Pediatric emergency medicine presentation Emergency Medicine Residency Thammasat University Hospital

2. Why so common in children?

5. Background
• Developmental milestones
– 6-9 months: creep, crawl, and pick up objects
– 9-12 months: pick up a pellet and put it in a hand
– 15 months: walking, pick up a pellet and put it in a bottle
– 18 months: able to consciously dump pellet from bottle
(e.g. Tylenol, aspirin, vitamins, adult prescription medications)

6. Epidemiology
• US Poison center reported 2.4 million calls/year
• 50% occurred in children ≤6 yrs old
• One to three yrs old peak incidence
• Less than 50 deaths annually
• 99% of ingestions by children under 6 are unintentional.
• Approx. 40% of adolescent ingestions reported are intentional.
• Approx. 56% of adolescent ingestions are by females

7. Epidemiology
• 10 Fold decrease in deaths since 1950
– Packaging legislation – child resistant closures
– Safer medications (tetracyclic > tricyclic)
– Consumer Product Safety measures
– Poison Centers
– Anticipatory Guidance

8. Most Common Pediatric Exposures

10. Common deadly ingestion medications
• Oral hypoglycemic drugs • Loperamide & Diphenoxylate
• Beta-blocker • Salicylates
• Calcium channel blocker • Quinine & Quinidine
• Alpha-2 adrenergic agonist • Camphor
• Cyclic antidepressants • Podophyllin & Colchicine
• Opioids • Acetylcholineesterase
• Buprenorphine inhibitor

11. Alpha-2 adrenergic agonist
• Resembles Opioids
– Bradycardia and hypotension
– Decreased LOC, miosis, and respiratory depression/apnea
• Clonidine (Catapress), Brimonidine (Alphagan®), Tetrahydrozoline
(Visine®), and Oxymetazoline (Iliadin®)
• Treatment involves atropine to increase heart rate and
intravenous fluid for euvolemic pressure support, may consider
vasopressor(Dopamine)
• Naloxone may reverse the effects of clonidine on µ-opioid
receptors

12. Oral hypoglycemics
• Clinically significant hypoglycemia may occur up to 18-24 hrs
• Glipizide, Glyburide, Glimepiride, Glibenclamide, Chlorpropamide
• Ingestion in a nondiabetic child requires admission for glucose
checks every 1-2 hours
• Supportive care/Decontamination
– Activated charcoal (ingestion < 1hr or extended release)
• Asymptomatic patients allowed to eat

14. • IV dextrose bolus and infusion for symptomatic patients
– 2 mL/kg of 25% dextrose for infant and children IV,IO,NG,PO
– 1 mL/kg of 50% dextrose for older children as to adults
– insulin release with breakthrough or rebound hypoglycemia
• Octreotide can directly inhibit insulin release
– Consider for cases refractory to IV dextrose
– 4-5 µg/kg/d SC divided Q 6hrs
• Consider IM glucagon (0.025-0.1 mg/kg) when unable to PO or IV
glucose

16. Ca-Channel Blocker
• Decrease cardiac inotropy, may increase vasodilation
• Overdose can block insulin secretion  Hyperglycemia
• Long-acting CCBs : should be admitted for 24 hours
• Common CCBs include: Amlodipine (Norvasc®), Nicardipine
(Cardene®), Verapamil (Isoptin®), and Diltiazem (Herbesser®)

18. • Treatment with high-dose insulinemia/euglycemia therapy
– 1 unit/kg intravenous bolus and 1 unit/kg/hr intravenously with
supplemental dextrose as needed (although it rarely is)
• Atropine/cardiac pacing
• Vasopressors
– Norepinephrine/Epinephrine
• Calcium gluconate
– 0.6 ml/kg IV bolus
– 0.6-1.5ml/kg/hr infusion
: refractory shock from amlodipine overdose

20. Beta-Blocker
• heart rate but fortunately are unlikely below its intrinsic rate
• Blockage of glycogenolysis Hypoglycemia
•  in mental status in the more lipid soluble agents that cross BBB
– Atenolol is more hydrophilic while Propanolol is most hydrophobic
• Symptomatic patients should be given glucagon (0.03-0.05 mg/kg),
bypassing beta-receptors to stimulate cAMP cascade, leading to
increased intracellular calcium for increased heart rate and
contractility.

