Poisoning in Children Norah Al Khathlan M.D. Consultant Pediatrician Consultant Pediatric...

Poisoning in ChildrenPoisoning in Children

Norah Al Khathlan M.D.Norah Al Khathlan M.D.Consultant PediatricianConsultant Pediatrician

Consultant Pediatric IntensivistConsultant Pediatric Intensivist02/02/0802/02/08


Goals:Goals:• Learn the pertinent aspects of the history and physical exam Learn the pertinent aspects of the history and physical exam

relative to acute poisoning with particular emphasis on clinical relative to acute poisoning with particular emphasis on clinical recognition of major toxic syndromes (toxidromes). recognition of major toxic syndromes (toxidromes).

• Understand the principles, methods, and controversies of Understand the principles, methods, and controversies of decontamination and enhancement of elimination of toxins. decontamination and enhancement of elimination of toxins.

• Learn the presenting signs, symptoms, laboratory findings, Learn the presenting signs, symptoms, laboratory findings, pathophysiology and treatment of common therapeutic drug pathophysiology and treatment of common therapeutic drug poisonings, drugs of abuse, natural toxins and general household poisonings, drugs of abuse, natural toxins and general household poisons. poisons.


Objectives:Objectives:At the end of this lecture the student will be able to :At the end of this lecture the student will be able to :1.1. Define poisoning.Define poisoning.2.2. Identify specific Toxidromes.Identify specific Toxidromes.3.3. Identify risk factors for pediatric toxidromes.Identify risk factors for pediatric toxidromes.4.4. Differentiate between the different classes of toxidromes.Differentiate between the different classes of toxidromes.5.5. Differentiate the routes of poisoning.Differentiate the routes of poisoning.6.6. Describe the general management of the toxidromes.Describe the general management of the toxidromes.7.7. Outline the management of specific toxidromes:Outline the management of specific toxidromes:

– IronIron– SalicylatesSalicylates– Paracetamole/ AcetaminophenParacetamole/ Acetaminophen– KeroseneKerosene


• Definition of Poisoning:Definition of Poisoning:– Exposure to a chemical or other agent that Exposure to a chemical or other agent that

adversely affects functioning of an organism.adversely affects functioning of an organism.

• Circumstances of Exposure can be intentional, Circumstances of Exposure can be intentional, accidental, environmental, medicinal or accidental, environmental, medicinal or recreational.recreational.

• Routes of exposure can be ingestion, injection, Routes of exposure can be ingestion, injection, inhalation or cutaneous exposure.inhalation or cutaneous exposure.

““All substances are poisons...the right dose separates poison All substances are poisons...the right dose separates poison

from a remedy.”from a remedy.”


• Ingestion of a harmful substance is among the Ingestion of a harmful substance is among the most common causes of injury to children less most common causes of injury to children less than six years of agethan six years of age

• Toxicology. . . is the science that studies the Toxicology. . . is the science that studies the harmful effects of drugs, environmental harmful effects of drugs, environmental contaminants, and naturally occurring substances contaminants, and naturally occurring substances found in food, water, air and soil.found in food, water, air and soil.

• Poisoning maybe a medical emergency Poisoning maybe a medical emergency depending on the substance involved.depending on the substance involved.


Constellation of signs & symptoms Constellation of signs & symptoms seen in poisoning characterized by seen in poisoning characterized by the type of substance.the type of substance.

Major four toxidromes are:Major four toxidromes are:– AnticholinergicAnticholinergic– SympathomimeticSympathomimetic– Opiates/Sedatives- Hypnotics/ AlcoholOpiates/Sedatives- Hypnotics/ Alcohol– CholinergicCholinergic


Examples:Examples:• ASAASA• AcetaminophenAcetaminophen• TCATCA• Narcotics & drugs of abuseNarcotics & drugs of abuse• BenzodiazepinesBenzodiazepines• Iron supplementsIron supplements• AlcoholAlcohol

Shannon M. N Engl J Med 2000;342:186-191

Agents Most Commonly Ingested by Children Less Than Six Years of Age, 1995 to 1998


Poisoning in ChildrenPoisoning in ChildrenImportant history pointsImportant history points

• What toxic agent/medications were found near the patient?What toxic agent/medications were found near the patient?

