicity can manifest as tachypnea and hyperpnoea, tachycardia, and altered mental status.
  • 53. c/f 4/3/2024 53  Signs of severe salicylate toxicity include hyperthermia, coma, and seizures.  Chronic salicylism can have a more insidious presentation, and patients can show marked toxicity at significantly lower salicylate levels than in acute toxicity.
  • 54. Mx 4/3/2024 54  Initial therapy focuses on aggressive volume resuscitation and prompt initiation of sodium bicarbonate therapy in the symptomatic patient  For the patient who presents soon after an acute ingestion, initial treatment should include gastric decontamination with activated charcoal  Urinary alkalinization.
  • 55. Hydrocarbons 4/3/2024 55  Hydrocarbons are organic substances that contain carbon and hydrogen.  Specific characteristics of each product determine whether exposure will produce systemic toxicity, local toxicity, both, or neither
  • 56. Hydrocarbons 4/3/2024 56  Classes of hydrocarbons  Aromatic hydrocarbons  Aliphatic hydrocarbons  Halogenated hydrocarbons  Terpene hydrocarbons
  • 57. Hydrocarbons 4/3/2024 57  Potential for toxicity  Low toxicity- asphalt, tars, mineral oil, petroleum jelly, motor oil, and axle grease.  Aspiration hazard – Clinical effects are typically limited to direct pulmonary damage and subsequent inflammation. Gasoline, kerosene, mineral seal oil (furniture polish), mineral spirits, or outdoor torch and cigarette lighter fluids.
  • 58. Hydrocarbons 4/3/2024 58 Systemic toxicity – Halogenated and aromatic hydrocarbons are absorbed readily through the gastrointestinal and/or respiratory systems.
  • 59. Determinants of pulmonary aspiration 4/3/2024 59  Volatility – The ability to vaporize or to exist in a gaseous form.  Surface tension – The adherence of molecules along a liquid surface. Lower surface tension allows compounds to spread over a larger area.  Viscosity – The resistance to flow through an orifice. Lower viscosity facilitates deeper penetration into the tracheobronchial tree.
  • 60. c/f 4/3/2024 60  Clinical manifestations of hydrocarbon ingestion depend largely on the specific profile of toxicity of the ingested substances.  The aspiration hazard of hydrocarbons is inversely related to viscosity and surface tension and directly related to volatility
  • 61. c/f 4/3/2024 61  Fever (30-60%), persistence beyond 48hr suggests super infection  tachypnea, dyspnea, cyanosis, wheezing, diminished resonance on percussion, rales, nasal flaring, and/or grunting respirations  asphyxia, necrotizing chemical pneumonitis, hemorrhagic pulmonary edema, which quickly progresses to shock and respiratory arrest
  • 62. c/f 4/3/2024 62  somnolence, headache, ataxia, dizziness, blurred vision, weakness, fatigue, lethargy, stupor, seizures, and coma  Cardiac dysrhythmias and myocardial dysfunction  Leukocytosis occurs early in the clinical course of hydrocarbon aspiration unrelated to pneumonitis and may last as long as one week
  • 63. Workup 4/3/2024 63  CXR – immediately and within 4-6 hrs after exposure  Blood gas  Complete blood count  Serum glucose  Serum electrolytes  Urinalysis
  • 64. Mx 4/3/2024 64  Successful management of hydrocarbon aspiration requires recognition of pulmonary toxicity and rapid initiation of appropriate supportive care  Stabilization  External decontamination  Treatment of hydrocarbon pneumonitis is supportive and includes oxygen and close monitoring of respiratory status.
  • 65. Indication for abcs 4/3/2024 65  Recurrence of fever after the first 48 hours  Increasing infiltrate in chest radiograph  Leukocytosis after the first 48 hours  Sputum or tracheal aspirate positive for bacteria
  • 66. Organophosphates 4/3/2024 66  Inhibitors of cholinesterase enzymes (acetyl cholinesterase, pseudo cholinesterase, and erythrocyte acetyl cholinesterase).  Most pediatric poisonings occur as the result of unintentional exposure to insecticides in and around the home or farm.
  • 67. Organophosphates 4/3/2024 67  Organophosphates and carbamates produce toxicity by binding to and inhibiting acetyl cholinesterase, preventing the degradation of acetylcholine and resulting in its accumulation at nerve synapses.  Diagnosis of poisoning is based primarily on history and physical exam findings
  • 69. Intermediate syndrome 4/3/2024 69  Ten to 40 percent of patients poisoned with organophosphates develop a distinct neurologic disorder 24 to 96 hours after exposure.  neck flexion weakness, decreased deep tendon reflexes, cranial nerve abnormalities, proximal muscle weakness, and respiratory insufficiency
  • 70. Delayed neurotoxicity 4/3/2024 70  Organophosphorus agent induced delayed neuropathy (OPIDN) typically occurs one to three weeks  transient, painful "stocking-glove" paresthesias followed by a symmetrical motor polyneuropathy characterized by flaccid weakness of the lower extremities, which ascends to involve the upper extremities.
  • 71. Mx 4/3/2024 71  Basic decontamination should be performed, including washing all exposed skin with soap and water and immediately removing all exposed clothing.  Basic supportive care should be provided, including fluid and electrolyte replacement and intubation and ventilation if necessary.
