POISONINGS AND ENVIRONMENTAL EXPOSURES

Board Review 12/17/2012

Test QuestionWhat topic should we do for January

Board Review?A. AdolescentB. Disorders of the eyeC. Sports Medicine and Physical Fitness

POISONING BASICS…

Poison Control Centers Multiple VERY helpful resources

Data on signs and symptoms of toxicities Can help identify unknown toxins Management of ingestions

1-800-222-1222 Always have a high level of suspicion with

an ingestion that there may be multiple agents involved i.e. check an acetaminophen level when

another ingestion is suspected Very few initial signs/symptoms but high potential

for poor outcome if missed

Basic Therapeutic Options for GI Decontamination Emetics (ie syrup of ipecac) Gastric Lavage Activated Charcoal Cathartics Whole bowel irrigation

Question #1A 4 year old is brought in by her parents because

20 minutes ago they found her playing with an empty bottle of grandmas atenolol which they knew previously had approximately 15 pills in it. You have a high suspicion that she ingested the medicine. She is anxious appearing but awake and alert with a heart rate of 70 and BP of 82/39. Which of the following would be the most appropriate action at this time?

A. Administer syrup of ipecacB. Observation C. Administer activated charcoalD. Administer N-acetylcysteineE. Draw an atenolol level

GI Decontamination Emetics (ie syrup of ipecac) or gastric lavage

No longer recommended for use in the home or ER Only possible use must meet these criteria:

Consultation with qualified medical personnel Substantial risk or serious toxicity of the substance

ingested No access to any alternative therapy for at least 1 hour Administration within 30-90 minutes of ingestion Administration will not adversely affect later treatment

(ie activated charcoal or N-acetylcysteine Absolute contraindications:

Severe HTN or bradycardia Risk of or current AMS Ingestion of caustic, corrosive or hydrocarbon

substance

GI Decontamination Activated Charcoal

Organic product with numerous micropores that allow a large surface area of absorption **ONLY method of GI decontamination

supported by poison control centers** Discussion about use in homes

Best if within 60 minutes of ingestion Not for use when ingested substances

are alcohols, corrosives, iron, or lithium; caution with hydrocarbons

Dosing:0.5-1g/kg (adult range 25-100g); 10:1 ratio of AC to ingested toxin

Can drink or give via OG/NG Contraindicated in patients with

unprotected airway

GI Decontamination Cathartics (laxatives)

Limited use; ? Benefit Sometimes given with dose of AC

Whole bowl irrigation Enteral administration of osmotically

balanced solution Can be used after AC Used for “body packers”

Question #2 A 3yo boy is brought to the ER at 7AM after his

parents found him unresponsive in bed. The last time they saw him was at 2AM while they were cleaning up from a cocktail party. On exam he has diaphoresis and moans to painful stimuli. His vitals are T96.4, HR145, RR20, BP 83/34, Sp02 98%. His pupils are mid-sized and sluggish. Of the following, what is the MOST important test to obtain at this time?

A. Acetylcholinesterase determinationB. Bedside glucoseC. Blood alcohol levelD. Serum osmolalityE. Urine toxicity

Ethanol (ethyl alcohol) Beverages, cough medications,

mouthwashes, aftershaves Multiple over-the-counter preparations

Clinical features Dose-related CNS depressant

Ingestion of 0.5g/kg (1.5ml/kg body weight) can produce intoxication in a young child

Induces hypoglycemia (especially in children)** Metabolism of ethanol creates a relative lack of

pyruvate blocks gluconeogenesis hypoglycemia Hypothermia, inebriation, vomiting, ataxia,

respiratory depression, coma, hypotension, death

Ethanol (ethyl alcohol) May mask toxicities from other ingestion

drugs** Effects of stimulants are blunted Effects of other depressants may be potentiated

Lab workup Ethanol level, serum electrolytes, glucose

Watch for hypokalemia Screen for other ingestions

Management Supportive, IVFs Correct electrolytes/glucose No antidote; good prognosis

Question #3Your 3yo child loves blueberry soda. You found

him in the garage with an empty bottle of Windex. Upon arrival to the ER the child is lethargic and minimally responsive to painful stimuli. An ABG shows 7.11/30/60/12. All of the following are possible treatment modalities for this child, EXCEPT:

