Pediatric Allergy and Asthma Brenda Beckett PAC Hypersensitivity

Pediatric Allergy and Asthma Brenda Beckett, PA-C

Hypersensitivity Disorders n Type I: Ig. E mediated. Allergies to anaphylaxis. n Type II: Ig. M, G or A. Complement cascade. Rh incompatability, Graves, etc. n Type III: Ag-Ab complexes, tissue injury. Vasculitis syndromes. n Type IV: Delayed. Sensitized T-cells recognize ag. Contact dermatitis.

Atopy n Atopic syndrome. n Allergic hypersensitivity (Type I) n Ig. E mediated – Atopic dermatitis – Allergic rhinitis – Asthma n Genetic and environmental causes

Atopic Dermatitis n Exaggerated cutaneous inflammatory response to triggers n Tissue inflammation n Acute or chronic

Atopic Dermatitis n 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 n 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 n Signs & Symptoms – Infantile: Intensely pruritic erythematous papules, excoriatied. Serous ooze – Childhood: Pruritis leads to erythematous excoriated scaling papules n Distribution – Infantile: Face, scalp, extensor surfaces. Diaper area spared, susceptible to Candida. – Childhood: flexural folds

Atopic Dermatitis n Longterm – Chronic lichenification n Triggers – Food and environmental allergens – Irritants: sweat, soap, detergents, alcohol, chemicals – Stress, anxiety – Climate

Atopic Dermatitis n Treatment – Patient education: written treatment plan – Avoid triggers – foods, environmental – Cleanse and hydrate skin – Moisturize, moisturize – Control itch – oral antihistamines – Topical steroids for flares only

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

Allergic Rhinitis n Etiology – Type I Ig. E mediated – Early: mast cells degranulate, release histamine, tryptase, leukotrienes, prostaglandins, etc – Late: Eosinophils, basophils, CD 4 T cells, etc – Chronic nasal inflammation

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

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

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

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

Allergic Rhinitis n Treatment: – Avoid triggers – Pharmagological: • • • Antihistamines, 2 nd generation Intranasal corticosteroids Decongestants ? Mast cell stabilizers Leukotriene modifiers

Allergic Rhinitis n Immunotherapy – For severe sx, unavoidable triggers, not controlled with pharmacological tx – Serum to desensitize and interfere with Ig. E production – longterm injections – Asthma needs to be in control – Should be observed for anaphylaxis – Can improve or resolve sx

Allergic Rhinitis n 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 n Prognosis – Seasonal: may not improve with age. – Patient needs to learn to self-manage sx n Prevention – Remove offending allergen (remove pet from home) – Air conditioning, close windows, HEPA filter, bed covering, etc

Asthma n Etiology: – Inflammatory cells, mediators and chemotactic factors lead to inflammation – Airway hyperresponsiveness: constriction in response to trigger – Edema, incr. mucus – Airway remodeling

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

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

Asthma n 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 n Pathogenesis – – – – Mast cell activation Inflammatory cell infiltration Edema Disruption of bronchial epithelium Collagen deposition beneath basement membrane Mucus hypersecretion Smooth muscle thickening

Asthma n So… Triggers airway hyperresponsiveness airflow limitation symptoms

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

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

Asthma n Laboratory Findings: – CXR: bilateral hyperinflation, flattening of diaphragms, peribronchial prominence, atelectasis – Spirometry (>5 yo): demonstrate reversible airway constriction ( FEV 1 after Bagonist) – PEF: establish personal best, compare effort to personal best, compare am & pm.

4 components of Asthma care n Assessment and monitoring n Patient education n Control of factors contributing to sx n Pharmacologic treatment

Asthma - Rx n Quick relief or rescue – Short acting beta 2 agonists (SABA) – Oral corticosteroids – Anticholinergics – short term only as additive (Ipatropium bromide >5 yo)

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

Asthma - Rx n Let’s look at the charts…

Asthma - Rx n SABA n ICS – low, med or high dose stepwise n LABA or Montelukast n Oral corticosteroids n 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 n Urticaria (hives), Angioedema – Ig. E mediated, activates mast cells – Pruritic – Acute or chronic – Triggers: foods, meds, insects, cold, dermatographism, idiopathic – Treat: Avoid triggers, 2 nd gen antihistamines

Anaphylaxis n Ig. E mediated, massive release of inflammatory mediators n Can be fatal n Avoidance of triggers – Foods (peanuts, tree nuts, mild, eggs, fish, shellfish, seeds, fruits, grains) – Drugs, venom, latex, vaccinations n Epi-pen (education), medicalert bracelet

Cystic Fibrosis n 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 n 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 n Clinical – Chronic, progressive – multiple complications related to viscous mucus, malabsorption, and infections – Colonization with bacteria (S. aureus, Hi. B, P. aeruginosa) – Digital clubbing – Chronic sinusitis – nasal polypsis

Cystic Fibrosis n 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