Pediatrics drug poisoning

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a lecture about Most common Pediatrics drugs poisoning.. Including Iron , acetaminophen & salicylates .

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Pediatrics drug poisoning

  1. 1. PEDIATRIC POISONINGS Dina F. El Wahaidi Supervised by: Dr. Mostafa El KahLout .
  2. 2. POISONING IN CHILDREN  Definition of Poisoning: Exposure to a chemical or other agent that adversely affects functioning of an organism.  Circumstances of Exposure can be intentional, accidental, environmental, medicinal or recreational.  Routes of exposure can be ingestion, injection, inhalation or cutaneous exposure. “All substances are poisons...the right dose separates poison from a remedy.” Parcelsus
  3. 3. EPIDEMIOLOGY  US Poison Centers receive 1.5 million calls a year regarding pediatric ingestions.  79% of these calls involve children younger than age six.  56% of pediatric exposures are from products around the house including medicines, cleaning agents, pesticides, plants and cosmetics.
  4. 4. EPIDEMIOLOGY 99% 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. EPIDEMIOLOGY
  6. 6. Major four toxidromes are: Anticholinergic Sympathomimetic Opiates/Sedatives- Hypnotics/ Alcohol Cholinergic
  7. 7. 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?  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?
  8. 8. 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
  9. 9.  Decontamination: 1. Ocular: – Flush eyes with saline 1. Dermal: – Remove contaminated clothing – Brush off – Irrigate skin 1. Gastro-intestinal: – Activated charcoal:  May Prevent /delay absorption of some drugs/toxins  Almost always indicated Only in the 1st hour !!!! – Naso/oro-gastric Lavage – Bowel Irrigation:  Recent ingestions  Awake alert patient  500 cc NS Children / 2000cc adults  Orally / Nasogastric tube  Contraindications…? ABC’S OF TOXICOLOGY:
  10. 10. in Children
  11. 11. IRON The most common cause of death in toddlers. Classically taught as having five clinical stages.
  12. 12. 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.
  13. 13. 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.  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 .
  14. 14. DIFFERENTIAL DIAGNOSES Metabolic Acidosis Other Problems to Be Considered Gastroenteritis Hepatic failure
  15. 15. 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 : 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.
  16. 16. 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 a repeat chemistry
  17. 17. 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
  18. 18. 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.
  19. 19. COMPLICATIONS Infectious -Yersinia enterocolitica septicemia Pulmonary - Acute respiratory distress syndrome (ARDS) Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis
  20. 20. ACETAMINOPH EN Acetaminophen is the most widely used analgesic- antipyretic medication taken by people in the United States and the world. or paracetamol, is also known by its chemical name, N -acetyl-p -aminophenol (APAP)
  21. 21. In Great Britain, acetaminophen toxicity is cited as the most common etiology of hepatic failure requiring liver transplantation
  22. 22. CLINICAL History : Patients with acetaminophen- induced hepatotoxicity present in 4 clinical stages :
  23. 23. Stage I 0-24 hrs Early symptoms Mild Neurologic, respiratory, and cardiac symptoms are rare in stage 1. If CNS involvement and/or severe metabolic acidosis (elevated anion gap) are present, consider co-ingestants Nausea, vomiting, malaise and diaphoresis. Normal bilirubin Transaminases and PT but may elevate after 12 hrs Post Ingestion
  24. 24. Stage 2 (24-72 h )  Stage 1 symptoms become less evident or resolve.  pain and tenderness in the right upper quadrant. (hepatomegaly) 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
  25. 25. Stage 3 (72-120 h)  Stage 3 develops 3-5 days after ingestion  Severe toxicity is evident on sera 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
  26. 26. Stage 4 (5-14 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. Hepatic histiologic can take as long as 3 months to resolve.  DOES NOT cause chronic hepatic dysfunction
  27. 27. 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.
  28. 28. Remember the Dose Aceta = 4 gday for adults = 80mgKgday for # Aceta =352-650mg every 4-6hrs for adults =10-15mgKg every 4-6 hrs for # For # Not more than 5 doses Not more than 2.6g Per Day # = Children < 12 Years Or < 50 Kg
  29. 29. DIFFERENTIAL DIAGNOSIS Pancreatitis Gastroenteritis Peptic ulcer Infections CMV Infection Hepatitis A , B Or C EBV or Varicella Amatoxin Wilson dis. Reye syndrome
  30. 30. WORKUP Measurement of acetaminophen serum concentration 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) hepatic injury is defined by elevation of the plasma transaminases more than 1000 IU/L  Others
  31. 31. TREATMENT  Medical Care 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) Oral N-acetylcysteine (Mucomys) 3) Intravenous (IV) NAC (Acetadote) INDICATIONs : altered mental status, GI bleeding and/or obstruction or a history of caustic ingestion, potential fetal toxicity from maternal toxicity, or an inability to tolerate oral SE : flushing, pruritus, and a rash (15%) Bronchospasm and hypotension (<2% of patients)
  32. 32. Probable toxicity should be treated with: N-acetylcysteine bolus 140 mg/kg Then 70 mg/kg Q 4 hrs for 17 doses. Assess hepatic function: On presentation  Daily Continue other support
  33. 33. SALICYLATES 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
  34. 34. 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
  35. 35.  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 %dehydration, Hypokalemia and hypocalcemia ( due to Resp. Alka. )  Hematologic effects Hypoprothrombinemia and platelet dysfunction  Musculoskeletal effects Rhabdomyolysis
  36. 36. 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), and/or ammonia levels 3) No other explanation for cerebral edema or hepatic abnormality 4) CSF with WBCs (usually lymphocytes) (8 X 109 /L or fewer) 5) Brain biopsy with cerebral edema without inflammation
  37. 37. 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.
  38. 38. 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
  39. 39. DIFFERENTIAL DIAGNOSES DKA SEPSIS Meningitis Encephalitis Other TOx
  40. 40. 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 useful and is seldom used by clinicians  Others . Repeat every 2 hrs till stabilization !
  41. 41. 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
  42. 42. 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 salicylate levels do not decrease despite charcoal, WBI should probably be used in addition to charcoal Urinary alkalization the U pH to 7.5-8 .Ion trapping : ions are poorly reabsorbed in the tubules and are excreted more readily. Correct hypokalemia and dehydration
  43. 43. 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

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