A. Ethylene glycolB. Sodium bicarbonateC. LeucovorinD. FolateE. Hemodialysis

Methanol Windshield wiper fluid, cooking fuel, perfumes Methanol itself causes n/v, inebriation Metabolites (formaldehyde and formic acid)

are more toxic CNS depression, anion gap acidosis (can cause

multiorgan dysfunction), optic changes Testing: methanol level, ABGs Treatment:

Sodium bicarb for acidosis Folate or leucovorin (can help eliminate formic acid) Ethanol: can help decrease formation of metabolites Hemodialysis for severe cases

Ethylene glycol Most commonly: Antifreeze Causes severe metabolic acidosis and

formation of calcium oxalate crystals in vital organs Hypocalcemia Nephrotoxicity

Treatment Gastric emptying (if within 1hr) Correction of acidosis and hypocalcemia Thiamine and pyridoxine

Cofactors in the non-toxic pathway of ethylene glycol metabolism

Hemodialysis

Hydrocarbons Gasoline is most

common exposure Irritating to GI and

respiratory tract Primary concern:

chemical pneumonitis Aspirated low-viscosity

hydrocarbons spread to large areas of lung; destroy surfactant; alveolar collapse; VQ mismatch; hypoxemia

Direct capillary damage also leads to pneumonitis

Question #4 A2yo boy is brought to the emergency department by

his father after they had spent several hours in the garage while the father worked on the car. The father reports that approximately 30 minutes ago he heard the child coughing and found him with an open bottle of lighter fluid in his hands. On exam, the child is awake and alert; temperature is 37.0°C, HR is 120 beats/min, RR is 24 breaths/min, BP is 90/60 mm Hg, and 02 sat 98%. Of the following, the MOST appropriate next step is to:

A. Obtain urine tox screenB. Perform gastric lavageC. Reassure the father and discharge the patient homeD. Obtain a STAT chest CTE. Place the child under observation

Hydrocarbons Clinical manifestations

Initial: oropharyngeal and gastric irritation Coughing and choking: could indicate inhalation of

fumes; does not necessarily imply aspiration Vomiting from gastric irritation

Aspiration: significant coughing and respiratory distress “petroleum” smell on breath, tachypnea, retractions,

bronchospasm, wheezing, rales, Fulminant chemical pneumonitis: marked SOB and

hypoxemia Fever within 6 hrs indicates tissue damage (not

infection) Pulmonary damage reaches peak at 3 days after

aspiration

Hydrocarbons Diagnosis

Based on history, signs/symptoms of respiratory involvement

If symptomatic: ABG, CXR CXR findings can lag 4-6hrs after aspiration

Management Asymptomatic patients: observe for 4-6 hrs

If abnormal CXR: consider admitting Symptomatic: admit

Supportive care; no use for abx or steroids Prognosis: good

Chemical pneumonitis often resolves completely Rarely will have long term problems (pneumatoceles)

Tricyclic antidepressants(TCA) Amitriptyline, clomipramine, desipramine, etc

Used in children to treat enuresis Block acetylcholine, prevent reuptake of

norepinephrine, and block sodium channels in the myocardium

Clinical toxicity begins with 6-8hrs of ingestion and peaks within 24hrs**

Clinical effects: Anticholinergic!

Dry mouth, ileus, dilated pupils, urinary retention, tachycardia, HTN, flushed

CNS: delirium, agitation, restlessness, hallucinations, convulsions

Life threatening toxicity due to cardiac dysrhythmias

Question #5You are called by the mother of a 3-year-old girl

because the child appears confused and is pale and sweating. The mother thinks the child may have taken some of her grandmothers imipramine. You advise her to call 911 to have her taken to the ER. Of the following, what is the most appropriate action to take in the ER?

