Pediatric Toxicology Pills and poisonous bites High Yield

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Pediatric ToxicologyPills and poisonous bites

High Yield

Eiman Abdulrahman MD/MPHPediatric Emergency Medicine Fellow

Emory University

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Outline

Important highlights in pediatric toxicology

Young children vs Adolescents Prevention Overview of pills potentially fatal in

children even in small amounts Approach to management Snake and spider bites

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Outline




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Epidemiology

1.25 million annual cases in <6years. 15,447 fatalities; 537 (3.7%) in <6yrs;

397 (2.6%) in <2yrs (since 1983) Of 27 deaths in 2004; 19 were caused by

pharmaceuticals (analgesics and opioids) of which 14 were in <2yrs

12 deaths were pre-hospital

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Outline




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Pediatric Toxicology Young children vs Teenagers

79% of all pediatric exposures occur in <6years and approx 99% are unintentional

Approx 40-45% of ingestions in adolescents are intentional and 56% are female (substance abuse vs suicide attempts)

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Young Children

Without suicidal intent Usually one substance Usually non-toxic Small amount Present for evaluation within one

hour

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Young children

Physiologic considerations High Metabolic Demands More permeable BBB until 4mos Decreased glycogen stores

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Adolescents

56% of seriously poisoned children Overdose from suicidal attempt Adverse effect while trying seeking

euphoria More frequently hospitalized than

younger children ( includes psych) 42% of AAPCC reported adolescent

fatalities from suicide vs 4% from medication errors and adverse reactions

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Outline




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Prevention The Poison Prevention Packaging Act

(PPPA) of 1972 has reduced pediatric mortality by 45% Mandatory child protective packaging

in household products, medicines, solvents

FDA 1997 regulation with packaging with blister packs of 30mg Iron tablets (overturned in 2003) Significant decline in iron overdose

Small amounts of some substances can extremely toxic to children

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Outline




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Lethal exposures

Analgesics Sedative/hypnotic/psychotics Antidepressants Stimulants and street drugs Cardiovascular drugs Alcohols Chemicals Gas and fumes Antihistamines

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Lethal Drugs

AntimalarialsAntidysrhythmicsBenzocaineβ-blockersCalcium channel blockers (CCBs)CamphorClonidine (and other imidazolines)

Lomotil (diphenoxylate/atropine)LindaneMethyl salicylateOpioids

SulfonylureasTheophyllineTricyclic antidepressants (TCAs)

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Outline




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General Approach

Airway Breathing Circulation Disability Drugs Decontamination

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Focused history

Three key questions: WHAT substance was ingested? WHEN did the ingestion occur? HOW MUCH was ingested?

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Key PE

Vital signs Level of consciousness, neuromuscular

status Eyes-pupils, EOM, fundi Mouth-corrosive lesions, odors CV- rate, rhythm, perfusion Resp- rate, chest excursion, air entry GI- motility Skin- color, bullae or burn, diaphoresis,

piloerection,

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Laboratory evaluation

CBC, co-oximetry ABG, serum osmolarity EKG/cardiac monitor CXR, abdominal xray Electrolytes, bun/cr, glucose,

calcium, LFT, UA Urine tox screen Quantitative tests (esp

acetaminophen)

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Assessment

Clinical findings Toxidromes Laboratory abnormalities

Anion gap: (Na + K)-(Cl + HCO3) Osmolarity: (2x Na)+ (Bun/2.8)+

(Glu/18) Osmolar gap: measured-calculated

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ToxidromesAnticholin-ergics

(Antihista-mines, Many

Others)

Organophosphates

(Insecticide Nerve Gases)

OpiatesClonidine

BarbituratesSedative-Hypnotics Salicylates

Theophylline

Sympathomimetics (Ampheta

mines, Cocaine)

MS/CNS Agitation, delirium, psychosis, convulsions

Delirium, psychosis, coma, convulsions

Confusion, fasciculations, coma

Euphoria, somnolence, coma

Somnolence, coma

Lethargy, convulsions

Agitation, tremor, convulsions

Heart rate Increased Increased Decreased (or increased)

