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Pediatrics_Nelson. + LABA High-dose ICS LABA + + Oral corticosteroids Oral corticosteroids Children 0–4 years of ageChildren 5–11 Years of Age Each Step: Patient Education and Environmental Control Each Step: Patient Education and Environmental Control, and Management of Comorbidities Steps 2–4: Consider subcutaneous allergen immunotherapy for patients who have persistent, allergic asthma.  SABA as needed for symptoms. Intensity of treatment depends on severity of symptoms.  With viral respiratory symptoms: SABA q 4–6 hours up to 24 hours (longer with physician consult). Consider short course of oral systemic corticosteroids if exacerbation is severe or patient has history of previous severe exacerbations. Caution: Frequent use of SABA may indicate the need to step up treatment. See text for recommendations on initiating daily long-term-control therapy. Caution: Increasing use of SABA or use >2 days a week for symptom relief (not prevention of EIB) generally indicates inadequate


Pediatrics_Nelson

Pediatrics_Nelson. text for recommendations on initiating daily long-term-control therapy. Caution: Increasing use of SABA or use >2 days a week for symptom relief (not prevention of EIB) generally indicates inadequate control and the need to step up treatment. OR Medium-dose ICS Medium-dose ICS LTRA or Theophylline + High-dose ICS LTRA or Theophylline + + High-dose ICSLTRA or Theophylline  SABA as needed for symptoms. Intensity of treatment depends on severity of symptoms: up to 3 treatments at 20-minute intervals as needed. Short course of oral systemic corticosteroids may be needed. replace, the clinical decision making required to meet individual patient needs.  If an alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up.  If clear benefit is not observed within 4–6 weeks, and patient’s/family’s medication technique and adherence are satisfactory, consider adjusting therapy or an alternative diagnosis.  Studies


Pediatrics_Nelson

Pediatrics_Nelson. If clear benefit is not observed within 4–6 weeks, and patient’s/family’s medication technique and adherence are satisfactory, consider adjusting therapy or an alternative diagnosis.  Studies on children 0–4 years of age are limited. Step 2 preferred therapy is based on Evidence A. All other recommendations are based on expert opinion and extrapolation from studies in older children.  Clinicians who administer immunotherapy should be prepared and equipped to identify and treat anaphylaxis that may occur. Key: Alphabetical listing is used when more than one treatment option is listed within either preferred or alternative therapy. ICS, Inhaled corti-costeroid; LABA, inhaled long-acting beta2-agonist; LTRA, leukotriene receptor antagonist, oral corti-costeroids, oral systemic corticosteroids; SABA, inhaled short-acting beta2-agonist  The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs.  If an


Pediatrics_Nelson

Pediatrics_Nelson. corticosteroids; SABA, inhaled short-acting beta2-agonist  The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs.  If an alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up.  Theophylline is a less desirable alternative due to the need to monitor serum concentration levels. Steps 1 and 2 medications are based on Evidence A. Step 3 ICS and ICS plus adjunctive therapy are based on Evidence B for efficacy of each treatment and extrapolation from comparator trials in older children and adults–comparator trials are not available for this age group; Steps 4–6 are based on expert opinion and extrapolation from studies in older children and adults.  Immunotherapy for Steps 2–4 is based on Evidence B for house-dust mites, animal danders, and pollens; evidence is weak or lacking for molds and cock roaches. Evidence is strongest for


Pediatrics_Nelson

Pediatrics_Nelson. and adults.  Immunotherapy for Steps 2–4 is based on Evidence B for house-dust mites, animal danders, and pollens; evidence is weak or lacking for molds and cock roaches. Evidence is strongest for immunotherapy with single allergens. The role of allergy in asthma is greater in children than adults. Clinicians who administer immunotherapy should be prepared and equipped to identify and treat anaphylaxis that may occur. Key: Alphabetical listing is used when more than one treatment option is listed within either preferred or alternative therapy. ICS, Inhaled corti-costeroid; LABA, inhaled long-acting beta2-agonist; LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta2-agonist


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Pediatrics_Nelson. Figure 78-1 Stepwise long-term approach for managing asthma in children, 0 to 4 years of age and 5 to 11 years of age. (From National Heart Lung Blood Institute, National Asthma Education and Prevention Program: Expert panel report 3: guidelines for the diagnosis and management of asthma. Summary report 2007, NIH Publication No. 08-5846, Bethesda, MD, 2007, U.S. Department of Health and Human Services, p 42, http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.pdf


Pediatrics_Nelson

Pediatrics_Nelson. Intermittent asthma Persistent asthma: Daily medication Consult with asthma specialist if Step 4 care or higher is required. Consider consultation at Step 3. Step 1 Preferred:SABA PRN Step 2 Preferred:Low-dose ICS Alternative:Cromolyn, LTRA, Nedocromil, or Theophylline Step 3 Preferred:Low-dose ICS + LABA ORMedium-dose ICS Alternative:Low-dose ICS + either LTRA, Theophylline, or Zileuton Step 4 Preferred:Medium-dose ICS + LABA Alternative:Medium-dose ICS + either LTRA, Theophylline, or Zileuton Step 5 AND Preferred:High-dose ICS + LABA Consider Omalizumab for patients who have allergies Preferred:Step 6 AND High-dose ICS + LABA + oral corticosteroid Consider Omalizumab for patients who have allergies Each step: Patient education, environmental control, and management of comorbidities. Steps 2–4: Consider subcutaneous allergen immunotherapy for patients who have allergic asthma (see Notes). Quick-relief medication for all patients  SABA as needed for symptoms. Intensity of treatment


Pediatrics_Nelson

Pediatrics_Nelson. 2–4: Consider subcutaneous allergen immunotherapy for patients who have allergic asthma (see Notes). Quick-relief medication for all patients  SABA as needed for symptoms. Intensity of treatment depends on severity of symptoms: up to 3 treatments at 20-minute intervals as needed. Short course of oral systemic corti costeroids may be needed.  Use of SABA >2 days a week for symptom relief (not prevention of EIB) generally indicates inadequate control and the need to step up treatment. AssesscontrolStep up if needed (first, check adherence, environmental control, and comorbid conditions) Step down if possible (and asthma is well controlled at least 3 months)


Pediatrics_Nelson

Pediatrics_Nelson. Figure 78-2 Stepwise approach for managing asthma in youths 12 years of age or older and adults. (From National Heart Lung Blood Institute, National Asthma Education and Prevention Program: Expert panel report 3: guidelines for the diagnosis and management of asthma. Summary report 2007, NIH Publication No. 08-5846, Bethesda, MD, 2007, U.S. Department of Health and Human Services, p 45, Key: Alphabetical order is used when more than one treatment option is listed within either preferred or alternative therapy. ICS, Inhaled corticosteroid; LABA, long-acting inhaled beta2-agonist; LTRA, leukotriene receptor antagonist; SABA, inhaled short-acting beta2-agonist Notes:  The stepwise approach is meant to assist, not replace, the clinical decision making required to meet individual patient needs.  If alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up.


Pediatrics_Nelson

Pediatrics_Nelson.  If alternative treatment is used and response is inadequate, discontinue it and use the preferred treatment before stepping up.  Zileuton is a less desirable alternative due to limited studies as adjunctive therapy and the need to monitor liver function. Theophylline requires monitoring of serum concentration levels.  In Step 6, before oral corticosteroids are introduced, a trial of high-dose ICS + LABA + either LTRA, Theophylline, or Zileuton may be considered, although this approach has not been studied in clinical trials.


Pediatrics_Nelson

Pediatrics_Nelson.  Step 1, 2, and 3 preferred therapies are based on Evidence A; Step 3 alternative therapy is based on Evidence A for LTRA, Evidence B for Theophylline, and Evidence D for Zileuton. Step 4 preferred therapy is based on Evidence B, and alternative therapy is based on Evidence B for LTRA and Theophylline and Evidence D Zileuton. Step 5 preferred therapy is based on Evidence B. Step 6 preferred therapy is based on (EPR–2 1997) and Evidence B for Omalizumab.  Immunotherapy for Steps 2–4 is based on Evidence B for house-dust mites, animal danders, and pollens; evidence is weak or lacking for molds and cockroaches. Evidence is strongest for immunotherapy with single allergens. The role of allergy in asthma is greater in children than in adults.  Clinicians who administer immunotherapy or Omalizumab should be prepared and equipped to identify and treat anaphylaxis that may occur. http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.pdf


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Pediatrics_Nelson. http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.pdf Most asthma exacerbations can be successfully managed at home. Status asthmaticus is an acute exacerbation of asthma that does not respond adequately to therapeutic measures and may require hospitalization. Exacerbations may progress over several days or occur suddenly and can range in severity from mild to life threatening. Significant respiratory distress, dyspnea, wheezing, cough, and a decrease in peak expiratory flow rate (PEFR) characterize deterioration in asthma control. During severe episodes of wheezing, pulse oximetry is helpful in monitoring oxygenation. In status asthmaticus, arterial blood gases may be necessary for measurement of ventilation. As airway obstruction worsens and chest compliance decreases, carbon dioxide retention can occur. In the face of tachypnea, a normal pCO2 (40 mm Hg) indicates impending respiratory arrest.


Pediatrics_Nelson

Pediatrics_Nelson. First-line management of asthma exacerbations includes supplemental oxygen, repetitive, or continuous administration of short-acting bronchodilators. Early administration of oral or intravenous corticosteroids (Fig. 78-4) is important in treating the underlying inflammation. Administration of anticholinergic agents (ipratropium) with bronchodilators decreases rates of hospitalization and duration of time in the emergency department. Intravenous magnesium sulfate is given in the emergency department if there is clinical deterioration, despite treatment with β2-agonists, ipratropium, and systemic glucocorticoids. The typical dose is 25 to 75 mg/kg (maximum 2.0 g) intravenously administered over 20 minutes. Epinephrine (intramuscular) or terbutaline (subcutaneous) is rarely used except when severe asthma is associated with anaphylaxis or unresponsive to continuous administration of short-acting bronchodilators.


Pediatrics_Nelson

Pediatrics_Nelson. For some children, symptoms of wheezing with respiratoryinfections subside in the preschool years, whereas othershave more persistent asthma symptoms. Prognostic indicators for children younger than 3 years of age who are at riskfor asthma include eczema, parental asthma, or two of the 90, 180, or 200 µg/inhalation Fluticasone HFA/MDI: 44, 110, or 220 µg/puff DPI: 50, 100, or 250 µg/inhalation Years of Age Years of Age Years of Age Years of Age Years of Age Years of Age >600–1,200 µg >1,200 µg 0.25–0.5 mg 1.0 mg 0.5 mg >0.5–1.0 mg >1.0 mg 2.0 mg 500–1,000 µg 1,000–1,250 >1,000–2,000 >1,250 µg >2,000 µg >1,500 µg >750–1,500 µg Key: DPI, Dry power inhaler; HFA, hydrofluoroalkane; MDI, metered-dose inhaler; NA, not available (either not approved, no data available, or safety and efficacy not established for this age group)


Pediatrics_Nelson

Pediatrics_Nelson. Key: DPI, Dry power inhaler; HFA, hydrofluoroalkane; MDI, metered-dose inhaler; NA, not available (either not approved, no data available, or safety and efficacy not established for this age group) Therapeutic Issues:  The most important determinant of appropriate dosing is the clinician’s judgment of the patient’s response to therapy. The clinician must monitor the patient’s response on several clinical parameters and adjust the dose accordingly. Once control of asthma is achieved, the dose should be carefully titrated to the minimum dose required to maintain control.  Preparations are not interchangeable on a µg or per puff basis. This figure presents estimated comparable daily doses. See EPR–3 Full Report 2007 for full discussion.  Some doses may be outside package labeling, especially in the high-dose range. Budesonide nebulizer suspension is the only inhaler corticosteroid (ICS) with FDAapproved labeling for children <4 years of age.


