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Pediatrics drug poisoning


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presentation and approach to general poisning and some common poisnings in pediatric population

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Pediatrics drug poisoning

  1. 1. 7We Care .“All substances are poisons...the right dose separates poison from a remedy.”
  2. 2. 7We Care Poisoning in Children • Definition of Poisoning: • A poison is an agent of injury to humans usually by chemical reaction, when a sufficient quantity is absorbed through epithelial lining such as skin or gut. • Circumstances of Exposure can be intentional, accidental, environmental, medicinal or recreational. • Routes of exposure can be ingestion, injection, inhalation or cutaneous
  3. 3. 7We Care Epidemiology • 0.64-11.6% of pediatric admissions and 0.6% of all pediatric deaths. • 79% of these involve children younger than age six. • 80% household products,21.8% drugs, agriculture pesticide 9.1%, industrial chemicals 7%,bites and stiings 3.2% of pediatric exposures.
  4. 4. 7We Care Epidemiology • 80% of ingestions by children under 6 are unintentional. • Approximately 40% of ingestions reported to the poison center by adolescents are intentional. • Approximately 56% of adolescent ingestions are by females.
  5. 5. 7We Care Recent advances • Stabilization of the patient is being considered as the main stay. • Gastrointestinal evacuation, is undergoing critical appraisal. • Ipecac and gastric lavage are being questioned • Activated charcoal is gaining importance . • Antidotal therapy is no more the mainstay of management • Antidotes for only about 5% poisons.
  6. 6. 7We Care Grouping the signs and symptoms produced by the poisons in to various toxidromes helps in rapid and effective management of the case. Major four toxidromes are: Anticholinergic Sympathomimetic Opiates/Sedatives- Hypnotics Cholinergic
  7. 7. 7We CareCommon Toxidrome Findings Physical Findings Adrenergi c Anti- cholinergi c Anti- cholineste rase OPIOID Sedative- hypnotic RR Increased No change No change Decreased Decreased HR Increased Increased Decreased Normal/ decreased Normal/ decreased Temp Increased Increased No change Normal/ decreased Normal/ decreased BP Increased NoChange /increased No change Normal/ decreased Normal/ decreased
  8. 8. 7We CareCommon Toxidrome Findings Physical Findings Adrenergi c Anti- cholinergi c Anti- cholinester ase OPIOID Sedative- hypnotic Mental status Alert/ agitated Depressed/ Confused/ hallucinate Depressed/ Confused/ Depressed Depressed pupils Dilated Dilated Constrict Constrict Normal Mucus membrane Wet Dry Wet Normal Normal skin Diaphoreti c Dry Diaphoreti c Normal Normal
  9. 9. 7We Care Symptoms and signs of common poisons Symptomalogy Important causes odor kerosene,cyanide ,phosphorus, organophosphates fever Salicylates,anticholinergics.kerosene hypothermia Opiates ,barbiturates delirium Dhatura,salicylates,barbiturates,antihistaminics Constricted pupils Opiates,organophosphates, early stages of barbiturates Dilated pupils atropine.,adernergic agents,antihistaminnics tachycardia Atropine,theophylline bradycardia Digitalis,beta blockers,quinidine
  10. 10. 7We Care Paralytic ilius Opiates, anticholinergics Metabolic acidosis Iron, salicylates,phenol hypotension Anticholinergic, barbiturates,opiates, phenothiazines,aluminium phosphide Cardiac arrhythmias Theophylline,tricyclic antidepressants,kerosene,digitalis,alumi nium phosphide.
  11. 11. 7We Care Important History Points • What toxic agent/medications were found near the patient? • What medications are in the home? • What approximate amount of the “toxic” agent was ingested? – How much was available before the ingestion? – How much remained after the ingestion?
  12. 12. 7We Care • When did the ingestion occur ? • Were there any characteristic odors at the scene of the ingestion? • Was the patient alert on discovery? – Has the patient remained alert since the ingestion? – How has the patient behaved since the ingestion? • Does the patient have a history of substance abuse?
  13. 13. 7We Care ABC’s of Toxicology: • Airway • Breathing • Circulation • Drugs: • Resuscitation medications if needed • Universal antidotes • Draw blood: • chemistry, coagulation, blood gases, drug levels • Decontaminate • Expose / Examine • Full vitals / Foley / Monitoring • Give specific antidotes / treatment
  14. 14. 7We Care ABC’s of Toxicology: • Decontamination: 1.Ocular: –Flush eyes with saline or tepid water for 15 min. 1.Dermal: –Remove contaminated clothing –Brush off –Wash skin with soap and water
  15. 15. 7We Care GI DECONTAMINATION GASTRO-INTESTINAL 1.EMESIS : use of emetics like syp of ipecac declined in recent past. Home remedy 2.GASTRIC LAVAGE • most effective if done within one hour. • Child in left lateral position with head end low. Use large orogastric tube with multiple holes at distal end and funnel at promixal end NS 15ml/kg(max 200-400)/per cycle till affluent is clear
  16. 16. 7We Care • In comatosed pts it should be done after intubation with cuffed ET tube. • Contraindications: corrosive ingestions like washing soda, detergents, alkalis and acids.
