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Pediatric Allergy and Asthma

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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 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
    – Maldigestionmalabsorption 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

				
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posted:10/7/2012
language:English
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