PEDIATRIC POISONING IN CHILDREN(part 01).pptx

Poisoning is a really concern to our society and hence a health practitioner must have the need to understand and have the knowledge of what poisoning, what are it's causes, it's effects and how should he/she approach a poisoned patient. This slides provides the definition/causes/approach to poisoning.

1. PEDIATRIC POISONING(PART 01) NAWA .M.S

2. OUTLINE DEFINITION CAUSES HISTORY EXAMINATION APPROACH PREVENTION PARACETAMOL IRON CHOLINESTERASE INHIBITING INSECTSIDES IBUPROFEN AND OTHER NSAIDS HYDROCARBON

3. DEFINITION Is inhalation or ingestion or injection and absorption of a toxic substance that can cause signs and symptoms of organ dysfunction leading to injury or death.

4. CAUSES 1 .) ACCIDENTAL- common in young children,occurs when parents or carers find their young children playing with tablets or households or garden substances or with some in their mouths. 2.) DELIBERATE/EXPERIMENTATION - with recreational substances by adoloscents and young people. 3.) IATROGENIC - as a result of drug errors occassionally made by health professions. 4.) INTENTIONAL -suicide attempts, drug abuse/misuse, by parents or carerers.

5. HISTORY WHAT TO ASK? 1.)DESCRIPTION OF TOXIN- should include product name, ingredient and concentration(which can be deduced from the lable), also deduce the toxin from child’s characteristic presentation. 2.) MAGNITUDE OF EXPOSURE- includes counting the tablet, measure the remaining volume and assume the worst case scenario. 3.) TIMING OF EXPOSURE- helps in decision making 4.) PROGRESSION OF SYMPTOMS- helps to determine intervention, prognosis and need for immediate life support.

6. EXAMINATION POSSIBLE SIGNS ON EXAMINATION

7. APPROACH

8. PREVENTION

9. ACETAMINOPHEN(PARACETAMOL) BACKGROUND most widely used antipyretic and analgesic in pediatrics. it is an important cause of acute liver failure in adoloscents. leading cause of intentional poisoning death. PATHOPHYSIOLOGY minimum toxic dose of Acetaminophen, posing significant risk of severe hepatotoxicity, are as follows: ADULTS and ADOLOSCENTS: 7.5-10g CHILDREN: 150mg/kg;200mg/kg in healthy children aged 1-6 years.

10. CLINICAL PRESENTATION

11. DIAGNOSIS SERUM STUDIES liver function tests-alanine aminotransferase(ALT), aspartate aminotransferase(AST), bilirubin,alkaline phosphotase. prothrombin time(PT) with INR glucose kidney function tests-electrolytres, BUN, creatinine lipase and amylase- patients presenting with abdominal pain human chorionic gonadotropin(HCG)- child bearing female salicylate levels- concern of co-ingestants arterial blood gas and ammonia- in clinically compromised patients urinalysis- to check for hematuria and proteinuria ECG-to detect additional clues for co-ingestants(not a serum study)

12. THE RUMACK-MATTHEW NOMOGRAM interprets the acetaminophen concentration(in nanograms per mililiter), in relation to time(in hours) after ingestion, and predicts possible hepatototxicity after single, acute ingestions of acetaminophen.

13. CASE 1: 14 YEAR OLD GIRL WITH VOMITING AND ABDOMINAL PAIN Jemima, a 14 year old girl, was brought to the emergency department in the morning by her mother as she has been vomiting and complains of severe abdominal pain. on examination she has a generally tender abdomen. blood tests reveals an extremely high alanine transminase concentration well above normal for her age. her clotting is so deranged with a prothrombin time of 17 seconds. 1.) what are your differential diagnoses? An initial diagnosis of hepatitis is made but on discussion with the consultant the lack of jaundice is considered atypical. 2.) what further questions would you ask jemima inorder to reach to your definitive diagnosis? on further questioning, jemima admits to have taken 22 tablets of a certain drug,the previous afternoon following an altercation with her boyfriend at school. 3.) what drug do you think jemima took and what is the toxic doseof the drug? 4.) what is the antidote of the drug mentioned in the scenario?

14. IRON POISONING BACKGROUND was a common cause of childhood poisoning deaths. the severity of an exposure is related to the amount of elemental iron ingested.ferrous sulpahate contains 20% elemental iron, ferrous gluconate 12%, ferrous fumarate 33%, ferrous chloride 28% and ferrous lactate 19%. note: iron tablets are particularly tempting to young children because they look like candy. PATHOPHYSIOLOGY TOXIC DOSE: >50mg/kg;> 60mg/kg but note= children may show signs of toxicity with ingestions of 10-20 mg/kg of elemental iron. Iron is corrosive to the GI mucosa, leading to hematemesis, melena, ulceration, infarction and potential perforation. causes mitcochindrial dysfunction(leads to cellular death), venodilation and increased capillary permeability.