• What medications are in the home?What medications are in the home?

• What approximate amount of the “toxic” agent was ingested?What approximate amount of the “toxic” agent was ingested?– How much was available before the ingestion?How much was available before the ingestion?– How much remained after the ingestion?How much remained after the ingestion?

• When did the ingestion occur ?When did the ingestion occur ?

• Were there any characteristic odors at the scene of the Were there any characteristic odors at the scene of the ingestion?ingestion?

• Was the patient alert on discovery?Was the patient alert on discovery?– Has the patient remained alert since the ingestion?Has the patient remained alert since the ingestion?– How has the patient behaved since the ingestion?How has the patient behaved since the ingestion?

• Does the patient have a history of substance abuse?Does the patient have a history of substance abuse?

Poisoning in ChildrenPoisoning in ChildrenManagementManagement

General measures:General measures:• Quick assessment & triageQuick assessment & triage

• Identify the culprit.Identify the culprit.

• Limit absorption:Limit absorption:– VomitingVomiting– LavageLavage– Activated charcoal instillationActivated charcoal instillation

Specific:Specific:


ABC’s of Toxicology:ABC’s of Toxicology:• AAirwayirway• BBreathingreathing• CCirculationirculation• DDrugs: rugs:

• Resuscitation medications if neededResuscitation medications if needed• Universal antidotesUniversal antidotes

• DDraw blood: raw blood: • chemistry, coagulation, blood gases, drug levelschemistry, coagulation, blood gases, drug levels

• DDecontaminateecontaminate• EExpose / Examinexpose / Examine• FFull vitals / Foley / Monitoringull vitals / Foley / Monitoring• GGive specific antidotes / treatmentive specific antidotes / treatment


• Decontamination:Decontamination:1.1. Ocular:Ocular:

– Flush eyes with salineFlush eyes with saline2.2. Dermal:Dermal:

– Remove contaminated clothingRemove contaminated clothing– Brush offBrush off– Irrigate skinIrrigate skin

3.3. Gastro-intestinal:Gastro-intestinal:– Activated charcoal:Activated charcoal:

– May Prevent /delay absorption of some drugs/toxinsMay Prevent /delay absorption of some drugs/toxins– Almost always indicatedAlmost always indicated

– Naso/oro-gastric LavageNaso/oro-gastric Lavage– Bowel Irrigation:Bowel Irrigation:

– Recent ingestions 4-6 hrsRecent ingestions 4-6 hrs– Awake alert patientAwake alert patient– 500 cc NS Children / 2000cc adults500 cc NS Children / 2000cc adults– Orally / Nasogastric tubeOrally / Nasogastric tube– Contraindications…?Contraindications…?


Agents Used for Gastrointestinal Decontamination in Children


Circumstances under Which Administration of Ipecac Syrup Should Be Avoided

Important pointsImportant points

Specific toxidromesSpecific toxidromes

• Acetaminophen:Acetaminophen:– Stage I 0-24 hrsStage I 0-24 hrs

• Early symptomsEarly symptoms– MildMild– Serum acetaminophen level 4 hrs post ingestionSerum acetaminophen level 4 hrs post ingestion– PLOT ON SPECIFIC NOMOGRAM.PLOT ON SPECIFIC NOMOGRAM.– No need to repeat levelsNo need to repeat levels

• If > 900 If > 900 µmol/L ---> POSSIBLE RISKµmol/L ---> POSSIBLE RISK• Nausea, vomiting, malaise and diaphoresis.Nausea, vomiting, malaise and diaphoresis.• Normal bilirubin Transaminases and PTNormal bilirubin Transaminases and PT

Acetaminophen poisoningAcetaminophen poisoning

• Stage II:Stage II:– 24-48 hrs after ingestion.24-48 hrs after ingestion.