Pediatrics_Nelson

Pediatrics_Nelson.  For children <4 years of age: The safety and efficacy of ICSs in children <1 year has not been established. Children <4 years of age generally require delivery of ICS (budesonide and fluticasone HFA) through a face mask that should fit snugly over nose and mouth and avoid nebulizing in the eyes. Wash face after each treatment to prevent local corticosteroid side effects. For budesonide, the dose may be administered 1–3 times daily. Budesonide suspension is compatible with Albuterol, Ipratropium, and Levalbuterol nebulizer solutions in the same nebulizer. Use only jet nebulizers, as ultrasonic nebulizers are ineffective for suspensions. For Fluticasone HFA, the dose should be divided 2 times daily; the low dose for children <4 years of age is higher than for children 5–11 years of age due to lower dose delivered with face mask and data on efficacy in young children. Potential Adverse Effects of Inhaled Corticosteroids:  Cough, dysphonia, oral thrush (candidiasis).


Pediatrics_Nelson

Pediatrics_Nelson. Potential Adverse Effects of Inhaled Corticosteroids:  Cough, dysphonia, oral thrush (candidiasis).  Spacer or valved holding chamber with non-breath-actuated MDIs and mouthwashing and spitting after inhalation decrease local side effects.  A number of the ICSs, including Fluticasone, Budesonide, and Mometasone, are metabolized in the gastrointestinal tract and liver by CYP 3A4 isoenzymes. Potent inhibitors of CYP 3A4, such as Ritonavir and Ketoconazole, have the potential for increasing systemic concentrations of these ICSs by increasing oral availability and decreasing systemic clearance. Some cases of clinically significant Cushing syndrome and secondary adrenal insufficiency have been reported.


Pediatrics_Nelson

Pediatrics_Nelson.  In high doses, systemic effects may occur, although studies are not conclusive, and clinical significance of these effects has not been established (e.g., adrenal suppression, osteoporosis, skin thinning, and easy bruising). In low-to-medium doses, suppression of growth velocity has been observed in children, but this effect may be transient, and the clinical significance has not been established.


Pediatrics_Nelson

Pediatrics_Nelson. Figure 78-3 Estimated comparative daily dosages for inhaled corticosteroids. (From National Heart Lung Blood Institute, National Asthma Education and Prevention Program: Expert panel report 3: guidelines for the diagnosis and management of asthma. Summary report 2007, NIH Publication No. 08-5846, Bethesda, MD, 2007, U.S. Department of Health and Human Services, p 49, http://www.nhlbi.nih.gov/ guidelines/asthma/asthsumm.pdf following: allergic rhinitis, wheezing with a cold, or eosino-teaching basic asthma facts, explaining the role of medica philia of greater than 4%. Atopy is the strongest predictor for tions, teaching environmental control measures, and improv wheezing continuing into persistent asthma (Table 78-4). ing patient skills in the use of spacer devices for metered dose inhalers and peak flow monitoring. Families should have an asthma management plan (Fig. 78-5) for daily care and for PREVENTION exacerbations.


Pediatrics_Nelson

Pediatrics_Nelson. PREVENTION exacerbations. Education plays an important role in helping patients and Peak flow monitoring is a self-assessment tool that is help- their families adhere to the prescribed therapy and needs to ful for children over 5 years of age. It is advisable for children begin at the time of diagnosis. Successful education involves who are poor perceivers of airway obstruction, have moderate FEV1 or PEF <40% (severe)  Oxygen to achieve SaO2 ˜90%  High-dose inhaled SABA plus Ipratropium by nebulizer or MDI plus valved holding chamber, every 20 minutes or continuously for 1 hour  Oral systemic corticosteroids FEV1 or PEF ˜40% (mild-to-moderate)  Oxygen to achieve SaO2 ˜90%  Inhaled SABA by nebulizer or MDI with valved holding chamber, up to 3 doses in first hour  Oral systemic corticosteroids if no immediate response or if patient recently took oral systemic corticosteroids


Pediatrics_Nelson

Pediatrics_Nelson. Initial assessment Brief history, physical examination (auscultation, use of accessory muscles, heart rate, respiratory rate), PEF or FEV1, oxygen saturation, and other tests as indicated Severe exacerbation FEV1 or PEF <40% predicted/personal best Physical exam: severe symptoms at rest, accessory muscle use, chest retraction History: high-risk patient No improvement after initial treatment  Oxygen  Nebulized SABA plus Ipratropium, hourly or continuous  Oral systemic corticosteroids  Consider adjunct therapies Moderate exacerbation FEV1 or PEF 40–69% predicted/personal best Physical exam: moderate symptoms  Inhaled SABA every 60 minutes  Oral systemic corticosteroid  Continue treatment 1–3 hours, provided there is improvement; make admit decision in <4 hours


Pediatrics_Nelson

Pediatrics_Nelson. Admit to hospital intensive care (see box below) Repeat assessment Symptoms, physical examination, PEF, O2 saturation, other tests as needed Good response  FEV1 or PEF ˜70%  Response sustained 60 minutes after last treatment  No distress  Physical exam: normal Incomplete response  FEV1 or PEF 40–69%  Mild-to-moderate symptoms Poor response  FEV1 or PEF <40%  PCO2 ˜42 mm Hg  Physical exam: symptoms severe, drowsiness, confusion Individualized decision re: hospitalization (see text) Discharge home  Continue treatment with inhaled SABA  Continue course of oral systemic corticosteroid  Consider initiation of an ICS  Patient education Review medications, including inhaler technique Review/initiate action plan Recommend close medical follow-up Admit to hospital ward  Oxygen  Inhaled SABA  Systemic (oral or intravenous) corticosteroid  Consider adjunct therapies  Monitor vital signs, FEV1 or


Pediatrics_Nelson

Pediatrics_Nelson. follow-up Admit to hospital ward  Oxygen  Inhaled SABA  Systemic (oral or intravenous) corticosteroid  Consider adjunct therapies  Monitor vital signs, FEV1 or PEF, SaO2 Improve Improve Admit to hospital intensive care  Oxygen  Inhaled SABA hourly or continuously  Intravenous corticosteroid  Consider adjunct therapies  Possible intubation and mechanical ventilation Discharge home  Continue treatment with inhaled SABAs.  Continue course of oral systemic corticosteroid.  Continue on ICS. For those not on long-term-control therapy, consider initiation of an ICS.  Patient education (e.g., review medications, including inhaler technique: review/initiate action plan and, whenever possible, environmental control measures; and recommend close medical follow-up).  Before discharge, schedule follow-up appointment with primary care provider and/or asthma specialist in 1–4 weeks. Key:


Pediatrics_Nelson

Pediatrics_Nelson. control measures; and recommend close medical follow-up).  Before discharge, schedule follow-up appointment with primary care provider and/or asthma specialist in 1–4 weeks. Key: FEV1, Forced expiratory volume in 1 second; ICS, inhaled corticosteroid; MDI, metered-dose inhaler; PCO2, partial pressure carbon dioxide; PEF, peak expiratory flow; SABA, short-acting beta2-agonist; SaO2, oxygen saturation Figure 78-4 Management of asthma exacerbations: emergency department and hospital-based care. (From National Heart Lung Blood Institute, National Asthma Education and Prevention Program: Expert panel report 3: guidelines for the diagnosis and management of asthma. Summary report 2007, NIH Publication No. 08-5846, Bethesda, MD, 2007, U.S. Department of Health and Human Services, p 55, http://www.nhlbi.nih.gov/guidelines/asthma/asthsumm.pdf


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Pediatrics_Nelson. Figure 78-5 Asthma self-management guideline. (From National Heart Lung Blood Institute, National Asthma Education and Prevention Program: Expert panel report 3: guidelines for the diagnosis and management of asthma. Summary report 2007, NIH Publication No. 05-5251, Bethesda, MD, 2007, U.S. Department of Health and Human Services, p 119, http://www.nhlbi.nih.gov/guidelines/asthma/asthgdln.pdf For: Doctor: Date: Doctor’s Phone Number Hospital/Emergency Department Phone Number Doing Well Take these long-term-control medicines each day (include an anti-inflammatory). No cough, wheeze, chest tightness, or Medicine How much to take When to take it shortness of breath during the day or night Can do usual activities And, if a peak flow meter is used, Peak flow: more than Identify and avoid and control the things that make your asthma worse, like (list here): (80 percent or more of my best peak flow)


Pediatrics_Nelson

Pediatrics_Nelson. And, if a peak flow meter is used, Peak flow: more than Identify and avoid and control the things that make your asthma worse, like (list here): (80 percent or more of my best peak flow) My best peak flow is: Before exercise, if prescribed, take: 45 to 60 minutes before exercise Asthma Is Getting Worse First Add: quick-relief medicine–and keep taking your GREEN ZONE medicine. Cough, wheeze, chest tightness, or puffs, 4every 20 minutes for up to 1 hour shortness of breath, or onceNebulizer, Waking at night due to asthma, or If applicable, remove yourself from the thing that made your asthma worse. Can do some, but not all, usual activities Second If your symptoms (and peak flow, if used) return to GREEN ZONE after 1 hour of above treatment: monitoring to be sure you stay in the green zone. ContinuePeak flow: to -Or(50 to 79 percent of my best peak flow) If your symptoms (and peak flow, if used) do not return to GREEN ZONE after 1 hour of above treatment: Take:


Pediatrics_Nelson

Pediatrics_Nelson. Add: mg per day. For (3–10) days (oral corticosteroid) the doctor hours after taking the oral corticosteroid.(phone) Medical Alert! Take this medicine: Very short of breath, or Nebulizer Quick-relief medicines have not helped, or (short-acting beta2-agonist) Cannot do usual activities, or mg Symptoms are same or get worse after (oral corticosteroid) 24 hours in Yellow Zone. Then call your doctor NOW. Go to the hospital or call an ambulance if You are still in the red zone after 15 minutes AND Peak flow: less than You have not reached your doctor. (50 percent of my best peak flow) Trouble walking and talking due to shortness of breath puffs of your quick-relief medicine 6AND Lips or fingernails are blue Go to the hospital or call for an ambulance NOW! Allergy Atopic dermatitis Allergic rhinitis Elevated total serum IgE levels (first year of life) Peripheral blood eosinophilia >4% (2–3 yr of age) Food and inhalant allergen sensitization


Pediatrics_Nelson

Pediatrics_Nelson. Allergy Atopic dermatitis Allergic rhinitis Elevated total serum IgE levels (first year of life) Peripheral blood eosinophilia >4% (2–3 yr of age) Food and inhalant allergen sensitization Girls Asthma associated with obesity and early-onset puberty Triad asthma (adulthood) Lower respiratory tract infection Respiratory syncytial virus, parainfluenza Severe bronchiolitis (e.g., requiring hospitalization) Pneumonia From Liu A, Martinez FD, Taussig LM: Natural history of allergic diseases and asthma. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice. St Louis, 2003, Mosby, p 15. to severe asthma, or have a history of severe exacerbations. Peak flow monitoring also can be useful in children who are still learning to recognize asthma symptoms.