15. CLINICAL PRESENTATION

16. DIAGNOSIS SERUM STUDIES serum iron levels should be measured 4-6hours after ingestion: <500mcg/dl, 4-8hours after ingestion has low risk of significant toxicity and >500mcg/dl indicates significant toxicity. full blood count= wbc > 15000/microliter arterial blood gas analysis serum glucose(>150mg/dl or > 8.3 mmol/l) liver function test coagulation profile IMAGING STUDIES abdominal x-ray= may show the pill, liquid preparations and chewable vitamins are not visible on radiographs. OTHER TESTS: deferoxamine challenge test= administer a single dose of deferoxamine, positive when urineis redish, indicating need for chelation. though not reliable test.

17. CASE 2: 10 KG CHILD WHO CONSUMED 10 TABLETS OF FERROUS GLUCONATE WITH ANSWER. a 5 year old male child is brought to the emergency department by her mother as he was vomiting and complained of severe abdominal pain. mother says child must have taken 10 tablets of the 20 remaining iron tablets in the container which was found lying down on the floor open. the mother then hands you the container which shows the following? FERROUS GLUCONATE: 320 mg(12% ELEMENTAL IRON PER TABLET). 1.) according to the mother(child took 10 tablets), calculate the amount of iron ingested by the child? answer: step 1: number of elemental iron per tablet= 320mg(ferrous gluconate) × 0.12(12%=12/100) elemental iron per tablet= 38.4 mg elemental per tablet. step 2: amount of iron ingested=(number of elemental iron per tablets ×number of tablets)/ childs weight= (38.4 mg × 10)/10kg=384mg/10kg= 38.4mg/kg .

18. what are the posible differential diagnoses of iron poisoning? answer: metabolic acidosis pediatric food poisoning pediatric gastroenteritis note: differentials for children with an unexplained anion gap metabolic acidosis remember MUDPILES . M= methanol U=uremia D=diabetic ketoacidosis P=paraaldehyde I=iron L=lactic acidosis E=ethylene glycol S=salicylates

19. CHOLINESTERASE INHIBITING INSECTICIDES BACKGROUND organophosphates and carbamates are the frequently used insecticides andboth are inhibitors of cholinesterase enzymes(acetyl cholinesterase, pseudocholinesterase and erythrocyte ACHE). occur as a result of unintentional exposure to insecticides in or around the homes or farms. organophosphates: malathion,monocrotophos, parathion, tertraethyl pyrophosphate(TEPP),mevinphos, dimethoate. carbamates: aldicarb, carbaryi(UMET and Sevin), propoxur, oxamyl,methomyl(Lannate) and tebucarb.

20. PATHOPHYSIOLOGY organophosphates and carbamates produce toxicity by binding and ihnibiting acetyl cholinesterase enzyme preventing the degradation of acetyl choline and resulting in accumulation at nerve synapses. if left untreated,organophosphates form an irrevesible bond, permanently inactivating the enzyme(process called aging ). this inactivation which allows accumulation of acetyl choline leads to overstimulation and disruption of nerve impulses. carbamates, form a temporal bond with the enzyme, allowing reactivation of ACHE within 24hrs.

21. CLINICAL PRESENTATION symptoms of carbamate are less severe than those seen in organophosphates. SYMPTOMS OF ORGANOPHOSPHATE POISONING are divided into: 1.)MUSCARINIC FINDINGS: DUMBBELS D= diarrhoea, diaphoresis B=bronchorrhea U=urination E=emesis M=miosis L=lacrimation B=bradycardia S=salivation OTHERS: wheezing, pulmonary oedema, sweating, abdominal cramping.

22. 2.) NICOTINIC FINDINGS: muscle fasciculations(twitching) tremors fatigue paralysis respiratory muscle weakness(hypoventilation due to diaphragm weakness) diminished respiratory effort tachycardia hypertension, dysrhythmias 3.) CNS FINDINGS: anxiety restlessness confusion headache, altered level of consciousness/hypotonia slurred speech ataxia seizures coma central respiratory paralysis NOTE: young children are more likely to present with altered consciousness than with the calssic DUMBBELS signs that are most commonly observed in adults.

