Allergic Diseases and Asthma
Leonard B. Bacharier
Avraham Beigelman
Anne E. Borgmeyer
Patti Gyr
Caroline Horner
Lila C. Kertz
ALLERGIC RHINITIS
Allergic rhinitis is a common disease that affects ˜40% of children and may have a significant affect on quality of life.
Children of parents with allergies and/or asthma are genetically predisposed to develop allergic rhinitis.
Pathophysiology
In the early phase, mediators (histamine, tryptase) are released from mast cells when allergen-specific immunoglobulin E (IgE) antibodies are cross-linked by allergens and cause acute mucosal edema, mucous secretion, vascular leakage, and stimulation of sensory neurons.
In the late phase, recruitment of inflammatory cells (neutrophils, eosinophils, and basophils) causes persistent inflammation, which may last for days.
History
Symptoms include rhinorrhea, nasal congestion, postnasal drainage, sneezing, and pruritus. Concomitant ocular symptoms often occur (see Allergic Conjuncitivitis below).
Common accompanying complaints are snoring, sore throat, frequent clearing of throat, cough, and hoarseness.
Determine whether symptoms are present throughout the year (perennial rhinitis), only during a particular season (seasonal rhinitis), or perennially with seasonal worsening. Also, determine whether symptoms are worse in a specific environment, such as at home with a pet, at daycare, or at school.
Identify measures that relieve symptoms, such as antihistamine usage and allergen avoidance.
Physical Examination
Close inspection of the skin, eyes, ears, nose, and throat is important.
Many children often have dark discoloration below the lower eyelids (allergic shiners) and prominent creases in the lower eyelid skin (Dennie-Morgan lines). A child who frequently rubs his or her nose (allergic salute) may develop a transverse nasal crease.
Findings on nasal examination include pale, boggy turbinates as a result of edema and clear nasal discharge.
Mouth breathing may be observed.
Cobblestoning in the posterior pharynx is a sign of follicular hypertrophy of mucosal lymphoid tissue.
Evaluation
Skin testing for environmental aeroallergens is sensitive and provides immediate information.
Serum allergen-specific IgE measurements are also available for common allergens. This testing is best used in children with dermatographism, with diffuse eczema, or with those who cannot discontinue the use of antihistamines or β-blockers.
Other findings supportive of a diagnosis of allergic rhinitis are peripheral blood eosinophilia, elevated total serum IgE, and eosinophils on nasal smear.
Rhinoscopy to directly visualize the nasal mucosa and upper airway is seldom used in the pediatric population.
Differential diagnosis
Other common causes of rhinitis are infectious, anatomic/mechanical, or nonallergic factors.
In younger children, it may be difficult to differentiate allergy symptoms from recurrent upper respiratory viral infections. In the presence of fevers, headache, myalgias, or purulent nasal discharge, an acute viral process or sinusitis should be considered.
Obstructive symptoms and unilateral purulent nasal discharge may suggest a retained foreign body.
History of mouth breathing and snoring may suggest coexistent adenoidal hypertrophy.
Presence of nasal polyps is atypical in childhood allergic rhnitis and should prompt evaluation for cystic fibrosis.
Treatment
Avoidance through environmental control
Effective, nonpharmacologic measures require a conscious effort from the parents to minimize allergen exposure.
For outdoor allergens, limit outdoor activity during peak pollen hours. Close windows and use air conditioning.
Homes cannot be made “allergen free,” but exposure to major indoor allergens can be reduced.
House dust mite avoidance includes changing bedding weekly and washing in hot water (>130°F); placing dust mite impermeable covers on the pillows, mattresses, and box springs; using a high efficiency particulate air (HEPA) filter vacuum; and removing carpeting in the bedroom.
If the child is allergic to a pet, removing the pet from the home is ideal. If patients reject this option, keeping the pet out of the bedroom and restricting the pet to certain areas of the home may be helpful.
HEPA filters reduce the amount of some airborne allergens.
Limiting ambient humidity and repairing water damage inhibit mold growth.
Pharmacotherapy (Table 13-1)
Antihistamines reduce rhinorrhea, sneezing, and pruritus but have little effect on congestion.
First-generation antihistamines are sedating and are available in many combination allergy medicines (chlorpheniramine and diphenhydramine). Most are well tolerated with the exception of sedation and potential anticholinergic effects.
Second-generation antihistamines (loratadine, desloratadine, cetirizine, levocetirizine, and fexofenadine) are less likely to cross the blood-brain barrier, minimizing sedation.