Pediatrics_Nelson

Pediatrics_Nelson. to severe asthma, or have a history of severe exacerbations. Peak flow monitoring also can be useful in children who are still learning to recognize asthma symptoms. To use a peak flow meter, a child should be standing with the indicator placed at the bottom of the scale. The child must inhale deeply, place the device in the mouth, seal the lips around the mouthpiece, and blow out forcefully and rapidly. The indicator moves up the numeric scale. The PEFR is the highest number achieved. The test is repeated three times to obtain the best possible effort. Peak flow meters are available as low range (<300 L/sec) and high range (<700 L/sec). It is important to provide the appropriate range meter so that accurate measurements can be obtained and children do not become discouraged because their exhalations barely move the indicator.


Pediatrics_Nelson

Pediatrics_Nelson. A child’s personal best is the highest PEFR achieved over a2-week period when stable. Based on the child’s personal best, a written action plan can be established, which is divided into three zones, similar to a stoplight. The green zone indicates aPEFR 80% to 100% of the child’s personal best value. In thiszone, the child is likely asymptomatic and should continuewith medications as usual. The yellow zone indicates a PEFR50% to 80% of the child’s personal best value, which generallycoincides with more asthma symptoms. Rescue medications,such as albuterol, are added. A call to the physician may be warranted if the peak flows do not return to the green zone within24 to 48 hours or if asthma symptoms are increasing. The redzone indicates a PEFR below 50% and is a medical emergency.Rescue medication should be taken immediately. If the PEFRremains in the red zone or the child has significant airway compromise, a call to the physician or emergency care is needed.


Pediatrics_Nelson

Pediatrics_Nelson. Children with asthma should be seen not only when they are ill but also when they are healthy. Regular office visits allow the health care team to review adherence to medication and control measures and to determine whether doses of medications need adjustment. Rhinitis describes diseases that involve inflammation of the nasal epithelium and is characterized by sneezing, itching, rhinorrhea, and congestion. There are many different causes of rhinitis in children, but approximately half of all cases of rhinitis are caused by allergies.


Pediatrics_Nelson

Pediatrics_Nelson. Allergic rhinitis, commonly known as hay fever, is caused by an IgE-mediated allergic response. During the early allergic phase, mast cells degranulate and release preformed chemical mediators, such as histamine and tryptase, and newly generated mediators, such as leukotrienes, prostaglandins, and platelet-activating factor. After a quiescent phase in which other cells are recruited, a late phase occurs approximately 4 to 8 hours later. Eosinophils, basophils, CD4 T cells, monocytes, and neutrophils release their chemical mediators, which leads to the development of chronic nasal inflammation.


Pediatrics_Nelson

Pediatrics_Nelson. Allergic rhinitis can be seasonal, perennial, or episodicdepending on the particular allergen and the exposure. Somechildren experience perennial symptoms with seasonal exacerbations. Seasonal allergic rhinitis is caused by airborne pollens,which have seasonal patterns. Typically trees pollinate in thespring, grasses in late spring to summer, and weeds in the summer and fall. The pollen, microscopic in size, can travel airbornehundreds of miles and be inhaled easily into the respiratory tract.Perennial allergic rhinitis is primarily caused by indoor allergens, such as house dust mites, animal dander, mold, and cockroaches. Episodic rhinitis occurs with intermittent exposure toallergens, such as visiting a friend’s home where a pet dwells.


Pediatrics_Nelson

Pediatrics_Nelson. Chronic rhinitis is one of the most common disorders encountered in infants and children. Overall allergic rhinitis is observed in 10% to 25% of the population, with children and adolescents more commonly affected than adults. The prevalence of physician-diagnosed allergic rhinitis may be 40%. Available @ StudentConsult.com Table 79-1 Classification of the Etiology of Rhinitis in Children ALLERGIC NONALLERGIC NONANATOMIC ANATOMIC Seasonal Nonallergic, noninfectious (vasomotor) rhinitis Adenoidal hypertrophy Episodic Nonallergic rhinitis with eosinophilia Choanal atresia CSF, Cerebrospinal fluid.


Pediatrics_Nelson

Pediatrics_Nelson. Episodic Nonallergic rhinitis with eosinophilia Choanal atresia CSF, Cerebrospinal fluid. The hallmarks of allergic rhinitis are clear: thin rhinorrhea; nasal congestion; paroxysms of sneezing; and pruritus of the eyes, nose, ears, and palate. Postnasal drip may result in frequent attempts to clear the throat, nocturnal cough, and hoarseness. It is important to correlate the onset, duration, and severity of symptoms with seasonal or perennial exposures, changes in the home or school environment, and exposure to nonspecific irritants, such as tobacco smoke.


Pediatrics_Nelson

Pediatrics_Nelson. The physical examination includes a thorough nasal examination and an evaluation of the eyes, ears, throat, chest, and skin. Physical findings may be subtle. Classic physical findings include pale pink or bluish gray, swollen, boggy nasal turbinates with clear, watery secretions. Frequent nasal itching and rubbing of the nose with the palm of the hand, the allergic salute, can lead to a transverse nasal crease found across the lower bridge of the nose. Children may produce clucking sounds by rubbing the soft palate with their tongue. Oropharyngeal examination may reveal lymphoid hyperplasia of the soft palate and posterior pharynx or visible mucus or both. Orthodontic abnormalities may be seen in children with chronic mouth breathing. Allergic shiners, dark periorbital swollen areas caused by venous congestion, along with swollen eyelids or conjunctival injection, are often present in children. Retracted tympanic membranes from eustachian tube dysfunction or serous otitis media also


Pediatrics_Nelson

Pediatrics_Nelson. by venous congestion, along with swollen eyelids or conjunctival injection, are often present in children. Retracted tympanic membranes from eustachian tube dysfunction or serous otitis media also may be present. Other atopic diseases, such as asthma or eczema, may be present, which helps lead the clinician to the correct diagnosis.


Pediatrics_Nelson

Pediatrics_Nelson. Allergy testing can be performed by in vivo skin tests or by in vitro serum tests (radioallergosorbent test [RAST], fluorescent enzyme immunoassay [FEIA], or enzyme linked immunosorbent assay [ELISA]) to pertinent allergens found in the patient’s environment (see Table 77-4). Skin tests (prick/puncture) provide immediate and accurate results. Positive tests correlate strongly with nasal and bronchial allergen provocative challenges. In vitro serum tests are useful for patients with abnormal skin conditions, for those with a tendency for anaphylaxis, or for those taking medications that interfere with skin testing. Disadvantages of serum tests include increased cost, inability to obtain immediate results, and reduced sensitivity compared with skin tests. Widespread screening with serum testing without regard to symptoms is not recommended. Measurement of total serum IgE or blood eosinophils generally is not helpful. The presence of eosinophils on the nasal smear suggests a diagnosis of


Pediatrics_Nelson

Pediatrics_Nelson. without regard to symptoms is not recommended. Measurement of total serum IgE or blood eosinophils generally is not helpful. The presence of eosinophils on the nasal smear suggests a diagnosis of allergy, but eosinophils also can be found in patients with nonallergic rhinitis with eosinophilia. Nasal smear eosinophilia is often predictive of a good clinical response to nasal corticosteroid sprays.


Pediatrics_Nelson

Pediatrics_Nelson. Rhinitis can be divided into allergic and nonallergic rhinitis (Table 79-1). Nonallergic rhinitis describes a group of nasal diseases in which there is no evidence of allergic etiology. It can be divided further into nonanatomic and anatomic etiologies. The most common form of nonallergic rhinitis in children is infectious rhinitis, which may be acute or chronic. Acute infectious rhinitis (the common cold) is caused by viruses, including rhinoviruses and coronaviruses, and typically resolves within 7 to 10 days (see Chapter 102). An average child has three to six common colds per year, with the most affected being younger children and children attending day care. Infection is suggested by the presence of sore throat, fever, and poor appetite, especially with a history of exposure to others with colds. Chronic infectious rhinosinusitis, or sinusitis, should be suspected if there is mucopurulent nasal discharge with symptoms that persist beyond 10 days (see Chapter 104). Classic signs


Pediatrics_Nelson

Pediatrics_Nelson. with colds. Chronic infectious rhinosinusitis, or sinusitis, should be suspected if there is mucopurulent nasal discharge with symptoms that persist beyond 10 days (see Chapter 104). Classic signs of acute sinusitis in older children include facial tenderness, tooth pain, headache, and fever. Classic signs are usually not present in young children who may present with postnasal drainage with cough, throat clearing, halitosis, and rhinorrhea. The character of the nasal secretions with infectious rhinitis varies from purulent to minimal or absent. Coexistence of middle ear disease, such as otitis media or eustachian tube dysfunction, may be additional clues of infection.


Pediatrics_Nelson

Pediatrics_Nelson. Nonallergic, noninfectious rhinitis (formerly known as vasomotor rhinitis) can manifest as rhinorrhea and sneezing in children with profuse clear nasal discharge. Exposure to irritants, such as cigarette smoke and dust, and strong fumes and odors, such as perfumes and chlorine in swimming pools, can trigger these nasal symptoms. Nonallergic rhinitis with eosinophilia syndrome is associated with clear nasal discharge and eosinophils on nasal smear and is seen infrequently in children. Cold air (skier’s nose), hot/spicy food ingestion (gustatory rhinitis), and exposure to bright light (reflex rhinitis) are examples of physical rhinitis. Treatment with topical ipratropium before exposure may be helpful.


Pediatrics_Nelson

Pediatrics_Nelson. Rhinitis medicamentosa, which is due primarily to overuse of topical nasal decongestants, such as oxymetazoline, phenylephrine, or cocaine, is not a common condition in younger children. Adolescents or young adults may become dependent on these over-the-counter medications. Treatment requires discontinuation of the offending decongestant spray, topical corticosteroids, and, frequently, a short course of oral corticosteroids. The most common anatomic problem seen in young children is obstruction secondary to adenoidal hypertrophy, which can be suspected from symptoms such as mouth breathing, snoring, hyponasal speech, and persistent rhinitis with or without chronic otitis media. Infection of the nasopharynx may be secondary to infected hypertrophied adenoid tissue.


