Pediatric Allergy and Asthma

Brenda Beckett, PA-C

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.

Atopy

Atopic syndrome. Allergic hypersensitivity (Type I) IgE mediated

– Atopic dermatitis– Allergic rhinitis– Asthma

Genetic and environmental causes

Atopic Dermatitis

Exaggerated cutaneous inflammatory response to triggers

Tissue inflammation Acute or chronic

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

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

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

Atopic Dermatitis

Longterm– Chronic lichenification

Triggers– Food and environmental allergens– Irritants: sweat, soap, detergents, alcohol,

chemicals– Stress, anxiety– Climate

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

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

Atopic Dermatitis

Severe AD – what can dermatologists offer?– UV light therapy (risk of later malignancy)– Cyclosporine

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

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

Allergic Rhinitis

Risk factors– Family history of atopy– Early introduction of foods (in atopic family)– Environmental tobacco smoke exposure– Heavy exposure to indoor allergens

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.

Allergic Rhinitis

History:– Itchy nose, eyes, pharynx– Clear rhinorrhea– Headache– Cough (nocturnal)– Snoring, sleep disturbances– Throat clearing, hoarseness– Fatigue, poor concentration

Allergic Rhinitis

PE:– Allergic shiners– Nasal crease– Pale, boggy nasal turbinates– Pharyngeal cobblestoning– Enlarged tonsils (and adenoids)– Scleral &/or conjunctival injection– Cervical adenopathy

Allergic Rhinitis

Differential Diagnosis:– NARES– Sinusitis– Foreign body– Septal deviation– Nasal polyps– Rhinitis medicamentosa– Vasomotor rhinitis*DX by history +/or skin and serum testing

Allergic Rhinitis

Treatment:– Avoid triggers– Pharmagological:

• Antihistamines, 2nd generation• Intranasal corticosteroids• Decongestants ?• Mast cell stabilizers• Leukotriene modifiers

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

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

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

Asthma

Etiology:– Inflammatory cells, mediators and

chemotactic factors lead to inflammation– Airway hyperresponsiveness: constriction

in response to trigger– Edema, incr. mucus– Airway remodeling

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

Asthma

Risk factors / History– Atopy– FH of asthma and/or allergy– Exposure to tobacco smoke– Low birth weight– Viral infections

Asthma

Asthma masqueraders:– Upper airway noise or congestion– Croup– Vocal cord dysfuntion– Gastroesophageal reflux– Foreign body aspiration– Cystic Fibrosis– Congenital abnormalities

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

Asthma

Pathogenesis– 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

Asthma

Symptoms:– Cough (nocturnal)– Wheeze– SOB and/or increased respiratory rate– Chest tightness– Fatigue, exercise intolerance or avoidance– Infants: difficulty feeding, grunting

Asthma

PE– Wheeze– Prolonged expiratory phase– Signs of atopy– Tachypnea / tachycardia– Nasal flaring– Retractions / use of accessory muscles– Cynaosis, lethargy

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.

4 components of Asthma care

Assessment and monitoring Patient education Control of factors contributing to sx Pharmacologic treatment

Asthma - Rx

Quick relief or rescue– Short acting beta 2 agonists (SABA)– Oral corticosteroids– Anticholinergics – short term only as

additive (Ipatropium bromide >5yo)

Asthma - Rx

Long term– Stepwise approach– Classify patient – severity and age– Asthma action plan– Education parent and patient

Asthma - Rx

Let’s look at the charts…

Asthma - Rx

SABA ICS – low, med or high dose stepwise LABA or Montelukast Oral corticosteroids Others

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

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

– Foods (peanuts, tree nuts, mild, eggs, fish, shellfish, seeds, fruits, grains)

– Drugs, venom, latex, vaccinations Epi-pen (education), medicalert bracelet

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

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)

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

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

Cystic Fibrosis

Diagnosis– Sweat chloride (two occasions)– CF genotyping (many different genotypes)

CF Treatment

Lung disease– Clearance techniques to remove mucus– Pharmacologic:

• Bronchodilators• Antibiotics

CF Treatment

Pancreatic insufficiency– Replacing pancreatic enzymes– Encouraging high caloric intake– Fat soluble vitamins in large doses

CF Treatment

Meconium ileus– May require surgery, may be treated with

enemas Intestinal obstruction

– Intestinal lavage or enema