Transcript Pediatric Allergy and Asthma

Pediatric Allergy
and Asthma
Brenda Beckett, PA-C
Hypersensitivity Disorders
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Type I: IgE mediated. Allergies to
anaphylaxis.
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Type II: IgM, G or A. Complement cascade.
Rh incompatability, Graves, etc.
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Type III: Ag-Ab complexes, tissue injury.
Vasculitis syndromes.
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Type IV: Delayed. Sensitized T-cells
recognize ag. Contact dermatitis.
Atopy
Atopic syndrome.
 Allergic hypersensitivity (Type I)
 IgE mediated
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– Atopic dermatitis
– Allergic rhinitis
– Asthma
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Genetic and environmental causes
Atopic Dermatitis
Exaggerated cutaneous inflammatory
response to triggers
 Tissue inflammation
 Acute or chronic
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Atopic Dermatitis
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Incidence
– 12-20% of children worldwide
– 80% will go on to develop asthma &/or
allergic rhinitis
– 60% symptomatic by 1 yo
– 85% by age 5
Atopic Dermatitis
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Presentation
– Chronically relapsing
– Pruritis
– Skin changes. Skin lacks lipids, susceptible
to water loss, makes it diffusely dry
– Prone to infections
• Bacterial: S. aureus
• Viral: HSV & molluscum
• Fungal
Atopic Dermatitis
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Signs & Symptoms
– Infantile: Intensely pruritic erythematous papules,
excoriatied. Serous ooze
– Childhood: Pruritis leads to erythematous
excoriated scaling papules
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Distribution
– Infantile: Face, scalp, extensor surfaces. Diaper
area spared, susceptible to Candida.
– Childhood: flexural folds
Atopic Dermatitis
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Longterm
– Chronic lichenification
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Triggers
– Food and environmental allergens
– Irritants: sweat, soap, detergents, alcohol,
chemicals
– Stress, anxiety
– Climate
Atopic Dermatitis
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Treatment
– Patient education: written treatment plan
– Avoid triggers – foods, environmental
– Cleanse and hydrate skin – Moisturize,
moisturize, moisturize
– Control itch – oral antihistamines
– Topical steroids for flares only
Atopic Dermatitis
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Treatment, continued:
– Topical corticosteroids. Ointments more
potent than creams, sting less
• Use lowest strength that works (fluticasone
0.05% approved down to 3 months)
– Topical Calcineurin Inhibitors
• Tacrolimus and pimecrolimus
• Immunomodulatory, inhibit allergic mediators
• Black box warning less than 2 yo
Atopic Dermatitis
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Severe AD – what can dermatologists
offer?
– UV light therapy (risk of later malignancy)
– Cyclosporine
Allergic Rhinitis
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Etiology
– Type I IgE mediated
– Early: mast cells degranulate, release
histamine, tryptase, leukotrienes,
prostaglandins, etc
– Late: Eosinophils, basophils, CD4 T cells,
etc
– Chronic nasal inflammation
Allergic Rhinitis
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Incidence:
– 20-40% of children in developed nations
– Prevalence peaks in adolescence
• Weeks/months/years to sensitize immune
system
• Rare in <6 mo old
• Usually >3 yo
Allergic Rhinitis
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Risk factors
– Family history of atopy
– Early introduction of foods (in atopic family)
– Environmental tobacco smoke exposure
– Heavy exposure to indoor allergens
Allergic Rhinitis
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Variations:
– Seasonal AR: cyclic exacerbations.
Airborne pollen – trees, grasses, weeds
– Perennial AR: Year round sx. Dust, dust
mites, animal dander, mold, cockroaches
– Mixed AR: Year round, seasonal
exacerbations
– Episodic AR: Exposure to allergen
aggravates sx.
Allergic Rhinitis
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History:
– Itchy nose, eyes, pharynx
– Clear rhinorrhea
– Headache
– Cough (nocturnal)
– Snoring, sleep disturbances
– Throat clearing, hoarseness
– Fatigue, poor concentration
Allergic Rhinitis
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PE:
– Allergic shiners
– Nasal crease
– Pale, boggy nasal turbinates
– Pharyngeal cobblestoning
– Enlarged tonsils (and adenoids)
– Scleral &/or conjunctival injection
– Cervical adenopathy
Allergic Rhinitis
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Differential Diagnosis:
– NARES
– Sinusitis
– Foreign body
– Septal deviation
– Nasal polyps
– Rhinitis medicamentosa
– Vasomotor rhinitis
*DX by history +/or skin and serum testing
Allergic Rhinitis
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Treatment:
– Avoid triggers
– Pharmagological:
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Antihistamines, 2nd generation
Intranasal corticosteroids
Decongestants ?
Mast cell stabilizers
Leukotriene modifiers
Allergic Rhinitis
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Immunotherapy
– For severe sx, unavoidable triggers, not
controlled with pharmacological tx
– Serum to desensitize and interfere with IgE
production – longterm injections
– Asthma needs to be in control
– Should be observed for anaphylaxis
– Can improve or resolve sx
Allergic Rhinitis
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Complications
– Asthma exacerbations
– Eustachian tube dysfunction
– Otitis media
– Tonsillar and adenoid hypertrophy
– Bacterial sinusitis
• All can lead to irritability, poor school
performance, etc
Allergic Rhinitis
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Prognosis
– Seasonal: may not improve with age.