  • 72. Mx 4/3/2024 72  Antidotes Atropine, which antagonizes the muscarinic acetylcholine receptor, is useful for both organophosphate and carbamate intoxication. (0.05mg/kg) Pralidoxime breaks the bond between the organophosphate and the enzyme, reactivating acetyl cholinesterase.
  • 73. Prognosis 4/3/2024 73  Without treatment, symptoms can persist for weeks, requiring continuous supportive care.  Even with treatment, some patients develop a delayed polyneuropathy and a range of chronic neuropsychiatric symptoms
  • 74. Phenobarbitone 4/3/2024 74  Classified as long acting barbiturate  Cause depression of the brainstem RAS with resultant generalized depression of the CNS  Onset of effects in 20-60min.  Slowly metabolized by liver microsomal enzymes & are eliminated, half lives of 2-6days
  • 75. c/f 4/3/2024 75  Respiratory depression and coma  Shock can occur secondary to myocardial depression and venodilation  Nausea ,vomiting nystagmus ataxia ,steven- johnson syndrome and hematologic abnormalities
  • 76. Mx 4/3/2024 76 General measure  Intubations and ventilatory support  Gastric lavage  Charcoal Toxic specific measures  Alklinization of the urine with NAHCO3  Hemodialysis  Multiple dose charcoal
  • 77. Carbon monoxide 4/3/2024 77  The most common gas involved in pediatric exposures  CO binds to Hg with an affinity >200 times that of oxygen, forming carboxyhemoglobin. In doing so, CO displaces oxygen and creates a conformational change in hemoglobin that impairs the delivery of oxygen to the tissues, leading to tissue hypoxia.
  • 78. Co 4/3/2024 78  Early symptoms are nonspecific and include headache, malaise, nausea, and vomiting.  At higher exposure levels, patients can develop mental status changes, confusion, ataxia, syncope, tachycardia, and tachypnea.  Severe poisoning is manifested by coma, seizures, myocardial ischemia, acidosis, cardiovascular collapse, and potentially death.
  • 79. Mx 4/3/2024 79  General supportive care, move pt to fresh air  Administration of 100% oxygen to enhance elimination of CO.  The average half-life of COHb is 4-6 hr, reduced to 60-90 min by providing 100% oxygen at normal atmospheric pressures via a non- re breather facemask.  Hyperbaric oxygen decreases the half-life of COHb to 20-30 minutes.
  • 80. Caustics 4/3/2024 80  Caustics include acids and alkalis  Strong acids and alkalis can produce severe injury even in small-volume ingestions.  Alkalis produce a liquefaction necrosis, allowing further tissue penetration of the toxin and setting the stage for possible perforation.  Acids produce a coagulative necrosis, which limits further tissue penetration, though perforation can still occur
  • 81. Caustics 4/3/2024 81  The severity of the corrosive injury depends on the pH and concentration of the product as well as the length of contact time with the product.  Agents with a pH of <2 or >12 are most likely to produce significant injury.
  • 82. C/f 4/3/2024 82  pain, drooling, vomiting, abdominal pain, and difficulty swallowing or refusal to swallow. Laryngeal injury can manifest as stridor and respiratory distress, necessitating intubation.  In the most severe cases, patients can present in shock after perforation of a hollow viscus.  Esophageal stricture.  Caustics on the skin or in the eye can cause significant tissue damage.
  • 83. ENDOSCOPIC APPEARANCE OF ESOPHAGEAL MUCOSA 4/3/2024 83 Grade 0 Normal mucosa Grade 1 Erythema Grade 2 Erythema, sloughing, ulceration, and exudates (not circumferential) Grade 3 Deep mucosal sloughing and ulceration (circumferential) Grade 4 Eschar, full thickness injury and perforation
  • 84. Mx 4/3/2024 84  Initial treatment of caustic exposures includes thorough removal of the product from the skin or eye by flushing with water.  Dilution by water or milk is recommended as acute treatment(15ml/kg, max 250ml.)  Emesis and lavage are contraindicated.  Endoscopic evaluation
  • 85. Prevention 4/3/2024 85  Use packages with safety closures and learn how to use them properly.  Keep household cleaning supplies, medicines, and insecticides out of the reach and sight of children. Lock them up whenever possible.  Never store food and cleaning products together. Store medicine and chemicals in original containers and never in food or beverage containers.
  • 86. Prevention cont’d 4/3/2024 86  Avoid taking medicine in children's presence. Never suggest that medicine is candy.  Read the label on all products, warnings and cautions. Never use medicine from an unlabeled or unreadable container.  If interrupted while using a product, take it with you—it takes only a few seconds for a child to get into it.
  • 87. Prevention cont’d 4/3/2024 87  Know what a child can do physically.  Non accidental poisoning is a psychiatric emergency that can be prevented by developing good communication and a supportive environment for the adolescents within the family  Poison control centers.
  • 89. 4/3/2024 89 What can be done in our setup?
  • 90. References 4/3/2024 90  Nelson 19th ed.  Text book of pediatric emergency 6th ed.  5 minute pediatric consult  Current diagnosis and management in pediatrics  Casarett and Dohul’s toxicology  Katzung pharmacology  Up to date 21.2