Pediatric Toxicology and Poisoning Management Guide
Epidemiology and Prevalence of Paediatric Poisoning
Occurrence Patterns: The vast majority of paediatric poisonings occur within the home environment.
Age and Gender Demographics:
Peak Age Range: 1-6 years of age.
Children: Male prevalence is higher than female (M > F).
Adolescents: Female prevalence is higher than male (F > M).
Intentionality: Poisonings involving young children are predominantly unintentional (exploratory), whereas adolescent cases are more frequently intentional.
Symptomatic Presentation: Fewer than of reported ingestion cases develop actual clinical symptoms.
Common Toxic Agents
Medications:
Over-the-Counter (OTC): Paracetamol, Ibuprofen, cold remedies, vitamins, and antihistamines.
Prescription/Illicit: Antidepressants, analgesics, and various illicit drugs.
Household Products: Detergents, disinfectants, and bleach.
Personal Care: Cosmetics and personal care products.
Biological/Environmental: Poisonous plants, gardening products, and pesticides.
Miscellaneous: Alcohol, glue, aromatic oils, batteries, and various chemicals.
Clinical Features and Toxicological Clues
Asymptomatic Presentation:
Ingestion is known or suspected based on environmental evidence (e.g., a toddler found with an open pill container/missing tablets) or disclosure by the patient or family.
General Symptoms: Decreased consciousness, arrhythmia, gastrointestinal (GI) upset (vomiting, abdominal pain, anorexia), behavioral changes, seizures, and metabolic acidosis (high anion gap).
Diagnostic Clues by Symptom:
Decreased Consciousness: If a child presents with an unusual or unexplained depressed state of consciousness, ingestion must always be queried.
Hypertension agents: Antidepressants, -blockers, opiates, and iron.
Hypotension agents: Cocaine and amphetamines.
Hypoglycemia agents: Iron poisoning, alcohol poisoning, and insulin.
Seizures agents: Tricyclic Antidepressants (TCA) and organophosphates (e.g., pesticides).
High Anion Gap Metabolic Acidosis: Salicylates/Aspirin, Iron, Ethanol, methanol, and ethylene glycol.
Hypokalemia: Salicylates.
Hyperkalemia: Digoxin and -blockers.
Assessments and History Taking
Initial Protocol: ABCD assessment (Airway, Breathing, Circulation, Disability), vitals monitoring, and rapid blood glucose check.
Collateral History Essentials:
Agent Identity: Type of agent ingested, specific preparation, and drug ingredients (examine the original bottle if possible).
Timing: Exact time the incident occurred.
Quantity: The amount ingested relative to the weight of the child.
Reliability: Healthcare providers must beware of inaccurate dose reporting during history taking; consider the possibility of mixed or undetermined ingestions.
General Management and Gastrointestinal Decontamination
Activated Charcoal:
Mechanism of Action (MOA): A highly adsorbent powder made from superheated, high surface area, porous particles. It adsorbs chemicals within minutes of contact to prevent GI absorption and toxicity. It can also interrupt the enterohepatic circulation of certain drugs (e.g., Aspirin, barbiturates).
Administration: Preferred within the first hour () of ingestion if the patient is conscious. For unpalatable doses (), it may be administered via NG/lavage tube.
Contraindications: Heavy metal poisoning (e.g., , lithium), alcohol ingestion, or ingestion of acids/alkalis (charcoal obscures endoscopy findings).
Side Effects: Severe lung damage if aspirated; the airway must be protected if consciousness is depressed.
Gastric Lavage:
Procedure: Large bore orogastric tube with normal saline irrigation.
Efficacy: Most effective within , removing up to of the toxin. Limited role with many complications.
Contraindications: Hydrocarbons, acids, and alkalis (risk of aspiration pneumonitis).
Complications: Aspiration pneumonia, esophageal/gastric perforation, laryngospasm, and hypoxia.
Whole Bowel Irrigation (WBI):
Procedure: Administration of osmotically balanced polyethylene glycol electrolyte solution (PEG-ES) to mechanically flush the GIT.
Indications: Potentially toxic ingestions of sustained-release or enteric-coated pills, or toxins not adsorbed by activated charcoal.
Contraindications: GI hemorrhage, intractable emesis, intestinal perforation, or obstruction.
Paracetamol (Acetaminophen) Poisoning
Exposure Patterns:
Unintentional: Young children, exploratory or inappropriate dosing by caregivers (e.g., adult formula given), or iatrogenic IV overdose.
Intentional: Predominantly girls > 10 years old; typically single-event high-dose ingestions for suicidal intent.
Pharmacokinetics:
Absorption: Rapidly absorbed from the GIT; peak serum concentrations usually occur at for immediate-release preparations.
Toxic Dose: Sharp threshold of for acute ingestion.