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Pediatrics_Nelson. Choanal atresia is the most common congenital anomaly of the nose and consists of a bony or membranous septum between the nose and pharynx, either unilateral or bilateral. Bilateral choanal atresia classically presents in neonates as cyclic cyanosis because neonates are preferential nose breathers. Airway obstruction and cyanosis are relieved when the mouth is opened to cry and recurs when the calming infant reattempts to breathe through the nose. Some newborns show respiratory difficulty while feeding only. Nearly half of infants with choanal atresia have other congenital anomalies as a part of the CHARGE association (coloboma, congenital heart disease, choanal atresia, retardation, genitourinary defects, ear anomalies). Unilateral choanal atresia may go undiagnosed until later in life and presents with symptoms of unilateral nasal obstruction and discharge.


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Pediatrics_Nelson. Nasal polyps typically appear as bilateral, gray, glistening sacs originating from the ethmoid sinuses and may be associated with clear or purulent nasal discharge. Nasal polyps are rare in children younger than 10 years of age but, if present, warrant evaluation for an underlying disease process, such as cystic fibrosis or primary ciliary dyskinesia. Triad asthma is asthma, aspirin sensitivity, and nasal polyps with chronic or recurrent sinusitis. Foreign bodies are seen more commonly in young children who place food, small toys, stones, or other things in their nose. The index of suspicion should be raised by a history of unilateral, purulent nasal discharge, or foul odor. The foreign body can often be seen on examination with a nasal speculum.


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Pediatrics_Nelson. Management of allergic rhinitis is based on disease severity, impact of the disease on the patient, and the ability of the patient to comply with recommendations. Treatment modalities include allergen avoidance, pharmacologic therapy, and immunotherapy. Environmental control and steps to minimize allergen exposure, similar to preventive steps for asthma, should be implemented whenever possible (see Table 78-3).


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Pediatrics_Nelson. Intranasal corticosteroids are the most potent pharmacologic therapy for treatment of allergic and nonallergic rhinitis. These include beclomethasone, budesonide, ciclesonide, flunisolide, fluticasone, mometasone, and triamcinolone. These topical agents work to reduce inflammation, edema, and mucus production. They are effective for symptoms of nasal congestion, rhinorrhea, itching, and sneezing but less helpful for ocular symptoms. Nasal corticosteroid sprays have been used safely in long-term therapy. Deleterious effects on adrenal function or nasal membranes have not been reported when these agents are used appropriately. The most common adverse effects include local irritation, burning, and sneezing, which occur in 10% of patients. Nasal bleeding from improper technique (spraying the nasal septum) can occur. Rare cases of nasal septal perforation have been reported.


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Pediatrics_Nelson. Antihistamines are the medications used most frequentlyto treat allergic rhinitis. They are useful in treating rhinorrhea, sneezing, nasal itching, and ocular itching but are lesshelpful in treating nasal congestion. First-generation antihistamines, such as diphenhydramine and hydroxyzine, easily cross the blood-brain barrier, with sedation as the mostcommon reported adverse effect. Use of first-generation antihistamines in children has an adverse effect on cognitive andacademic function. In very young children, a paradoxicalstimulatory central nervous system effect, resulting in irritability and restlessness, has been noted. Other adverse effectsof first-generation antihistamines include anticholinergiceffects, such as blurred vision, urinary retention, dry mouth,tachycardia, and constipation. Second-generation antihistamines, such as cetirizine, loratadine, desloratadine, fexofenadine and levocetirizine, are less likely to cross the blood-brainbarrier, resulting in less sedation.


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Pediatrics_Nelson. Second-generation antihistamines, such as cetirizine, loratadine, desloratadine, fexofenadine and levocetirizine, are less likely to cross the blood-brainbarrier, resulting in less sedation. Cetirizine, fexofenadine,and loratadine are over-the-counter medications. Azelastine and olopatadine, topical nasal antihistamine sprays,are approved for children older than 5 years and older than6 years, respectively.


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Pediatrics_Nelson. Decongestants, taken orally or intranasally, may be used to relieve nasal congestion. Oral medications, such as pseudoephedrine and phenylephrine, are available either alone or in combination with antihistamines. Adverse effects of oral decongestants include insomnia, nervousness, irritability, tachycardia, tremors, and palpitations. For older children participating in sports, oral decongestant use may be restricted. Topical nasal decongestant sprays are effective for immediate relief of nasal obstruction but should be used for less than 5 to 7 days to prevent rebound nasal congestion (rhinitis medicamentosa). Topical ipratropium bromide, an anticholinergic nasalspray, is used primarily for nonallergic rhinitis and rhinitis associated with viral upper respiratory infection. Leukotrienemodifiers have been studied in the treatment of allergic rhinitis. Montelukast is approved for use in seasonal allergicrhinitis.


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Pediatrics_Nelson. If environmental control measures and medication intervention are only partially effective or produce unacceptable adverse effects, immunotherapy may be recommended. The mechanism of action for allergen immunotherapy is complex but includes increased production of an IgG-blocking antibody, decreased production of specific IgE, and alteration of cytokine expression produced in response to an allergen challenge. Immunotherapy is effective for desensitization to pollens, dust mites, and cat and dog proteins. Use in young children may be limited by the need for frequent injections. Immunotherapy must be administered in a physician’s office with 20 to 30 minutes of observation after the allergen injection. Anaphylaxis may occur, and the physician must be experienced in the treatment of these severe adverse allergic reactions.


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Pediatrics_Nelson. Approximately 60% of children with allergic rhinitis have symptoms of reactive airways disease/asthma (see Chapter 78). Chronic allergic inflammation leads to chronic cough from postnasal drip; eustachian tube dysfunction and otitis media; sinusitis; and tonsillar and adenoid hypertrophy, which may lead to obstructive sleep apnea. Children with allergic rhinitis may experience sleep disturbances, limitations of activity, irritability, and mood and cognitive disorders that adversely affect their performance at school and their sense of well-being. Seasonal allergic rhinitis is a common and prominent condition that may not improve as children grow older. Patients become more adept at self-management. Perennial allergic rhinitis improves with allergen control of indoor allergens.


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Pediatrics_Nelson. Removal or avoidance of the offending allergen is advised. The only effective measure for minimizing animal allergens from pets is removal of the pet from the home. Avoidance of pollen and outdoor molds can be accomplished by staying indoors in a controlled environment. Air conditioning and keeping windows and doors closed lower exposure to pollen. High-efficiency particle air filters reduce exposure to allergens (e.g., pet dander). Sealing the mattress, pillow, and covers in allergen-proof encasings is the most effective strategy for reduction of mite allergen. Bedding should be washed in hot water (>130 °F) every week.


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Pediatrics_Nelson. Atopic dermatitis is a chronic, pruritic, relapsing inflammatory skin condition. The pathogenesis is multifactorial and involves a complex interplay of factors, including genetic predisposition, immunologic abnormalities, disturbances in skin barrier function, environmental interactions, and infectious triggers. Several genes encoding epidermal (filaggrin) or other epithelial structural proteins and genes encoding major elements of the immune system play a major role in atopic dermatitis.


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Pediatrics_Nelson. Several immunoregulatory abnormalities have been described in patients with atopic dermatitis. There is an exaggerated cutaneous inflammatory response to environmentaltriggers, including irritants and allergens. Activated Langerhanscells in the dermis expressing surface-bound IgE stimulate Tcells. In acute lesions, activated Th2 lymphocytes infiltrate the dermis. They initiate and maintain local tissue inflammationprimarily through interleukin-4 (IL-4) and IL-13, which promote IgE production, and IL-5, which promotes eosinophil differentiation. As the disease progresses from an acute to a chronicphase, there is a switch from Th2 to Th1/Th0 cellular response.Chronic lesions are characterized by increased IL-12 and IL-18.


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Pediatrics_Nelson. Patients with atopic dermatitis have hyperirritable skin,and many factors can cause the disease to worsen or relapse. Known triggers include anxiety and stress, climate (extremes of temperature and humidity), irritants, allergens, and infections. Approximately 35% to 40% of infants and young children with moderate to severe atopic dermatitis have coexisting food allergies. The more severe the atopic dermatitis and the younger the patient, the more likely a food allergy will be identified as a contributing factor. Egg allergy is the most common cause of food-induced eczematous reactions.


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Pediatrics_Nelson. The prevalence of atopic dermatitis increased twofold to threefold over the past 30 years. Approximately 15% to 20% of children and 2% to 10% of adults are affected. Atopic dermatitis oftenstarts in early infancy. Approximately 50% of affected childrenshow symptoms in the first year of life, and 80% of these childrenexperience disease onset before 5 years of age. Atopic dermatitisis often the first manifestation of other atopic diseases. Approximately 80% of children with atopic dermatitis develop otherallergic diseases, such as asthma or allergic rhinitis. Symptomsof dermatitis often disappear at the onset of respiratory allergy.


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Pediatrics_Nelson. The clinical manifestations of atopic dermatitis vary with age. In infants, atopic dermatitis involves the face, scalp, cheeks, and extensor surfaces of the extremities (Fig. 80-1). The diaper area is spared. In older children, the rash localizes to the antecubital and popliteal flexural surfaces, head, and neck. In adolescents and adults, lichenified plaques are seen in the flexural areas (Fig. 80-2) and the head and neck regions. Itching or pruritus has a significant impact on the child and family’s quality of life; it is often worse at night, interrupting sleep. Physical examination may show hyperlinearity of the palms and soles, white dermatographism, pityriasis alba, creases under the lower eyelids (Dennie−Morgan folds or Dennie lines), and keratosis pilaris (asymptomatic horny follicular papules on the extensor surfaces of the arms).


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Pediatrics_Nelson. Figure 80-1 Atopic dermatitis typical cheek involvement. (From Eichenfield LF, Frieden IJ, Esterly NB: Textbook of Neonatal Derma-tology, Philadelphia, 2001, Saunders, p 242.) Figure 80-2 Rubbing and scratching the inflamed flexural areas cause thickened (lichenified) skin. (From Habif T: Clinical Dermatology, ed 4, Philadelphia, 2004, Elsevier.) The diagnosis of atopic dermatitis is based on clinical features rather than laboratory tests (Table 80-1). Skin biopsy is of little value, but it may be used to exclude other skin diseases that mimic atopic dermatitis. Skin testing or, alternatively, CAP fluorescent immunoassay (also known as FEIA) may be helpful in assessing the contribution of food or environmental allergies to disease expression.