A. CXR to evaluate for pulmonary edemaB. EKG to monitor for dysrhythmiaC. ECHO to assess cardiac functionD. EEG to identify a seizure focusE. Serum measurement of imipramine

TCAs Work-up

Can check serum levels, but results do not contribute to treatment decisions

EKG** Can help identify significant conduction defects

Prolonged PR Widened QRS

Single most useful prognostic indicator for convulsions or dysrhythmias

OTc prolongation Rightward shift of axis AV block Ventricular dysrhythmias

TCAs Management

Activated charcoal for GI decontamination CNS toxicity (convulsions) respond to benzos Serial EKGs/monitor for the first 6 hrs after ingestion For cardiac dysrhythmias:

Cardiac monitoring Continued until all toxic effects have resolved for 24hrs

Sodium bicarb (1-2Meq/kg) Prognosis is good

Resolution of toxicity generally in 24-48hrs Can have late (2-5days after overdose) fatal

dysrhythmia but this is found in seriously ill patients

Question #6A 16yo girl is brought to the ER by her parents

after she admitted to taking two handfulls of acetaminophen (500mg) because her boyfriend broke up with her. Which of the following is the MOST important piece of information you must obtain in order to determine your next course of action?

A. The name and address of the boyfriend B. History of previous suicide attemptsC. How long ago the ingestion took placeD. A blood gas measurementE. Glucose measurement

Acetaminophen One of most common medications used

to treat fever and pain in children Most common analgesic overdose in

children less than 6yo Toxicity arises from metabolism of the

drug During hepatic metabolism of large doses, a

toxic metabolite accumulates in the hepatocyte and causes damage to liver cells

Minimum toxic dose: 140mg/kg Severe toxicity for ingestions >250mg/kg

Acetaminophen Initial signs/symptoms: nonspecific;

nausea/vomiting Within 18-24hrs hepatic damage may

become evident with increased LFTs If not treated, hepatic damage may worsen Either gradually resolves OR if severe, will

progress to severe hepatic damage hepatic failure Hepatic failure:

Coagulation abnormalities Encephalopathy

In young children: altered ‘sleep/wake’ cycles, irritability

Acetaminophen Only accurate predictor

of hepatic toxicity from acetaminophen is measurement of a level 4-10hrs after overdose Levels that fall above

nomogram line may be associated with hepatic damage

Treatment N-acetylcysteine

Should be started within 10 hours of ingestion

Question #7A 7 yo boy is brought to the ER due to altered mental

status. He was well when he came home from school, but when he came inside for dinner after playing outside with friends he complained of abdominal pain and had an episode of NBNB emesis. Over the next 30 min he became increasingly lethargic. In the ER, he is unresponsive and drooling. Temp is 98.8, HR is 50, RR is 36, BP is 100/60. Sp02 is 82% on room air. Pupils are small and sluggish. Breath sounds are coarse bilaterally with increased WOB. You suspect a toxin exposure. What is the most appropriate treatment?

A. AtropineB. N-actylcysteineC. NaloxoneD. PhysostigmineE. Ethanol

Organophosphates Found in a wide array of products

Herbicides, pesticides, lawn care 70% of exposures occur due to ingestion of

improperly stored products Mechanism of action: (Cholinergic poisoning)

Irreversibly inhibits acetylcholinesterase leads to accumulation of acetylcholine excess acetylcholine overstimulates muscarinic, nicotinic, central receptors Muscarinic: “SLUDGE” (salivation, lacrimation,

urination, diarrhea, gastric emesis), miosis, bronchorrhea/resp distress, sweating, bradycardia, hypotension

Nicotinic: muscle twitching, weakness, paralysis Central: confusion/AMS, HA, tremor, seizure, coma

Organophosphates Treatment

Decontamination Skin washing, activated charcoal

Blocking effects of excess acetylcholine Atropine: give every 10-30min until

muscarinic effects gone Reactivating acetylcholinesterase

Pralidoxime: best if given within 24-48hrs Supportive measures

Ventilation, IVFs, vasopressors

Question #8A 2-year-old boy is brought to the emergency department

after his father found him with the leaf from a foxglove plant in his mouth. He has had one episode of emesis and is complaining of abdominal pain. On physical examination, his heart rate is 140 beats/min, respiratory rate is 24 breaths/min, blood pressure is 100/60 mm Hg, and oxygen saturation is 100%. His pupils are 4 mm and briskly reactive to 2 mm. The remainder of his examination findings are normal. After administering activated charcoal, what is the most appropriate next step?

