this PowerPoint discusses all details of poisoning on a specific topic like organophosphate, hydrocarbons, salicylate, carbon monoxide...atc

1. Seminaron
AcutePoisoning

2. CONTENTS
Approachto ThePoisoned
Patient
Objectives
Introduction
Selected compoundscommonly
involvedinpediatricsPoisoning

3. Objectives
- Understand what poison is
- How to approach a child
withacute poisoning
- know common poisons with
their clinical manifestation
and managements.

4. INTRODUCTION
Poisons are substances that cause disturbances to organisms, usually by
chemical reaction or other activity on the molecular scale, when a sufficient
quantity is absorbed by an organism.
Poisoning in children may be:
• accidental– commonin young
children (peak upto 30 months)
• due to deliberate self-harm or
experimentation with recreational
substances – by adolescents
(>12yrs)and youngpeople
• Iatrogenic – as a result of drug
errors occasionally made by health
professionals
• Intentional – by parents or carers,
thoughthis is rare.

5. - Poisoning is the number 1 cause of injury
death in the United States
Routes
• Ingestion accounts for the vast majority of
exposures, with a minority occurring via the
dermal, inhalational, and ophthalmic routes.
• In 2012, carbon monoxide and analgesics
(acetaminophen and salicylate) were the
leading causes of poison-related fatalities in
youngchildren.
• Inour country,Organophosphatepoisoning
and Poisoning from household cleaning
agentsare the most common.
INTRODUCTION

6. APPROACHTOTHEPOISONED
PATIENT
1INITIALEVALUATION
Stabilizing the patient and
identifying thecause.
2 MANAGEMENTPRINCIPLES
BasicManagmentstepsincluding
Antidotes, Decontamination and
increasedexceretion
3 SUPPORTIVECARE
IncludingABC’s of life

7. HISTORY
Description of toxic agent-Product names and ingredients
along with their concentrations
Amountingested
Time androute ofexposure
Progression of symptoms
Past Medical History
SocialHistory

8. PHYSICAL
EXAMINATION
MENTALSTATUS
SKIN
Pupils(size,reactivity)
nystagmus,
THEVITALSIGNS
BOWELSOUNDS
Odors

9. TOXIDROMES
Sympathomimetic
VITAL SIGN
Hypertension,
tachycardia,
hyperthermia
MENTALSTATUS
Agitation,psychosis,
delirium, violence
PUPILS
Dilated
SKIN
Diaphoretic
BOWEL SOUNDS
Normal to
increased
Anticholinergic
VITAL SIGN
Hypertension,
tachycardia,
hyperthermia
MENTALSTATUS
Agitated, delirium,
coma, seizures
PUPILS
Dilated
SKIN
Dry, hot
BOWEL SOUNDS
Diminished
* Ileus urinary
retention
Opioids
VITALSIGN
Respiratory depression
bradycardia,
hypotension,
hypothermia
MENTAL STATUS
Depression, coma,
euphoria
PUPILS
Pinpoint
SKIN
Normal
BOWEL SOUNDS
Hyperactive
POSSIBLE TOXINS
Amphetamines,
cocaine,PCP, bath
salts (cathinones),
ADHD medication
POSSIBLE TOXINS
Antihistamines, tricyclic
antidepressants,
atropine, jimson
weed
Cholinergic
VITAL SIGN
Bradycardia BPand
temp typically
normal
MENTALSTATUS
Confusion,coma,
fasciculations
PUPILS
Small
SKIN
Diaphoretic
BOWEL SOUNDS
Hyperactive
*Diarrhea, urination,
bronchospasm,
emesis, lacrimation,
salivation
POSSIBLE TOXINS
Organophosphates,
carbamates
POSSIBLE TOXINS
Methadone, morphine,
oxycodone, heroin,etc.

