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

10. APPROACH

11. PREVENTION

12. 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.

14. CLINICAL PRESENTATION

15. 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)

16. 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.

17. 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?

19. 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.

20. CLINICAL PRESENTATION

21. 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.

22. 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.

23. • 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

24. 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.

26. 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.

28. 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.

29. • 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.

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

31. 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

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

33. 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.

34. 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.

36. 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).

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

38. 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

39. 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.

41. 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.

43. 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).

45. 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.

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

47. 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

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