A. Abdominal xrayB. EKGC. Serum creatine phosphokinaseD. Serum sodiumE. Head CT

Toxic Plants Ingestions most common in children < 6yo

Fewer than 10% result in need for medical treatment Most ingestions are small in quantity and

symptoms are generally short-lived GI effects are most common

Treatment based on suspected ingestion/symptoms ABCs Decontamination: activated charcoal Reversal:

Physostigmine for anticholinergic ingestion Cardiac monitoring for cardiac glycoside ingestion

Call poison control for ANY question** They can help identify unknown plant

Plant Toxic part

Toxin/Class Clinical Features

Datura (jimson weed) Atropa belladonna (nightshade

All parts Atropine, scopolamine, hyoscyamine (anticholinergics)

CNS: hallucinations, agitationCardiac: HTN, tachycardiaOther: blurred vision, dry mouth, flushing, hyperthermia

Solanum (tomatoes, potatoes, eggplant)

Blossoms or unripe buds

Anticholinergics As above

Tobacco plant parasympathetic Miosis, bronchorrhea, GI distress, neuromuscular derangement

Digitalis (foxglove), Convallaria (lily of the valley) Nerium (oleander)

All, especially seeds

Cardiac glycosides CNS: sedationCardiac: conduction abnormalities (PR prolongation, QT shortening, bradycardia, ventricular arrhythmia)Hyperkalemia

Mistletoe berries Berries GI distress

Prunus (cherries, apricots, peaches, apples, plums)

Seeds, pits Cyanide Potentially lethal

Mushrooms (ie Amanita)

amatoxins Nausea, vomiting, diarrhea Late onset: fulminant hepatitis

Question #9A 2 year old boy is brought to the ER because he

has been difficult to arouse for an hour. The child is somnolent and responsive only to pain. His temperature is 101.5, HR 130, RR 56, and BP 90/60. ABG reveals pH 7.28/CO2 20/HCO3 15. The patient and his mom have been staying with grandma for the holidays. Mom is healthy, but the grandma takes a few different medications. The most likely explanation for this child’s findings is

A. Intracranial hemorrhageB. Acetaminophen ingestionC. Metoprolol ingestionD. SepsisE. Aspirin ingestion

SALICYLATES

Aspirin Toxicity Remains one of the most serious

ingestions in the pediatric population

Toxic dose for a child = >150mg/kg

Salicylates are found in various household products (not just in Aspirin tablets) Mouthwash Face cleanser Powders Bismuth compounds ETC…

Clinical Manifestations Symptoms

Nausea and vomiting from DIRECT gastric irritation.

Altered hearing…usually tinnitus Fever Altered mental status

Agitation Seizures Stupor and coma

Signs Tachypnea Tachycardia Non-cardiac pulmonary edema (due to increased

vascular permeability)

Laboratory Findings Anion gap metabolic acidosis!!

Methanol toxicity Uremia Diabetic Ketoacidosis Paraldehyde ingestion Iron/INH toxicity Lactic acidosis Ethylene glycol ingestion SALICYLATES So be sure to rule these things out!

Respiratory alkalosis **in young children the metabolic acidosis tends

to predominate

Laboratory Findings Global hypokalemia due to K+ excretion in the

urine Initial alkaline urine

HCO3 excreted in response to the respiratory alkalosis Later…acidic urine as the kidney tries to preserve

K+ in exchange for H+ (which is excreted) Paradoxic aciduria in the face of respiratory alkalosis is

a hallmark of aspirin toxicity Salicylate levels

Peak 4-6 hours after ingestion Correlate poorly with clinical symptoms Should be followed q2-4 hours until decreasing or

<30mg/dL

Question #10You are admitting a patient to the PICU with

findings suspicious for Aspirin toxicity. The patient was initially awake upon presentation and was already given activated charcoal. The initial salicylate level was 80mg/dL. You know that aside from supportive care, the next BEST step to enhance salicylate elimination is…

A. Gastric lavageB. Alkalinization of the urineC. N-acetylcysteineD. 100% OxygenE. Acidification of the urine

Treatment Upon presentation

Activated charcoal if the patient is alert Gastric lavage is NOT usually recommended UNLESS

Ingestion was a large, life-threatening dose Brought to medical attention within 1 hour

Correction of metabolic derangements and dehydration Fluid boluses Alkalinization to enhance salicylate elimination

Goal serum pH 7.5 , goal urine pH >7.5 Rec: 1-2 mEq/kg bolus of NaHCO3 followed by a NaHCO3

drip **Add K+ to fluids of patients without renal failure

Dialysis if level >100mg/dL or other worrisome signs Intubation can suppress hyperventilation and may be

dangerous!