Decreased — — Increased

Blood pressure

Increased Increased — Decreased Decreased — Increased

Temp Increased Increased — Decreased Decreased Increased Increased

Respirations

— — Increased Decreased Decreased Increased Increased

Pupils Large, reactive

Large, sluggish

Small Pinpoint — — Large

Bowel sounds

Present Diminished Hyperactive — — — —

Skin Dry skin Flushed, dry Diaphoresis — — — Diaphoresis

Misc — — “SLUDGE”a — — Vomiting Vomiting

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Detoxification

Reassess ABCDs GI decontamination:

Dilution, gastric emptying, Activated charcoal, catharsis, whole bowel irrigation

Urgent antidotal therapy Consider excretion enhancement

Diuresis, urine alkalinization, dialysis, hemoperfusion

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Case 1 “lethargic”

4 year old w/ ALOC Grandmother called 911 when girl

was not arousable VS: T 37.6 HR 60 RR 18 BP 80/60

Pulse Ox 98%

Differential?

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MNEMONIC FOR ALOC A- Alcohol E- Epilepsy I- Insulin/intussusception O-Overdose U- Uremia T- Trauma I- Infection P- Psychiatric S- Shock

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PE: 1mm pupils reactive Dry skin No trauma except for “bandaid” on

Rt knee

Diagnosis?

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Clonidine patch on Rt knee Fluid resuscitation- NS20ml/kg Naloxone w/ no effect Admitted to PICU D/C next day

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Outline




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Brown Recluse Spider(Loxosceles)

Southern and mid-western states Brown violin shaped mark on

dorsum of cephalothorax Usually outdoors, but make indoor

nests in closets Shy and will only attack when

provoked Venom is cytotoxic and hemolytic

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Clinical presentation 2-8 hours

Local reaction with mild-moderate pain (stinging sensation)

Erythema, central blister or pustule 24 hours

Fever, chills, malaise weakness, N/V, rash with petechiae, joint pain, DIC, hematuria, renal failure

Subcutaneous discoloration that spreads over 3-4 days

Spreads to 10-15 cm Pustule drains leaving ulcerated crater that scars

Scar formation is rare after 72 hrs Reaction varies according to amount of envenomation

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Management Unless spider is brought for ID, definitive

diagnosis cannot be made Good local wound care If systemic symptoms, then CBC with platelets,

U/A, BUN, creatinine Vigorous supportive care in PICU

Surgical excision and skin grafting after necrosis is demarcated

Steroids, heparin, and hyperbaric O2 don’t work No Dapsone for kids – methemoglobinemia No antivenom available Have wound rechecked daily for progression

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Black Widow Spider(Latrodectus)

Shiny black spider with brilliant red hourglass marking on abdomen

Only the female bite is dangerous Male spiders are ¼ the size of

females and bite cannot penetrate human skin

Females not aggressive unless provoked or guarding egg sac

Produces a neurotoxin

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Clinical presentation

No local symptoms 1-8 hours after bite

Generalized pain and muscle rigidity Cramping pain to abdomen, flanks, thighs,

chest Chills Urinary retention Priapism Death from cardiovascular collapse

Mortality 50% in young children

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Management Supportive ABC’s Tetanus Treatment of spasm with narcortics and

benzo’s Children < 40kg: Antivenin given as

soon as bite confirmed Dose: 2.5ml (one vial)

Children >40kg: not as urgent to give immediately unless having respiratory difficulty or significant hypertension

Admit to PICU

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Other Spiders…

Tarantulas Do not bite unless provoked Venom is mild and not a problem

Wolf Spider and Jumping spider Mild venom only causes local

reaction Treatment is good local wound

care

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Snake characteristics cold blooded (seeks shelter at 55

degrees) - poor vision, great smell - slow but can strike 11 feet/sec. - Rattles are interlocking keratin rings - Jacobson’s organ at end of the forked

tongue used to ID prey - venom with potent enzymes that effect

coagulation, multi-organ function Play major role in ecosystem as rodent

predators

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Snakes Bites

Epidemiology approx 400,000 bites worldwide Approx 45,000 bites in USA Approx 8,000 poisonous bites 5-15 deaths annually

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Snake Types Over 95% in the pit viper

(Crotadilae) family: Eastern

diamondback rattlesnake (Crotalus)

Copperhead (Agkistrodon)

Cottonmouth (Agkistrodon)

- 1% Coral snake(elapidae) family

Georgia is home to 41 different snakes of which 6 are venomous

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Pit Vipers (Crotalinae) Rattlesnakes,

cottonmouths, water moccasins

Proteolytic enzymes and anticoagulant esterases=> digest victim!!

