The Allergy Report

The Allergy Report
Volume 1
Overview of Allergic Diseases:

Diagnosis, Management, and Barriers to Care Introduction Background Prevention Diagnostic Testing Management of Allergic Diseases
Environmental Control Pharmacologic Therapy Allergen Immunotherapy Patient Education
Recommendations for Policy and Interventions Volume 2
Diseases of the Atopic Diathesis

Introduction Rhinitis Asthma Atopic Dermatitis Associated Disease: Rhinosinusitis Associated Disease: Chronic or Recurrent Otitis Media Volume 3
Conditions That May Have an Allergic Component

Introduction Conjunctivitis Urticaria and Angioedema Contact Dermatitis Drug Reactions Food Reactions Insect Sting Reactions Latex Reactions Anaphylactic and Anaphylactoid Reactions
Copyright 2000. The American Academy of Allergy, Asthma & Immunology, Inc. All rights reserved. The material contained in this publication is the exclusive property of the American Academy of Allergy, Asthma & Immunology, Inc. (AAAAI) and, as to copyrighted works of others which are contained herein, such other copyright owners. This work is protected under U.S. copyright law and other international treaties and conventions. Except as stated herein, none of the material contained in this publication may be copied, reproduced, distributed, republished, downloaded, displayed, posted or transmitted in any form or by any means, including, but not limited to, electronic, mechanical, photocopying, recording, or otherwise, without the prior written permission of AAAAI or, as to copyrighted material of others, the copyright owner. Any inquiries regarding such permission should be directed to: Ms. Amy Stone American Academy of Allergy, Asthma & Immunology, Inc. 611 East Wells Street Milwaukee, WI 53202 Phone: (414) 272-6071 Fax: (414) 272-6070 Certain material in this publication is taken or derived from NIH Publication Nos. 974051 (Guidelines for Diagnosis and Management of Asthma) (July 1997) and 97-4053 (Practical Guide for Diagnosis and Management of Asthma) (October, 1997) of the U.S. Department of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung and Blood Institute. AAAAI gratefully acknowledges the assistance of the Academic Services Consortium, University of Rochester, in the preparation of this publication. Permission is granted to display, copy, distribute and download the materials in this publication for personal, non-commercial use only provided that such materials are not altered or modified and AAAAIs copyright notice is displayed thereon. DISCLAIMER: This publication and the material and information contained herein have been produced for informational purposes as a service to members and the general public and are provided as is, without warranty of any kind, either express or implied, including, without limitation, implied warranties of merchantability and fitness for a particular purpose. AAAAI shall not be liable for direct, indirect, special, incidental or consequential damages related to the users decision to use this publication or any material or information contained herein.
CONTENTS
Introduction .. 13
Rhinitis...... .. 21
Classification of Rhinitis ............................ .. 21 Allergic Rhinitis .... 22 Seasonal Allergic Rhinitis . 22 Perennial Allergic Rhinitis .... 22 Nonallergic Rhinitis .... 23 Nonallergic Eosinophilic Rhinitis .... Infectious Rhinitis.... Idiopathic Nonallergic or Vasomotor Rhinitis .. Rhinitis Medicamentosa .... Hormonal Rhinitis.... Anatomic Rhinitis ....... 23 23 24 24 24 24
Natural History of Allergic Rhinitis .... 25 Allergic rhinitis often coexists with other allergic disorders... 25 Allergic rhinitis and asthma often coexist ....... Inflammatory components common to allergic rhinitis and asthma. Common symptoms of allergic rhinitis and their mediators(chart).. Allergic rhinitis and rhinosinusitis frequently coexist and are definitely linked........ 25 25 26 27
Diagnosing the Patient with Allergic Rhinitis .. 27 Medical History .................. ... 27 Physical Examination .......................... 28 Diagnostic Testing ........................... 30 Nasal Smears................... 30 Imaging .............. 31 Considerations for Diagnosing Seasonal Allergic Rhinitis .. 31
Considerations for Diagnosing Perennial Allergic Rhinitis .. 31 Managing the Patient with Allergic Rhinitis .... 33 Four general principles of allergy management. .... 33 1. Avoid factors that cause symptoms ....... 33 2. Use appropriate treatments . 33 Antihistamines . 34 Decongestants ..... 35 Antihistamine-decongestant Combination Products..... 36 Corticosteroids............. 36 Intranasal Corticosteroid s......... 36 Oral Corticosteroids............... 36 Mast Cell Stabilizers .............. 38 Anticholinergics . 38 General pharmacologic management (chart). . 39 Stepwise approach to pharmacotherapy for seasonal allergic rhinitis (chart) .. 40 Stepwise approach to pharmacotherapy for perennial allergic rhinitis (chart)... 41 Stepwise approach to pharmacotherapy for perennial nonallergic rhinitis (chart). 42 Medications to Treat Rhinitis ... 43 Oral antihistamines (charts) ......... 43 Oral antihistamine-decongestant combinations (charts).. 43 Intranasal antihistamines (chart) .... 44 Intranasal mast cell stabilizers (chart )... 44