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Pediatrics_Nelson. Many conditions share signs and symptoms of atopic dermatitis (Table 80-2). Infants presenting in the first year of life with failure to thrive, recurrent skin or systemic infections, and scaling, erythematous rash should be evaluated for immunodeficiency disorders. Wiskott-Aldrich syndrome is an X-linked recessive syndrome characterized by atopic The diagnosis requires evidence of itchy skin (or parental report of scratching or rubbing) plus three or more of the following: 1. History of involvement of skin creases 2. History of asthma or allergic rhinitis (or history of atopic disease in a first-degree relative if child is <4 years of age) 3. History of generally dry skin in the past year 4. Onset in a child <2 years of age (criterion not used if child is <4 years of age) 5. Visible flexural dermatitis (including dermatitis affecting cheeks, forehead, and outer aspects of limbs in children <4 years of age)


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Pediatrics_Nelson. Visible flexural dermatitis (including dermatitis affecting cheeks, forehead, and outer aspects of limbs in children <4 years of age) Modified from Williams HC, Burney PG, Hay RJ, et al: Diagnostic criteria for atopic dermatitis. III. Independent hospital validation. Br J Dermatol 131:406–416, 1994. Zinc deficiency Pyridoxine (vitamin B6) and niacin deficiency Multiple carboxylase deficiency, phenylketonuria From Leung DYM: Atopic dermatitis. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric allergy: principles and practice, St Louis, 2003, Mosby, p 562. IPEX, Immunodeficiency polyendocrinopathy X-linked.


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Pediatrics_Nelson. IPEX, Immunodeficiency polyendocrinopathy X-linked. dermatitis, thrombocytopenia, small-sized platelets, and recurrent infections. Langerhans cell histiocytosis is characterized by hemorrhagic or petechial lesions. Scabies is an intensely pruritic skin condition caused by the human scabies mite. The presence of a burrow found in the web spaces of the fingers, the flexor surfaces of the wrists, elbows, axilla, or genitals is pathognomonic. Burrows may be few in number or absent, however.


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Pediatrics_Nelson. The goals of therapy are to reduce the number and severity of flares and to increase the number of disease-free periods. Successful management involves skin hydration, pharmacologic therapy to reduce pruritus, and identification and avoidance of triggers. Patients with atopic dermatitis have a decrease in skin barrier function and enhanced transepidermal water loss. Daily, lukewarm baths for 15 to 20 minutes followed immediately by the application of fragrance-free emollients to retain moisture are a major component of therapy. Prevention of xerosis is important for control of pruritus and for maintaining the integrity of the epithelial barrier. Emollients should be ointments or creams, such as petrolatum, Aquaphor, Eucerin, or Cetaphil. Lotions are not as effective because they contain water or alcohol and may have a drying effect owing to evaporation. A mild nonsoap cleanser also is recommended.


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Pediatrics_Nelson. Topical anti-inflammatory agents, including corticosteroids and immunomodulators, are the cornerstone of therapy for acute flares and prevention of relapses. Topical corticosteroids are used for reducing inflammation and pruritus; they are effective for the acute and chronic phases of the disease. Ointments generally are preferred over creams and lotions because of enhanced potency and skin penetration. Corticosteroids are ranked by potency into seven classes. The least potent corticosteroid that is effective should be used. Higher potency corticosteroids may be necessary to diminish the dermatitis flare but should be used for limited periods. Low-potency, nonfluorinated corticosteroids should be used on the face, intertriginous areas (groin, axilla), and large areas to reduce the risk of adverse effects. Reduced efficacy of topical corticosteroids may be related to disease severity rather than glucocorticoid resistance. Local adverse effects, such as skin atrophy and striae, and


Pediatrics_Nelson

Pediatrics_Nelson. of adverse effects. Reduced efficacy of topical corticosteroids may be related to disease severity rather than glucocorticoid resistance. Local adverse effects, such as skin atrophy and striae, and systemic adverse effects, such as hypothalamic-pituitary-adrenal axis and growth suppression and hyperglycemia, are related to the potency, length of use, and extent of medication application. In infants and younger children, the possibility of corticosteroid-induced adverse effects may be greater. When control of inflammatory lesions is achieved, most patients can be managed with emollients and low-potency topical corticosteroids.


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Pediatrics_Nelson. The topical immunomodulating drugs, tacrolimus and pimecrolimus, are approved as second-line agents for short-term and intermittent treatment of atopic dermatitis in patients unresponsive to or intolerant of other therapies. They are approved for use in children older than 2 years of age. These agents may be used on all body locations and are especially useful on delicate skin sites, such as the face, neck, and axilla without the adverse effect of cutaneous atrophy seen with topical corticosteroids. These medications have a potential increased cancer risk, and their long-term safety has not been established. Other less serious adverse effects include local burning and the need for sun protection.


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Pediatrics_Nelson. Defective cell-mediated immunity leads to increased susceptibility to many bacterial, viral, and fungal infections of the skin. More than 90% of patients with atopic dermatitis have colonization of lesional skin with Staphylococcus aureus, and more than 75% of patients have colonization of uninvolved skin. Colonization and infection by S. aureus are associated with disease severity. S. aureus secretes exotoxins that act as a superantigen, stimulating T cells and increasing IgE production. Secondarily infected atopic dermatitis often presents as impetiginous, pustular lesions with crusting and honey-colored exudate. Topical antibiotics, such as mupirocin or retapamulin, can be used to treat local areas of infection, or oral antibiotics (such as cephalexin, dicloxacillin, or amoxicillin-clavulanate) can be used for multifocal disease or for infection around the eyes and mouth that is difficult to treat topically. Bacterial cultures may be helpful in patients who do not respond to oral


Pediatrics_Nelson

Pediatrics_Nelson. can be used for multifocal disease or for infection around the eyes and mouth that is difficult to treat topically. Bacterial cultures may be helpful in patients who do not respond to oral antibiotics or who have infection after multiple antibiotic courses. The incidence of community-acquired methicillin-resistant S. aureus is increasing.


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Pediatrics_Nelson. Herpes simplex superinfection of affected skin, or Kaposi varicelliform eruption or eczema herpeticum, results in vesiculopustular lesions that appear in clusters and can become hemorrhagic. Herpes simplex virus infection can be misdiagnosed as bacterial infection and should be considered if skin lesions fail to respond to antibiotics. In individuals with atopic dermatitis, smallpox vaccination or exposure to a vaccinated individual may lead to eczema vaccinatum, a localized vaccinial superinfection of affected skin. Eczema vaccinatum may progress to generalized vaccinia with vaccinial lesions appearing at sites distant from the inoculation. In patients with underlying immunodeficiencies, it may be life threatening. Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis.


Pediatrics_Nelson

Pediatrics_Nelson. Widespread infections with human papillomavirus (warts) and molluscum contagiosum are also common in children with atopic dermatitis. Atopic dermatitis is a chronic, relapsing skin disorder that tends to be more severe and prominent in young children. Symptoms become less severe in two thirds of children, with complete remission for approximately 20%. Early onset disease that is more widespread, concomitant asthma and allergic rhinitis, family history of atopic dermatitis, and elevated serum IgE levels may predict a more persistent course. Patients and families should be taught that a single cause and cure for atopic dermatitis is unlikely but that good control is possible for the majority of affected patients.


Pediatrics_Nelson

Pediatrics_Nelson. An important step in the management of atopic dermatitis is to identify and avoid allergens and irritants. Common irritants include soaps, detergents, fragrances, chemicals, smoke, and extremes of temperature and humidity. Wool and synthetic fabrics can be irritating to the skin; 100% cotton fabric is preferred. Sweating is a recognized trigger. Fingernails should be trimmed frequently to minimize excoriations from scratching. In infants and younger children who do not respond to the usual therapies, identifying and removing a food allergen from the diet may lead to clinical improvement. Food allergy is not a common trigger for older patients. Other environmental exposures, such as dust mites, pet dander, or pollens, can also contribute to the disease state. URTICARIA, ANGIOEDEMA, AND ANAPHYLAXIS


Pediatrics_Nelson

Pediatrics_Nelson. URTICARIA, ANGIOEDEMA, AND ANAPHYLAXIS Urticaria, commonly referred to as hives, is swelling of the dermis and one of the most common skin conditions seen in clinical practice. Angioedema results from a process similar to urticaria, but the reaction extends below the dermis. Urticaria and angioedema occur in response to the release of inflammatory mediators, including histamine, leukotrienes, platelet-activating factor, prostaglandins, and cytokines from mast cells present in the skin. A variety of stimuli can trigger mast cells and basophils to release their chemical mediators. Typically mast cells degranulate when cross-linking of the membrane-bound IgE occurs. Release of these mediators results in vasodilation, increased vascular leakage, and pruritus. Basophils from the circulatory system also can localize in tissue and release mediators similar to mast cells. Patients with urticaria have elevated histamine content in the skin that is more easily released.


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Pediatrics_Nelson. Anaphylaxis is mediated by IgE, whereas anaphylactoid reactions result from mechanisms that are due to nonimmunologic mechanisms. Both reactions are acute, severe, and can be life threatening due to a massive release of inflammatory mediators. Urticaria, angioedema, and anaphylaxis are best considered as symptoms because they have a variety of causes. Not all mast cell activation is IgE-mediated. Immunologic, nonimmunologic, physical, and chemical stimuli can produce degranulation of mast cells and basophils. Anaphylatoxins,C3a and C5a, can cause histamine release in a non–IgE-mediated reaction. Anaphylatoxins are generated in serum sickness (reactions to blood transfusions) (see Chapter 82) and in infectious, neoplastic, and rheumatic diseases. In addition mast cell degranulation can occur from a direct pharmacologic effect or physical or mechanical activation, such as urticaria after exposure to opiate medications, and dermatographism.


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Pediatrics_Nelson. Urticaria/angioedema can be classified into three subcategories: acute, chronic, and physical. By definition acute urticaria and angioedema are hives and diffuse swellingthat last less than 6 weeks. Often the history is quite helpfulin eliciting the cause of the acute reaction (Table 81-1). AnIgE mechanism is more commonly found in acute urticariathan in chronic urticaria. Chronic urticaria and angioedemaare characterized by persistence of symptoms beyond 6 weeks(Table 81-2). Some have daily symptoms of hives and swelling, whereas others have intermittent or recurrent episodes.Chronic urticaria can be idiopathic with unknown causal Foods Egg, milk, wheat, peanuts, tree nuts, soy, shellfish, fish, strawberries (direct mast cell degranulation) Medications Suspect all medications, even over-thecounter or homeopathic medications Insect stings Hymenoptera (honeybee, yellow jacket, hornets, wasp, fire ants), biting insects (papular urticaria)


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Pediatrics_Nelson. Insect stings Hymenoptera (honeybee, yellow jacket, hornets, wasp, fire ants), biting insects (papular urticaria) Infections Bacterial (group A streptococcus pharyngitis, Mycoplasma, sinusitis); viral (hepatitis B, mononucleosis [EBV], coxsackieviruses A and B); parasitic (Ascaris, Ancylostoma, Echinococcus, Fasciola, Filaria, Schistosoma, Strongyloides, Toxocara, Trichinella); fungal (dermatophytes, Candida) Contact allergy Latex, pollen, animal saliva, nettle plants, caterpillars Transfusion reactions Blood, blood products, or IVIG administration From Lasley MV, Kennedy MS, Altman LC: Urticaria and angioedema. In Altman LC, Becker JW, Williams PV, editors: Allergy in Primary Care, Philadelphia, 2000, Saunders, p 232. EBV, Epstein-Barr virus; IVIG, intravenous immunoglobulin. Idiopathic 75%–90% of cases 25%–50% of adult patients have IgG, anti-IgE, and anti-FcεR1 (high-affinity IgE receptor alpha chain) autoantibodies


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Pediatrics_Nelson. Idiopathic 75%–90% of cases 25%–50% of adult patients have IgG, anti-IgE, and anti-FcεR1 (high-affinity IgE receptor alpha chain) autoantibodies Angioedema Hereditary angioedema (autosomal dominant inherited deficiency of Cl-esterase inhibitor) From Lasley MV, Kennedy MS, Altman LC: Urticaria and angioedema. In Altman LC, Becker JW, Williams PV, editors: Allergy in Primary Care, Philadelphia, 2000, Saunders, p 234. factors; 35% to 40% of chronic urticaria cases have an autoimmune process due to IgG autoantibodies binding directly toIgE or to the IgE receptor. Physical urticaria and angioedemaare characterized by known eliciting external factors that mayinclude pressure, cold, heat, exercise, or exposure to sun or water.