23. SYMPTOMS OF CARBAMATES:SLUDGE S=salivation L=lacrimation U=urination D=defecation G=gi distress E=emesis

24. DIAGNOSIS LABS full blood count- to rule out infectious causes Electrolytes- to rule out electrolyte imbalance Red blood cell cholinesterase tests( confirmatory )- reveals decreased activity. IMAGING chest radiography- to rule out pulmonary oedema nonenhanced head CT scan- to rule out structural lesions(if altered mental status is present). OTHERS ECG-to evaluate cardiac arrhythmias

25. DIFFERENTIAL DIAGNOSIS phosgene toxicity paraquat toxicity lead/mercury/household cleaners. meningitis encephalitis nerve agents(sarin, tabun, soman) poisoning

26. IBUPROFEN AND OTHER NONSTEROIDAL ANTI-INFLAMMATORY DRUGS(NSAIDS) BACKGROUND are prostaglandin synthesis inhibitors. often involved in unintentional and intentional overdose because of their widespread availability. commonly used as antipyretics and analgesics. have a wide therapeutic index, hence serious effects after an acute overdose is rare.

27. PATHOPHYSIOLOGY ibuprofen,the primary NSAID used in paediatrics, is well tolerated, even in overdose. NOTE: acute doses of <200mg/kg= rarely cause toxicity, but >400mg/kg= more serious effects including, altered mental status, seizures and coma, metabolic acidosis. reversibly inhibits the cyclooxygenase enzyme, which is primarily responsible for prostaglandin synthesis. side effcts =GI irritation, reduced renal blood flow and platelet dysfunction.

28. CLINICAL PRESENTATION symptoms usually develop within 4-6hours and resolve within 24hours. MANIFESTATIONS, IF TOXICITY OCCURS: nausea vomiting abdominal pain gi beeding and ulcers, with chronic use. cns depression, anion gap metabolic acidosis,renal insufficiency and respiratory depression(rare), with massive ingestion. seizures, with overdose of mefanemic acid. occassionally, anaphylactoid reaction(in of pruritus,circulatory collapse and angioedema).

29. DIAGNOSIS SERUM STUDIES full blood count arterial blood gas analysis renal function tests acetaminophen serum levels- in case co-ingestants

30. DIFFERENTIAL DIAGNOSIS encephalitis stevens-johnson syndrome toxic epidermal necrolysis(TEN) peptic ulcer disease co-ingestion with acetaminophen and salicylate electrolyte abnormalities-hyperkalemia, hypophosphotemia, hypocalcemia, hypernatremia. acute kidney injury

31. HYDROCARBON POISONING BACKGROUND organic compounds that only contain hydrogen and carbon. aspiration of even small amounts of certain hydrocarbons can lead to serious, potentially life threatening toxicity. they include mineral spirits, kerosene, lamp oil,turpentine, gasoline.

32. PATHOPHYSIOLOGY Inactivate type 2(II) pneumocytes, which results in sufactant deficiency. important manifestation is aspiration pneumonitis. only small quantities (<1ml) of such chemicals need to be aspirated to produce significant injury.

33. CLINICAL PRESENTATION transient, cns depression apiration characterized by cough= usually is the 1st early clinical finding chest xray abnormalities after 6hours post aspiration pneumatoceles can develop 2-3 weeks post aspiration respiratory symptoms can remain mild or progress to acute respiratory distress syndrome and respiratory failure. fever leukocytosis dysrhythmias and sudden death ( after inhalational exposure to halogented hydrocarbons). type IV acute renal tubular necrosis ( with recurrent inhalation of aromatic hydrocarbon toluene). acute myelogenous leukemia/aplastic anemia (chronic benzene exposure).

34. DIAGNOSIS VITALS pulse oximetry- to evaluate oxygenation. SERUM STUDIES full blood count- check for anemia and leukocytosis. blood urea nitrogen(BUN) and serum creatinine. glucose arterial blood gas analysis. electrolyte levels serum creatinine kinase level- to assess for rhabdomyolysis IMAGING chest xray- symptomatic patients OTHERS ECG- to assess for dysrhythmias.

35. DIFFERENTIAL DIAGNOSIS inhalational injury acute respiratory distress syndrome carbonmonoxide poisoning alcohol toxicity barbituarate toxicity benzodiazepene toxicity toluene toxicity aspiration

36. REFERENCES NELSONS TEXTBOOK OF PEDIATRICS(20TH EDITION).POISONING POISONING IN CHILDREN BY DR CHANDA KAPOMA PEDIATRIC BOARD STUDY GUIDE A LAST MINUTE REVIEW BY OSAMA NAGA. ILLUSTRATED TEXTBOOK OF PEDIATRICS(5TH EDITION). ACCIDENTS AND POISONING EMEDICINE.MEDSCAPE.COM

37. THANK YOU THANK TOU THANK YOU NEXT SLIDE: PEDIATRIC POISONING(PART 02): MANAGEMENT.