Intranasal anticholinergics (chart)....... 44 Intranasal corticosteroids (chart)..... 45 3. Evaluate for immunotherapy .................. 46 Consider immunotherapy for allergic rhinitis ... 46 4. Educate and follow-up ............. 47 Consultation/comanagement with an allergy/immunology specialist or otolaryngologic allergy specialis t... 47 Considerations for Special Populations........... 48 Managing the Child with Allergic Rhinitis ..... 48 Managing the Elderly Patient with Allergic Rhinitis ....... 49 Managing Allergic Rhinitis During Pregnancy ..... 49 References ...................... 50
Asthma ............ 53
Asthma is often associated with allergy.... 53 Rhinitis and asthma involve a common respiratory mucosa.............. 53 Pathogenesis ...................... 54 Progression to airway remodeling (figure)....... 55 Natural History ........................... 56 Diagnosing the Patient with Asthma ..... 56 Medical History ........ 57 Physical Examination ....................... 59 Objective Measurements ....................... 59 When is peak expiratory flow (PEF) used?...... 60
Two ways to use a peak flow meter for measuring PEF variability .. 61 Differential Diagnosis .............................. 62 Masqueraders of asthma in children and adults (chart).. 62 Classification of Asthma Severity.................. 63 How do you classify asthma severity? . 64 Classifying asthma severity BEFORE treatment (chart) ..... 64 Classifying asthma severity AFTER treatment........ 65 Patients with asthma may need additional tests to aid and/or confirm the diagnosis (chart) .. 65 Managing the Patient with Asthma ................... 66 The four components of asthma management.... 66 Component 1. Measures of Assessment and Monitoring. 66 Spirometry should be performed ..... 67 Peak expiratory flow monitoring may be helpfu l..... 67 Measure PEF in the office ............ 67 Measure PEF at home............ 68 Cutpoints for PEF monitoring ......... 69 Monitor the quality of life/functional status...... 69 Component 2. Controlling Factors Contributing to Asthma Severity...... 71 Allergens are common causal factors .. 71 Common causal factors of asthma (chart)....... 72 Component 3. Pharmacologic Therapy .... 74 Two approaches to initiating step-care therapy .... 74
When do you step up, or increase long-term control medications? 75 How do you help the patient regain control of his/her asthma?.. 75 When and how do you step down long-term control therapy?................ 75 Reduce therapy gradually ................ 76 What medications are used to treat asthma?...... 77 Long-term Control Medications... Inhaled Corticosteroids ..... Cromolyn Sodium/Nedocromil Sodium. Leukotriene Modifiers ....... Long-acting Beta2 -agonists..... Methylxanthines (theophylline) ...... .... Oral Corticosteroids..... Quick-Relief Medications....... Short-acting Beta2 -agonists ... Oral Corticosteroids........ .. Anticholinergics (Ipratropium Bromide ).... 77 77 78 78 79 80 80 81 81 81 81
Stepwise approach for managing infants and young children (5 years of age) with acute or chronic asthma symptoms (chart) .................. ... 82 Stepwise approach for managing asthma in patients > 5 years of age with acute or chronic asthma symptoms (chart). ... 84 Medication Tables ........... Long-Term Control Medications (charts)...... Quick-Relief Medications (charts) ...... New Medications (charts) ......... 86 87 91 93
Types of inhalation devices for asthma medications (chart).. 94 Advantages of Using Spacers and Holding Chambers96 Treat asthma exacerbations promptly and aggressively... 97
Assessing the severity of an asthma exacerbation... 98 Risk factors for death from asthma ........... 98 Managing Asthma Exacerbations in the Home.... 99 rgent Care (Clinicians Office or Emergency Department) for Managing Asthma Exacerbations ... 100 Referral to an asthma specialist for consultation or comanagement ....102 Special Considerations for Managing Asthma ..... 103 Managing Exercise-induced Bronchospasm (EIB).... 103 Preventing anticipated episodes of asthma symptoms (other than exercise) .. 104 Treating asthma symptoms due to upper viral respiratory infections (URIs) ... 104 Treating the child with asthma ...... Children < 2 years ............ Children between 3 and 5........ For School-age children ..... Adolescents................... The childs schedule and giving asthma medications..... Asthma, inhaled corticosteroids, and linear growth .... Managing asthma in the elderly ..... . Managing the pregnant patient with asthma.. Managing bronchopulmonary aspergillosis in the patient with asthma...... 105 106 106 107 107 108 108 109 110
111
Managing work-aggravated asthma and occupational Asthma.. 111 Some examples of compounds causing asthma (chart). ..
112
Component 4. Educations for a Partnership in Asthma Care Take a proactive approach to asthma educatio n.. What can you and your staff do in a single asthma visit? ........... Focus on what is doable to improve adherence with asthma therapy ... Education Recommendations (chart)..... Asthma Management Plan for Long-term Control and Exacerbations .... Asthma and the School ...... ... Teachers, coaches, and school health personnel need to know .. .. How asthma friendly is your school? . School Asthma Management Plan ... References .................. ....
113 113 114 114 116 118 119 119 120 121 123
Atopic Dermatitis.......... ... ....