CARBON MONOXIDE

Carbon Monoxide Has no color, odor, or taste

Has come to be known as the “silent killer”

Accounts for most of the poisoning deaths in the US 300-500 people die annually from

unintentional poisoning We, as pediatricians, need to be able to

recognize the signs and symptoms

Pathophysiology CO is inhaled and absorbed into the

bloodstream Forms carboxyhemoglobin by binding to

hemoglobin with an affinity 250x that of oxygen Unable to transport oxygen Reduces oxygen delivery to the tissues by

interfering with the dissociation of oxygen from the remaining oxyhemoglobin molecules

People (and organs) with higher metabolic rates are affected most Infants and children are at a greater risk Neurologic, cardiac, and pulmonary

manifestations are seen more often

Clinical Manifestations People living in the same home present with

similar, nonspecific symptoms Fatigue Dizziness Headache Nausea Irregular breathing or dyspnea on exertion Palpitations Irritability/confusion/irrational behavior

Patients may appear pale or cyanotic Symptoms can progress to LOC and death Symptoms may improve when patient leaves

the place of exposure

Question #11A 5 year old boy is brought to the ED for 2 days of HA,

nausea, and vomiting. He is afebrile and does not have diarrhea. Everyone at home, including the dog, has the same symptoms. On PE, he is mildly irritable but alert and oriented, and his mucous membranes appear bright red. His lung exam is clear, but he does have some mild increased WOB. Sats are 100% on RA. What is the MOST appropriate next step?

A. Admit the patient for continuous pulse ox monitoringB. Place the patient on 2L of O2 at 40% FiO2C. Obtain a carboxyhemoglobin measurementD. Administer IV Methylene BlueE. Arrange for emergent hyperbaric oxygen therapy

Diagnosis Measurement of carboxyhemoglobin levels

can confirm exposure. Extent of exposure and/or measure CO-Hb

levels may not correspond to severity

O2 saturations obtained by routine pulse ox is falsely normal because O2-Hb and CO-Hb cannot be differentiated on standard pulse ox techniques

ABG: metabolic acidosis with a normal PaO2

Management Separate patient from the source of CO

exposure Decrease oxygen consumption by maintaining

bedrest and diminishing anxiety Oxygen

Should be provided until symptoms resolve and CO-Hb levels decrease to 5% or less

100% O2 via non-rebreather mask Decreases elimination half-life of CO to 1 hour

Ventilatory support if needed Hyperbaric oxygen

Indications for use are debatable EKG monitoring for cardiac dysrhythmia

Prevention Counsel parents on important sources of

exposure for children Traveling in vehicles Living in homes with poorly ventilated gas

cooking and heating appliances Vehicles idling in attached garages

Carbon monoxide detectors Show promise Effect on saving lives has not been

demonstrated

CORROSIVES

Corrosive Ingestion Corrosives are concentrated acid, alkaline,

or oxidizing agents Many are common household products

Laundry detergent Toilet bowl cleaner Stain and mildew removers Various cleaners Batteries Bleaches ETC!

These products are often attractive to children and easily accessible in the home.

Clinical Manifestations Depend on the amount and pH of the

substance and the nature of the contact Drooling, dysphagia Stridor or wheezing Burns on the mucosa, lips, chin, hands, nose,

and chest Odynophagia Dysphonia Nausea/vomiting Chest pain Hoarseness Hematemesis

Question #12A 3 year old boy was admitted for inpatient

observation after presenting to the ER with a suspected corrosive ingestion. The patient was initially stable with no mucosal burns in his oropharynx. In fact, his examination on admit was normal except for fussiness. 48 hours later, the patient begins with gross hematemesis. Which agent was MOST likely ingested?