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Pediatrics_Nelson. The most common physical urticaria is dermatographism, affecting 2% to 5% of persons. Dermatographism means “writing on the skin” and is easily diagnosed by firmly scratching the skin with a blunt point, such as the wooden tip of a cotton swab or tongue depressor. It is characterized by an urticarial reaction localized to the site of skin trauma. It has been suggested that trauma induces an IgE-mediated reaction causing histamine to be released from the mast cells. Cholinergic urticaria, characterized by the appearance of 1to 3-mm wheals surrounded by large erythematous flares after an increase in core body temperature, occurs commonly in young adults. Lesions may develop during strenuous exercise, after a hot bath, or emotional stress. The lack of airway symptoms differentiates it from exercise-induced anaphylaxis.


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Pediatrics_Nelson. Cold urticaria occurs with exposure to cold and may develop within minutes on areas directly exposed to cold or on rewarming of the affected parts. Ingestion of cold drinks may result in lip swelling. Cold urticaria syndromes can be categorized into acquired and familial disorders. Severe reactions resulting in death can occur with swimming or diving into cold water. Patients must never swim alone, avoid total body exposure to cold, and have injectable epinephrine available.


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Pediatrics_Nelson. Hereditary angioedema (HAE) is an autosomal dominant disease due to a deficiency of Cl inhibitor. The genetic defect may be caused by spontaneous mutation; approximately 25% of cases occur in patients without any family history. The disease is estimated to affect approximately 10,000 persons in the United States. It is characterized by unpredictable, recurrent attacks of episodic swelling that involves the face, peripheral extremities, genitalia, abdomen, oropharynx, and pharynx. Episodes are often triggered by trauma. Asphyxiation from laryngeal attacks is a significant cause of mortality. Patients with HAE rarely have urticaria associated with angioedema. The majority of patients (85%) have type I disease, which is due to decreased production of Cl-esterase inhibitor. A minority of patients (15%) have type II disease, which is due to production of dysfunctional Cl-esterase inhibitor. A low C4 level serves as an initial screening test. Patients with reduced C4 should have


Pediatrics_Nelson

Pediatrics_Nelson. of patients (15%) have type II disease, which is due to production of dysfunctional Cl-esterase inhibitor. A low C4 level serves as an initial screening test. Patients with reduced C4 should have quantitative and functional levels of Cl-esterase inhibitor measured. C2 levels are low during an acute attack. Type III HAE patients have normal laboratory evaluation. These patients are more typically females, but some males have been reported in the literature. Three products are approved to treat HAE attacks: Berinert (for acute facial or abdominal attacks in children ≥13 years old), Kalbitor (for acute attacks in children ≥16 years of age), and Cinryze (for prophylaxis in adolescents and adults).


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Pediatrics_Nelson. Anaphylactic reactions are type I, IgE-mediated reactions and result from many causes (Table 81-3). Cross-linking of the IgE molecule with the allergen leads to IgE receptor activation on the mast cell and basophil and release of mediators, including histamine, tryptase, tumor necrosis factor, platelet-activating factor, leukotrienes, prostaglandins, and cytokines. Other cell types involved in the reactions include monocytes, macrophages, eosinophils, neutrophils, and platelets. The mediator release results in the clinical picture of anaphylaxis. From Young MC: General treatment of anaphylaxis. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 644. *In order of frequency.


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Pediatrics_Nelson. From Young MC: General treatment of anaphylaxis. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 644. *In order of frequency. Anaphylactoid reactions are due to nonimmunologic mechanisms. Mast cells and basophils can be activated by direct, nonspecific stimulation, although the exact underlying mechanism is unknown. Reactions to agents, such as opiates and radiocontrast material, are classic examples. Complement system activation also can result in mast cell and basophil activation. Anaphylatoxins, C3a and C5a, are named because of their ability to trigger mediator release and are generated in serum sickness. The most common cause of this type of reaction is transfusion with blood products. There are other causes of anaphylactoid reactions for which the mechanism has not been clarified.


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Pediatrics_Nelson. Urticaria and angioedema are common skin conditions affecting 15% to 25% of individuals at some point in their lives. Most cases of urticaria are self-limited, but, for some patients, they are chronic. In approximately 50% of patients, urticaria and angioedema occur together. In the remaining 50%, 40% have urticaria alone and 10% have angioedema alone. The incidence of anaphylaxis in children is unknown. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com Raised, erythematous lesions with pale centers that are intenselypruritic characterize urticaria, commonly called hives (Fig. 81-1). The lesions vary in size and can occur anywhere on the body. Typically urticaria arises suddenly and may resolvewithin 1 to 2 hours or may persist for 24 hours. Angioedemais a similar process that involves the deeper dermis or subcutaneous tissue, with swelling as the principal symptom. Generally angioedema is not pruritic, may be mildly painful, andpersists for longer than 24 hours. In rare cases it may becomelife threatening if swelling affects the upper airway.


Pediatrics_Nelson

Pediatrics_Nelson. The clinical manifestations of anaphylaxis and anaphylactoid reactions are the same for children and adults. The signs and symptoms vary and can range from mild skin findings to a fatal reaction. Ninety percent of patients present with cutaneous symptoms, including urticaria, angioedema, flushing, and warmth; the absence of dermal symptoms does not exclude the diagnosis of anaphylaxis. Other affected organ systems include the respiratory tract (rhinorrhea, oropharyngeal edema, laryngeal edema, hoarseness, stridor, wheezing, dyspnea, and asphyxiation), cardiovascular system (tachycardia, hypotension, shock, syncope, and arrhythmias), gastrointestinal tract (nausea, abdominal pain, crampy diarrhea, and vomiting), and neurologic system (syncope, seizure, dizziness, and a sense of impending doom). The severity of an anaphylactic reaction is often proportionate to the speed of symptom onset.


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Pediatrics_Nelson. The laboratory evaluation of patients with urticaria and angioedema must be tailored to the clinical situation. Acute urticaria and angioedema do not require specific laboratory evaluation except to document the suspected cause. For patients with chronic urticaria and angioedema, laboratory evaluation should be performed to exclude underlying diseases (Table 81-4). Patients with recurrent angioedema without urticaria should be evaluated for HAE (Table 81-5). Measurement of the mast cell mediators, histamine and tryptase, may be helpful when the diagnosis of anaphylaxis isin question. A tryptase level is a more useful test because histamine is released quickly, has a short half-life, and is often difficult to detect in the serum. Serum tryptase levels peak 1 to 1.5 hours after anaphylaxis. Elevated levels may be helpful in Figure 81-1 Examples of urticaria. (From Zitelli BJ, Davis HW, editors: Pediatric Physical Diagnosis Electronic Atlas, Philadelphia, 2004, Mosby.)


Pediatrics_Nelson

Pediatrics_Nelson. Figure 81-1 Examples of urticaria. (From Zitelli BJ, Davis HW, editors: Pediatric Physical Diagnosis Electronic Atlas, Philadelphia, 2004, Mosby.) Complete blood count with If vasculitis is suspected differential Erythrocyte sedimentation rate Antinuclear antibody Urinalysis Skin biopsy From Zuraw B: Urticaria and angioedema. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 580. establishing the diagnosis, but normal tryptase levels do not ruleout the diagnosis. It is best to measure a serum tryptase level 1to 2 hours after the onset of symptoms. It also can be orderedretrospectively on stored serum that is less than 2 days old.


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Pediatrics_Nelson. The diagnosis of urticaria and angioedema is straightforward;finding the etiology may be more difficult. Other dermatologic conditions can mimic urticaria. Erythema multiforme has target-shaped, erythematous, macular or papular lesionsthat may look similar to urticaria, but the lesions are fixedand last for several days. Other dermatologic diseases includedermatitis herpetiformis and bullous pemphigoid, which arequite pruritic, and early on, the lesions may resemble urticaria. Mastocytosis is characterized by mast cell infiltrationof various organs, including the skin. Some patients have skin lesions similar in appearance to urticaria rather than theclassic urticaria pigmentosa. Urticaria pigmentosa appears ashyperpigmented, red-brown macules, which may coalesce. From Zuraw B: Urticaria and angioedema. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 580.


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Pediatrics_Nelson. From Zuraw B: Urticaria and angioedema. In Leung DYM, Sampson HA, Geha RS, et al, editors: Pediatric Allergy: Principles and Practice, St Louis, 2003, Mosby, p 580. When these lesions are stroked, they urticate, which is calledthe Darier sign. A rare disorder that should be included in the differential diagnosis of urticaria is Muckle-Wells syndrome. It is an autosomal dominant disorder characterized by episodic urticaria presenting in infancy, with sensorineuraldeafness, amyloidosis, arthralgias, and skeletal abnormalities.Another rare syndrome is Schnitzler syndrome, which is characterized by chronic urticaria, macroglobulinemia, bonepain, anemia, fever, fatigue, and weight loss. Urticarial vasculitis is a small vessel vasculitis with histologic features of aleukocytoclastic response. The main distinguishing feature isthat the lesions last longer than 24 hours, may be tender, andleave behind skin pigmentation. Skin biopsy is required fordefinitive diagnosis.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of anaphylaxis is usually apparent from the acute and often dramatic onset of multisystem involvement of the skin, respiratory tract, and cardiovascular system. Sudden cardiovascular collapse in the absence of cutaneous symptoms suggests vasovagal collapse, seizure disorder, aspiration, pulmonary embolism, or myocardial infarction. Laryngeal edema, especially with abdominal pain, suggests HAE. Many patients with anaphylaxis are initially thought to have septic shock (see Chapter 40).