Diagnosing the Patient with Atopic Dermatitis...... .. Medical History ......................... . Distribution of lesions (figure) .............
131
135 135 136
Ask the patient about what causes symptoms...... 137 Physical Examinatio n........ .. 137 Characteristics of atopic dermatitis lesions... 138
Distinguishing features of seborrheic and atopic dermatitis in infancy (chart) .............. 140 Masqueraders of atopic dermatitis.... 140 Diagnostic Testing .......... ... Elimination diets ........... .. Managing the Patient with Atopic Dermatitis........ 141 141 142
Four general principles of allergy management.... 142 1. Avoid factors that cause symptoms .... 142 Avoiding causal factors .............. 142 Skin care is important for palliation of symptoms... 143
2. Use appropriate medications ............ 145 Corticosteroid s............................ Topical Corticosteroids.............. Topical Corticosteroids (charts) ...... 145 145 147
Oral Corticosteroids ............ 149 Oral Antihistamines ....................... Tar preparations......... .. 149 149
A Protocol for Treating Atopic Dermatitis ... 150 Special Considerations for Treating Atopic Dermatitis ... Antibiotics ....... .. Antiviral Agents ............ Antifungal Agents (topical or oral).... 3. Evaluate for immunotherapy ............... 150 150 151 151 151
4. Education and regular follow-up are important ..... 151 Consultation/comanagement with an allergy/immunology specialist ..... Referral to an allergy/immunology and/or dermatology specialist.... .
152
152
Tips for patients with Atopic Dermatitis ..... 153 References .................................... .... 154
Associated Disease: Rhinosinusitis ....157