  17. 17. 7We Care ACTIVATED CHARCOL • Made by pyrolysis of organic matter like wood pulp activated by an oxidizing process. • Used in all cases except in iron , cyanide and when orally adminstered antidotes are used. • Dose 01 gm/kg/dose mixed in sufficient amount of water to make slurry. • Contraindicated in paralytic ilius, intestinal perforation and orally adminstered antidotes.
  18. 18. 7We Care Whole bowel irrigation • Recent addition to emergency treatment of poisninmg • Removes unabsorbed drug from entire gut and possibly absorbed one from gut mucosa • Contraindicated in intestinal obstruction, perforation or hemorrhage.
  19. 19. 7We Care • Isotonic balanced salt solution containing propylene glycol at 30 ml/kg/hr in childern by NG tube or orally. • Continued till effluent fluid from rectum is clear. • Indications are poor binding of toxin to activated charcol, massive ingestion,late presentation,sustained release formulations. • Useful in iron poisning and sustained release/enteric coated formulations.
  20. 20. 7We Care Enhancing excreation • Diuresis • Dialysis • Hemoperfusion diuresis : osmotic agents like 20% mannitol in initial doses of 0.5gm/kg and then repeated to ensure a UO of 6-9 ml/kg/hr. useful when poisning sgent is excreted primarily through renal route.
  21. 21. 7We Care • Alkaliztion or acidification of urine enhances excretion of toxin and enhances the efficacy of diuretics. • Alkaliztion is achieved with soduim bicorbonte 1-2 meq/kg infusion over 1-2 hrs. useful in salicylates and barbiturates.
  22. 22. 7We Care • Acidification is done with ammonium chloride in a dose of 75mg/kg/dose to keep urine PH 5 or less. • Useful in week bases like amphetamine,strychnine ,quinine.
  23. 23. 7We Care Dialysis • particularly useful if electrolyte or acid base abnormalities exist. • Indications : 1 anticipated prolonged coma and liklyhood of complications. 2.renal failure 3. Progressive clinical deterioration 4. Plasma levels of toxin in potentially fatal range.
  24. 24. 7We Care Hemodialysis is useful in poisning with • Salicylates • Acetaminophen • Chloroquine • Propranolol • Vancomycin • Snake bite
  25. 25. 7We Care Hemoperfusion and hemofilteration • hemoperfusion is useful in toxins with low water solubility and with high affinity for the absorbant like carbmazepine,barbiturates and theophylline • Hemofilteration in toxins with high molecular wt used in poisning with aminoglycosides,theophyline iron and lithium
  26. 26. 7We Care in Children
  27. 27. 7We Care Acetaminophen Acetaminophen is the most widely used analgesic- antipyretic medication taken by people in the world.
  28. 28. 7We Care
  29. 29. 7We Care Acetaminophen toxicity is one of the most common etiology of hepatic failure requiring liver transplantation
  30. 30. 7We Care Clinical patients with acetaminophen induced hepatotoxicity present in 4 clinical stages :
  31. 31. 7We Care Stage I 0-24 hrs Nausea, vomiting, malaise and diaphoresis with cold skin
  32. 32. 7We Care Stage 2 (24-48 h ) • The clinical evidence of hepatic dysfunction supervenes. • jaundice,pain and tenderness in the right upper quadrant can be present. Some patients may report oliguria. • Serum studies reveal elevated ALT and AST levels, PT, and bilirubin values. • RF may also be present and indicate nephrotoxicity
  33. 33. 7We Care Stage 3 (48-96 h) • the symptoms of stage 1 reappear and hepatic coma supervenes with gross evidence of hepatic dysfunction • Severe toxicity is evident on laboratory studies. Lactic acidosis, prolonged PT or (INR), markedly elevated ALT and AST (>10,000 IU/L ) • Death is most common during stage 3, with multiorgan failure as the primary cause
  34. 34. 7We Care • Stage 4 (4-14 d) • This stage can last as long as 21 days. • Patients either have a complete recovery or they die. • the period to normalization may take several weeks. • DOES NOT cause chronic hepatic dysfunction
  35. 35. 7We Care Physical exam • Stage 1 : non specific (Pallor, diaphoresis, & dehydration ) • Stage 2 : RUQ Tenderness, tachycardia & hypotension • Stage 3 : hepatic injury (abdominal pain, jaundice, and GI bleeding ) Encephalopathy and cerebral edema& MOF • Stage 4 : resolve or death occurs.