Mojave rattlesnake only pit viper with neurotoxin venom

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Clinical Presentation Local effects:

edema within 1 hr (mod-severe bites) spreads centrally over 8-24hrs.

Ecchymosis, Petechiae and Hemorrhagic bullae

Systemic Effects: Nausea, vomiting, paresthesias,

dizziness, and diaphoresis. In severe envenomations-hypotension, rhabdomyolysis, renal failure and AMS

Coagulopathy: Increase in PT, PTT, thrombocytopenia

and hemolysis. DIC in severe cases

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Coral snakes

Eastern coral snake:AR, NC, SC, FL, GA, LA, MS, TX

Local damage usu mild and doesn’t correlate with severity of envenomation

All confirmed coral snake envenomations are defined as severe and require antivenom

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Clinical Presentation

Mild local finding Venom potent neurotoxin

Paresthesia, weakness, cranial nerve dysfunction, confusion, fasciculations, and lethargy

Common early sx:diplopia, ptosis, and dysarthia

Nausea, vomiting, and salivation are also common

Respiratory paralysis common cause of death

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Lab evaluation

CBC, coagulation studies, DIC panel

CK, renal function, UA Type and crossmatch in severe

envenomations

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Prehospital treatment

Prehospital Remove from vicinity of snake Immobilize bite site below heart

level Minimize all physical activity

(decrease absorption) DO not incise bite marks Transport to nearest hospital

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ED management ABC, IV hydration Coral snakes: monitor neurologic sx

(intubate if resp compromise) Antivenom (moderate to severe pit vipers

and all confirmed eastern coral snake bites)

Admission criteria: admit all pts w/ confirmed coral snake bites; if no envenomation observe for 6hr; if local pain or erythema, observe for 12hr; admit all pts with progressive symptoms to ICU; bitten by Mojave rattlesnake or exotic snake

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Question 1

The four major steps in treatment of any poisoned patient include all of the following EXCEPT: A. prompt hemodialysis or hemoperfusion B. decontamination and prevention of absorption,

while preventing contamination of health care workers

C. support of vital signs (ABCs) and symptomatic treatment specific antidote, if available

D. enhancement of toxin excretion or elimination

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Question 2

Syrup of Ipecac is the first line

therapy for gastric decontamination

of the poisoned patient: A. True B. False

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Question 3

Very few drugs are fatal for a 10 kgtoddler upon ingestion of onecommercially available dose unit.Examples of drugs in which ingestionof one dose can be potentially fatal inthis population include all of thefollowing EXCEPT:A. ChloroquineB. TCAC. Calcium Channel BlockersD. SSRI’s

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Question 4

Which of the following statements is TRUEregarding intentional overdoses? A. Intentional overdoses are most

commonly seen in the preschool age group.

B. These overdoses are usually of one agent known to be lethal.

C. Intentional overdoses frequently involve more than one agent Intentional overdoses are seldom fatal.

D. None of the above are TRUE.

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THANK YOU

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Reference Fine SJ. Pediatric Principles. Goldfrank LR et al.

editors Goldfrank’s Toxicologic Emergencies. 8th Edition. Mc Graw-Hill;

Henry K, Harris CR. Deadly Ingestions. Pediatr Clin N Am 53 (2006) 293-315

Ranniger C. Roche C. Are one or two dangerous? Calcium Channel Blocker Exposure in Toddlers. Journal of Emergency Medicine. Vol 33 No.2. 145-154, 2007

Eldridge DL, Van Eyk J, Kornegay C. Pediatric Toxicology. Emerg Med Clin N Am 15 (2007) 283-308

Carson RH. The toxicology handbook for clinicians. Mosby, 2006

Pediatric Toxicology Pills and poisonous bites High Yield

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