Pathogenesis (NAPQI): Hepatotoxicity occurs when excessive intake leads to the depletion of glutathione stores and increased CYP450 activity, resulting in NAPQI poisoning and liver damage. Younger children are generally less susceptible, but fasting or malnutrition increases risk.
Clinical Stages:
Stage 1 (): Often asymptomatic; occasionally nausea, vomiting, lethargy, and malaise.
Stage 2 (): Right subcostal pain, hepatic necrosis, liver decompensation, acute tubular necrosis, and renal failure.
Management:
Check Levels: Measure paracetamol levels, Liver Function Tests (LFT), and INR at exactly post-ingestion.
Antidote: N-acetylcysteine (NAC) administered IV or PO if the serum concentration is above the "treatment" line on the acetaminophen poisoning nomogram. Extremely effective if given within .
Alcohol and Illicit Drug Overdose
Epidemiology: Alcohol is common and easily available; polypharmacy (mixed drugs) is frequent in paediatric Emergency Departments.
Alcohol Toxicity Thresholds:
Infant/Young Child Toxic Dose: of ethanol (peak serum ethanol of ).
Severe Toxicity: Ingestion of of ethanol.
Clinical Features:
CNS Depression: Dose-dependent ataxia, lethargy, and coma. Profound respiratory failure if co-ingested with benzodiazepines or barbiturates.
Hypoglycemia: Ethanol-induced hypoglycemia (<2.22\,\text{mmol/L}) can occur hours later due to glycogen store issues, potentially leading to seizures and death.
Metabolic: Metabolic acidosis (pyruvate to lactate conversion), hypokalemia, and hypothermia (suppressed shivering).
Management: Purely supportive (ABCD); temperature regulation; IV dextrose bolus for hypoglycemia. Activated charcoal is of no benefit for pure alcohol.
Iron Poisoning
Toxic Dosages (Elemental Iron):
>20\,\text{mg/kg}: Toxicity possible.
>60\,\text{mg/kg}: Serious toxicity.
>150\,\text{mg/kg}: Fatal.
The Five Phases of Iron Toxicity:
GI Phase (): Abdominal pain, vomiting, diarrhea, hematemesis, melena, lethargy, and hypovolemic shock.
Latent Phase (): Apparent stability as iron redistributes. May still show tachycardia and hyperventilation.
Shock/Acidosis Phase (): Cardiovascular toxicity, coagulopathy, and profound metabolic acidosis. Cardiogenic shock may develop within .
Hepatotoxicity Phase (): Hepatic failure as liver cells passively absorb high concentrations of iron from portal circulation.
Bowel Obstruction Phase (): Pyloric stenosis or gastric outlet obstruction due to scarring where tablets aggregated.
Antidote: IV Deferoxamine (). It chelates ferric iron () into water-soluble ferrioxamine, creating "vin ros\u00e9" (orange-reddish) urine.
Aspirin (Salicylate) Poisoning
Kinetics: Rapidly absorbed but induces gastric stasis, potentially allowing recovery of material up to post-ingestion. Toxic dose is .
Pathogenesis: Uncoupling of oxidative phosphorylation leading to metabolic acidosis, hyperpyrexia, and hypoglycemia. Initial stimulation of the medulla causes respiratory alkalosis.
Symptom Phases:
Phase 1 (): Anxiety, sweating, hyperventilation, respiratory alkalosis, and alkaline urine.
Phase 2: Paradoxical aciduria (acidic urine despite alkalosis) once potassium () stores are depleted.
Phase 3 (up to ): Dehydration, metabolic acidosis, pulmonary oedema, and respiratory failure.
Management:
Urine Alkalization: IV sodium bicarbonate to achieve a urine \text{pH} > 7.5 to enhance elimination.
Caution: Avoid intubation if possible as it is dangerous in salicylate poisoning.
Caustic and Button Battery Ingestion
Pathogenesis: Lodge in GIT mucosa causing burns, mucosal ulceration, and perforation through electrical discharge, leakage of alkaline contents, or pressure necrosis.
Critical Site: The esophagus is the most common site of impaction. Damage can occur within .
Radiographic Diagnosis: Button batteries show a "halo" or double-ring sign on an AP view and a "step-off" at the anode/cathode separation on a lateral view, unlike coins which have sharp edges.
Management:
Forbidden: NO emesis, NO lavage, NO charcoal.
First Aid (if asymptomatic and >1 yr): Immediate PO honey to neutralize pH and reduce burn severity.
Emergency: Surgical review and emergency endoscopic removal (OGD).
Follow-up and Prevention
National Poisons Information Centre (NIPC): Located at Beaumont Hospital for reporting and consultation.
Social Inquiry: Assess why the ingestion happened. Investigate supervision, neglect, housing, and social worker involvement. Deliberate ingestion requires Psychiatry involvement.
Prevention Rules:
Child-resistant locks; store poisons out of reach.
Never refer to medications as "sweeties."
Never store poisons in drink bottles.
Discard old batteries and medications.
Do not cultivate poisonous plants at home.