22. CCB Vs. BB
• Different mechanisms of action, but toxic effects are similar
(hypotension and bradycardia)
• CNS
– BB (lipophylic): sedation, seizure
– CCB: alert
• Respiratory
– BB: bronchospasm
• Metabolic
– BB: hypoglycemia, mild hyperkalemia
– CCB: hyperglycemia

23. TCA
• Block fast Na channels leading to intraventricular conduction
delay, widening of the QRS (with subsequent prolongation of QTc),
and rightward axis deviation
• QRS > 100 msec with a prominent terminal R in aVR is predictive of
both ventricular arrhythmia onset and seizure activity
• Imipramine, Desipramine, Amitriptylline are regularly prescribed
• A child who ingested TCA should be admitted for cardiac
monitoring and serial ECGs

25. Overall effects
• Sodium Channel blockage
• Potassium channel antagonist
• Anticholinergic effect : competitive inhibitor of Ach at Central and
Peripheral muscarinic receptor
• Antihistaminic effect: Central and Peripheral
• Inhibition of Amine reuptake (NE, serotonin)
• Inhibition of postsynaptic Central and Peripheral alpha adrenergic
receptors
• GABA-A receptor antagonist

26. Cardiotoxicity
• Delayed conduction : Na Channel blockade
– QRS prolongation
– AV block
• Arrthymia
– Anticholinergic : Sinus tachycardia
– Re-entry : Ventricular tachycardia
– Prolonged repolarization : Torsade de pointes
• Hypotension
– Na Channel blockade : Decreased contractility
– Alpha adrenergic blockade : Vasodilatation

27. • Repeated activated charcoal
• Serum alkalinization with NaHCO3 to reverse acidic cardiac toxicity
– Bolus 1-2 mEq/kg IV and infusion 1-2 mEq/kg/hr
– Serum pH 7.45-7.55
• Hyperventilation : if NaHCO3 is contraindicated
• Seizure : Benzodiazepine, Barbiturate, Propofol But Not Phynetoin
• Levophed(NE) is vasopressor of choice if unresponsive to IV, NaHCO3
• No Physostigmine !!!
• No Flumazenil especially in BZD coingestion!!!

28. Opioids/Narcotics
• Depression in mental status and respiration directly in center
• Mostly death due to apnea, hypoxia
• A long-acting opioid like OxyContin® peak effects 18-24 hrs
• Common narcotics : Oxycodone + Acetaminophen (Percocet®),
Oxycodone (OxyContin), Hydrocodone + Acetaminophen (Vicodin®),
Fentanyl patches, Methadone, and Hydromorphone (Dilaudid®)
• Careful monitoring, supportive care, and administration of
naloxone as needed

29. Buprenorphine
• The opioid agonist/antagonist
• Active ingredient in Suboxone® (8 mg) and Subutex® (agents used
to treat opioid addiction)
• Significant respiratory depression in children after only 1 lick
• Any pediatric exposure requires a 24-hr hospital admission for
respiratory monitoring and administration of naloxone as needed

30. Loperamide & Diphenoxylate
• The synthetic opioids, active ingredients
decreasing peristalsis in certain antidiarrheals
(Lomotil®, Imodium®, and Tincture of opium)
• Too much can cause opioid toxicity
• Lomotil® intox. classically “Biphasic reaction”
– Initial antimuscarinic symptoms in 2 – 3 hours
– Delayed opioid symptoms
• Symptomatic patients should receive naloxone
and be admitted 24hr for expectant mx

31. Salicylates
• Widely available in OTC products
– Most often as Aspirin (acetylsalicylic acid)
– Oil of wintergreen (methyl salicylate)
– Pepto-bismol (bismuth subsalicylate)

32. Salicylates
• Minimal toxic ingested dose in children: 150 mg/kg
• 1 tsp of 98% methyl salicylate contains 7000 mg of salicylate = 90
Baby ASA = > 4 times potentially toxic dose for 10-kg child
• Infants : may show just dehydration, rapid breathing
• Older kids : GI symptoms (Nausea, Vomiting), CNS depression
• Metabolic derangement that induces cerebral and lung edema,
seizures, and death