10. All intoxicantlevels mustbeinterpretedin
conjunction with thehistory.
- Specific bloodconcentrationsonly helpful for few
drugs like paracetamol,iron,salicylates,andalcohol
-Generalbloodtests(e.g.full bloodcount,renaland
liverfunction) dependent on mechanism and
likelihood oftoxicity
-Specific Investigations like ECG fordrugswith
cardiovasculartoxicity,Chestx-rayforPneumonitis,
Abdominalx-rayforthepresenceofleadpaintchips
orotherforeignbodies.
-Urine toxicologyscreen nothelpfulintheacute
situationbutmayhelpto confirmdiagnosis
INVESTIGATOINS

11. Theprinciplesof managementofthepoisoned
patientare
- Supportivecare
- Antidotes(for those which have antidotes)
- Decontaminationand
- Enhancedelimination
MANAGEMENT

12. • Careful attention is paid first to the “ABCs” of airway,
breathing andcirculation
• there should be a low threshold to aggressively manage the
airway of a poisoned patient. For example
• Endotracheal intubation  For neuroleptics
• If hypotensionpersists after 1 or 2 standard boluses of
crystalloid,  direct-acting vasopressor
(norepinephrine or epinephrine)
• Treating Seizure
• Treating Dysrhythmia
SUPPORTIVECARE

13. COMMON
ANTIDOTES
Acetaminophen N-Acetylcysteine(Mucomyst),
N-Acetylcysteine(Acetadote)
Anticholinergics Physostigmine
Carbonmonoxide Oxygen
Iron Deferoxamine
Opioids Naloxone
Organophosphates Atropine, Pralidoxime(2-PAM)
Salicylates Sodiumbicarbonate
Tricyclic antidepressants Sodiumbicarbonate

14. • The goal of decontamination is to minimizeabsorption of the
toxic substance. But, it should not be routinely employedfor
everypoisonedpatient.
• ForDermalandOcular– Removalofanycontaminated
matterandWashing.
• Forinhalational- movingthepatienttofreshairand
administeringsupplementaloxygenifindicated.
• GIdecontaminationstrategiesaremostlikelytobe
effectiveinthe1sthourafteranacuteingestion.
• GIdecontaminationafter1hrmaybeindicatedif
• agents slow GI motility (anticholinergic, opioid)
• massive pillingestions
• sustained-release
• preparations ingestions of agents that can form
pharmacologic bezoars (e.g., enteric-coated
salicylates)
DECONTAMINATION

15. • Improvesclearance of a poison that has already been
absorbed.
• Urinary Alkalinization
• Hemodialysis
• Multiple-Dose Activated Charcoal
• Intralipid Emulsion Therapy
ENHANCEDELIMINATION

16. SELECTED
COMPOUNDS
COMMONLYINVOLVED
IN PEDIATRIC
POISONINGS

17. CARBONMONOXIDE
● The most common gas involved in pediatric exposures is CO.
● CO is a colorless, odorless gas produced during the
combustion of any carbon-containing fuel;
Wood-burning stoves, kerosene heaters, old furnaces, hot-
water heaters, closed-space fires, and automobiles are a few
of the potential sources of CO.
● It impairs the delivery of oxygen to the tissues, leading to
tissue hypoxia.

18. CLINICALANDLAB
MANIFESTATION
EARLY symptoms are nonspecific and include headache, malaise,
nausea, andvomiting.
● At higher exposure levels, patients can develop mental status
changes, confusion, ataxia, syncope, tachycardia, and tachypnea.
● Severe poisoning is manifested by coma, seizures, myocardial
ischemia, acidosis, cardiovascular collapse, and potentially death.

19. ● Physical examination should focus on the cardiovascular and
neurologic systems.
● Emergency department evaluation shouldinclude:-
● arterial or venous blood gas analysis with HbCO determined by
CO-oximetry,
● CK level in severely poisoned patients,
● pregnancy test,and
● ECG in any patient with cardiac symptoms.

20. MANAGEMENT
● Remove patient from the source.
● Give 100% oxygen to accelerate removal of carbon monoxide (note
patient can look pink but still be hypoxemic) until signs of hypoxia
disappear.
● Severely poisoned patients might benefit from hyperbaric oxygen
(HBO).
● Indications of HBO include syncope, coma, seizure, altered mental
status, acute coronary syndrome, HbCO level >25%, abnormal
cerebellar
examination, andpregnancy.

21. CONT…
● Sequelaeof CO poisoning include persistent and
delayed cognitive and cerebellar effects.
● such sequelae is minimized through the delivery of
100% oxygen at 3 atm of pressure
● Patients typically receive oxygen, by non-rebreather
mask or hyperbaric chamber, for 6-24 hr.

