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Board Review 12/17/2012
What topic should we do for January Board
Review?
A. Adolescent
B. Disorders of the eye
C. Sports Medicine and Physical Fitness

Multiple VERY helpful resources
 Data on signs and symptoms of toxicities
 Can help identify unknown toxins
 Management of ingestions
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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
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Emetics (ie syrup of ipecac)
Gastric Lavage
Activated Charcoal
Cathartics
Whole bowel irrigation
A 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 ipecac
B. Observation
C. Administer activated charcoal
D. Administer N-acetylcysteine
E. Draw an atenolol level
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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:
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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
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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
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Cathartics (laxatives)
 Limited use; ? Benefit
 Sometimes given with dose of AC
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Whole bowl irrigation
 Enteral administration of osmotically balanced
solution
 Can be used after AC
 Used for “body packers”
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 determination
B. Bedside glucose
C. Blood alcohol level
D. Serum osmolality
E. Urine toxicity
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Beverages, cough medications, mouthwashes,
aftershaves
 Multiple over-the-counter preparations
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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
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May mask toxicities from other ingestion drugs**
 Effects of stimulants are blunted
 Effects of other depressants may be potentiated
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Lab workup
 Ethanol level, serum electrolytes, glucose
 Watch for hypokalemia
 Screen for other ingestions
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Management
 Supportive, IVFs
 Correct electrolytes/glucose
 No antidote; good prognosis
Your 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 glycol
B. Sodium bicarbonate
C. Leucovorin
D. Folate
E. Hemodialysis
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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
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Testing: methanol level, ABGs
Treatment:
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Sodium bicarb for acidosis
Folate or leucovorin (can help eliminate formic acid)
Ethanol: can help decrease formation of metabolites
Hemodialysis for severe cases
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Most commonly: Antifreeze
Causes severe metabolic acidosis and formation of
calcium oxalate crystals in vital organs
 Hypocalcemia
 Nephrotoxicity
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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
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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
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 screen
B. Perform gastric lavage
C. Reassure the father and discharge the patient home
D. Obtain a STAT chest CT
E. Place the child under observation
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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
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Diagnosis
 Based on history, signs/symptoms of respiratory
involvement
 If symptomatic: ABG, CXR
 CXR findings can lag 4-6hrs after aspiration
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Management
 Asymptomatic patients: observe for 4-6 hrs
 If abnormal CXR: consider admitting
 Symptomatic: admit
 Supportive care; no use for abx or steroids
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Prognosis: good
 Chemical pneumonitis often resolves completely
 Rarely will have long term problems (pneumatoceles)
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Amitriptyline, clomipramine, desipramine, etc
 Used in children to treat enuresis
 Block acetylcholine, prevent reuptake of norepinephrine,
and block sodium channels in the myocardium
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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
You 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 edema
B. EKG to monitor for dysrhythmia
C. ECHO to assess cardiac function
D. EEG to identify a seizure focus
E. Serum measurement of imipramine
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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
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OTc prolongation
Rightward shift of axis
AV block
Ventricular dysrhythmias
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Management
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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)
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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
A 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 attempts
C. How long ago the ingestion took place
D. A blood gas measurement
E. Glucose measurement
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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
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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
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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
A 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. Atropine
B. N-actylcysteine
C. Naloxone
D. Physostigmine
E. Ethanol
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Found in a wide array of products
 Herbicides, pesticides, lawn care
 70% of exposures occur due to ingestion of improperly
stored products
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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
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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
A 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.
B.
C.
D.
E.
Abdominal xray
EKG
Serum creatine phosphokinase
Serum sodium
Head CT
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Ingestions most common in children < 6yo
 Fewer than 10% result in need for medical treatment
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Most ingestions are small in quantity and symptoms
are generally short-lived
 GI effects are most common
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Treatment based on suspected ingestion/symptoms
 ABCs
 Decontamination: activated charcoal
 Reversal:
 Physostigmine for anticholinergic ingestion
 Cardiac monitoring for cardiac glycoside ingestion
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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, agitation
Cardiac: HTN, tachycardia
Other: blurred vision, dry mouth,
flushing, hyperthermia
Solanum (tomatoes,
potatoes, eggplant)
Blossoms or
unripe buds
Anticholinergics
As above
parasympathetic
Miosis, bronchorrhea, GI
distress, neuromuscular
derangement
Cardiac glycosides
CNS: sedation
Cardiac: conduction
abnormalities (PR prolongation,
QT shortening, bradycardia,
ventricular arrhythmia)
Hyperkalemia
Tobacco plant
Digitalis (foxglove),
Convallaria (lily of the
valley) Nerium (oleander)
All, especially
seeds
Mistletoe berries
Berries
Prunus (cherries, apricots,
peaches, apples, plums)
Seeds, pits
Mushrooms (ie Amanita)
GI distress
Cyanide
Potentially lethal
amatoxins
Nausea, vomiting, diarrhea
Late onset: fulminant hepatitis
A 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 hemorrhage
B. Acetaminophen ingestion
C. Metoprolol ingestion
D. Sepsis
E. Aspirin ingestion