Classification of Rhinosinusitis ..................... Acute Rhinosinusitis ....................................... 157 157
Recurrent Acute Rhinosinusitis............ Subacute (persisting acute) Rhinosinusitis .... . Chronic Rhinosinusitis .................. Tips to distinguish chronic from acute rhinosinusitis .... Who is at risk for rhinosinusitis? ............. Clinical and environmental factors that predispose an individual to infectious rhinosinusitis (chart)... ... Diagnosing the Patient with Rhinosinusitis ......
157 157 157 158 159
159 160
Signs and Symptoms Associated with Rhinosinusitis ....... 160 Differentiating acute infectious rhinosinusitis from seasonal allergic rhinitis (chart) ....... 160 The signs and symptoms of rhinosinusitis may reveal which sinus is primarily affected ........ Diagnostic Procedures ................................ Imaging ...................................................... Nasal Endoscopy ...................................... Other diagnostic tests may be considered in some circumstances Tips for diagnosing rhinosinusitis ...... Managing the Patient with Infectious Rhinosinusitis .....
161 161 161 162
162 163 164
Palliative Treatment ...................................... 164 Pharmacologic Management ....................... Antibiotic Therap y.................................. Intranasal Corticosteroids.................... Decongestants .......................................... Oral Mucolytics ...................................... 164 164 .165 165 166
Surgery .............................................................. 166
Specific Considerations for Treating Rhinosinusitis ... Acute Rhinosinusitis.............................. Recurrent Acute Rhinosinusitis ........... Subacute (Persisting Acute Rhinosinusitis........... Chronic Infectious Rhinosinusitis ....... Additional Management Considerations .... Special Considerations for Treating Rhinosinusitis in Children..
167 167 167 167 168 168 169
Consider referral to an allergy/immunology or an otolaryngologic allergy specialist for consultation and/or comanagement......... 171 When is referral to an otolaryngologic allergy specialist preferred?.... References ............................................................... Associated Disease: Recurrent or Chronic Otitis Media .......
171 172 175
Characteristic Signs and Symptoms .............. 175 Natural History of Otitis Media ........................ 176 Risk Factors for Otitis Media (chart) 176
Diagnosing the Patient with Otitis Media ....... 177 Allergy Evaluation ........................................ Managing the Patient with Otitis Media ...... Preventive Therapies ................................... Therapeutic Treatments ............................... Referral to an allergy/immunology specialist or otolaryngologic allergy specialist ......................................................... References ............................................................... 179 179 179 180 180 181
Resource Organizations ................................. 183
Glossary .................... ..... 185
The Allergy Report

Introduction
o improve the health and well being of allergy sufferers, the American Academy of Allergy, Asthma, and Immunology (AAAAI) in partnership with the National Institute of Allergy and Infectious Diseases (NIAID) and 20 other medical associations, advocacy groups, and government agencies, has undertaken a comprehensive initiative Allergic Disorders: Promoting Best Practice. The goal of this initiative is to ensure that a broad spectrum of healthcare providers learns about, understands, and implements clinical and best practice information for diagnosing and managing patients with allergic diseases. The Allergy Report represents the outcome of a first step of the initiative: development of an evidence-based, practical and easy-toaccess guide to allergic disorders to help family practice physicians, internists, pediatricians, nurse practitioners, school nurses, and others who manage or interact with patients with allergies. The Allergy Report provides guidance on the clinical management of allergic disorders, examines the barriers to effective care, and addresses future research needs for allergy mechanisms and clinical approaches to treatment. The Report is organized into three volumes. This Volume provides information on the diseases of atopic diathesis: rhinitis, asthma, and allergic dermatitis. It also includes sections on two commonly associated diseases: rhinosinusitis and recurrent or chronic otitis media. Volume 1 provides an overview of the allergic process, the principles in common to the diagnosis and management of all allergic diseases, and discusses potential interventions for improving care for patients with allergic disorders. Volume 3 focuses on the conditions in which there may be an allergic component, including: conjunctivitis, urticaria and angioedema, contact dermatitis, drug reactions, food reactions, insect sting reactions, latex reactions, and anaphylactic/anaphylactoid reactions.
Introduction i
Overview of Sections of Volume 2: Diseases of the Atopic Diatheses Rhinitis