Pediatrics_Nelson

Pediatrics_Nelson. Avoidance of triggering agents is important in the management of urticaria and angioedema. The mainstay of pharmacologic treatment is H1 antihistamines. Second-generation H1 antihistamines, such as cetirizine, desloratadine, fexofenadine, levocetirizine, and loratadine, are preferred because they have fewer adverse effects. If a second-generation H1 antihistamine, by itself, does not provide adequate relief, the next step is to add a sedating H1 antihistamine at bedtime or H2 antihistamines, such as cimetidine or ranitidine. Tricyclic antidepressants, such as doxepin, exhibit potent activity at both H1 and H2 receptors. Corticosteroids are effective in treating urticaria and angioedema, although adverse effects from long-term use mandate the lowest dose for the shortest time. When urticaria is resistant to treatment, the leukotriene receptor blocker montelukast has been used in several case studies. Other immunomodulating agents, such as cyclosporine, hydroxychloroquine, methotrexate,


Pediatrics_Nelson

Pediatrics_Nelson. is resistant to treatment, the leukotriene receptor blocker montelukast has been used in several case studies. Other immunomodulating agents, such as cyclosporine, hydroxychloroquine, methotrexate, cyclophosphamide, and intravenous immunoglobulin, have been used; however, data supporting their use are limited, and they require laboratory monitoring due to potential adverse effects.


Pediatrics_Nelson

Pediatrics_Nelson. Anaphylaxis is a medical emergency; prompt recognition and immediate treatment are crucial (Fig. 81-2). Early administration of intramuscular epinephrine is the mainstay of therapy and should be given at the same time that basic measures of cardiopulmonary resuscitation are being performed. If the child is not in a medical setting, emergency medical services should be called. Supplemental oxygen and intravenous fluid should be administered with the child lying in supine position. An airway must be secured; intubation or tracheotomy may be required. Additional pharmacologic therapies, such as corticosteroids, antihistamines, H2-receptor antagonists, and bronchodilators, may be given to improve symptoms. Up to 20% of people with anaphylaxis have biphasic or protracted anaphylaxis.


Pediatrics_Nelson

Pediatrics_Nelson. A person with biphasic anaphylaxis has both earlyandlate-phase reactions. The biphasic reaction is a recurrence ofanaphylactic symptoms after an initial remission, occurringwithin 8 to 72 hours after the initial reaction. A person with protracted anaphylaxis has signs and symptoms that persist for hours or even days despite treatment, although thisis rare.


Pediatrics_Nelson

Pediatrics_Nelson. Prevention of urticaria, angioedema, and anaphylaxis focuses on avoidance of known triggers. A referral to an allergy specialist for a thorough history, diagnostic testing, and recommendations for avoidance is suggested for patients following severe reactions or anaphylaxis. Skin testing and serum IgEspecific testing are available for foods, inhalants, insect venoms, drugs (penicillin), vaccines, and latex. Educating the patient and family members about the signs and symptoms of anaphylaxis and using self-administered epinephrine early result in better outcomes. Fatal anaphylaxis has occurred despite timely and appropriate treatment. A MedicAlert bracelet with appropriate information should be worn. Medications such as β-blockers, angiotensin-converting enzyme inhibitors, and monoamine oxidase inhibitors should be discontinued because they may exacerbate anaphylaxis or interfere with its treatment. ACUTE TREATMENT, Health care setting LONG-TERM RISK REDUCTION, Community setting


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Pediatrics_Nelson. ACUTE TREATMENT, Health care setting LONG-TERM RISK REDUCTION, Community setting TREATMENT, IF NEEDED  Allergen-specific –Immunotherapy with insect venom –Desensitization to ˜-lactam antibiotics, NSAIDs, other  Allergen non-specific –Idiopathic anaphylaxis: consider glucocorticoid treatment EMERGENCY PREPAREDNESS Epinephrine autoinjector Anaphylaxis Emergency Action Plan (www.aaaai.com) Medical ID    ASSESS/TREAT COMORBIDITIES ALLERGEN AVOIDANCE www.foodallergy.org www.latexallergyresources.org www.aaaai.org www.acaai.org     ASSESS NEED FOR CO-MEDICATIONS Asthma Cardiovascular disease Mastocytosis Other     Nonselective ˜-blockers Other


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Pediatrics_Nelson. Figure 81-2 Summary of anaphylaxis management. Acute treatment is the same regardless of the mechanism or trigger involved in anaphylaxis. In contrast, for long-term risk reduction, avoidance measures and immunomodulation are trigger-specific; currently immunomodulation is available only for a minority of individuals with anaphylaxis. All at-risk individuals need to have comorbidities and comedications assessed, be taught the importance of emergency preparedness, and be instructed in the use of self-injectable epinephrine. ACLS, Advanced cardiac life support; CPR, cardiopulmonary resuscitation; CVS, cardiovascular; GI, gastrointestinal; ID, identification (e.g., bracelet, wallet card); IV, intravenous. (From Simon FER: Anaphylaxis, J Allergy Clin Immunol 121:S405, 2008.) *The skin should be inspected, and weight estimation is important, especially in infants and children, and also in overweight and obese teens and adults, in order to calculate an optimal dose of epinephrine and other


Pediatrics_Nelson

Pediatrics_Nelson. be inspected, and weight estimation is important, especially in infants and children, and also in overweight and obese teens and adults, in order to calculate an optimal dose of epinephrine and other medications needed in treatment and resuscitation.


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Pediatrics_Nelson. †Supine position, as tolerated, to prevent empty ventricle syndrome. ‡Call 911/emergency medical services for anaphylaxis occurring in community health care facilities such as medical, dental, or infusion clinics, where optimal backup might not be available for resuscitation. Serum sickness is a type III hypersensitivity reaction (see Table 77-1). The patient’s immune system recognizes the proteins in the drug or antiserum as foreign and produces antibodies against them. The newly formed antibodies bind with the foreign protein to form antigen-antibody or immune complexes, which may enter the circulation and be deposited in blood vessels and in filtering organs. These complexes cause tissue injury by activating the complement cascade and recruiting neutrophils, resulting in increased capillary permeability, toxic mediator release, and tissue damage.


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Pediatrics_Nelson. Immune complexes were first described after administration of heterologous serum, such as horse serum for diphtheria. The availability of human-derived biologics, bioengineered antibodies, and alternative pharmacotherapies has greatly reduced the incidence of serum sickness. Common inciting agents include blood products and foreign proteins, such as antithymocyte globulin and antivenoms. Medications frequently implicated include penicillin, sulfonamides, minocycline, cefaclor, hydantoins, and thiazides. Available @ StudentConsult.com


Pediatrics_Nelson

Pediatrics_Nelson. Available @ StudentConsult.com The symptoms of serum sickness typically occur 7 to 21 daysafter the administration of drugs, foreign proteins, or infections.Symptom onset may be more rapid (within 1 to 4 days) in previously sensitized individuals. The classic clinical manifestationsconsist of fever, polyarticular arthralgias, lymphadenopathy, andcutaneous symptoms. Cutaneous lesions vary and may includeurticaria, angioedema, erythema multiforme, morbilliformrash, and a palpable purpura or serpiginous rash at the interfaceof the dorsal and palmar or plantar aspects of the hands and feet. Carditis, glomerulonephritis, Guillain-Barre syndrome, encephalomyelitis, and peripheral neuritis are rare complications.


Pediatrics_Nelson

Pediatrics_Nelson. Carditis, glomerulonephritis, Guillain-Barre syndrome, encephalomyelitis, and peripheral neuritis are rare complications. Laboratory tests may show an elevated erythrocyte sedimentation rate, presence of circulating immune complexes, and depressed complement (C3 and C4) levels. Skin biopsy specimens show immune deposits of IgM, IgA, IgE, or C3. Hematuria or proteinuria or both may be present. The diagnosis is established by history of exposure to an inciting cause, characteristic clinical manifestations, and laboratory testing showing circulating immune complexes and depressed complement levels.


Pediatrics_Nelson

Pediatrics_Nelson. Serum sickness is self-limited and resolves within 1 to 2 weeks; therefore, treatment is symptomatic relief. Antihistamines may be administered to relieve pruritus. Nonsteroidal anti-inflammatory drugs are given for fever and joint pain, and, if necessary, prednisone (1 to 2 mg/kg orally daily) is administered with a tapering dose. Allergy skin testing does not predict the likelihood of serum sickness development. The primary means of prevention is to avoid exposure to the implicated cause.


Pediatrics_Nelson

Pediatrics_Nelson. The primary means of prevention is to avoid exposure to the implicated cause. Systemic allergic reactions usually result from stinging insectsof the order Hymenoptera, which include apids (honeybee and bumblebee), vespids (yellow jacket, wasp, yellow-face, and white-face hornets), and formicids (fire and harvester ants).Honeybees have a barbed stinger that remains embedded aftera sting. Yellow jackets are responsible for most allergic reactions in most parts of the United States, whereas wasps are themost frequent cause of sting reactions in Texas. Fire ants are found in the southeastern and south central United States.


Pediatrics_Nelson

Pediatrics_Nelson. Biting insects rarely cause anaphylaxis. Anaphylaxis has been described, however, after the bites of a kissing bug (Triatoma), bed bug, blackfly, and deerfly. Large local reactions from biting insects, such as mosquitoes, fleas, and flies, are a more common occurrence. The reaction appears urticarial and is caused by the salivary secretions deposited by the biting insect and does not represent an allergic response. Insect sting allergy may develop at any age and typically manifests after several uneventful stings. Although children are stung more frequently than adults, systemic allergic reactions occur in only about 1% of children and 3% of adults. Reactions in adults are generally more severe than in children and can result in death. Large local reactions to insect stings are more common in children, with an estimated incidence of 20% for children and 10% for adults.


Pediatrics_Nelson

Pediatrics_Nelson. The diagnosis of insect sting allergy is dependent on the history of the reaction and the presence of venom-specific IgE. Normal reactions to insect stings, which are observed in 90% Large local reaction >2 inches in diameter Swelling contiguous to the site Duration 2–7 days Nonlife-threatening Immediate generalized reaction confined to the skin (erythema, urticaria, angioedema) Life-threatening Immediate generalized reaction not confined to the skin with respiratory (laryngeal edema, bronchospasm) or cardiovascular (hypotension, shock) symptoms Toxic Follows multiple stings, produced by exogenous vasoactive amines in venom Unusual Serum sickness, vasculitis, nephrosis, neuritis, encephalitis Symptoms start several days to weeks after the insect sting.


Pediatrics_Nelson

Pediatrics_Nelson. of children, include localized pain, swelling, and erythema at the sting site that usually subside within 24 hours. Large local reactions occur in approximately 10% of patients. They are usually late-phase, IgE-mediated reactions, with large swelling, contiguous to the sting site that develops over 24 to 48 hours and resolves within 2 to 7 days. Virtually all individuals with large local reactions have similar reactions with subsequent stings. Systemic reactions are IgE mediated and occur in 1% of children. They can be mild and nonlife-threatening with cutaneous symptoms only or life-threatening with respiratory, cardiovascular, or neurologic symptoms of anaphylaxis (see Chapter 81). Toxic reactions may result if a person receives a large number of stings (50 to 100). Symptoms include malaise, nausea, and emesis resulting from the toxic effects of the venom. Unusual reactions, such as vasculitis, nephrosis, neuritis, serum sickness, and encephalitis, rarely are associated with insect


Pediatrics_Nelson

Pediatrics_Nelson. nausea, and emesis resulting from the toxic effects of the venom. Unusual reactions, such as vasculitis, nephrosis, neuritis, serum sickness, and encephalitis, rarely are associated with insect stings (Table 83-1).


