Engidaw Ambelu

1. APPROACH & Mx OF ACUTE CHILDHOOD
POISONING
Mehretie Kokeb,MD
Asst.Professor of Pediatrics & Child Health
September, 2007

2. • EPIDEMIOLOGY
• GENERAL Mx PRINCIPLES
• SELECTED POISONS

3. Poisoning cont…..
• Epidemiology
– Each day a child is exposed to potential
toxin
– Age
• most common in<5yrs(50-60%)
– Cause
• most(93-99%) are accidental

4. Types:
 Deliberate
 Overdose as self-harm or suicide attempt.
 Most episodes of pediatric poisoning.
 Accidental
 Dosage error
• Iatrogenic
• Patient error
 Recreational use
 Environmental:
• Plants
• Food
 Venomous stings/bites
 Industrial exposures

5. Common substances
• Non-drugs
– Cosmetics
– Cleaning
– Hydrocarbons
– Insecticides
– Caustics
• Drugs
– Analgesics
– Vitamins
– Minerals

6. Route of Exposure
 Ingestion = 78%
 Dermal = 6.8%
 Ophthalmic = 5.9%
 Inhalation = 5.4%
 Parenteral = 0.3%

7. Mx Principles:
 Description of toxins
 Magnitude of exposure
 Time of exposure
 Progression of symptoms
 Medical Hx

8. Mx …..
Initial medical care/Resuscitation
A-ir way
B-reathing
C-irculation
D-isability
-rug
-econtamination
Occular → copious saline
Skin → water, soap
GI → consider options

9. Laboratory:
• CBC
• serum electrolyte
• LFT, RFT
• screening
• RBS
• SO2

10. REMOVAL OF POISON:
• Inhaled
– O2
• External surface
– water
• Injected
– Tourniquet, surgical removal/suction

11. GI decontamination/Prevention of absorption:
Dilution (water or milk)
 Emesis
• commonly used agent is ipecac syrup,but saline,
lookwarm water can be used
• should be used within3-4hrs of ingestion

12. Contraindications:
 Caustics
 Coma
 Seizure
 Hydrocarbons
 age <6mo

13. Gastric Lavage if
• emesis fails
• Contraindication of emesis
• Ineffective after 3-4hrs
• plain water, saline
Whole bowel Irrigation
Activated charcoal
Catharsis/enemas

14. • Dilution
water or milk
• for corrosives & irritants
• may increase absorption of drugs
• Emesis (ipecac, apomorphine)
removes 1/3 of stomach content
Ineffective after 3-4hrs
Removes particulate & tablets
can be done at home

15. Gastric Lavage
plain water
NS
Large orogastric tube
pt. on left side
head slightly lower than feet
50-100ml(total500-1000ml)
decrease risk of aspiration
critically ill,extremely toxic,massive dose,not bound to
AC & no effective antidote
Contraindications
• caustics
• hydrocarbons

16. Activated charcoal for all cases
In severe cases → Repeated doses
 Poorly (not) adsorbed by AC
• Electrolytes
• Hydrocarbons
• Fe
• Alcohols
• Most solvents

17. Catharsis
after emesis or lavage and/or Ac
• Saline
• MgSo4
• Sorbitol
• Mg Citrate
Contraindications:
 caustics
 absent bowel sounds
 recent bowel surgery

18. Whole Bowel Irrigation (WBI)
• Intestinal irrigation with large volumes & flow
rates of a Polyethylene glycol-balanced
electrolyte solution (Colyte, Goletely)
• useful for
Fe
Massive poisoning
late presenters
 Mouth or NGT(500ml/hr)

19. Enhanced excretion:
A. Diuresis
 forced diuresis
 osmotic diuresis
 loop diuretics
 ionized diuresis
B. Dialysis & Exchange transfusion
C. Antidote
 only few
 specific/nonspecific

20. Selected Poisons:
• Drugs
 Acetaminophen
 Salicylate
 Iron
 Digoxin
 Phenobarbitone
• Insecticides
 Organophosphate
 Carbamates
• Hydrocarbons
• Caustics