Allergic rhinitis is the most common allergic disease in the U.S. affecting about 40 million people. It is associated with direct costs of about $4.5 billion annually and indirect costs that reflect approximately 4 million days of lost time and productivity at work and school. Discussion includes differentiating allergic and non-allergic rhinitis, appropriate methods for diagnostic testing, and suggestions for managing the allergic rhinitis patient. Specific medications are described in terms of their effects on symptoms and potential impact on daily activities. For example, the older antihistamines are effective treatments but in many patients cause drowsiness and/or loss of concentration and may affect psychomotor performance. In these cases, the newer nonsedating antihistamines are appropriate therapeutic choices. There are other medications that have some sedating side effects, but less than the older antihistamines (hence, they are referred to as the lesssedating antihistamines). Stepwise protocols for treatment are given for both seasonal and perennial allergic rhinitis and nonallergic rhinitis.
Asthma
Asthma is a chronic inflammatory disease of the airways characterized by airway obstruction which is at least partially reversible with or without medication, and increased bronchial responsiveness to a variety of stimuli. Asthma is often associated with allergy, and atopy is the strongest identifiable predisposing factor for the development of asthma. This section provides an overview of the diagnostic and treatment recommendations for asthma based on the Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (EPR-2) published by the National Asthma Education and Prevention Program (National Heart Lung and Blood Institute) in 1997.
Atopic Dermatitis
Atopic dermatitis is a chronic or recurrent atopic inflammatory skin disease that usually begins in the first few years of life. It is often the initial clinical manifestation of an atopic predisposition, and often precedes allergic rhinitis and asthma in children. Up to 15% of the
Introduction ii
population in the U.S. is affected by atopic dermatitis at some time during childhood, and the prevalence is increasing. Clinical criteria for diagnosis are given including the morphology and distribution of lesions in relation to age and/or ethnicity, consideration of appropriate diagnostic tests, and the distinguishing features of common dermatoses of infancy that should be distinguished from atopic dermatitis. Nonpharmacologic and pharmacologic approaches to treatment are included. The use of topical corticosteroids is discussed in detail.
Associated Disease: Rhinosinusitis

Rhinosinusitis is an inflammation of the paranasal sinuses that occurs with rhinitis and is common in patients with perennial allergic and nonallergic rhinitis and in patients with moderate to severe asthma. Diagnosis depends on a constellation of signs and symptoms. Suggestions for diagnosis and for managing the patient with rhinosinusitis are provided.
Associated Disease: Chronic or Recurrent Otitis Media