Azelastine and olapatadine are available as topical (intranasal) antihistamines.
Intranasal corticosteroids are potent anti-inflammatory agents that relieve rhinorrhea, sneezing, pruritus, and congestion.
These agents are indicated for both perennial and seasonal allergic rhinitis.
To optimize benefits, administer daily.
Side effects include epistaxis, burning/stinging, and oropharyngeal irritation. Review of proper intranasal administration or temporary discontinuation usually resolves these problems.
The leukotriene receptor antagonist montelukast is effective for allergic rhinitis, either alone or in combination with an antihistamine.
Montelukast is most effective in patients who experience from nasal congestion.
It is well tolerated with minimal adverse effects and may be indicated in children as young as 6 months.
A short (3-5 day) course of systemic corticosteroids may rarely be used for severe symptoms, particulary during the peak of pollen seasons.
Topical and systemic decongestants (oxymetazoline hydrochloride, pseudoephedrine, and phenylephrine) are effective for short-term relief of symptoms, such as rhinorrhea and congestion. Restrict the use of topical decongestants to 3-5 days to avoid rhinitis medicamentosa.
Intranasal mast cell stabilizers (cromolyn) inhibit mast cell degranulation, are best used prophylactically, and are well tolerated with minimal adverse effects.
Immunotherapy
The exact mechanism of immunotherapy remains unclear, but it reduces the levels of circulating specific IgE and increases allergen-specific IgG levels.
It is indicated in children who are not responsive to maximal pharmacotherapy and in some children with asthma.
Treatment is individualized and based on identified sensitizations to allergens. Immunotherapy requires long-term commitment from the parents and child.
With the known risk of anaphylaxis, immunotherapy should be prescribed only by physicians trained in allergy and immunotherapy.
TABLE 13-1 Medications Used in the Treatment of Allergic Rhinitis | ||||||||||||||||||||||||||||||||||
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ALLERGIC CONJUNCTIVITIS
Allergic conjunctivitis is frequently seen concomitantly with allergic rhinitis.
Symptoms inlcude watery eyes, itching, sensitivity to light, redness, and eyelid swelling.
Pathophysiology is similar to that for allergic rhinitis and involves the same mediators and inflammatory cells.
History and Physical Examination
Diagnosis begins with a history and physical examination.
Allergic conjunctivitis is characterized by acute onset, bilateral involvement, clear watery discharge, and pruritus.
On examination, there is bilateral hyperemia and edema of the conjunctivae.
Evaluation
Demonstration of allergen-specific IgE, by either skin testing or in vitro testing, are both sensitive diagnostic approaches for identifying relevant allergens.
Ocular allergen challenge is sensitive but seldom used clinically.
Differential diagnosis
Bacterial conjunctivitis is characterized by acute onset, thick purulent discharge, minimal pain, and history of exposure. It often occurs as unilateral disease that may subsequently infect the contralateral side.
Viral conjunctivitis is characterized by acute/subacute onset, clear watery discharge (often bilateral), and history of recent upper respiratory infection.
Keratoconjunctivitis
Vernal keratoconjunctivitis is chronic bilateral inflammation of conjunctiva with the presence of giant papillae on the superior tarsal conjunctiva with ropy mucous discharge. Itching is the most common symptom, with photophobia, foreign body sensation, tearing, and blepharospasm as other reported symptoms.
Atopic keratoconjunctivitis is bilateral inflammation of conjunctiva and eyelids associated with atopic dermatitis. The most common symptom is bilateral itching of the eyelids, and symptoms are perennial.
Both vernal and atopic keratoconjunctivitis are sight-threatening disorders and should prompt immediate referral to an ophthalmologist.
Treatment
Identification and avoidance of the identified allergen(s) is necessary, but not always feasible (such as tree pollen).
Artificial tear substitutes provide a barrier function, wash away allergens, and dilute inflammatory mediators.
Topical antihistamines (azelastine, emadastine, epinastine, olapatadin) provide relief of acute symptoms and prevent symptom development when used prophylactically. They have a rapid onset of action.
Mast cell stabilizers (cromolyn, ketotifen, lodoxamine, pemirolast) inhibit mast cell degranulation and the release of inflammatory mediators (Table 13-2).
Topical vasoconstrictors (naphazoline, pheniramine) reduce injection but have little effect on pruritus or swelling. Continued use may cause conjunctivitis medicamentosa.
Topical corticosteroids are usually not necessary for allergic conjunctivitis. In severe cases uncontrolled with the above approaches, referral to an ophthalmologist is generally indicated.
