Senior lecturer Department of pediatrics ETIOLOGY The most common agents ingested by young children include family members medications The most common poisonings that lead to hospitalization are due to acetaminophen lead and antidepressant ID: 915211
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Slide1
poisoning
Dr.mushriq
A.hussein
Senior lecturer
Department of pediatrics
Slide2ETIOLOGYThe most common agents ingested by young children include family members'
medications
.
The
most common poisonings that lead to hospitalization are due to acetaminophen, lead, and antidepressant
medications.
Fatal
childhood poisonings are commonly caused by carbon monoxide, hydrocarbons, medications (iron, cardiovascular drugs, cyclic anti-depressants), drugs of abuse, and caustic
ingestions.
Slide3EPIDEMIOLOGY
more than 50% of poisoning annually occur in children <6 yr old
..
Poisoning exposures in children 6-12 yr old are much less common, involving only ~ 6%
of reported
pediatric exposures
.
Slide4More than 90% of toxic exposures in children occur in the home, produce no (82%) or minor (17%) toxicity;
Approximately
50% of cases involve nondrug substances, such as cosmetics, personal care items, cleaning solutions, plants, and foreign
bodies.
COMMON NONTOXIC AND MINIMALLY TOXIC*
PRODUCTS
Antacids,
non-
salicylate
-containing
topical Antibiotics
,
topical
Antifungals
,
Slide5Approach to the patient
The
initial approach to the patient with a witnessed or suspected poisoning should be no different than that in any other sick child, starting with stabilization and rapid assessment of the airway, breathing, circulation, and mental status
.
History
:
historical features such as age of the child (toddler or adolescent), acute
onset
Slide6of symptoms without prodrome, sudden alteration of mental status, multiple system organ dysfunction, or highs levels of household stress
Slide7Description of the Exposure Whether
wittnessed
in the
site,referred
from other hospital
Time,amount
of substance
ingested,it
is better to be overestimated.
Symptoms
1.ODOR
:
Bitter almonds
Acetone
Garlic
Slide82.OCULAR SIGNS
:
Miosis
Mydriasis
Nystagmus
Lacrimation
Retinal hyperemia
3.CUTANEOUS
SIGNS
Diaphoresis
Alopecia
Erythema
Cyanosis (unresponsive to oxygen)
Slide94.ORAL SIGNS
Salivation
Oral Burns
Gum lines
5.GASTROINTESTINAL
SIGNS
:
Diarrhea
Hematemesis
6.CARDIAC SIGNS:
Bradycardia
Hypertension
Hypotension
tachycardia
Slide107.RESPIRATORY SIGNS
Depressed respirations
Tachypnea
8. CNS Signs.
Past Medical History
Social History
Physical Examination
COMPLICATIONS
A poisoned child can exhibit any one of six basic clinical patterns: coma, toxicity, metabolic acidosis, heart rhythm aberrations, gastrointestinal symptoms, and
seizures.
Slide11Laboratory Evaluation For select intoxications (salicylates, some
anticonvulsants),
additional labs tests that may be helpful include electrolytes and renal function (an elevated anion gap suggests a number of ingestions), serum
osmolarity
,complete
blood count, liver function tests, urinalysis (crystals), co-oximetry, and a serum
creatine
kinase level
.
Slide12Additional Diagnostic Testing An
electrocardiogram (ECG) is a quick and noninvasive bedside test that can yield
important
clues to diagnosis and
prognosis
.
Chest
x-ray may reveal signs of
pneumonitis (e.g., hydrocarbon ingestion),
pulmonary edema (e.g., salicylate toxicity), or a foreign body. Abdominal x-ray can suggest the presence of a bezoar,
Slide13demonstrate radiopaque tabletsRADIOPAQUE SUBSTANCE ON KUB (MNEMONIC = CHIPPED), or reveal drug packets in a body packer.
Slide14Hospital admission Children
who have features of poisoning should generally be admitted to hospital
.
Children
who have taken poisons with delayed actions should also be admitted, even if they appear
well.Delayed
-action
poisons include aspirin, iron,
paracetamol
,
tricyclic
antidepressants, and co-
phenotrope
(
diphenoxylate
with atropine,
Lomotilc
);
the
effects
of modified-release
preparations are also delayed
Slide15Principles of Management The four principles of management of the poisoned patient are decontamination, enhanced elimination, antidotes, and supportive
care.
Decontamination
The goal of decontamination is to prevent absorption of the toxic
substance
decontamination should not be routinely employed for every poisoned
patien
.
Slide16Dermal and ocular decontamination begin with removal of any contaminated clothing and particulate matter, followed by flushing of the affected area with tepid water or normal
saline.
Dermal decontamination, especially after exposure to adherent or lipophilic (e.g., organophosphates) agents, should include thorough cleansing with soap and water.