A. An acidic corrosiveB. EthanolC. An alkaline corrosiveD. Diet cokeE. Acetaminophen

Clinical Manifestations Alkaline ingestions

Cause deep, more extensive burns that may take longer to heal

Cause liquefactive necrosis and tissue edema that affects the squamous epithelium

Tend to injure the esophagus and pharynx Acidic ingestions

Burn the top layer or skin, so children tend to stop drinking these substances more quickly

Cause coagulation necrosis Squamous epithelium of OP and esophagus are fairly

resistant MORE likely be transported straight to the stomach and

manifest a little later Severe hematemesis, gastritis, strictures, gastric outlet

obstruction

Question #13A 2-year-old boy is brought to the emergency department after his mother found him with an open bottle of toilet bowl cleaner. She reports that he had spilled some on his shirt and had some on his face, but she does not know if he drank any of it. The child is awake and alert, and his vital signs are normal. He is drooling slightly, but examination of his oropharynx reveals no lesions.Of the following, the MOST appropriate next step is to

A. Administer activated charcoalB. Give syrup of ipecacC. Perform a gastric lavageD. Observe overnight and the DC without further

interventionE. Consult GI for an urgent endoscopy

Management ABCs…with particular attention to airway! NO syrup of ipecac NO gastric lavage

Re-exposes damaged mucosa to same corrosive agent

Can lead to more necrosis and further damage Labs/Imaging

Electrolytes, BUN/Cr, ABG if respiratory distress CXR to ensure no signs of aspiration

pneumonitis, mediastinitis, or pleural effusion Endoscopy

Within 12-48 hours!!! Assess extent of injury and look for

burns/stricture/bleeding

Anticipatory Guidance All household products should be

moved up and our of the reach of children

Corrosives should NOT be placed in unlabeled containers or food containers. They should be kept in the original packaging.

Large labels/symbols of poison should be marked on the product, and kids should be taught the meaning of these symbols.

1-800-222-1222 kept close to phone

ENVIRONMENTAL CONTAMINANTS

Environmental Contaminants Most health conditions associated with contaminants in food, water, the home, and the community present initially to the primary care physician.

Children’s susceptibility to environmental contaminants differs from adults. Fetal development is affected by exposure to drugs,

chemicals, and infections. Carcinogenic cells have more time to develop into

tumors. Children eat more food, drink more water, and breathe

more air than adults on a per kilogram basis…so they receive a “higher dose” of contaminant.

Unique developmental stages increase their exposure to certain contaminants.

Question #14What is the BEST method to screen for ALL types of environmental exposure in your general pediatrics patients?

A. Obtain lead levels every 2 years on all patients

B. Send a heavy metal screen on everyoneC. Sample the drinking water of your patientsD. Obtain a thorough environmental exposure

historyE. Do a personal assessment of all patient

homes

Exposure History One of the most important tools in discerning the

importance of environmental hazards for health consequences or to prioritize anticipatory guidance is the environmental history!

Ask about generally recognized exposures of concern Tobacco smoke, lead, radon, pesticides, parents’ occupations

Also focus on more locally relevant factors Toxic waste sites, wood smoke, well water, sports fishing

In the context of illness or disease, an environmental history helps discern the link between environmental factors and the nature, onset, worsening, and improvement of symptoms.

Exposure History

Drinking Water Contaminants

Community or public drinking water supplies are regularly monitored under the Safe Drinking Water Act.

This oversight does not apply to the 15-20% of households in the U.S. that obtain their water from private wells.

Asking patients about their sources of drinking water, such as whether it is from a public source or private well is a key component of the environmental history.

Question #15What are the two MOST COMMON microbiologic WATER contaminants of concern for children?

A. Salmonella and ListeriaB. E. coli and CampylobacterC. Toxoplasma and Bacillus cereusD. E. coli and cryptosporidiumE. H. pylori and Clostridium difficile

Drinking Water Contaminants

Arsenic Known human carcinogen and potential neuro-developmental

toxin Lead

20% of child’s exposure is attributable to drinking water Leaches into drinking water from lead-containing pipes “run water for 2 minutes before drinking…”

Bacteria E. coli and cryptosporidium are the 2 most common Boiling water for at least 1 minute is required for decontamination

(due to small size of cryptosporidium) Nitrate

Common contaminant in well water from sewage contamination or fertilizer

Young infants are at risk for METHEMOGLOBINEMIA due to the conversion of nitrate nitrate in their stomachs

Trichloroethylene and perchloroethylene (industrial solvents)

Community Exposures Community characteristics, such as proximity to

pesticide-treated fields, high-traffic roadways, industrial sites, or waste sites should be assessed because contaminants can affect the health of children. Pesticides Industrial wastes Traffic pollutants

The Air Quality Index can provide local information on daily air quality and help guide decisions on outdoor activities.