– Patient needs to learn to self-manage sx
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Prevention
– Remove offending allergen (remove pet
from home)
– Air conditioning, close windows, HEPA
filter, bed covering, etc
Asthma
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Etiology:
– Inflammatory cells, mediators and
chemotactic factors lead to inflammation
– Airway hyperresponsiveness: constriction
in response to trigger
– Edema, incr. mucus
– Airway remodeling
Asthma
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Epidemiology:
– Most common chronic disease of childhood
– Estimated 6 million children in USA
– 80% of children with asthma diagnosed by
age 5
– 40% of children who wheeze as babies
Asthma
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Risk factors / History
– Atopy
– FH of asthma and/or allergy
– Exposure to tobacco smoke
– Low birth weight
– Viral infections
Asthma
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Asthma masqueraders:
– Upper airway noise or congestion
– Croup
– Vocal cord dysfuntion
– Gastroesophageal reflux
– Foreign body aspiration
– Cystic Fibrosis
– Congenital abnormalities
Asthma
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Triggers:
– Viral respiratory infections
– Environmental irritants and allergens:
Tobacco or wood smoke, dust mites, pet
dander, mold, cockroaches
– Exercise
– Weather changes
– Coexisting aggravating conditions
Asthma
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Pathogenesis
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Mast cell activation
Inflammatory cell infiltration
Edema
Disruption of bronchial epithelium
Collagen deposition beneath basement membrane
Mucus hypersecretion
Smooth muscle thickening
Asthma
So…
Triggers 
airway hyperresponsiveness 
airflow limitation  symptoms
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Asthma
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Symptoms:
– Cough (nocturnal)
– Wheeze
– SOB and/or increased respiratory rate
– Chest tightness
– Fatigue, exercise intolerance or avoidance
– Infants: difficulty feeding, grunting
Asthma
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PE
– Wheeze
– Prolonged expiratory phase
– Signs of atopy
– Tachypnea / tachycardia
– Nasal flaring
– Retractions / use of accessory muscles
– Cynaosis, lethargy
Asthma
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Laboratory Findings:
– CXR: bilateral hyperinflation, flattening of
diaphragms, peribronchial prominence,
atelectasis
– Spirometry (>5 yo): demonstrate reversible
airway constriction ( FEV1 after Bagonist)
– PEF: establish personal best, compare
effort to personal best, compare am & pm.
4 components of Asthma care
Assessment and monitoring
 Patient education
 Control of factors contributing to sx
 Pharmacologic treatment
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Asthma - Rx
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Quick relief or rescue
– Short acting beta 2 agonists (SABA)
– Oral corticosteroids
– Anticholinergics – short term only as
additive (Ipatropium bromide >5yo)
Asthma - Rx
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Long term
– Stepwise approach
– Classify patient – severity and age
– Asthma action plan
– Education parent and patient
Asthma - Rx
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Let’s look at the charts…
Asthma - Rx
SABA
 ICS – low, med or high dose stepwise
 LABA or Montelukast
 Oral corticosteroids
 Others
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Asthma reference: great reading!
National Asthma Education and
Prevention Program expert Panel 3:
Guidelines for the Diagnosis and
Prevention of Asthma (summary)
www.nhlbi.nih.gov/guidelines/asthma
More on Allergies
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Urticaria (hives), Angioedema
– IgE mediated, activates mast cells
– Pruritic
– Acute or chronic
– Triggers: foods, meds, insects, cold,
dermatographism, idiopathic
– Treat: Avoid triggers, 2nd gen
antihistamines
Anaphylaxis
IgE mediated, massive release of
inflammatory mediators
 Can be fatal
 Avoidance of triggers
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– Foods (peanuts, tree nuts, mild, eggs, fish,
shellfish, seeds, fruits, grains)
– Drugs, venom, latex, vaccinations
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Epi-pen (education), medicalert bracelet
Cystic Fibrosis
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Epidemiology:
– Autosomal recessive
– Most common life-limiting recessive
disease in whites
– 1 in 3,200 white newborns in US
– 1 in 15,000 in African Americans
Cystic Fibrosis
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Physiology:
– Mutation of CFTR leads to dysfunctional
epithelial transport
– Secretory and absorptive characteristics of
epis affected. Impaired mucociliary
transport
– CFTR is a chloride channel – Cl and
possibly Na transport affected (respiratory
and GI)
Cystic Fibrosis
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Clinical
– Chronic, progressive
– multiple complications related to viscous
mucus, malabsorption, and infections
– Colonization with bacteria (S. aureus, HiB,
P. aeruginosa)
– Digital clubbing
– Chronic sinusitis – nasal polypsis
Cystic Fibrosis
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Clinical, cont.
– Pancreatic insufficiency due to inspissation
of mucus in pancreatic ducts
– Maldigestionmalabsorption steatorrhea
– Vitamin deficiencies
– Failure to thrive (ravenous appetite)
– Meconium ileus
– Intestinal obstruction
Cystic Fibrosis
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Diagnosis
– Sweat chloride (two occasions)
– CF genotyping (many different genotypes)
CF Treatment
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Lung disease
– Clearance techniques to remove mucus
– Pharmacologic:
• Bronchodilators
• Antibiotics
CF Treatment
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Pancreatic insufficiency
– Replacing pancreatic enzymes
– Encouraging high caloric intake
– Fat soluble vitamins in large doses
CF Treatment
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Meconium ileus
– May require surgery, may be treated with
enemas
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Intestinal obstruction
– Intestinal lavage or enema