Otitis media is an acute or chronic inflammation of the middle ear that is often associated with allergic rhinitis, particularly in children over 3 years of age. Risk factors for otitis media, evaluation of the patient, and preventative and therapeutic approaches to treatment are discussed.
Comment on Terminology
The Allergy Report represents the collaboration and team effort of 22 organizations (see page vi). Eight drafts of the document were developed, reviewed, and revised by some or all of the Task Force before the final sign-off and endorsement. Several terms had different definitions and/or interpretations by members of different groups. As a result, it was necessary for the Task Force to reach consensus on the following: Allergy: In most of The Allergy Report, the term: Allergen refers to substances that can induce IgE antibody responses.
Allergy refers to IgE antibody responses to allergens.
Introduction iii
Allergic disease is the resulting clinical manifestations generated
by IgE antibody responses. Allergens include generally harmless materials such as: Pollens Cockroaches
Mold spores Animal danders House dust mites Penicillin and other drugs Foods Latex Insect venoms
In several places in The Report, the terms allergy and allergic disease are more broadly encompassing and include altered immunologic reactivity that may be either IgE-mediated or non-IgE-mediated. The reader should note that this broader definition is used selectively. Examples of this can be seen in the following sections in Volume 3: Drug Reactions and Food Reactions describe clinical responses that are both IgE-mediated and non-IgE-mediated.
Contact Dermatitis describes specific, non-IgE-mediated immune cell
reactions (i.e., T-cell responses to contact antigens). Another term that is frequently confused with allergy is atopy. Atopy refers to the genetic tendency to develop the classical allergic diseases, namely, allergic rhinitis, asthma, and atopic dermatitis. Atopy is typically associated with a genetically determined capacity to mount IgE responses to common allergens, especially inhaled allergens and food allergens. Recently, it has been shown that IgE responses to latex are more frequent in atopic families, and thus, latex allergy may be considered an atopic disease. In contrast, IgE responses to insect venom and drugs are not more common in atopic families. Hence, these disorders are considered allergic, but not atopic, diseases. Specialist: The Allergy Report identifies many clinical situations in which referral to a specialist is warranted. Specialists may include: Allergy/immunology specialists
Dermatologists Infectious disease specialists Ophthalmologists
Introduction iv
Otolaryngologists Otolaryngologic allergy specialists Pulmonologists
In many cases, the type of specialist varies with the provider network and the geography/community. For example, the Asthma section (page 82) uses the term asthma specialist in the same manner used by the National Asthma Education and Prevention Program1 to refer to a fellowship-trained allergist or pulmonologist or, occasionally, other physicians with experience in asthma management developed through additional training and experience. Similar complexities exist in identifying specialists for management of such diseases as atopic dermatitis, rhinosinusitis, otitis media, conjunctivitis, urticaria and angioedema, and contact dermatitis. Therefore, consultation or comanagement is recommended, as appropriate, with the type of specialist determined by the referring healthcare provider and taking into account the patients health insurance coverage and the healthcare resources available in the community. Allergies are the sixth leading cause of chronic disease in the United States, costing the healthcare system over $18 billion annually. Each year more than 50 million Americans suffer from allergic disease, and these numbers are increasing. On a daily basis, allergies cause time lost from work, school, and leisure activities and decrease productivity at work, in school, and at home; but they dont have to! Learning what triggers allergies and understanding how to treat the diseases may make the difference between a chronic debilitating illness and a productive, healthy lifestyle. To help healthcare professionals bridge the gap between current knowledge and practice, The Allergy Report presents basic recommendations for the diagnosis and management of allergic diseases. It is the hope of the Task Force responsible for developing The Allergy Report, and those who have reviewed it, that this initiative will improve healthcare and productivity for patients with allergic diseases.
Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma: Clinical Practice Guidelines. NIH Publication No. 97-4051, page 10.
Introduction v
Acknowledgements
The Task Force acknowledges the support of Schering/Key, which provided an unrestricted educational grant for development, publication, and distribution of The Allergy Report.
Chairs
Harold S. Nelson, M.D., FAAAAI American Academy of Allergy, Asthma and Immunology National Jewish Medical and Research Center Denver, CO Gary S. Rachelefsky, M.D., FAAAAI American Academy of Allergy, Asthma and Immunology Allergy Research Foundation, Inc. University of California at Los Angeles Los Angeles, CA
Task Force Members