33. • Uncouple oxidative phosphorylation
– Electron transport occurs without ATP synthesis
– Increased heat production  Hyperthermia increased energy
demand  Glycogenolysis, Lipolysis  Ketones, Hyperglycemia
– Impaired gluconeogenesis  Hypoglycemia
• Inhibits dehydrogenase enzymes in Krebs cycle  Anaerobic
metabolism  Lactate and Pyruvate accumulation

34. • Initial respiratory alkalosis
– Direct stimulation of medulla
– Rarely seen in infants or young children
• Metabolic acidosis
– Accumulation of organic acids from anaerobic metabolism
– Acidemia (pH<7.4) implies a severe toxicity with high morbidity
• Children can progress to metabolic acidosis w/o an alkalotic phase

36. • Initial treatment can start with the activated charcoal (1 g/kg PO)
• Fluid resuscitation
• Levels 20 mg/dL require urine alkalinization with NaHCO3 1-2
meq/kg/hr mixed in D5W or D5½NS depending on age to enhance
renal elimination
• Prevent acidemia : Avoid sedation, Hyperventilation if intubated
• Extracorporeal Removal (Hemoperfusion, Hemodialysis, Exchange
transfusion)
– Require hemodialysis for acute critical levels (above or approaching
60 mg/dL), patients with ARF, Severe salicylism (Pulmonary edema,
altered mental status)

37. Quinine & Quinidine
• Na-channel blockade, leading to QRS widening and arrhythmias
• Hypokalemia-related QTc prolongation and Torsades de pointes
• Mild cinchonism : Blurred vision, Hearing impairment, and Flushing
• Severe : Deafness, Blindness, and Cardiac arrhythmias
• Quinine's derivatives : Chloroquine & Hydrochloroquine similar toxic
• Treatment includes NaHCO3 when QRS is widened, replenishment of
electrolytes, and supportive cares
• Chloroquine toxicity is treated with diazepam 2 mg/kg

38. Camphor
• Initially nausea and vomiting and can quickly progress to delirium,
hallucinations, seizures, and cerebral edema
• It is used for its anti-itch, moth repellant, cough suppressant, and
muscle-soothing properties in products : Tiger Balm®, Modern
(nonnaphthalene) mothballs, Vicks® VapoRub®, and Mentholatum®
Ointment
• Cause of death : Respiratory depression, Status epilepticus
• Treat seizures with benzodiazepines and institute supportive care

40. Podophyllin & Colchicine
• Nausea, vomiting, and diarrhea but can progress to hypotension,
tachycardia, metabolic acidosis, and coma mimicking septic shock
• Pancytopenia often nadirs 4-7 days after exposure
• Dermal overdose can delay presentation up to 24 hrs
• Ingestions of greater than 0.5 mg/kg can cause marrow aplasia;
as little as 7 mg total has been reported to cause death in adult
• Overdose of either agent should be treated with aggressive
supportive measures

41. Acetylcholinesterase inhibitors
• Oral AchEIs lead to cholinergic poisoning
• Nicotinic effects of hypotonia, miosis, and "floppiness"
• Often absent Muscarinic signs : DUMBBELSS
• Organophosphate : Insecticides and warfare nerve agents (sarin
and VX) are an unlikely exposure risk for toddlers
• Oral AchEIs Rivastigmine, Donepezil, Tacrine, and Galantamine used
for treatment of Alzheimer dementia are commonly found
• Treat muscarinic effects, if present, with atropine
• Treat nicotinic effects with pralidoxime

43. DUMBBELSS

44. References
• Michael JB, Sztajnkrycer MD. Deadly pediatric poisons: nine
common agents that kill at low doses. Emerg Med Clin North Am.
2004 Nov;22(4):1019-50.
• Matteucci MJ. One pill can kill: assessing the potential for fatal
poisonings in children. Pediatr Ann. 2005 Dec; 34(12):964-8.

46. Thank you!