22. • Paracetamol administered for therapy is about 15-
20mg/kg/dose
• The single toxic dose of PCM IS>200 mg/kg for children and
>7.5to 10 gram in adolescents and adults.
• paracetamol toxicity remains the most common cause of acute
liver failure and is the leading cause of intentional poisoning
death.
• Exposure can be intentional or unintentional(exploratory or
inappropriate dosing by a care giver).
CLINICALANDLABMANIFESTATIONS
• Diagnosis of the PCM toxicity is through the combination of
the patients history ,symptoms and lab findings.
ACETAMINOPHEN
(PARACETAMOL)

23. CLINICAL MANIFESTATION
AcuteExposures:-
• Stage I (up to 24 hours after overdose) –Asymptomatic,
but less commonly: nausea, vomiting, and, in patients
with very large doses, lethargy and malaise
• Stage II (24 to 72 hours after overdose) – RUQ pain,
elevation in liver enzymes, prothrombin time (PT) and
INR of PT, and, in severe cases, evidence of
nephrotoxicity and/or pancreatitis .
• Stage III (72 to 96 hours) – Evidence of liver failure ,
renal failure and MOSF; death most commonly occursin
this stage.
• Stage IV (4 to 14 days) – Recovery

24. LABFINDINGS
• Serum APAP LEVELS 4hrs after the time of
ingestion.
• A stat APAP LEVELS for those present to medical
care more than 4hrs after ingestion.
testsinclude
• Hepatic transaminases,
• Renal function tests, and
• Coagulation Parameters

25. ● After assessment of theABCs, it ishelpful to place the patient into
oneof thefollowing four categories.
1, THE PROPHYLACTIC:
● These patient has normalAST.
● IF APAP level is known and ingestion is within 24hrs ,the treatmentdecision
is based on where the level falls on the Rumack-Matthewnomogram
● Any patient with a serum APAP level in the possible or probable
hepatotoxicity range per the nomogram should be treated with N -
acetylcysteine (NAC) as either oral Mucomyst or IV Acetadote for 24 or 21
hr, respectively.
● If the AST remains normal and the APAP becomes nondetectable,treatment
may be discontinued.
If the AST becomes elevated, the patient moves into the next categoryof
treatment (injury).

26. CONT…
 If APAP is still present, treatment should be continued until
the level is nondetectable.
In the case of a patient with a documented APAP level,
normal AST, and an unknown time of ingestion, treatment
should ensue until the level is nondetectable, with normal
transaminases.
No patient, regardless of the size of the ingestion, who
receives NAC within 8 hr of overdose should die from liver
failure.
● The longer from the 8 hr mark the initiation of therapy is
delayed, the greater the risk of acute liver failure.

27. CONT…
● 2, Hepatic injury .
● Any patient in this category requires therapy with NAC (IV or oral).
To discontinue the therapy ,the transaminases and INR have peaked and
fallen significantly “toward” normal
3,Acute liver failure.
● TheKing'sCollegecriteria for consideration of liver transplant.These criteriainclude:-
■ acidemia(serum pH <7.3)after adequate fluid resuscitation,
■ coagulopathy(INR >6),
■ renal dysfunction (creatinine >3.4mg/dL), and
■ grade IIIor IV hepatic encephalopathy.
.A serum lactic acid >3mmol/L (after IV fluids) adds to both sensitivity and
specificity of the criteria to predict death without liver transplant.

28. Cont…
4 Repeated SupratherapeuticIngestion
● Inthe asymptomatic patient, if the AST is normal and the APAP is <10
µg/mL, no therapy is indicated.
A normal AST and an elevated APAP warrants NAC dosing for at least
long enough for the drug to metabolize while the AST remains normal .

30. MANAGEMENT
● Give activated charcoal within 4 hours of ingestion.
Decide if antidote is required to prevent liver damage: ingestions of
150 mg/kg or more, or toxic 4 hour paracetamol level where this is
available.
● Antidote is more often required for older children who deliberately
ingest paracetamol or when parents overdose children by mistake.
● If within 8 hours of ingestion give oral methionine or IV
acetylcysteine.
● Methionine can be used if the child is conscious and not vomiting (<6
years:1 gram every 4 hours for 4 doses; 6 years or older: 2.5 grams
every 4 hours for 4 doses).

31. Cont….
● If more than 8 hours after ingestion, or the child cannot take
oral treatment, give IV acetylcysteine.
● For children <20 kg give the loading dose of 150 mg/kg in 3
ml/kg of 5%glucose over 15 minutes, followed by 50 mg/kg in 7
ml/kg of 5%glucose over 4 hours, then 100 mg/kg IV in 14 ml/kg
of 5%glucose over 16 hours
● The volume of glucose can be scaled up for larger children.
● Continue infusion of acetyl cysteine beyond 20 hours if late
presentation or evidence of liver toxicity.
● If liver enzymes can be measured and are elevated, continue IV
infusion until enzyme levels are falling.

