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Pediatric Allergy and Asthma
Brenda Beckett, PA-C
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Hypersensitivity Disorders
Type I: IgE mediated. Allergies to anaphylaxis.
Type II: IgM, G or A. Complement cascade. Rh incompatability, Graves, etc.
Type III: Ag-Ab complexes, tissue injury. Vasculitis syndromes.
Type IV: Delayed. Sensitized T-cells recognize ag. Contact dermatitis.
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Atopy
Atopic syndrome. Allergic hypersensitivity (Type I) IgE mediated
– Atopic dermatitis– Allergic rhinitis– Asthma
Genetic and environmental causes
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Atopic Dermatitis
Exaggerated cutaneous inflammatory response to triggers
Tissue inflammation Acute or chronic
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Atopic Dermatitis
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
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Atopic Dermatitis
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
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Atopic Dermatitis
Signs & Symptoms– Infantile: Intensely pruritic erythematous papules,
excoriatied. Serous ooze– Childhood: Pruritis leads to erythematous
excoriated scaling papules
Distribution– Infantile: Face, scalp, extensor surfaces. Diaper
area spared, susceptible to Candida.– Childhood: flexural folds
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Atopic Dermatitis
Longterm– Chronic lichenification
Triggers– Food and environmental allergens– Irritants: sweat, soap, detergents, alcohol,
chemicals– Stress, anxiety– Climate
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Atopic Dermatitis
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
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Atopic Dermatitis
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
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Atopic Dermatitis
Severe AD – what can dermatologists offer?– UV light therapy (risk of later malignancy)– Cyclosporine
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Allergic Rhinitis
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
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Allergic Rhinitis
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
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Allergic Rhinitis
Risk factors– Family history of atopy– Early introduction of foods (in atopic family)– Environmental tobacco smoke exposure– Heavy exposure to indoor allergens
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Allergic Rhinitis
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.
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Allergic Rhinitis
History:– Itchy nose, eyes, pharynx– Clear rhinorrhea– Headache– Cough (nocturnal)– Snoring, sleep disturbances– Throat clearing, hoarseness– Fatigue, poor concentration
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Allergic Rhinitis
PE:– Allergic shiners– Nasal crease– Pale, boggy nasal turbinates– Pharyngeal cobblestoning– Enlarged tonsils (and adenoids)– Scleral &/or conjunctival injection– Cervical adenopathy
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Allergic Rhinitis
Differential Diagnosis:– NARES– Sinusitis– Foreign body– Septal deviation– Nasal polyps– Rhinitis medicamentosa– Vasomotor rhinitis*DX by history +/or skin and serum testing
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Allergic Rhinitis
Treatment:– Avoid triggers– Pharmagological:
• Antihistamines, 2nd generation• Intranasal corticosteroids• Decongestants ?• Mast cell stabilizers• Leukotriene modifiers
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Allergic Rhinitis
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
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Allergic Rhinitis
Complications– Asthma exacerbations– Eustachian tube dysfunction– Otitis media– Tonsillar and adenoid hypertrophy– Bacterial sinusitis
• All can lead to irritability, poor school performance, etc
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Allergic Rhinitis
Prognosis– Seasonal: may not improve with age.– Patient needs to learn to self-manage sx
Prevention– Remove offending allergen (remove pet
from home)– Air conditioning, close windows, HEPA
filter, bed covering, etc
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Asthma
Etiology:– Inflammatory cells, mediators and
chemotactic factors lead to inflammation– Airway hyperresponsiveness: constriction
in response to trigger– Edema, incr. mucus– Airway remodeling
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Asthma
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
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Asthma
Risk factors / History– Atopy– FH of asthma and/or allergy– Exposure to tobacco smoke– Low birth weight– Viral infections
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Asthma
Asthma masqueraders:– Upper airway noise or congestion– Croup– Vocal cord dysfuntion– Gastroesophageal reflux– Foreign body aspiration– Cystic Fibrosis– Congenital abnormalities
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Asthma
Triggers:– Viral respiratory infections– Environmental irritants and allergens:
Tobacco or wood smoke, dust mites, pet dander, mold, cockroaches
– Exercise– Weather changes– Coexisting aggravating conditions
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Asthma
Pathogenesis– Mast cell activation– Inflammatory cell infiltration– Edema– Disruption of bronchial epithelium– Collagen deposition beneath basement membrane– Mucus hypersecretion– Smooth muscle thickening
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Asthma
So…
Triggers
airway hyperresponsiveness
airflow limitation symptoms
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Asthma
Symptoms:– Cough (nocturnal)– Wheeze– SOB and/or increased respiratory rate– Chest tightness– Fatigue, exercise intolerance or avoidance– Infants: difficulty feeding, grunting
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Asthma
PE– Wheeze– Prolonged expiratory phase– Signs of atopy– Tachypnea / tachycardia– Nasal flaring– Retractions / use of accessory muscles– Cynaosis, lethargy
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Asthma
Laboratory Findings:– CXR: bilateral hyperinflation, flattening of
diaphragms, peribronchial prominence, atelectasis
– Spirometry (>5 yo): demonstrate reversible airway constriction ( FEV1 after B-agonist)
– PEF: establish personal best, compare effort to personal best, compare am & pm.
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4 components of Asthma care
Assessment and monitoring Patient education Control of factors contributing to sx Pharmacologic treatment
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Asthma - Rx
Quick relief or rescue– Short acting beta 2 agonists (SABA)– Oral corticosteroids– Anticholinergics – short term only as
additive (Ipatropium bromide >5yo)
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Asthma - Rx
Long term– Stepwise approach– Classify patient – severity and age– Asthma action plan– Education parent and patient
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Asthma - Rx
Let’s look at the charts…
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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
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More on Allergies
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
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Anaphylaxis
IgE mediated, massive release of inflammatory mediators
Can be fatal Avoidance of triggers
– Foods (peanuts, tree nuts, mild, eggs, fish, shellfish, seeds, fruits, grains)
– Drugs, venom, latex, vaccinations Epi-pen (education), medicalert bracelet
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Cystic Fibrosis
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
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Cystic Fibrosis
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)
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Cystic Fibrosis
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
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Cystic Fibrosis
Clinical, cont.– Pancreatic insufficiency due to inspissation
of mucus in pancreatic ducts– Maldigestionmalabsorption steatorrhea– Vitamin deficiencies– Failure to thrive (ravenous appetite)– Meconium ileus– Intestinal obstruction
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Cystic Fibrosis
Diagnosis– Sweat chloride (two occasions)– CF genotyping (many different genotypes)
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CF Treatment
Lung disease– Clearance techniques to remove mucus– Pharmacologic:
• Bronchodilators• Antibiotics
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CF Treatment
Pancreatic insufficiency– Replacing pancreatic enzymes– Encouraging high caloric intake– Fat soluble vitamins in large doses
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CF Treatment
Meconium ileus– May require surgery, may be treated with
enemas Intestinal obstruction
– Intestinal lavage or enema