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Poisonings in Paediatrics
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POISONINGS IN PAEDIATRICS
Definitons Poisoning: Exposure to a chemical or other agents that adversely affects functioning of an organ
Poison: A poison is any agent of self injury absorbed into the body through epithelial surfaces.
Toxin : Toxin are poisons produced by a natural biological process.
Venom : Venoms are toxins that are injected by a bite or sting to cause their effect.
Incidences:Poisoning represents one of the most common medical emergencies.Circumstances of Exposure can be unintentional,intentional, accidental, environmental, or medicinal.Total hospital admissions 0.33%-7.6%Unintentional exposure 80%-90% in infants to preschool children.Intentional exposure higher in older children and adolescents.
Developing countries ingestion of pesticides and plants.
Developed countries pharmceuticals and chemicals.
Children under 5 years are at higher risk.
Incidences: Of total poison cases., 50% cases occur in children <6yrs.
All are unintentional exposures to toxic substances.
90% toxic exposure home
Major ingestion route
Minor dermal, inhalational, ophthalmic routes
50% cases non-drug causes like cosmetics, plants, foreign bodies, etc.
Pharmaceutical products remains the cause for rest of the exposures.
Vit. C is most commonly reported drug exposure.
Incidences:
Only 6% of children's are affected in 6-12yrs of age.
Adolescents intentional exposure (suicide, abuse or misuse of substances)
These intentional exposures leads to severe toxicity stages.
Non toxic & minimal toxic chalk, crayons, ball point ink, ant-acids (except salicylates),etc.
Toxic B-blockers, CCB, camphor, Anti-malarial drugs, etc.
Recently, Carbon monoxide gas, CVS drugs, Anti-depressants, Anti-Psychotics Leading
Toxidromes:
It is the association of several clinically recognizable features, signs, symptoms, phenomena or characteristics which often occur together.
Clinical significant in single drug exposure.
Toxins Toxidromes
Sympathomimetic Hypertension, Tachycardia, Delirium, Dilated pupils, Diaphoretic skin,
Anticholinergic Hypertension , Tachycardia, Hyperthermia, Delirium, Mumbling Speech, Dilated pupils, Dry skin
Cholinergic Bradycardia, Confusion, coma, Fasciculation, Small Pupil, Diaphoretic skin
Opioids Respiratory depression, Bradycardia, Hypotension, Depression, Coma, Pinpoint Pupil, Normal Skin
Sedative- Hypnotics Respiratory depression, Coma, Small pupil, Normal Skin
Serotonin syndrome Hyperthermia, Tachycardia, Hypertension, Hypotension, Agitation, Confusion, Coma, Dilated pupil, Diaphoretic skin
Salicylates Tachypnea, Hyperpnea, Tachycardia, Hyperthermia, Agitation, Confusion, Coma, Normal pupil, Diaphoretic skin
Withdrawal Tachycardia, tachypnea, Hyperthermia, Lethargy, confusion, Delirium, Dilated pupils, Diaphoretic skin
Analgesics Acetaminophen Salicylates Ibuprofen & other NSAIDS Oral opioids
CVS drugsB-Adrenergic
receptor blockers
CCB Clonidine Digoxin
Iron
Oral hypoglycemics
Compounds:
Psychiatric medications
• Anti-depressants
• SSRI• Atypical Anti-
depressants• MOI• Anti-
psychotics
House hold products
• Caustics• Cholinesterace
inhibitor insecticides
Hydrocarbons
• Kerosene• Tar• Turpentine
Toxic alcohol
• Methanol• Ethylene
glycol
Compounds:
Acetaminophen (ACT) poisoning:Pathophysiology
N-acetyl-p-benzoquinone (NAPQI)
Cytochrome P450 enzyme
Glutathione
Non-toxic mercaptopuric acid
OverdosesGlutathione stores
overwhelmed
Free NAPQI combine with hepatic macromolecules
Induces hepatic damage
Dosages:Acute toxic dose:
Children >200mg/kg
Adolescents 7.5 – 10g
Doses >75mg/kg/day for consecutive days hepatic failure
Stages of acteminophen toxicity: Stage 1,2,3,4
Assessment:S.Acetaminophen levels 4hrs after ingestion.
Others Heaptic transaminases, RFT, Coagulation parameters.
Runmack- Matthew nomogram plot of S.acetaminophen levels vs time
Used within 24hrs of exposure with known ingestion time.
NAC is used, if in hepatotoxic range
Any other drugs combined 2nd S.ACT are taken in 6-8hrs .
Unknown cases S.ACT, Hepatic Trans., coagulation parameters
NAC normal LVT with ,10ug/ml & signs of hepatotoxcity with low or non-detectable ACT.
Treatment: 1-2hrs decontamination with activated charcoal
Antidote – NAC (N-acetyl cysteine)
-- restores glutathione stores
PO : 140mg/kg loading,
70mg/kg q4h *17doses
IV : 150mg/kg over 1hr,
followed by 50mg/kg over 4hr,
followed by 100mg/kg over 16hrs (mostly preffered)
Hypersensitivity IgE diphenhydramine, epinephrine, albuterol
Non responsive liver transplantation done based on King’s college criteria.