Topical medications are well tolerated. The difficulty of administrating eyedrops in a child and the frequency of dosing are the most common limiting factors.
ATOPIC DERMATITIS (ECZEMA)
Atopic dermatitis is a chronic relapsing and remitting inflammatory skin disease characterized by dermatitis with typical morphology and distribution.
Eczema is a generic term for a constellation of clinical signs, whereas atopic dermatitis is a term that specifically connotes an allergic contribution to the etiology of the eczema.
The overall prevalence of atopic dermatitis in the United States is 17% among school-aged children, leading to considerable disease-related morbidity, including irritability, secondary skin infections, sleep disturbance, school absenteeism, and poor self-image.
History
Age of onset is a consideration, with 45% of affected individuals manifesting atopic dermatitis in the first 6 months of life, 60% by the first year, and 85% by school age.
Pruritus is a cardinal feature of eczema, often described as the “itch that rashes.” Scratching leads to further compromise in the skin barrier and augments inflammation.
Xerosis (dry skin) also involves nonlesional skin. (In other conditions, commonly mistaken for atopic dermatitis [seborrheic dermatitis, nummular eczema, and psoriasis], the uninvolved skin is generally healthy.)
Patients may have a personal and family history of atopy (asthma, hay fever, food allergy).
Exacerbating factors include food allergens (most frequently egg, milk, wheat, soy, peanut, tree nuts, shellfish) and inhalant allergens (e.g., pet dander, house dust mite).
Systemic involvement, with failure to thrive, chronic diarrhea, and/or recurrent infections should prompt consideration of underlying systemic disease, such as immunodeficiency (e.g., Wiskott-Aldrich syndrome, Netherton syndrome, immune dysregulation polyendocrinopathy enteropathy X-linked [IPEX] syndrome, and hyper-IgE syndrome), or malabsorption (e.g., zinc deficiency or cystic fibrosis).
TABLE 13-2 Medications Used in the Treatment of Allergic Conjunctivitis | ||||||||||||
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Physical Examination
Xerosis
Morphology of lesions
Acute lesions: pruritic papules with excoriation and serous exudation
Chronic lesions: lichenified papules and plaques
Superficial linear abrasions from scratching
Indistinct lesional borders, unlike that of psoriasis
Areas of involvement. Although atopic dermatitis may appear anywhere on the body, characteristic patterns include:
Infants: cheeks, forehead, and extensor surface of extremities
Children/adolescents: flexor surface of extremities popliteal and antecubital fossae, and ventral surface of wrists and ankles
Atypical areas: diaper region (difficult for child to scratch) and nasolabial folds (commonly involved in seborrheic dermatitis)
Evaluation
Diagnosis is based on clinical features. Skin biopsy is not essential for diagnosis.
Identify factors that exacerbate atopic dermatitis.
Food allergy
One-third of children with moderate to severe atopic dermatitis experience worsening of eczema when exposed to food allergens.
Percutaneous skin tests, food-specific serum IgE, and oral food challenges may help identify specific foods.
Aeroallergen sensitivity
Infections
Bacteria. Staphylococcus aureus colonizes (cutaneous, nasal, or both) 80%-90% of individuals with atopic dermatitis, potentially leading to superinfection and/or production of superantigens and augmenting cutaneous inflammation.
Cutaneous viruses
Herpes simplex virus (eczema herpeticum). These vesicles and/or individual “punched out” lesions have an erythematous base. Confirm by herpes simplex virus polymerase chain reaction test from a newly unroofed vesicle.
Molluscum contagiosum
Malassezia sympodialis (formerly Pityrosporum ovale): Consider in individuals with recalcitrant eczema, especially with lesions concentrated on the head, neck, and upper torso. Sensitivity to M. sympodialis (by skin prick test or specific IgE determination) is diagnostic. Treatment is oral antifungal therapy (itraconazole).
Differential diagnosis
Dermatologic disease: seborrheic dermatitis, psoriasis, nummular eczema, irritant or allergic contact dermatitis, keratosis pilaris, ichthyosis, lichen simplex chronicus, and Netherton syndrome
Infections: scabies, tinea corporis, tinea versicolor, and HIV-associated eczema
Metabolic disease: zinc or biotin deficiency and phenylketonuria
Immunodeficiency: see earlier discussion
Neoplastic disease: mycosis fungoides (cutaneous T-cell lymphoma) and Langerhans histocytosis
Treatment
Limiting exposure to triggers
Nonspecific irritants. Wear nonocclusive clothing, and avoid wool or synthetic material.
