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Approach to childhood poisoning.tmp 12

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Poisoning in children
Poisoning in children
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Approach to childhood poisoning.tmp 12

  1. 1. APPROACH & Mx OF ACUTE CHILDHOOD POISONING Mehretie Kokeb,MD Asst.Professor of Pediatrics & Child Health September, 2007
  2. 2. • EPIDEMIOLOGY • GENERAL Mx PRINCIPLES • SELECTED POISONS
  3. 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. 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. 5. Common substances • Non-drugs – Cosmetics – Cleaning – Hydrocarbons – Insecticides – Caustics • Drugs – Analgesics – Vitamins – Minerals
  6. 6. Route of Exposure  Ingestion = 78%  Dermal = 6.8%  Ophthalmic = 5.9%  Inhalation = 5.4%  Parenteral = 0.3%
  7. 7. Mx Principles:  Description of toxins  Magnitude of exposure  Time of exposure  Progression of symptoms  Medical Hx
  8. 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. 9. Laboratory: • CBC • serum electrolyte • LFT, RFT • screening • RBS • SO2
  10. 10. REMOVAL OF POISON: • Inhaled – O2 • External surface – water • Injected – Tourniquet, surgical removal/suction
  11. 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. 12. Contraindications:  Caustics  Coma  Seizure  Hydrocarbons  age <6mo
  13. 13. Gastric Lavage if • emesis fails • Contraindication of emesis • Ineffective after 3-4hrs • plain water, saline Whole bowel Irrigation Activated charcoal Catharsis/enemas
  14. 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. 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. 16. Activated charcoal for all cases In severe cases → Repeated doses  Poorly (not) adsorbed by AC • Electrolytes • Hydrocarbons • Fe • Alcohols • Most solvents
  17. 17. Catharsis after emesis or lavage and/or Ac • Saline • MgSo4 • Sorbitol • Mg Citrate Contraindications:  caustics  absent bowel sounds  recent bowel surgery
  18. 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. 19. Enhanced excretion: A. Diuresis  forced diuresis  osmotic diuresis  loop diuretics  ionized diuresis B. Dialysis & Exchange transfusion C. Antidote  only few  specific/nonspecific
  20. 20. Selected Poisons: • Drugs  Acetaminophen  Salicylate  Iron  Digoxin  Phenobarbitone • Insecticides  Organophosphate  Carbamates • Hydrocarbons • Caustics
  21. 21. INSECTICIDES: • Most commonly used are – organophosphates and – carbamates • Both are cholinesterase inhibitors
  22. 22. Pathophysiology:  bind to the enzyme preventing degradation of Ach accumulation of Ach at nerve synapses affecting: – CNS – Neuromuscular junctions – Sympathetic & Parasympathetic NS
  23. 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. 24. Mx :- Supportive GID AC Antidotes (atropine, pralidoxime)
  25. 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. 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. 27. Mx :-  Correction of hypoxia & acidosis  NO emesis  NO lavage  NO prophylactic Antibiotic  NO STEROIDS
  28. 28. Caustics • Alkaline and Acids Examples; Battery liquid Metal cleansing products Bleaches
  29. 29. C/M :-  Causes burn to the mouth, esophagus and GI • Dysphagia • Odynophagia • Chest pain • Abdominal pain • Nausea and vomiting
  30. 30. Mx :- No emesis No lavage No neutralization No steroid Dilution (water, milk) for solid alkaline materials Airway Mx Antacids (Cimetidine, omeperazole)
  31. 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. 32. Paracetamol → conjugation (sulfate,Glucuronide) Reactive Metabolite → Gluthatione → NAC (NAPQI) Binding to Hepatic macromolecules → Necrosis
  33. 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. 34. • Mx -Supportive -emesis/lavage -Ac -NAC/Mucomyst
  35. 35. SALICYLATE POISONING Toxic dose>150mg/kg • Pathphysiology  directly/indirectly affects most organs by: -direct stimulation of the respirstory center Hyperventilation & respiratory Alkalosis
  36. 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. 37. • C/M – younger children are at more risk – nausea & vomiting – agitation,restlessness,confusion – coma may develop – In severe cases,pul.hemorrhage
  38. 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. 39.  Mx Supportive GID,AC Ion trapping Dialysis (severe cases)
  40. 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. 41. • C/M – nausea,vomiting,dirrhea,& abd.pain – hematemesis & bloody dirrhea – drwsiness,& coma – gastric scarring & pyloric stenosis (2-4wk after ingestion)
  42. 42. • Laboratory – serum Fe – RBS – LFT – coagulation studies – Abd.X-ray • Mx -supportive & symptomatic care -emesis -Ac (not useful) -WBI -endoscopy/surgery
  43. 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. 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. 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. 46. Late limbs become flaccid DTR disappear pupils become constricted Sometimesbullous eruptions Terminal phase shallow & periodic respiration decreased BP-Shock
  47. 47. Mx Supportive GID AC Saline catharsis Diuresis Alkalinization Dialysis
  48. 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. 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. 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. 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. 52. • Mx of digitoxicccity D/C the drug GID AC,cathartic Rx of dysrhythmia (phenytoin. lidocain) Rx of hyperkalemia Antidotes (Digibind)

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