Slide17Gastrointestinal (GI) decontamination is a controversial
,
In general, 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
,massive
pill ingestions, sustained-release preparations, and ingestions of agents that can form pharmacologic
bezoars
Slide18Described methods of GI decontamination include induced emesis with ipecac, gastric
lavage
, cathartics, activated charcoal, and whole-bowel irrigation
(WBI).
Syrup of
ipecac
.
Criteria for use:
the
ipecac can be administered within 30-90 min of the ingestion.
There is a substantial risk of serious toxicity to the patient.
There are no contraindications to the use of ipecac
.
There is no alternative therapy available to decrease GI absorption.
The use of ipecac will not adversely affect more definitive therapy that may be provided at the hospital.
Gastric Lavage
in most clinical scenarios, the use of gastric
lavage
is no longer
recommended?
Single-Dose
Activated Charcoal
:
activated charcoal is thought to potentially be the most
useful.
toxins are adsorbed onto its surface, thus preventing absorption from the GI tract.
Charcoal is most likely to be effective when given within 1 hr of ingestion
.
The dose of activated charcoal is 1 g/kg in children
Slide20Some toxins, including heavy metals, iron, lithium, hydrocarbons, cyanide, and low-molecular-weight alcohols, are not significantly bound to charcoal.
one
must
ensure that the patient's airway is intact or protected and that he or she has a benign abdominal
exam
. Cathartics
(sorbitol, magnesium sulfate, magnesium citrate) have been used in conjunction with activated charcoal to prevent constipation and accelerate evacuation of the charcoal-toxin complex.
Slide21WBI involves instilling large volumes (35 mL
/kg/hr in children or 1-2 L/hr in adolescents) of a polyethylene glycol electrolyte solution (e.g.,
GoLYTELY
) to “cleanse” the entire GI
tract.Complications
of WBI include vomiting,
abdominal
pain, and abdominal
distention
Enhanced Elimination
Multiple-Dose Activated Charcoal
MDAC is typically given as 0.5 g/kg every 4-6 hr (for ≤24 hr) and continued until there is significant clinical
improvement.
the airway and abdominal exam
should be assessed before each
dose.
Slide22Urinary Alkalinization
:Urinary
alkalinization
is accomplished with a continuous infusion of sodium bicarbonate–containing intravenous fluids, with a goal urine pH of 7.5-8.
Alkalinization
of the urine is most useful in managing
salicylate
and
methotrexate
toxicity.
Alkalinization
may also be beneficial in managing
phenobarbital
toxicity
Slide23Dialysis:Toxins that are amenable to dialysis have the following properties: low volume of distribution (<1 L/kg), low molecular weight, low degree of protein binding, and high degree of water
solubility.
toxins for which dialysis may be useful include
methanol and ethylene glycol, as well as large symptomatic ingestions of
salicylates
,
theophylline
, bromide, or
lithium
Slide24Intralipid Emulsion TherapyA potentially life-saving intervention of infusing
Intralipid
emulsions is a means of sequestering fat-soluble drugs and decreasing their impact at target organs
Lipophilic
drugs are potentially bound by
Intralipidemulsions
, including calcium channel blockers (
verapamil
and
diltiazem
)
and
tricyclic
antidepressants.
Antidote:
Slide25Glucagon and/or insulin and glucose
Calcium channel antagonists
Diphenhydramine and/or benztropine
Dystonic reactions
Calcium salts
Fluoride, calcium channel blockers
Protamine
Heparin
Folinic acid
Methotrexate, trimethoprim, pyrimethamine
Sodium bicarbonate
Sodium channel blockade (tricyclic antidepressants, type 1 antiarrhythmics)
Acetaminophen
N
-Acetylcysteine
physostigmine
anticholinergic
Slide26Supportive Care The goal is to support the vital functions of the patient until the patient can eliminate the toxin from the
system. If the level of consciousness is depressed, and a toxic substance is suspected, glucose (1 g/kg IV), 100% oxygen, and
naloxone
should be administered.
PROGNOSIS :
Mortality from poisoning is rare
.The
most common exposures resulting in death include carbon monoxide, hydrocarbons, and opioids (all of which interfere with oxygen delivery to tissues).
Slide27PREVENTIONProperly educating parents to use childproof medication containers, to store toxic substances in locked cabinets, and to label toxic chemicals properly is necessary for preventing ingestions
Slide28Why Not Ipecac?
Variable percentage of removal of toxic medication
In adult volunteers:
51-83% removal (5 minutes after ingestion)
2-59% removal (30 minutes after ingestion)
May cause persistent vomiting, lethargy, and diarrhea
Vomiting may preclude later administration of oral antidotes
Slide29Why Not Ipecac?
Lethargy and vomiting together increase risk of aspiration
Inappropriate use-following ingestion of acid .
Misuse-children with eating disorders
Misuse-Munchausen by proxy