Pediatrics_Nelson

Pediatrics_Nelson. A positive skin test to Hymenoptera venom extract demonstrates the presence of venom-specific IgE in the context of a positive sting reaction history and helps identify specific insects to which an individual is allergic. Venom-specific IgE antibodies also may be measured by in vitro serum tests. Both testing methods should be considered complementary because neither test alone detects all patients with insect sting allergy. Future reactions correlate more with past individual patterns than the level of sensitivity of venom skin testing or serum specific IgE testing. A history of an immediate systemic reaction is necessary before venom testing and immunotherapy should be considered. Identification of the offending insect is often unreliable. Honeybee stings may be identified by the stinger that remains in place. Vespid stings are usually unprovoked and occur at summer’s end when the insects are more aggressive.


Pediatrics_Nelson

Pediatrics_Nelson. Local reactions should be treated by cleaning the site,applying cold compresses, and administering oral antihistamines and analgesics. Occasionally large local reactionsmay be mistaken for cellulitis. Infection is unlikely if reaction occurs within 24 to 48 hours after a sting. Treatment iswith an oral corticosteroid for 4 to 5 days rather than oralantibiotics. Treatment of systemic reactions is guided by the severity of the reaction, but epinephrine is the cornerstone of therapy and should be administered without delay. Antihistamines may be administered concurrently with epinephrine. Corticosteroids should be given to prevent recurrent or prolonged symptoms. For severe reactions, intravenous fluids and epinephrine, oxygen, and respiratory support in an intensive care unit may be needed. After acute care of a systemic sting reaction, patients should be provided an epinephrine autoinjector, referral to an allergist/immunologist, and instructions on prevention of insect stings.


Pediatrics_Nelson

Pediatrics_Nelson. At least 50 to 100 fatalities per year in the United States are attributed to insect sting reactions. Most deaths (80%) occur in adults older than 40 years of age, and only 2% occur in individuals younger than 20 years of age. Approximately one half of deaths occur in persons without any history of a prior sting reaction. Successfully avoiding the stinging insect is the most important prognostic factor. More than 85% of adults who complete 5 years of immunotherapy tolerate challenge stings without systemic reactions for 5 to 10 years after completion. Measures to reduce the chance of accidental sting include exterminating infested areas; not eating or drinking outdoors; wearing long pants and shoes; and avoiding brightly colored clothing, fragrances, or hairspray when outdoors. Common insect repellents are not effective against Hymenoptera.


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Pediatrics_Nelson. Current recommendations are to administer venom immunotherapy to individuals who have had a systemic life-threatening reaction from an insect sting and have positive venom skin tests or elevated levels of venom-specific IgE. All persons with a history of systemic reactions to insects should be instructed in the use of an epinephrine autoinjector and encouraged to wear a MedicAlert bracelet. Children younger than 16 years of age who have had only a cutaneous reaction generally do not require immunotherapy because their prognosis is benign and can be managed with the availability of epinephrine.


Pediatrics_Nelson

Pediatrics_Nelson. An adverse reaction to food is a generic description of anyuntoward reaction after food ingestion, including toxic reactions such as food poisoning and nontoxic reactions, which canbe subdivided further into nonimmune and immune reactions. Lactose intolerance is a nonimmune reaction. Food allergy orhypersensitivity reactions encompass immune reactions to foodand can be divided further into IgE-mediated reactions, whichare typically rapid in onset, and non-IgE-mediated reactions.


Pediatrics_Nelson

Pediatrics_Nelson. Oral tolerance is the process of suppression of the immune response to the array of dietary elements ingested daily. Food allergy or hypersensitivity reactions are the result of immune reactions to glycoproteins and develop in genetically predisposed individuals. In children, cow’s milk, eggs, peanuts, soybean, wheat, tree nuts, fish, and shellfish cause 90% of IgE-mediated reactions. In older children and adults, peanuts, tree nuts, fish, and shellfish account for most reactions. Exposure to the allergenic food protein results in cross-linking of the IgE receptor found on the mast cells and basophils, which become activated and degranulate, releasing numerous potent mediators and cytokines. Non-IgE-mediated reactions typically occur hours to days after the allergen ingestion and are manifest as gastrointestinal symptoms. A cell-mediated immune mechanism may be responsible. Approximately 6% to 8% of children are affected with food allergy. In adults this declines to 1% to 2%.


Pediatrics_Nelson

Pediatrics_Nelson. Approximately 6% to 8% of children are affected with food allergy. In adults this declines to 1% to 2%. Symptoms of hypersensitivity reactions vary from involvement of the skin, gastrointestinal tract, and respiratory tract to anaphylaxis. Non-IgE-mediated food allergy typically presents during infancy as proctitis/proctocolitis, enteropathy, or enterocolitis (Table 84-1). In acute IgE reactions, skin prick allergy testing and serum testing to foods may help confirm the suspected food allergy.


Pediatrics_Nelson

Pediatrics_Nelson. In acute IgE reactions, skin prick allergy testing and serum testing to foods may help confirm the suspected food allergy. A careful history focuses on symptoms, the time interval fromingestion to onset of symptoms, the quantity of food necessaryto evoke the reaction, the most recent reaction, patterns of reactivity, and associated factors such as exercise and medicationuse. Skin prick testing can be performed to confirm IgE-mediated food allergies. A negative skin test virtually excludes anIgE-mediated reaction (unless the clinical history suggests asevere reaction after an isolated ingestion of the food). A positive skin test indicates sensitization but does not prove clinicalreactivity and must be interpreted, based on the history.


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Pediatrics_Nelson. Table 84-1 Gastrointestinal Food Allergic Disorders DISORDER AGE GROUP CHARACTERISTICS DIAGNOSIS PROGNOSIS/COURSE IgE-MEDIATED Acute gastrointestinal hypersensitivity Any Onset: minutes to 2 h Nausea, abdominal pain, emesis, History, positive PST, and/ or serum food-IgE Variable, food-dependent Milk, soy, egg, and wheat Allergic eosinophilic esophagitis Any, but especially infants, children, adolescents Children: chronic/intermittent symptoms of gastroesophageal reflux, emesis, dysphagia, abdominal pain, irritability Adults: abdominal pain, dysphagia, food impaction History, positive PST, and/ or food-IgE in 50%, but poor correlation with clinical symptoms Patch testing may be of value Elimination diet and OFC Endoscopy, biopsy provides conclusive diagnosis and response to treatment information Variable, not well established, improvement with elimination diet within 6–8 wk Elemental diet may be required Often responds to swallowed topical steroids


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Pediatrics_Nelson. Biopsy diagnostic: villus Lifelong atrophy Screening with serum IgA antitissue transglutaminase and antigliadin Resolution of symptoms with gluten elimination and relapse on oral challenge From Adkinson NF Jr, Bochner BS, Busse WW, et al: Middleton’s Allergy: Principles and Practice, ed 7, Philadelphia, 2008, Mosby. OFC, Oral food challenge; PST, prick skin test. Adapted from Sampson HA: Food allergy, J Allergy Clin Immunol 111:S544, 2003.


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Pediatrics_Nelson. An in vitro serum specific IgE assay can be used to helpconfirm clinical allergy as well. Many allergists and laboratories regard the ImmunoCAP system as the method of choice.This method uses a quantitative fluorescent immunoassay,which is more sensitive than other assays; this method also has improved specificity and reproducibility compared toother assays. These tests provide supplementary informationto skin tests. Researchers have tried to determine concentrations of food-specific IgE at which clinical reactions are highlylikely to occur (Table 84-2). Patients with allergen specific IgElevels greater than 95% of the predictive value may be considered allergic, and there is no need for an oral food challenge.Monitoring the allergen specific IgE level may be helpful in predicting whether a child has outgrown the food allergy.Oral food challenges remain the standard of diagnosis andcan be performed to determine whether a child can eat thefood safely.


Pediatrics_Nelson

Pediatrics_Nelson. Management of food allergies consists of educating the patient to avoid ingestion of the responsible allergen and to initiate therapy if ingestion occurs. For mild symptoms limited to the skin only, such as mild itching or hives in the area of allergen contact, oral antihistamines such as diphenhydramine or cetirizine can be administered. If symptoms extend beyond skin, including but not limited to difficulty breathing or swallowing, tongue or throat swelling, vomiting, and fainting or symptoms not responding to diphenhydramine within 20 minutes, injectable epinephrine should be administered and immediate medical attention pursued. Types of injectable epinephrine include EpiPen (0.3 mg), EpiPen Jr. (0.15 mg), and Twinject (0.3 or 0.15 mg). Anaphylaxis is the most serious complication of allergic food reactions and can result in death (see Chapter 81).


Pediatrics_Nelson

Pediatrics_Nelson. Anaphylaxis is the most serious complication of allergic food reactions and can result in death (see Chapter 81). Hypersensitivity to egg, milk, wheat, and soy resolves within the first 5 years of life in approximately 80% of children. Sensitivity to certain foods, such as peanuts, tree nuts, fish, and shellfish, tends to be lifelong. However 20% of children who manifested peanut allergy younger than 2 years of age may outgrow it. Avoidance of the suspect food is crucial. Careful reading of food labels is a priority. A MedicAlert bracelet with appropriate information should be worn. The Food Allergy Research & Education organization ( www.foodallergy.org ) is a useful educational resource for families and physicians.


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Pediatrics_Nelson. Recommendations for prevention of allergic diseases aimed at the high-risk newborn who has not manifested atopic disease include (1) breastfeeding for the first 4 to 6 months or (2) using a hydrolyzed casein formula (e.g., Alimentum or Nutramigen) or partially hydrolyzed whey formula (e.g., Good Start) (if supplementing) for the first 4 to 6 months and delaying introduction of solid foods until 4 to 6 months of age. Other approaches, such as maternal avoidance diets during pregnancy and during lactation, as well as avoidance of allergenic foods for infants beyond 6 months of age, are unproven.


Pediatrics_Nelson

Pediatrics_Nelson. An adverse drug reaction is defined as an unwanted, negative consequence associated with the use of a drug or biologic agent. Drug reactions can be classified as immunologic or nonimmunologic reactions (Table 85-1). Nearly 75% to 80% of adverse drug reactions are caused by a predictable, nonimmunologic mechanism, and between 5% and 10% of all drug reactions are explained by an immune-mediated mechanism. The remaining drug reactions are caused by an unpredictable mechanism, which may or may not be immune-mediated. The Gell and Coombs classification can be used to describe some drug-induced allergic reactions (see Table 77-1). Many drug reactions cannot be classified because the exact immune mechanism has not been defined. Most drugs cannot elicit an immune response because of their small size; rather, the drug or a metabolite acts as a hapten and binds to larger molecules, such as tissue or serum proteins, a process called haptenation.The multivalent hapten-protein complex forms a new


Pediatrics_Nelson

Pediatrics_Nelson. rather, the drug or a metabolite acts as a hapten and binds to larger molecules, such as tissue or serum proteins, a process called haptenation.The multivalent hapten-protein complex forms a new immunogenic epitope that elicits Tand B-lymphocyte responses.