21. INSECTICIDES:
• Most commonly used are
– organophosphates and
– carbamates
• Both are cholinesterase inhibitors

22. Pathophysiology:
 bind to the enzyme preventing degradation
of Ach accumulation of Ach at
nerve synapses affecting:
– CNS
– Neuromuscular junctions
– Sympathetic & Parasympathetic NS

23. C/Ms :-
• Muscarinic s/Sx
 Diaphoresis, emesis,
 Incontinence (urine, fecal),
 Tearing, bronchorrhea & bronchospasm
 Meiosis, hypotension, bradycardia
• Nicotinic S/S
 Muscle weakness, tremors, fasciculation,
 Hypoventilation, HTN, tachycardia, dysarhythmias
• CNS effects
 confusion, delirium, coma, Seizure, anxiety, restlessness
Common acronym=SLUDGE

24. Mx :-
Supportive
GID
AC
Antidotes (atropine, pralidoxime)

25. Hydrocarbon poisoning
• Type of toxic response depends on:
– amount of ingestion
– volatility(viscosity)
• Pathophysiology
– Cause toxicity in 2 ways :
a. Aspiration (most common) results in
→ Spasm, edema, inflammatory rxn, and necrosis of the
respiratory passages & alveoli.
→ Vascular thrombosis & hemorrhage with chemical
pneumonitis, atelectasis, & emphysema, also
bacterial pneumonia

26. b. Systemic effects
– volatile or low viscosity → degenerative changes in various
organs (mostly CNS)
C/M :-
 Choking
 Coughing
 vomiting & diarrhea, which may be bloody
 dyspnea and cyanosis
 mild tracheobronchitis, severe necrotizing bronchopneumonia &
pul.hemmorrhage
 atelectasis , pneumatocele, bacterial infection (secondary),
pneumomediastinum
 mild to moderate fever within 48hrs
 CNS -tremors, irritability, confusion, drowsiness, sz,& coma

27. Mx :-
 Correction of hypoxia & acidosis
 NO emesis
 NO lavage
 NO prophylactic Antibiotic
 NO STEROIDS

28. Caustics
• Alkaline and Acids
Examples;
Battery liquid
Metal cleansing products
Bleaches

29. C/M :-
 Causes burn to the mouth, esophagus and GI
• Dysphagia
• Odynophagia
• Chest pain
• Abdominal pain
• Nausea and vomiting

30. Mx :-
No emesis
No lavage
No neutralization
No steroid
Dilution (water, milk) for solid alkaline
materials
Airway Mx
Antacids (Cimetidine, omeperazole)

31. ACETAMINOPHEN POISONING
• mostly used & available at home
• Toxic dose>200mg/kg
• Pathophysiology
 due to toxic metabolite N-acetyl-P-benzoquinonemine (NAPQI), produced by
P450 enzyme.

32. Paracetamol → conjugation (sulfate,Glucuronide)
Reactive Metabolite → Gluthatione → NAC
(NAPQI)
Binding to Hepatic macromolecules → Necrosis

33. • C/m
 if untreated, poisoned patient passes through 4 stages;
• Stage I: 30-24hrs
– anorexia,nausea
– Vomiting
– diaphoresis
• Stage II:24-48hrs
– resolution of symptoms
– RUQ.abd. Pain
– increased LFT, bilirubin,PT
• Stage III:72-96hrs
– peak LFTabnormality
– anorexia,malaise
– Vomiting may reappear
• Stage IV:4days-2wks
– total resolution or liver failure

34. • Mx
-Supportive
-emesis/lavage
-Ac
-NAC/Mucomyst

35. SALICYLATE POISONING
Toxic dose>150mg/kg
• Pathphysiology
 directly/indirectly affects most organs by:
-direct stimulation of the respirstory center
Hyperventilation & respiratory Alkalosis