Remains one of the most serious ingestions in the
pediatric population
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Toxic dose for a child = >150mg/kg
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Salicylates are found in various household products
(not just in Aspirin tablets)
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Mouthwash
Face cleanser
Powders
Bismuth compounds
ETC…
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Symptoms
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Nausea and vomiting from DIRECT gastric irritation.
Altered hearing…usually tinnitus
Fever
Altered mental status
 Agitation
 Seizures
 Stupor and coma
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Signs
 Tachypnea
 Tachycardia
 Non-cardiac pulmonary edema (due to increased vascular
permeability)
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Anion gap metabolic acidosis!!
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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

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
You 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 lavage
B. Alkalinization of the urine
C. N-acetylcysteine
D. 100% Oxygen
E. Acidification of the urine

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
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Dialysis if level >100mg/dL or other worrisome signs
Intubation can suppress hyperventilation and may be
dangerous!

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

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

People living in the same home present with similar,
nonspecific symptoms
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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
A 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 monitoring
B. Place the patient on 2L of O2 at 40% FiO2
C. Obtain a carboxyhemoglobin measurement
D. Administer IV Methylene Blue
E. Arrange for emergent hyperbaric oxygen therapy

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
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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
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EKG monitoring for cardiac dysrhythmia

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

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Corrosives are concentrated acid, alkaline, or
oxidizing agents
Many are common household products
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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.

Depend on the amount and pH of the substance and
the nature of the contact
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Drooling, dysphagia
Stridor or wheezing
Burns on the mucosa, lips, chin, hands, nose, and chest
Odynophagia
Dysphonia
Nausea/vomiting
Chest pain
Hoarseness
Hematemesis
A 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 corrosive
B. Ethanol
C. An alkaline corrosive
D. Diet coke
E. Acetaminophen

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

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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
A 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.
B.
C.
D.
E.
Administer activated charcoal
Give syrup of ipecac
Perform a gastric lavage
Observe overnight and the DC without further intervention
Consult GI for an urgent endoscopy
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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

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

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.
What is the BEST method to screen for ALL types of
environmental exposure in your general pediatrics
patients?
A.
B.
C.
D.
E.
Obtain lead levels every 2 years on all patients
Send a heavy metal screen on everyone
Sample the drinking water of your patients
Obtain a thorough environmental exposure history
Do a personal assessment of all patient homes

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.

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.
What are the two MOST COMMON microbiologic
WATER contaminants of concern for children?
A.
B.
C.
D.
E.
Salmonella and Listeria
E. coli and Campylobacter
Toxoplasma and Bacillus cereus
E. coli and cryptosporidium
H. pylori and Clostridium difficile

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 characteristics, such as proximity to pesticidetreated 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.”

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!!

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”

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



Most children will be asymptomatic
Nausea/vomiting
Management:
 Supportive care for GI upset
 Obtain additional history for possibility of co-ingestion
(especially in adolescents)

Clinical signs





Depressed sensorium
Bradycardia
Hypotension
+/- diaphoresis
Management
 Observation on a CR monitor

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

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


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

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

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

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