Hydrocarbons poisoning:Even smaller doses causes life threatening toxicity.
Classes of hydrocarbons Aliphatic / straight chain : acetone, butane, propane, isopropane Aromatic/ cyclic structures: benzene, toluene, xylene Toxic/ Halogenated : Carbon tetrachloride, trichloro ethylene Petroleum distillates: Kerosene, gasoline, furniture polish
Saybolt Universal Seconds (SUS) – aspirational potential of a hydrocarbon
Hydrocarbons poisoning:The propensity of hydrocarbon is inversely proportional to its viscosity
Compounds with low viscosity spread rapid affect large areas when aspirated
<1mL produce significant injury
Gasoline & kerosene poorly absorbed but cause GI mucosal irritation
Certain hydrocarbons have unique toxicities:
Carbon tetrachloride – hepatic toxicity
Methylene chloride – carbon monoxide
Benzene – AML
Nitrobenzene, aniline - Methhemoglobinemia
Aspiration pneumonitis
(cough or gag)
Inactivation of type2
pneumocytes
Surfactant deficiency
Contd.. Kerosene & paraffin oils young children
Kerosene toxicity neonates Transdermal absorption also cause toxicity
IV kerosene drug abusers major lung injury
Halogenated hydrocarbons sensitizes myocardium endogenous catecholamines
This may result in dysarythmia and ‘sudden sniffing death’
Chronic abuse cerebral atrophy , peripheral neuropathy , kidney disease,etc
Clinical & Lab manifestations: Mild CNS depression is common & sometimes ventricular dysrhythmias are associated
Aspiration cough
Chest X-Ray shows abnormality within 6hrs of exposure,
pneumatocele appear after 2-3weeks of exposure,
x-ray remains abnormal even after patient is clinically normal.
Resp. symptoms ARDS or respiratory failure
Fever & leucocytosis common signs in patients with pneumonitis
Treatment: Contraindicated emesis & gastric lavage
Activated charcoal not useful
Management is symptomatic with preservation of airway in unconscious patients.
Standard Mech. Ventilation, High Freq. Ventilation & ECMO ARDS , resp. failure, pneumonitis
Dysrythmias b-blockers usually esmolol
Organophosphorus poisoning: MC organophosphates & carbamates cholinesterase enzymes unintentional
Pathophysiology : binds & inhibits AchE increased Ach at synapses
If untreated, OrgP. Forms permanent bonds to AchE ’aging’
Carbamates form temporary bonds with enzymes.
Reactivation weeks to months , in organophosphates.
<24hrs, in carbamates .
Clinical & Lab manifestations: Clinical effects depends on accumulations at peripheral nicotinic & muscarinic synapses.
Symptoms : carbamates < organophospahtes
Symptoms for cholinergic excess “ DUMBBLES”
Nicotinic signs muscle weakness, fasciculations, tremors , hypoventilation, hypertension ,
tachycardia, dysrhythmias, coma, seizures, respiratory failures.
Diagnosis history & physical findings
Early reported cases RBC cholinesterase & pseudocholinesterase in labs.
Treatment: Basic decontamination with washing with soap, water & removing exposed clothes immediately.
Activated charcoal controversial based on recent suggestions of its limited values
Fluid & electrolyte replacement is done.
TWO antidotes : atrophine & pralidoxime
Atrophine 0.05-0.1 mg/kg repeated q5-10min as needed (IV/ET)
Pralidoxime 25-50 mg/kg over 5-10 min (max,200 mg/min); can be repeated
after 1-2 hr, then q10-12hr as needed. (IV/IM)
Contd.. Large doses of atrophine intermittent bolus or through infusions to control symptoms,
targeted to resolve respiratory secretions & bronchospasm.
Tachycardia can result from nicotinic effects
Pralidoxime breaks bond b/w organophosphate and the reactivating enzymes,
effective only before permanent bond is formed.
In carbamtes, pralidoxime is not needed as the bond degrades spontaneously.
Without treatment, symptoms persist for weeks which require supportive care.
Even with treatment, patients may develop delayed polyneuropathy.
Iron Intoxication
• GI Toxicity• Stability for 48hrs• Ciruclatory shock• Metabolic acidosis &
Myocardial dysfunction
Ferrous Sulfate
Longterm hepatic fibrosis &GI scaring
GI symptoms are seen 15 to 30mg/kg
No significant toxicity <50mg/kg
Lethal dose 200 to 500mg/kg
Increased serum iron levels >500ug/dl casuses severe toxicity
Child develops complication after few hours or after a latent period of 1-2hrs.
Vomiting , diarrohea, S.glucose,leukocyte, abdominal radiograpgh iron levels >300ug/dl
Treatment:Gastric emptying stomach wash with sodium bicarbonate
IV sod. Bicarbonate 3mg/kg diluted with 5% dextrose acidosis
Fluid resuscitation may be necessary
Iron chelated with IV deferoxamine (15mg/kg/hr) until S.iron lowers <300ug/dl or stoppage vine rose color urine
Renal failure dialysis is required to remove deferoxamine iron complexes.
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