Review – Kaplan Pediatrics: Allergy

Dec 5, 2019 admin NHI KHOA 0

Review – Kaplan Pediatrics: Allergy

Allergic Rhinitis

  • Generally established by 6 years of age
  • Increased risk—early introduction of formula (versus breast milk) or solids, mother smoking before child is 1 year old, heavy exposure to indoor allergens
  • Most perennial or mixed; increased symptoms with greater exposure

Presentation

  • Diagnosis suggested by typical symptoms (nasal congestion/pruritus, worse at night with snoring, mouth-breathing; watery, itchy eyes; postnasal drip with cough; possible wheezing; headache) in absence of URI or structural abnormality
  • Allergic salute (rhinorrhea and nasal pruritus) → nasal crease
  • Vigorous grinding of eyes with thumb and side of fist
  • Allergic shiners (venous stasis)—blue-gray-purple beneath lower eyelids; often with Dennie lines—prominent symmetric skin folds
  • Conjunctival injection, chemosis (edema), stringy discharge, “cobblestoning” of tarsal conjunctiva
  • Transverse nasal crease (from allergic salute)
  • Pale nasal mucosa, thin and clear secretions, turbinate hypertrophy, polyps
  • Postnasal drip (posterior pharynx)
  • Otitis media with effusion is common
  • Food allergies more common (nuts, seafood) in young children (then skin, gastrointestinal, and, less often, respiratory)
  • Family history of allergic disease (atopy, asthma)

Treatment

Nonpharmacologic 

  • Environmental control plus removal of allergen is most effective method
  • Avoidance of biggest triggers—house dust mite, cat, cockroach
  • Dehumidifiers, HEPA-filtered vacuuming, carpet removal, pillow and mattress encasement
  • Remove pets
  • No smoking
  • No wood-burning stoves/fireplaces

Pharmacologic  

  1. Antihistamines (first-line therapy):
    1. First generation— cross blood-brain barrier—sedating
    2. Second generation now preferred
    3. Oral antihistamines are more effective than cromolyn but significantly less than intranasal steroids; efficacy ­ when combined with an intranasal steroid
  2. Intranasal corticosteroids—most effective medication, but not first-line:
    1. Effective for all symptoms
    2. Add to antihistamine if symptoms are more severe
  3. Leukotriene-receptor antagonists
  4. Chromones—cromolyn and nedocromil sodium:
    1. Least effective
    2. Very safe with prolonged use
  5. Decongestants—topical forms (oxymetazoline, phenylephrine) significant rebound when discontinued.
  6. Immunotherapy:
    1. Major indication—duration and severity of symptoms are disabling in spite of routine treatment (for at least two consecutive seasons). This, however, is the treatment of choice for insect venom allergy.
    2. Should NOT be used for (lack of proof):
      1. Atopic dermatitis
      2. Food allergy
      3. Latex allergy
      4. Urticaria
      5. Children <3 years old (too many systemic symptoms)
    3. Need several years of treatment; expensive
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Insect Venom Allergy

  1. Etiology/pathophysiology—systemic allergic responses are IgE-mediated and are almost always due to stings from the order Hymenoptera (yellow jackets most notorious—aggressive, ground-dwelling, linger near food)
  2. Clinical presentation
    1. Local—limited swelling/pain <1 day
    2. Large local area—develop over hours to days; extensive swelling
    3. Systemic—urticaria/angioedema, pruritus, anaphylaxis
    4. Toxic—fever, malaise, emesis, nausea
    5. Delayed/late response—serum sickness, nephrotic syndrome, vasculitis, neuritis, encephalitis
  3. Diagnosis—for biting/stinging insects, must pursue skin testing
  4. Treatment
    1. Local—cold compresses, topical antipruritic, oral analgesic, systemic antihistamine; remove stingers by scraping
    2. If anaphylaxis—epinephrine pen, ID bracelet, avoid attractants (e.g., perfumes)
    3. Indication for venom immune therapy—severe reaction with + skin tests (highly effective in decreasing risk)
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Food Reactions

  • Most infants and young children outgrow milk and egg allergy (half in first 3 years); majority with nut or seafood allergies retain for life:
  • Most food allergies are—egg, milk, peanuts, nuts, fish, soy, wheat, but any food may cause a food allergy.
  • Food allergic reactions are most common cause of anaphylaxis seen in emergency rooms
  • With food allergies, there is an IgE and/or a cell-mediated response.