32. HYDROCARBONS
● Hydrocarbons include a wide array of chemical
substances found in thousands of commercial
products.
● produce systemic toxicity, local toxicity, or both.
● Nevertheless, aspiration of even small amounts of
certain hydrocarbons can lead to serious, potentially
life-threatening toxicity.
● The most important manifestation of hydrocarbon
toxicity is aspiration pneumonitis.

33. • Aspiration usually occurs at the time of ingestion, when
coughing and gagging are common, but can also be
secondary to vomiting.
• The propensity of a hydrocarbon to cause aspiration
pneumonitis is inversely proportional to its viscosity.
• Only small quantities (<1 mL) of low-viscosity
hydrocarbons need be aspirated to produce significant
injury.
• Gasoline and kerosene often cause considerable
gastrointestinal mucosal irritation as they pass through the
intestines.

34. CLINICALANDLABORATORY
MANIFESTATION
 Transient, mild CNS depression
 Coughing, mild to severe respiratory distress
 Feverand leukocytosis.
 Abnormality on CXR:- will be positive after 6hr
 Inhalational exposure to halogenated hydrocarbons
can cause ventricular dysrhythmias.

35. Treatment
● Emesis and lavage are contraindicated becauseof
the risk of aspiration.
● If gastric lavage (only in case of highly toxic HCs
such as CCl4) is to be performed, the patient
should be intubated with a ballon cuffed tube to
protect the airway from further aspiration.
● Activated charcoal also is not useful.

36. ● If hydrocarbon-induced pneumonitis develops,
respiratory treatment is supportive
● Corticosteroids and Prophylactic antibiotics should not
be given because bacterial pneumonia occurs in only a
very small percentage of cases.
● Patients with dysrhythmias in the setting of halogenated
inhalation should be treated with B blockers.

37. ORGANOPHOSPHATEANDCARBAMATE
POISONING
 These are commonly used insecticides and herbicides
 E.g. organophosphorus (malathion, parathion, TEPP,
mevinphos/Phosdrin)
and carbamates (methiocarb and carbaryl)
 These compounds can be absorbed through the skin,
ingested orinhaled.
 The child may complain central nervous system
symptoms (dizziness,
headache, ataxia, convulsions, and coma)

38.  Muscarinic effects of these poisons can be memorized with
mnemonic
"DUMBBELS"
– Diarrhea
– Urination
– Miosis
– Bradycardia, Bronchorrhea/Bronchospasm
– Emesis
– Lacrimation
– Salivation

39. ● Nicotinic signs and symptoms include muscle
weakness, fasciculation, tremors, hypoventilation
(diaphragm paralysis), hypertension, tachycardia,
and dysrhythmias.
● CNS effects include confusion, delirium, seizures,
and coma.
● Symptoms caused by carbamate toxicity are usually
less severe than those seen with organophosphates.

40. Management
 Remove poison by irrigating eye or washing skin (if in eye
or on skin).
 Give activated charcoal within 1 hours of ingestion,
however it could be given up to 4 hours after ingestion of
the poison.
 Ina serious ingestion where activated charcoal cannot be
given, consider careful aspiration do gastric lavage (the
airway should be protected).

41. ● After decontamination, antidotal therapy begins
withadministration of
atropine sulfate
● Give a dose of 0.05 to 0.1 mg per kg to children and 2
to 5 mg for adolescents IV or IM.
 This dose should be repeated every 10 to 30 minutes
or as needed until chest secretions and pulmonary
rales cleared.
 Therapy is continued until all absorbed
organophosphate has been metabolized and may
require 2 mgto more than 2,000 mgof atropine may
be required for a few hours to several days.

42. ● If muscle weakness develops after
atropinization, give pralidoxime
(cholinesterase reactivator) 25–50mg/kg
diluted with 15 ml water by IV infusion over
30 minutes repeated once or twice, or
followed by an intravenous infusion of 10 to
20 mg/kg/hour, as necessary.