•Better, less symptoms.Better, less symptoms.

•Elevated bilirubin, transaminases and PTElevated bilirubin, transaminases and PT


• Stage III Stage III – 48-96 hrs ( 2- 4 days) after ingestion:48-96 hrs ( 2- 4 days) after ingestion:

•Hepatic dysfunctionHepatic dysfunction

•(Rarely hepatic failure)(Rarely hepatic failure)

•Peak elevations in:Peak elevations in:– BilirubinBilirubin– Transaminases may reach > 1000 IU/LTransaminases may reach > 1000 IU/L– Prolonged PT Prolonged PT


• Stage VI Stage VI – 168- 192 hrs (7-8 days)168- 192 hrs (7-8 days)– Clinical improvementClinical improvement– LFTs returning to normalLFTs returning to normal


• Probable toxicity should be treated Probable toxicity should be treated with:with:– N-acetylcysteine bolus 140 mg/kgN-acetylcysteine bolus 140 mg/kg– Then 70 mg/kg Q 4 hrs for 17 doses.Then 70 mg/kg Q 4 hrs for 17 doses.– Assess hepatic function:Assess hepatic function:

•On presentationOn presentation

• DailyDaily

– Continue other supportContinue other support

Iron PoisoningIron Poisoning

• Five Stages but variableFive Stages but variable– Stage Stage 11

•Gastro-intestinal stage: within several hrs of Gastro-intestinal stage: within several hrs of ingestion:ingestion:

– V/D. Hematochezia and abdominal painV/D. Hematochezia and abdominal pain– Severe: fluid loss, bleeding, shock(acidosis, Severe: fluid loss, bleeding, shock(acidosis,

tachycardia +/- hypotension)tachycardia +/- hypotension)– Fever. Lethargy. ComaFever. Lethargy. Coma


• Stage Stage 22– Quiescent stage: 4-48hrsQuiescent stage: 4-48hrs

•Clinical improvementClinical improvement

•Subtle hemodynamic changes:Subtle hemodynamic changes:– TachycardiaTachycardia– Decreased U.O.P.Decreased U.O.P.


• Stage Stage 33::– Circulatory collapse : 48-96 hrsCirculatory collapse : 48-96 hrs

•Metabolic acidosis, hypotension, low Cardiac Metabolic acidosis, hypotension, low Cardiac output.output.

•CoagulopathyCoagulopathy

•Multiorgan system failureMultiorgan system failure


• Stage 4:Stage 4:– Hepatic failure: 96 hrsHepatic failure: 96 hrs

• Increased mortalityIncreased mortality

•Rarely fulminant hepatic failureRarely fulminant hepatic failure

•Hepatic necrosisHepatic necrosis

– Liver transplant can save lives Liver transplant can save lives


• STAGE 5:STAGE 5:– Bowel obstruction 2-6 wksBowel obstruction 2-6 wks– Due to scarringDue to scarring

•Gastric outlet obstructionGastric outlet obstruction

•Small intestinal obstructionSmall intestinal obstruction

– May not pass through stage 4May not pass through stage 4


Management:Management:1.1. Gastric decontamination:Gastric decontamination:

• Forced emesisForced emesis• Gastric lavage with 5% NaHCO3Gastric lavage with 5% NaHCO3• No activated char coalNo activated char coal

2.2. Secure good IV Secure good IV 3.3. Get initial the 4hrs levels and TBCGet initial the 4hrs levels and TBC4.4. Chelate with Deferoxamine if levels> Chelate with Deferoxamine if levels>

300mg/dL300mg/dL


• Chelate with Deferoxamine:Chelate with Deferoxamine:– Stable pts : levels< 500 mg/dL 40mg/kg Stable pts : levels< 500 mg/dL 40mg/kg

IM/IVIM/IV– Unstable: bleeding/ level > 500Unstable: bleeding/ level > 500

•Give 20cc/kg NS/RLGive 20cc/kg NS/RL

•Deferoxamine at 15 mg/kg IV over 1hrDeferoxamine at 15 mg/kg IV over 1hr

•Continuous drip at 15mg/kg/hrContinuous drip at 15mg/kg/hr

•Continue till “vin rose” urine color Continue till “vin rose” urine color disappears.disappears.