Manifestations:

  • Skin—urticaria/angioedema and flushing, atopic dermatitis; 1/3 of children with atopic dermatitis have food allergies, but most common is acute urticaria/ angioedema
  • Gastrointestinal—oral pruritus, nausea, vomiting, diarrhea, abdominal pain, eosinophilic gastroenteritis (often first symptoms to affect infants):
    1. Predominantly a cell-mediated response, so standard allergy tests are of little value
    2. Food protein–induced enterocolitis/proctocolitis—presents with bloody stool/diarrhea (most cow milk or soy protein allergies)
  • Respiratory—nasal congestion, rhinorrhea, sneezing, laryngeal edema, dyspnea, wheezing, asthma
  • Cardiovascular—dysrhythmias, hypotension

Diagnosis

  • Skin tests, IgE-specific allergens are useful for IgE sensitization.
  • A negative skin test excludes an IgE-mediated form, but because of cell-mediated responses, may need a food elimination and challenge test in a controlled environment (best test)

Treatment

  • Only validated treatment is elimination
  • Epinephrine pens for possible anaphylaxis
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Urticaria and Angioedema

Pathophysiology

  1. Acute, IgE-mediated (duration <6 weeks)
    1. Activation of mast cells in skin
    2. Systemically absorbed allergen: food, drugs, stinging venoms; with allergy, penetrates skin → hives (urticaria)
  2. Non IgE-mediated, but stimulation of mast cells
    1. Radiocontrast agents
    2. Viral agents (especially EBV, hepatitis B)
    3. Opiates, NSAIDs
  3. Physical urticarias; environmental factors—temperature, pressure, stroking, vibration, light
  4. Hereditary angioedema
    1. Autosomal dominant
    2. C1 esterase-inhibitor deficiency
    3. Recurrent episodes of nonpitting edema

Diagnosis mainly clinical; skin tests, IgE-specific allergens (blood)

Treatment

  • Most respond to avoidance of trigger and oral antihistamine
  • Severe—epinephrine, short-burst corticosteroids
  • If H1 antagonist alone does not work, H1 plus H2 antagonists are effective; consider steroids
  • For chronic refractory angioedema/urticaria → IVIg or plasmapheresis
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Anaphylaxis

  • Sudden release of active mediators with cutaneous, respiratory, cardiovascular, gastrointestinal symptoms
  • Most common reasons
    1. In hospital—latex, antibiotics, IVIg (intravenous immunoglobulin), radiocontrast agents
    2. Out of hospital—food (most common is peanuts), insect sting, oral medications, idiopathic
  • Presentation—reactions from ingested allergens are delayed (minutes to 2 hours); with injected allergen, reaction is immediate (more gastrointestinal symptoms)
  • What the patient should do immediately:
    1. Injectable epinephrine
    2. Oral liquid diphenhydramine
    3. Transport to ER
  • Medical:
    1. Oxygen and airway management
    2. Epinephrine IM (IV for severe hypotension); intravenous fluid expansion; H1 antagonist; corticosteroids; nebulized, short-acting beta-2 agonist (with respiratory symptoms); H2 antagonist (if oral allergen)
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Atopic Dermatitis (Eczema)

Clinical presentation

  • Half start by age 1 year; most by age 1 and 5 years; chronic or relapsing
  • Intense cutaneous reactivity and pruritus; worse at night; scratching induces lesions; becomes excoriated
  • Exacerbations with foods, inhalants, bacterial infection, decreased humidity, excessive sweating, irritants

Patterns for skin reactions:

  • Acute: Erythematous papules; Intensely pruritic; Serous exudate, excoriation
  • Subacute—erythematous, excoriated, scaling papules
  • Chronic—lichenification (thickening, darkening)

Distribution pattern:

  • Infancy: face, scalp, extensor surfaces of extremities
  • Older, long-standing disease: flexural aspects
  • Often have remission with age, but skin left prone to itching and inflammation when exposed to irritants