Pets and people can track pesticide residues from treated fields to the indoor area and contaminate surfaces where children crawl and play…”take –home pathway.”

Chemical Exposures at Home Children spend most of their time indoors at home. More than 90% of the 2 million poisonings reported each

year occur in the home Daily, low-dose exposure to contaminants may increase

chronic health risks such as asthma or cognitive/behavioral problems

Mold Leaks and water damage increase risk May result in URI symptoms, cough/wheeze/asthma in

sensitized individuals Radon

Estimated to cause 21,000 lung cancer deaths each year Comes from the radioactive decay of naturally occurring

uranium in soil, rock, and water can infiltrate through holes in foundation.

All homes below the 3rd floor should be tested!!

Chemical Exposures at Home Carbon Monoxide Improper or inadequate ventilation can allow build-up

from household combustion sources (furnace, fireplace, attached garage)

Discussion of a functioning CO detector should be a part of anticipatory guidance

Household members that work Exposures may be brought home as dust or residues

on clothing or shoes, so it is important to ask about parents’ occupations.

Examples: farmers with pesticide exposure, painters, renovation workers, chemical plants, etc.

Hygeine practices of removing work clothes/shoes and showering before entering the home can reduce the “take-home pathway”

Home Renovations Improper remediation and repair may result in

concerning indoor exposures. Asbestos

Friable ceiling material or degraded insulation around pipes, boilers, and furnaces

Use of asbestos-containing building materials has declines since the 1970s

Lead Exposure is associated with a reduced IQ and behavioral

problems, including ADHD Deteriorating lead-containing paint is the most common

cause in young children Lead dust can form when paint is scraped, sanded, or

heated Dust accumulates in windowsills, on floors, and in the soil

Lead-based paint banned in 1978 Home repairs/renovations should be performed by trained

individuals to apply special containment methods

EXTRA CONTENT SPECS

NSAIDs Most children will be asymptomatic Nausea/vomiting Management:

Supportive care for GI upset Obtain additional history for possibility of

co-ingestion (especially in adolescents)

Antihypertensives Clinical signs

Depressed sensorium Bradycardia Hypotension +/- diaphoresis

Management Observation on a CR monitor

Coin ingestion Most common foreign body ingested:

COINS 95% will pass within 4-6 days If do not progress past the stomach in 24

hrs they should be removed Esophogeal

Proximal esophagus: should be removed ASAP via endoscopy

Middle-lower esophagus: observe for 12-24 hrs if asymptomatic Endoscopy if the coin does not pass

Button Battery Management depends on location of

battery AP and lat radiographs from mouth to anus

Esophageal Batteries lodged in the esophagus should be

immediately removed with direct endoscopic visualization

Stomach Usually pass in 48hrs Reimage after 48hrs

If still present remove

Iron Toxic ingestion occurs at doses >40mg/kg of

elemental iron Clinical manifestations

Phase 1: vague GI complaints (v/d/abd pain) within 6hrs

Phase 2: Decreased GI symptoms; deceptive improvement (hours 6-24)

Phase 3: multisystem effects Metabolic acidosis Coagulopathy Cardiovascular collapse

Phase 4: obstruction due to scarring/stricture

Iron Management

ANY symptoms within 6 hours bring to medical attention

Serum iron level >350, WBC >15, glucose >150 = BAD

Symptomatic patient Abdominal films to identify iron tablets

Chelation For severe symptoms, anion gap acidosis, iron level

>500, pills visible on abdominal film Deferoxamine chelation

Causes urine to be pink/red Can be stopped once urine returns back to normal color

Terrorism Anthrax

Virtually all cases are cutaneous form Lesions: pruritic papule central bullous lesion becomes

necrotic central black painless eschar Surrounding tissue is swollen and red; no tenderness Eschar falls off in 1-2weeks

Extra pearls It is important to ask about

complimentary/alternative medicines Especially in children with complex medical

conditions such as autism Over-the-counter cough and cold

preparations have not been adequately studied in children <6yo Not recommended for use to treat common cold

Active ingredients for cold medicines Dextromethorphran, antihistamines,

pseudoephedrine, guaifenesin Multiple side effects

YAY! WE’RE DONE THANKS!!!