  36. 36. 7We Care Remember the Dose >150mg/kg or >10gm in adults can lead to serious toxicity. normal dose: 350-650mg every 4-6hrs for adults 10-15mg/Kg every 4-6 hrs for childern
  37. 37. 7We Care Workup • Measurement of acetaminophen serum concentration. • Levels >200micgm/ml at 4hrs, >100micgm/ml at 8 hrs and >50micgm/ml at 16 hrs and hepatic transaminases >1000u/ml associated with serious hepatic damage. • Any serum sample drawn 4 hours or longer after a single ingestion may be plotted on (Rumack- Matthew nomogram) to estimate the risk of hepatotoxicity • Measurement of hepatic (ALT) and (AST). • Others
  38. 38. 7We Care
  39. 39. 7We Care Treatment 1)Consider decontamination with activated charcoal in any patient who presents within 4 hours of ingestion. Consider gastric lavage if ingestion occurred within 1 hour of evaluation 2)Supportive treatment: correction of hypoglycemia maintenece of hydration electrolyte balance treatment of coagulopathy
  40. 40. 7We Care N-acetylcysteine NAC:acts by enhancing glutathione stores and Anhancing nontoxic sulfate conjugation in the liver. oral NAC is as effective as IV 150mg/kg iv over 15 min followed by same dose over next 20 hrs. 75mg/kg orally every 4-6 hrs for 2-3 days. SE : flushing, pruritus, and a rash (15%) Bronchospasm and hypotension (<2% of
  41. 41. 7We Care Poor prognostic factors • PH < 7.3 • PT > 100 sec • Grade III or more of hepatic encephalopathy • Raised serum bilirubin > 04 mg/dl • SGOT > 1000 IU/L • Factor VIII : Factor V > 30 (indicates the worst outcome)
  42. 42. 7We Care THANKS
  43. 43. 7We CareIron • The most common cause of death in toddlers. • Classically taught as having five clinical stages.
  44. 44. 7We Care Iron • Toxic doses occur at 10-20mg/Kg of elemental iron. • Prenatal vitamins typically contain about 65 mg of elemental iron. • Children's vitamins contain about 10-18 mg of elemental iron.
  45. 45. 7We Care The Five Stages : • Stage 1 ( first 6 hrs ) – Nausea, vomiting, abdominal pain and diarrhea. • Stage 2 ( 6- 12 hrs ) – This is the latent phase often between 4-12hours as the patient resolves GI symptoms • Stage 3 ( 12 - 24 hrs ) – Shock stage involving multiple organs including coagulopathy, poor cardiac output, Hypovolemia, lethargy and seizures.
  46. 46. 7We Care • Stage 4 (2-3 days) – Continuing of hepatic failure and ongoing oxidative damage by the iron in the reticuloendothelial system • Stage 5 ( 2 -6 weeks ) – Gastric outlet obstruction secondary to scarring & Liver Cirrhosis
  47. 47. 7We Care Differential Diagnoses • Metabolic Acidosis Other Problems to Be Considered Gastroenteritis Hepatic failure
  48. 48. 7We Care Workup Laboratory Studies• It is a clinical diagnosis • Little is known about the absorption rate of iron in an overdose or the timing of peak serum iron level • Serum levels Of iron : Mild - Less than 300 µg/dL Moderate - 300-500 µg/dL Severe - More than 500 µg/dL • TIBC has no utility in the acute overdose setting.
  49. 49. 7We Care Management • Detailed history and physical including a rectal exam for frank blood. • Aggressive fluid resuscitation and intravenous access. • Whole bowel irrigation and KUB to Look for pills. • Laboratory analysis for CBC, chemistry, and iron levels (peak around 4 hours) Will often require repeat levels with
  50. 50. 7We Care Indications for Deferoxamine treatment - shock, altered mental status, persistent GI symptoms, metabolic acidosis, pills visible on radiographs, serum iron level greater than 500 µg/dL, or estimated dose greater than 60 mg/kg of elemental iron - if a serum iron level is not available and symptoms are present
  51. 51. 7We Care • If the patient is in shock, remember to at least type and screen (if not cross match) for blood. • Deferoxamine was derived from streptomyces pilosus. • Ferrioxamin :This complex imparts a reddish, vin rosé, color to the urine • Hypotension and allergic reactions are seen. • ARDS is a known complication and usually limit its use to 24 hours or less.