Treatment

  • Identify and eliminate causative factors
  • Lukewarm soaking baths followed by application of occlusive emollient (hydrophilic ointments)
  • Topical corticosteroids
    1. Seven classes—the higher potency classes are not to be used on face or intertriginous areas and only for short periods
    2. Goal—emollients and low-potency steroids for maintenance
  • Topical immunomodulators; tacrolimus (calcineurin inhibitor):
    1. Inhibits activation of key cells
    2. Ointment safe and effective
    3. Safe on face
    4. Can use as young as 2 years of age
  • Tar preparations
  • Phototherapy—UV light
  • Systemic: antihistamines (sedating at night; for pruritus); glucocorticoids; cyclosporine (refractory to all other treatment); interferon (if all else fails)
  • Treat with antibiotics for bacterial superinfection

Complications

  • Secondary bacterial infection, especially S. aureus; increased incidence of T. rubrum, furfur
  • Recurrent viral skin infections—Kaposi varicelliform eruption (eczema herpeticum) most common
  • Warts/molluscum contagiosum
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Contact Dermatitis

  • Irritant
    1. Nonspecific injury to skin
    2. Results from prolonged or repetitive contact with various substances (e.g., diaper rash)
  • Allergic
    1. Delayed hypersensitivity reaction (type IV); provoked by antigen applied to skin surface
    2. Intense itching; chronically can mimic atopic dermatitis
    3. Distribution provides clue to diagnosis
    4. Causes—jewelry (especially nickel), shoes, clothing, and plants (poison ivy)
  • Diagnosis—clinical
  • Treatment—supportive; eliminate contact with allergen; cool compresses
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ASTHMA

Most with onset <6 years of age; most resolve by late childhood

Two main patterns:

  • } Early childhood triggered primarily by common viral infections
  • } Chronic asthma associated with allergies (often into adulthood; atopic)

Some risk factors for persistent asthma:

  • } Perennial allergies
  • } Atopic dermatitis, allergic rhinitis, food allergy
  • } Severe lower respiratory tract infections
  • } Wheezing other than with URIs (exercise, emotions)
  • } Environmental tobacco smoke exposure
  • } Low birth weight

Clinical presentation

  • Diffuse wheezing, expiratory then inspiratory
  • Prolonged expiratory phase
  • Decreased breath sounds
  • Rales/rhonchi → excess mucus and inflammatory exudate
  • Increased work of breathing
  • Exercise intolerance

Diagnosis

  • In children, no lab or challenge tests for diagnosis; but may be for following

Lung function:

  • Gold standard = spirometry during forced expiration. FEV1/FVC <0.8 = airflow obstruction (the forced expiratory volume in 1 second adjusted to the full expiratory lung volume, i.e., the forced vital capacity) in children age ³ 5 yrs
  • Bronchodilator response to inhaled beta-agonist—improvement in FEV1 to >12%
  • Exercise challenge—worsening in FEV1 of at least 15%
  • Home tool—peak expiratory home monitoring (PEF)
    • } a.m. and p.m. PEF for several weeks for practice and to establish personal best and to correlate to symptoms
    • } Based on personal best, divide PEFs into zones: Green: 80–100%, Yellow: 50–80% Red: <50%

Radiology (no routine use):

  • Hyperinflation—flattening of the diaphragms
  • Peribronchial thickening
  • Use to identify other problems that may mimic asthma (e.g., aspiration with severe gastroesophageal reflux) and for complications during severe exacerbations (atelectasis, pneumonia, air leak)

Treatment—based on asthma severity classification

  • Intermittent: symptoms ≤2 days/week and ≤2 nights/mo
    1. No need for daily controller
  • Persistent (mild → moderate → severe) symptoms > intermittent
    1. Need daily controller

Table 9-1. Severity Classification and Treatment 

 

Class

 Daytime Symptoms Nighttime Symptoms  

Treatment
Intermittent ≤2´/week ≤2´/month Short-acting b agonist PRN
Mild persistent >2´/week >2´/month Inhaled steroids, beta-agonist for breakthrough
Moderate persistent Daily >1´/week Inhaled steroids
Long-acting b agonist
Short-acting b for breakthrough Leukotrine-receptor antagonists
Severe persistent Continual; limited activities; frequent exacerbations Frequent High-dose inhaled steroid Long-acting beta-agonist Short-acting b agonist Systemic steroids
Leukotrine-receptor antagonists

 

Quick-relief medications:

  • Short-acting beta-2 agonists—albuterol, levalbuterol (nebulized only), terbutaline, metaproterenol:
    1. } Rapid onset, may last 4–6 hours
    2. } Drug of choice for rescue and preventing exercise-induced asthma
    3. } Inadequate control if need >1 canister/month
  • Anticholinergics:
    1. } Ipratropium bromide
    2. } Much less potent than beta agonists
    3. } Mostly for added treatment of acute severe asthma—ER and hospital
  • Short-course systemic glucocorticoids:
    1. } Outpatient—with moderate–severe flare-up; prednisone 3–7 days
    2. } Hospital—methylprednisolone IV recommended

Long-term controller medications:

  • Cromoglycates
    1. } Cromolyn sodium, nedocromil sodium
    2. } Only for mild–moderate asthma
    3. } Must be administered frequently (2–4´/day)
    4. } Not as effective as preferred medicines → now considered an alternative
  • Inhaled corticosteroids (ICS):
    1. } Treatment of choice for persistent asthma
    2. } Six FDA-approved inhaled steroids: Beclomethasone, flunisolide, triamcinolone (first generation); Budesonide, fluticasone, mometasone (second generation → greater topical-to-systemic potency = better therapeutic index)
    3. } Nebulized budesonide—only FDA-approved for ≤1 year duration; 1–2´/day
  • Long-acting beta agonists (LABA):
    1. } Salmeterol and formoterol
    2. } No rescue! No monotherapy (i.e., must use with ICS!)
    3. } Dose q 12 hours (not BID)
    4. } Major role = add-on medication
  • Leukotriene-modifying agents—two classes:
    1. } Inhibitors of synthesis (zileuton; >12 years old)
    2. } Receptor antagonists: montelukast, zafirlukast
    3. } Not as effective as ICS
    4. } Add-on med
  • Systemic steroids:
    1. } For severe asthma
    2. } Prednisone, prednisolone, methylprednisolone
    3. } Steroid-induced adverse effects
  • Theophylline:
    1. } Rarely used anymore
    2. } In oral form for steroid-dependent asthma for some steroid-sparing effects
    3. } Need routine levels (narrow therapeutic window)

Emergency Management of asthma exacerbations

  • Monitor, oxygen as needed
  • Inhaled albuterol q 20 minutes for one hour—add ipratropium if no good response for second dose
  • Corticosteroids PO or IV
  • Can go home if sustained improvement with normal physical findings and SaO2 >92% after 4 hours in room air; PEF ≥70% of personal best
  • Home on q 3–4 hour MDI + 3–7-day oral steroid

Hospital—for moderate–severe flare-ups without improvement within 1–2 hours of initial acute treatment with PEF <70% of personal best or SaO2 <92% on room air:

  • Oxygen
  • Nebulized albuterol (very frequently or continuous)
  • Add ipratropium q 6 hours
  • Intravenous  corticosteroids
  • May need intravenous fluids
  • Mechanical ventilation (rare)

Bronchiolitis vs. Asthma

Feature Bronchiolitis Asthma
Etiology Most RSV Reversible bronchoconstriction with chronic inflammation
Age Infants (especially <1 year) Most start age <5 years
Timing Winter All year

Most with URI in winter
Diagnosis Key Words URI from another household contact

Getting worse

Fever

Tachypnea

Bilateral expiratory wheezing ± respiratory distress

Apnea

 Repeated episodes of expiratory wheezing

Chronic non-productive cough

Chest tightness

Respiratory distress

May have other atopic disease + family history

May occur primarily with URIs

Cannot make diagnosis of asthma for firsttime wheezing in infant with fever (diagnosis is bronchiolitis)
Best Initial Test Clinical Dx

CXR only if severe and therefore possibility of secondary bacterial pneumonia

 Worsening of FEV1/FVC with exercise and improvement with beta-agonist
Most Accurate Test NP rapid test or PCR for organism

ABG only for severe to evaluate possible need for ventilation

 Repeated episodes that improve with betaagonist
Treatment Oxygen, if needed

Supportive Rx

May try beta-agonist

Ribavirin in severe or worsening cases MAY prevent the need for intubation and ventilation

 Oxygen

Short-acting beta-agonist

Add oral steroid for acute attack

May need chronic maintenance Rx

 

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