36. • Inhibts Kreb’s cycle enzymes
• Uncoupling oxidative phosphorylation
• Inhibts aa synthesis
• Decrease platelet adhesiveness
• Inhibit Vit K dependent factors synthesis
• Increase capillary permeability
• Gastric irritation

37. • C/M
– younger children are at more risk
– nausea & vomiting
– agitation,restlessness,confusion
– coma may develop
– In severe cases,pul.hemorrhage

38. • Death results from:
pul.edema & RF
cerebral edema
sevsere electrolyte imbalance
CV collapse
• Lab
serum salicylate
urine PH & volume
Plasma PH ,glucose, K
LFT
Clotting studies

39.  Mx
Supportive
GID,AC
Ion trapping
Dialysis (severe cases)

40. IRON POISONING
• Fe-containing products are common & often resemble candy
• Severity is based on the amount of elemental Fe
• Toxic dose>60mg/kg
 Pathophysiology
• corrosive to the GI
• Accumulates in the mitochondria & tissues-cellulr damage
& systemic toxicity
• Causes venodilation & increased capillary permeability-
hypotention
• Hepatic necrosis (in severe cases)

41. • C/M
– nausea,vomiting,dirrhea,& abd.pain
– hematemesis & bloody dirrhea
– drwsiness,& coma
– gastric scarring & pyloric stenosis (2-4wk after ingestion)

42. • Laboratory
– serum Fe
– RBS
– LFT
– coagulation studies
– Abd.X-ray
• Mx
-supportive & symptomatic care
-emesis
-Ac (not useful)
-WBI
-endoscopy/surgery

43. PHENOBARTINOE POISONING
• Pathphysiology
– 50% of phenobabitone is non-protein-bound, available to
equilibrate with tissues.
– ability to cross cell memrane(BBB) is inversely
correlated with its degree of ionization.
– cause depression of the brainstem RAS with resultant
generalised depression of the CNS

44. • May result in :
mild sedation, sleep or
high doses—coma,& respiratory arrest
 Absorbed from oral ingestion
 onset of effects in 20-60min.
 Slowly metabolized by liver microsomal enzymes & are
eliminated –half-lives of 2-6days

45. C/M
 Early
Euphoria
Disinhibition
Ataxia
Dysarthric
Nystagmus
slow respiration but adequate
superficial reflexes disappear
corneal reflexes present
pupils react briskly to light

46. Late
limbs become flaccid
DTR disappear
pupils become constricted
Sometimesbullous eruptions
Terminal phase
shallow & periodic respiration
decreased BP-Shock

47. Mx
Supportive
GID
AC
Saline catharsis
Diuresis
Alkalinization
Dialysis

48. DIGITOXICITY
• Digoxin is commonly used drug
• absobed from GI
90-100%-liqid preparation
60-80%-tablets
• Widely distributed to body tissues, esp.heart & skeletal muscles
• Eliminated by:
renal excretion(80%)
hepatic metabolism(20%)

49. o Physiologic effects are mediated through:

Inhibition of the Na-K ATPase enzyme system resulting
in:
Positive inotropic effect
Negative chronotropic
Enhanced vagal tone
Increased automaticity(ventricles,purkinje fibers)

50.  Toxic effects result from :
 excessive vagal tone
 Inhibition of Av nodal conductivity
 Hyperkalemia
 Enhanced automaticity
 Factors increasing toxicity are:
hypomagnesemia
Hypercalcemia
myocarditis
Prematurity
hypokalemia

51. Evidence of Digitoxicity
 Clinical and ECG
 arhythmias(most common)
bradycardia,AV or BBB,ectopic beats(atrial,ventricular),short
QRS,prolonged PR,Depression of ST with inversion of t-wave.
 Nausea,anorexia,vomiting,diarrhea
 Neurologic signs:
Visual(blurredvvision,scoioma,photophobia,transient blindness)
Neurobehavioral(confusion,hallucinatio,delirium)

52. • Mx of digitoxicccity
D/C the drug
GID
AC,cathartic
Rx of dysrhythmia (phenytoin. lidocain)
Rx of hyperkalemia
Antidotes (Digibind)