43. SALICYLATESTOXICITY
● The acute toxic dose of salicylates is generally considered to be
>150 mg/kg.
● More significant toxicity is seen after ingestions of >300 mg/kg, and
● severe, potentially fatal, toxicity is described after ingestions of
>500 mg/kg.
Clinical and LaboratoryManifestations.
○ Mild acute salicylisminclude nausea, vomiting, diaphoresis, and
tinnitus.
○ Moderate salicylate toxicitycan manifest as tachypnea
&hyperpnea,tachycardia, and altered mental status.
○ Severe salicylate toxicityinclude mild hyperthermia, coma, and
seizures.

44. Labfinding
● primary respiratory alkalosis and a primary, elevated anion
gap metabolicacidosis.
● Hyperglycemia (early) and hypoglycemia (late)
● Serial serum salicylate levels should be closely monitored
(every 2-4 hr initially) until they are consistently
downtrending.
● Serum and urine pH and electrolytes should be followed
closely.
● A chest radiograph is recommended in any patient in
respiratory distress.

45. Treatment
● gastric decontamination with activated charcoal.
aggressive volume resuscitation and
● prompt initiation of sodium bicarbonate therapy in the symptomatic
patient
The primary mode of therapy for salicylate toxicity is urinary
alkalinization
.ThegoalsoftherapyincludeaurinepHof7.5-8,aserumpHof7.45-
7.55, anddecreasingserumsalicylatelevels.
Add potassium to bicarbonate drip,to prevent hypokalemia .
● Parenteral glucose .
● In patients with severe toxicity, hemodialysis may be required.

46. CONT…
● Indications fordialysisinclude:-
○ severe acid-base abnormalities (specifically severe acidosis
and acidemia),
○ a rising salicylate level (despite adequate decontamination
and properly alkalinized urine)
○ pulmonary edema,
○ cerebral edema,
○ seizures, and
○ renal failure.

47. IBUPROFENTOXICITY
● Ibuprofen and other NSAIDs are often involved in
unintentional and intentional overdoses.
● Fortunately, serious effects after acute NSAID overdose are
rare because of their wide therapeutic index.
But ,ingestions of >400 mg/kg can produce more serious
effects, including altered mental status and metabolic acidosis.
ClinicalandLaboratoryManifestations
Symptoms usually develop within 4-6 hr of ingestion and resolve
within 24 hr.

48. CONT…
● If toxicity does develop, it is typically manifested as nausea, vomiting, and
abdominal pain.
After massive ingestions, patients can develop
■ marked CNSdepression,
■ anion gap metabolic acidosis,
■ renal insufficiency,and
■ (rarely) respiratorydepression.
Renal functionstudies,
■ acid-base balance,
■ complete blood count (CBC), and
coagulation parameters should be monitored after very large ingestions.

49. TREATMENT
● use of antiemetics and acid blockade as indicated, is
the primary therapy for NSAID toxicity.
● Decontamination with activated charcoal should be
considered if a patient presents within 1-2 hr of a
potentially toxicingestion.
● There is no specific antidote for this class of drugs
Patients who remain asymptomatic for 4-6 hr after
ingestion may be considered medically cleared.

50. PHENOBARBITALPOISONING
● Phenobarbital is primarily used as anticonvulsant.
● The therapeutic range for phenobarbital is 15 to 40
μg/mL.
● It’s overdose results in central nervous depression
with respiratory distress and suppression of skeletal,
cardiac and smooth muscles
● Poisoned child may present with respiratory
depression and deranged vital signs (hypotension,
bradycardia and hypothermia)
● Pupils may constrict early but dilate later

51. Management…
● Initial management issupportive andstabilization ofABC.
● Check bloodglucoseandtreatif hypoglycemic.
● Give activated charcoal 1g/kgfor achild (foradolescents give
■ 50g).
● For patients whohaveacompromised airway, endotracheal
intubation isadvised prior togivingcharcoal.
● With very largeoverdoses, antecedent gastric lavagemaybe
■ considered.
● Since Phenobarbital undergoes enterohepatic circulation,(MDAC)
should begivento decreasethehalflife of thedrugandincrease its
clearance.

52. PREVENTION
• Safety closure
• Keep out of the reach of children
• Never store food and cleaning products together
• Discard unused medicine and toxic products
together
• Keep a bottle of syrup of ipecac and learn how to
use it

53. REFERENCES
● Jillian L. Theobald, Mark A. Kostic
Poisoning. Nelson text book of
pediatrics 21st edition ,2020
● UpToDate 2018
● POCKET BOOK Guidelines for the
management of common illnesses in
hospitals second edition, 2016
● Emergency triage Assessment and
Treatment

54. THANKYOU!!