  52. 52. 7We Care Complications • Infectious -Yersinia enterocolitica septicemia • Pulmonary - Acute respiratory distress syndrome (ARDS) • Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis
  53. 53. 7We Care Thanks
  54. 54. 7We Care
  55. 55. 7We Care
  56. 56. 7We CareSalicylates • One teaspoon of 98% methyl salicylate contains 7000 mg of salicylate, the equivalent of nearly 90 baby aspirin and more than 4 times the potentially toxic dose for a child who weighs 10 kg ! • consider salicylate poisoning when topical herbal medicinal oil is involved
  57. 57. 7We Care Pathophysiology  acetylsalicylic acid is rapidly converted to salicylic acid, its active moiety  salicylic acid is metabolized by the liver and eliminated in 2-3 hours  Salicylate poisoning is manifested clinically by disturbances of several organ systems  Salicylates directly or indirectly affect most organ systems in the body by uncoupling oxidative phosphorylation, inhibiting Krebs cycle enzymes, and inhibiting amino acid synthesis but lipid metabolism is stimulated
  58. 58. 7We Care • GI tract & Hepatic effects : Nausea and vomiting. Hepatitis at or above 30.9 mg/d & Rey syndrome • CNS effects : tinnitus, hearing loss at serum levels of 30-45 mg/dl, seizures, cerebral edema, hyperthermia, coma, cardiorespiratory depression • Acid-base status :normal anion-gap acidosis does not exclude salicylate. • Respiratory system effects 35 mg/dL • Glucose metabolism • Fluid and electrolyte effects : 5-10
  59. 59. 7We Care • Reye syndrome is characterized by acute noninflammatory encephalopathy and hepatic failure of unknown etiology , typically occurs after a viral illness, partic. an (URTI), influenza, Varicella or GE & it is associated with the use of aspirin during the illness . • Diagnostic criteria from the (CDC) : 1) Acute noninflammatory encephalopathy with an altered level of consciousness 2) Hepatic dysfunction with a liver biopsy showing fatty metamorphosis or a more than 3-fold increase in (ALT), (AST),
  60. 60. 7We Care Clinical and laboratory manifestations • Phase 1 : hyperventilation respiratory alkalosis and compensatory alkaluria. Both K & NaHCO3 are excreted in the urine. may last as long as 12 hours • phase 2 : paradoxic aciduria occurs when sufficient potassium has been lost from the kidneys. may begin within hours & may last 12-24 hours • Phase 3 : includes dehydration, hypokalemia, and progressive metabolic acidosis. This phase may begin 4-6 hours after ingestion in a young infant or 24 hours or more after ingestion in an adolescent or adult.
  61. 61. 7We Care History • When possible take : – Type of salicylate – Amount – Approximate time of ingestion – Possibility of long-term ingestion – Potential co-ingestants – Presence of other medical conditions (eg, cardiac, renal diseases) • The presence of tinnitus is a clue for salicylate ingestion. Tachypnea, tachycardia, and elevated temperature can be detected by evaluating vital sign
  62. 62. 7We Care Differential Diagnoses • DKA • SEPSIS • Meningitis • Encephalitis • Other TOx
  63. 63. 7We Care Workup Laboratory Studies • Bedside ferric chloride testing (No longer) • ABG: the most common abnormality is a mixed acid-base disturbance • Salicylate concentration: Therapeutic range of salicylate is 15-30 mg/Dl • the peak serum concentration may not occur for 4-6 hours . A 6-hour salicylate level higher than 100 mg/dL is considered potentially lethal and is an indication for hemodialysis • the Done nomogram is regarded as not very
  64. 64. 7We Care potential severity and morbidity of an acute, single event, nonenteric-coated, salicylate ingestion: • less than 150 mg/kg - ranges from no toxicity to mild toxicity • From 150-300 mg/kg - Mild-to-moderate toxicity • From 301-500 mg/kg - Serious toxicity • Greater than 500 mg/kg - Potentially lethal toxicity
  65. 65. 7We Care Treatment • Gastric lavage and activated charcoal are useful for acute ingestions but not in chronic salicylism. • ABCs & lactated Ringer or isotonic Na Cl solution for volume expansion at 10-20 cc/kg/h until a 1-1.5-cc/kg/h urine flow is established • GI tract decontamination :initial dose of activated charcoal is 1 g/kg of body weight to a maximum of 50 g in children and 1-2 g/kg to a maximum of 100 g in adults . If enteric-coated aspirin has been ingested or
  66. 66. 7We Care Hemodialysis Indications : 1. serum level greater than 120 mg/dL (acutely) or greater than 100 mg/dL (6 h postingestion) 2. refractory acidosis, 3. coma or seizures, 4. noncardiogenic pulmonary edema, 5. volume overload 6. renal failure. • In chronic overdose, for a symptomatic patient with a serum salicylate level greater than 60 mg/dL. • Peritoneal dialysis is only 10-25% as efficient as
  67. 67. 7We Care