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

a remedy.”

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Poisoning in Children

• Definition of Poisoning:• A poison is an agent of injury to humans usually

by chemical reaction, when a sufficient quantity is absorbed through epithelial lining such as skin or gut.

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

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

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Epidemiology

• 0.64-11.6% of pediatric admissions and 0.6% of all pediatric deaths.

• 79% of these involve children younger than age six.

• 80% household products,21.8% drugs, agriculture pesticide 9.1%, industrial chemicals 7%,bites and stiings 3.2% of pediatric exposures.

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Epidemiology

• 80% 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.

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Recent advances • Stabilization of the patient is being considered as

the main stay.• Gastrointestinal evacuation, is undergoing critical

appraisal. • Ipecac and gastric lavage are being questioned• Activated charcoal is gaining importance .• Antidotal therapy is no more the mainstay of

management • Antidotes for only about 5% poisons.

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Care Grouping the signs and symptoms produced by the poisons in to various toxidromes helps in rapid and effective management of the case.

Major four toxidromes are:AnticholinergicSympathomimeticOpiates/Sedatives- HypnoticsCholinergic

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Common Toxidrome FindingsPhysical Findings Adrenergi

c

Anti-

cholinergic

Anti-

cholinesterase

OPIOIDSedative-

hypnotic

RR Increased No change No change Decreased Decreased

HR Increased Increased Decreased Normal/

decreased

Normal/

decreased

Temp Increased Increased No change Normal/

decreased

Normal/

decreased

BP Increased NoChange/increased

No change Normal/

decreased

Normal/

decreased

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Common Toxidrome FindingsPhysical Findings Adrenergi

c

Anti-

cholinergic

Anti-

cholinesterase

OPIOIDSedative-

hypnotic

Mental status

Alert/

agitated

Depressed/

Confused/

hallucinate

Depressed/

Confused/

Depressed Depressed

pupils Dilated Dilated Constrict Constrict Normal

Mucus membrane

Wet Dry Wet Normal Normal

skin Diaphoretic

Dry Diaphoretic

Normal Normal

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Symptoms and signs of common poisons

Symptomalogy Important causes

odor kerosene,cyanide ,phosphorus, organophosphates

fever Salicylates,anticholinergics.kerosene

hypothermia Opiates ,barbiturates

delirium Dhatura,salicylates,barbiturates,antihistaminics

Constricted pupils Opiates,organophosphates, early stages of barbiturates

Dilated pupils atropine.,adernergic agents,antihistaminnics

tachycardia Atropine,theophylline

bradycardia Digitalis,beta blockers,quinidine

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Paralytic ilius Opiates, anticholinergics

Metabolic acidosis

Iron, salicylates,phenol

hypotension Anticholinergic, barbiturates,opiates, phenothiazines,aluminium phosphide

Cardiac arrhythmias

Theophylline,tricyclic antidepressants,kerosene,digitalis,aluminium phosphide.

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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?

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Care• 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?

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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

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ABC’s of Toxicology:• Decontamination:

1.Ocular:– Flush eyes with saline or tepid water for 15

min.

2.Dermal:– Remove contaminated clothing– Brush off– Wash skin with soap and water

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GI DECONTAMINATION GASTRO-INTESTINAL1.EMESIS : use of emetics like syp of ipecac declined in recent past.

Home remedy

2.GASTRIC LAVAGE• most effective if done within one hour.• Child in left lateral position with head end low. Use large orogastric tube with multiple holes at distal end

and funnel at promixal endNS 15ml/kg(max 200-400)/per cycle till affluent is clear

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Care• In comatosed pts it should be done after intubation with cuffed ET tube.

• Contraindications: corrosive ingestions like washing soda, detergents, alkalis and acids.

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ACTIVATED CHARCOL

• Made by pyrolysis of organic matter like wood pulp activated by an oxidizing process.• Used in all cases except in iron , cyanide and

when orally adminstered antidotes are used.• Dose 01 gm/kg/dose mixed in sufficient

amount of water to make slurry.• Contraindicated in paralytic ilius, intestinal

perforation and orally adminstered antidotes.

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Whole bowel irrigation

• Recent addition to emergency treatment of poisninmg

• Removes unabsorbed drug from entire gut and possibly absorbed one from gut mucosa

• Contraindicated in intestinal obstruction, perforation or hemorrhage.

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Care• Isotonic balanced salt solution containing propylene glycol at 30 ml/kg/hr in childern by NG tube or orally.

• Continued till effluent fluid from rectum is clear.• Indications are poor binding of toxin to activated

charcol, massive ingestion,late presentation,sustained release formulations.

• Useful in iron poisning and sustained release/enteric coated formulations.

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Enhancing excreation

• Diuresis • Dialysis • Hemoperfusion diuresis : osmotic agents like 20% mannitol in

initial doses of 0.5gm/kg and then repeated to ensure a UO of 6-9 ml/kg/hr.

useful when poisning sgent is excreted primarily through renal route.