• Observe for:Observe for:– Systemic BPSystemic BP– ECGECG– CVPCVP

• Signs of hepatic failure:Signs of hepatic failure:– BleedingBleeding– Glucose intoleranceGlucose intolerance– HyperammonemiaHyperammonemia– EncepalopathyEncepalopathy

SALICYLATESSALICYLATES

• Oral ingestion commonestOral ingestion commonest

• Transdermal lessTransdermal less

• Peak levels at 12 hrsPeak levels at 12 hrs– Early : hyperpnea Early : hyperpnea respiratory respiratory

alkalosisalkalosis– Then metabolic acidosisThen metabolic acidosis– Severe cases: Cerebral edema and Severe cases: Cerebral edema and

increased ICPincreased ICP

SALICYLATESSALICYLATES

• MANAGEMENTMANAGEMENT– Treat electrolyte imbalanceTreat electrolyte imbalance– IV hydrationIV hydration– Forced alkaline diuresisForced alkaline diuresis– HemodialysisHemodialysis– DiureticsDiuretics

HydrocarbonsHydrocarbons

• Kerosene ingestion:Kerosene ingestion:– Risk of aspirationRisk of aspiration– GIT & Respiratory effects.GIT & Respiratory effects.– Burning sensation, nausea, belching and Burning sensation, nausea, belching and

diarrheadiarrhea– Cough, chocking, gagging and grunting.Cough, chocking, gagging and grunting.– CXR 2-8 hrs later: Pulmonary infiltrates or CXR 2-8 hrs later: Pulmonary infiltrates or

perihilar densities. perihilar densities. – pneumatoceles, pleural effusion or pneumatoceles, pleural effusion or

pneumothorax and bacterial superinfection pneumothorax and bacterial superinfection – Resolution 2-7 days.Resolution 2-7 days.

HydrocarbonsHydrocarbons

• Treatment:Treatment:– Do not induce vomitingDo not induce vomiting– Do not attempt gastric lavageDo not attempt gastric lavage– Risk of aspiration outweighs any benefit Risk of aspiration outweighs any benefit

from removal of substancefrom removal of substance– CXR around 2-4 hrs “not before 2hrs”CXR around 2-4 hrs “not before 2hrs”– Observe in ER for 6-8 hrs if no Observe in ER for 6-8 hrs if no

symptoms symptoms discharge. discharge.


““Prevention is the vaccine for the Prevention is the vaccine for the disease of injury.”disease of injury.”

• HostHost

• AGENTAGENT A causal A causal

relationship!relationship!

• EnvironmentEnvironment


““Prevention is the vaccine for the Prevention is the vaccine for the disease of injury.”disease of injury.”

• HostHost

• AGENTAGENT A causal A causal

relationship!relationship!

• EnvironmentEnvironment


PreventionPrevention• The reduction in the incidence of childhood poisonings in the The reduction in the incidence of childhood poisonings in the

past half-century has been dramatic. past half-century has been dramatic. • This reduction is largely the result of the combination of This reduction is largely the result of the combination of

highly effective active and passive methods of intervention.highly effective active and passive methods of intervention.

– Passive interventions eg: introduction of child-resistant Passive interventions eg: introduction of child-resistant containers for drugs and other dangerous household products. containers for drugs and other dangerous household products. Child-resistant containers have been particularly effective in Child-resistant containers have been particularly effective in reducing the incidence of death from the ingestion of reducing the incidence of death from the ingestion of prescription drugs by children.prescription drugs by children.

– Active interventions, which require a change in behavior by Active interventions, which require a change in behavior by parents and caretakers, include the safe storage of household parents and caretakers, include the safe storage of household products. products.

Thank youThank you

Norah Khathlan M.D.Norah Khathlan M.D.

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