Allergens. Eliminate contact with established allergic triggers (food or aeroallergen) if identified.
Topical therapy
Emollients. Rehydration of the skin is key to stopping the “itch-scratch” cycle by the “soak and seal” method. Daily baths with lukewarm water for 10-20 minutes followed by application of a thick emollient are necessary. Minimize use of soap and products with fragrances.
Topical corticosteroids, which are the gold standard of therapy for treatment of acutely inflamed areas
Use mild to moderate potency corticosteroids in children (e.g., hydrocortisone 1% ointment and triamcinolone 0.1% ointment, respectively).
Use only mild potency corticosteroid on face, genital, and intertriginous areas.
Topical calcineurin inhibitors, such as pimecrolimus and tacrolimus
Nonsteroidal topical agents effective in treating atopic dermatitis and are approved for children 2 years of age and older
A U.S. Food and Drug Administration “black box” warning for topical calcineurin inhibitors, recommending these drugs as second-line treatment options
Wet-wrap therapy. This involves applying a damp wet layer of cotton dressing (or cotton pajamas) over the topical emollients and then placing a layer of dry clothing above.
Antimicrobial therapy
Topical antiseptics (mupirocin, triclosan, or chlorhexidine) may be applied to open excoriated areas. Intranasal mupirocin may be used to eradicate nasal carriage of S. aureus if detected. Neomycin should be avoided because it can cause contact dermatitis.
Bleach baths, which may decrease colonization. Add 1-2 cups of household bleach per bathtub (adding a cup of table salt may diminish the stinging sensation).
Systemic antibiotics
Systemic corticosteroids. These agents are effective in short courses, but the systemic side-effect profile limits long-term applicability.
Systemic antihistamines
The major therapeutic value of systemic antihistamines resides in the sedative effect of first-generation histamine blockers, which helps minimize scratching and discomfort at night. Nonsedating antihistamines may provide a modest reduction in pruritus.
Topical antihistamines should be avoided because they may cause sensitization and worsen disease.
Other therapies: ultraviolet light (PUVA), systemic cyclosporine, azathioprine, and immunotherapy
Special Considerations
Associated atopic disorders. Atopic dermatitis in early childhood may herald progression toward other allergic conditions. This is known as the atopic march (allergic rhinitis and asthma).
Prevention
Exclusive breastfeeding for at least 4 months reduces the risk of atopic dermatitis, although the protective effect wanes by 3 years of age.
Natural history. Among children with onset of atopic dermatitis before 2 years of age, 60% experience complete remission, 20% have intermittent symptoms, and 20% have persistent disease by 7 years of age.
ASTHMA
Definition
Asthma is a reversible obstructive lung disease that is characterized by airway inflammation and hyperreactivity with airway mucosal edema, bronchoconstriction, and mucous plugging.
Clinically, asthma presents with recurrent episodes of wheezing, coughing, chest tightness, shortness of breath, and increased work of breathing.
Diagnosis is based on history, presence of wheezing, coughing, and increased work of breathing that resolves in response to treatment with bronchodilators and corticosteroids. Many conditions may present with wheezing and must be considered, especially in patients who present with a first episode of wheezing and/or are not responsive to asthma therapy (Table 13-3).
History
History of current episode: precipitating factors, onset and progression of symptoms, treatment, and response to treatment
Chronic history
Age of first episode, age at time of diagnosis, and course of the illness over time; typical signs and symptoms as well as precipitating factors (triggers)
Medication use: dosage, frequency, route, and schedule of all quick relief and control medications; effect of missed doses of medications; side effects; and adverse reactions. Review inhaled medication administration technique.
Assessment of chronic asthma severity (the intrinsic intensity of the disease process) to initiate therapy
Determine severity by quantifying frequency of daytime symptoms, nighttime symptoms, rescue β-agonist use, and interference with activity.
See Table 13-4, assessing both domains of impairment (frequency and intensity of symptoms and functional impairment the patient is currently experiencing or has recently experienced) and risk (the likelihood of asthma exacerbations, progressive decline in lung function or growth, or risk of adverse effects of medications). This classification scheme is most appropriate for patients who are not receiving controller therapy.
Assessment of asthma control to adjust therapy
Determine number of school days missed because of asthma; number of previous emergency visits and admissions, including intensive care with or without intubation; prior use of oral corticosteroids, including number of previous corticosteroid bursts and date of last corticosteroid course; and frequency of albuterol usage.
Use Table 13-5, assessing both domains of impairment and risk, to determine level of asthma control. This approach is most appropriate for patients already receiving controller therapy.
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