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Care• Alkaliztion or acidification of urine enhances excretion of toxin and enhances the efficacy of diuretics.

• Alkaliztion is achieved with soduim bicorbonte 1-2 meq/kg infusion over 1-2 hrs.

useful in salicylates and barbiturates.

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Care• Acidification is done with ammonium chloride in a dose of 75mg/kg/dose to keep urine PH 5 or less.

• Useful in week bases like amphetamine,strychnine ,quinine.

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Dialysis

• particularly useful if electrolyte or acid base abnormalities exist.

• Indications : 1 anticipated prolonged coma and liklyhood of

complications. 2.renal failure 3. Progressive clinical deterioration 4. Plasma levels of toxin in potentially fatal range.

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Care Hemodialysis is useful in poisning with • Salicylates• Acetaminophen• Chloroquine• Propranolol• Vancomycin• Snake bite

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Hemoperfusion and hemofilteration

• hemoperfusion is useful in toxins with low water solubility and with high affinity for the absorbant like carbmazepine,barbiturates and theophylline

• Hemofilteration in toxins with high molecular wt used in poisning with aminoglycosides,theophyline iron and lithium

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in Children

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AcetaminophenAcetaminophen is the most widely used

analgesic-antipyretic medication taken by people in the world.

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Acetaminophen toxicity is one of the most common etiology of hepatic failure requiring liver transplantation

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Clinical

patients with acetaminophen induced hepatotoxicity present in 4 clinical stages :

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Stage I 0-24 hrs

Nausea, vomiting, malaise and diaphoresis with cold skin

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Stage 2 (24-48 h )

• The clinical evidence of hepatic dysfunction supervenes.

• jaundice,pain and tenderness in the right upper quadrant 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

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Stage 3 (48-96 h)

• the symptoms of stage 1 reappear and hepatic coma supervenes with gross evidence of hepatic dysfunction

• Severe toxicity is evident on 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

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• Stage 4 (4-14 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.

• DOES NOT cause chronic hepatic dysfunction

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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.

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Remember the Dose >150mg/kg or >10gm in adults can

lead to serious toxicity. normal dose: 350-650mg every 4-6hrs for adults 10-15mg/Kg every 4-6 hrs for childern

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Workup • Measurement of acetaminophen serum

concentration.• Levels >200micgm/ml at 4hrs,

>100micgm/ml at 8 hrs and >50micgm/ml at 16 hrs and hepatic transaminases >1000u/ml associated with serious hepatic damage.

• 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).• Others

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Treatment

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)Supportive treatment: correction of hypoglycemia maintenece of hydration electrolyte balance treatment of coagulopathy hemodialysis for ARFManagement of hepatic failure

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Care N-acetylcysteine NAC:acts by enhancing glutathione stores and Anhancing nontoxic sulfate conjugation in the liver.

oral NAC is as effective as IV 150mg/kg iv over 15 min followed by same dose

over next 20 hrs. 75mg/kg orally every 4-6 hrs for 2-3 days.SE : flushing, pruritus, and a rash (15%) Bronchospasm and hypotension (<2% of patients)

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Poor prognostic factors

• PH < 7.3• PT > 100 sec• Grade III or more of hepatic encephalopathy• Raised serum bilirubin > 04 mg/dl• SGOT > 1000 IU/L• Factor VIII : Factor V > 30 (indicates the worst

outcome)

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THANKS

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Iron• The most common

cause of death in toddlers.

• Classically taught as having five clinical stages.

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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.

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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.

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Care• 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

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Differential Diagnoses

• Metabolic Acidosis

Other Problems to Be Considered Gastroenteritis

Hepatic failure

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WorkupLaboratory 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 iron :Mild - Less than 300 µg/dLModerate - 300-500 µg/dLSevere - More than 500 µg/dL• TIBC has no utility in the acute overdose setting.

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Management• Detailed history and physical including a rectal exam for frank blood.

• Aggressive fluid resuscitation and intravenous access.

• Whole bowel irrigation and KUB toLook for pills.

• Laboratory analysis for CBC, chemistry, and iron levels (peak around 4

hours) Will often require repeat levels with a repeat chemistry

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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

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• 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.

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Complications

• Infectious -Yersinia enterocolitica septicemia

• Pulmonary - Acute respiratory distress syndrome (ARDS)

• Gastrointestinal - Fulminant hepatic failure, hepatic cirrhosis, pyloric or duodenal stenosis

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Thanks

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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

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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

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• 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

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• 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

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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.

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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

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Differential Diagnoses

• DKA• SEPSIS• Meningitis • Encephalitis• Other TOx

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WorkupLaboratory 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 !

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potential severity and 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

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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

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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 overload6. 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 hemodialysis

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