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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 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 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