John Bernick, M.D., Ph.D. American College of Occupational and Environmental Medicine A. Wesley Burks, M.D. American Academy of Pediatrics Don Cui, PA-C, C.M.C.M. American Academy of Physicians Assistants Mark Dykewicz, M.D., F.A.C.P . American College of Physicians American Society of Internal Medicine Ivor Emanuel, M.D. American Academy of Otolaryngic Allergy John Georgitis, M.D., F.C.C.P . American College of Chest Physicians Peter Gergen, M.D. Agency for Health Care Policy and Research James A. Hadley, M.D., F.A.C.S. American Academy of Otolaryngology/ Head and Neck Surgery Sharon Hipkins, R.N., M.S.N. Asthma and Allergy Foundation of America Joel Karlin, M.D. American Medical Association Monica Kraft, M.D. American Thoracic Society Barry Lampl, D.O. American Osteopathic College of Allergy and Immunology
Introduction vi
Doris Luckenbill, R.N., M.S., C.R.N.P . National Association of School Nurses Bryan Martin, D.O. American Osteopathic College of Allergy and Immunology Anne Muoz-Furlong The Food Allergy Network Donna Nativio, Ph.D., C.R.N.P ., F.A.A.N. American College of Nurse Practitioners Marshall Plaut, M.D. National Institute of Allergy and Infectious Diseases, National Institutes of Health
Stephen Redd, M.D. Centers for Disease Control and Prevention Daniel Rotrosen, M.D. National Institute of Allergy and Infectious Diseases, National Institutes of Health Nancy Sander Allergy and Asthma Network Mothers of Asthmatics, Inc. William Storms, M.D. American College of Allergy, Asthma and Immunology Karen Tietze, Pharm.D. American Pharmaceutical Association Barbara Yawn, M.D. Specialist in Family Medicine
Outside Reviewers
The panel of content experts who reviewed the draft document included: Leonard Bielory, M.D., FAAAAI; S. Allan Bock, M.D., FAAAAI; William W . Busse, M.D., FAAAAI; Harold M. Friedman, M.D., FAAAAI; Mitchell Friedlaender, M.D., FAAAAI; Anthony Gaspari, M.D.; David B. K. Golden, M.D., FAAAAI; Michael A. Kaliner, M.D., FAAAAI; Michael A. LeNoir, M.D.; Mark T. O'Hollaren, M.D., FAAAAI; Harold C. Pillsbury, III, M.D.; Thomas E. Platts-Mills, M.D., Ph.D., FAAAAI; Hugh Sampson, M.D., FAAAAI; Gail Shapiro, M.D., FAAAAI; F. Estelle R. Simons, M.D., FAAAAI; David Skoner, M.D.; Stuart Stoloff, M.D.; Abba Terr, M.D., FAAAAI; John Warner, M.D.; Jill Warner, Ph.D.; Robert Zeiger, M.D., Ph.D., FAAAAI.
Introduction vii
Rhinitis
Rhinitis is an inflammation of the mucous
membranes of the nose.

The characteristic symptoms of rhinitis are: o Sneezing o Itching o Nasal discharge o Congestion Rhinitis can be allergic, nonallergic, or both. Rhinitis is often associated with other chronic
conditions, including:
o Asthma o Eustachian tube dysfunction and otitis media o Rhinosinusitis o Nasal polyposis o Allergic conjunctivitis o Atopic dermatitis
Rhinitis can be allergic, nonallergic, or both. Rhinitis is often associated with other chronic conditions. The same inflammatory processes may affect the mucosa of the:
Nasal passages Lower airways Sinuses Eustachian tube
Classification of Rhinitis
Classification of Rhinitis
Allergic rhinitis: Seasonal allergic rhinitis Perennial allergic rhinitis Nonallergic rhinitis: Infectious rhinitis Idiopathic nonallergic or vasomotor rhinitis Rhinitis medicamentosa Hormonal rhinitis Anatomical causes of rhinitis
Rhinitis with prolonged nasal inflammation and eustachian tube dysfunction can be a factor in the development of otitis media.
Rhinitis
Allergic Rhinitis
Patients with allergic rhinitis are usually sensitive to nonspecific irritants (e.g., perfumes, tobacco smoke).
Repeated allergen
Involves IgE-mediated reactions of the nasal mucosa to
one or more allergens. May be seasonal, perennial, or both. Repeated allergen exposures primes the nasal mucosa, resulting in hypersensitivity so that symptoms occur: o At lower allergen levels. o To nonspecific irritants.
exposure primes the nasal mucosa resulting in hypersensitivity. o Symptoms occur at lower allergen levels. o Symptoms occur with nonspecific irritants.
Seasonal Allergic Rhinitis

Patients experience an IgE-mediated reaction of the
Plants that depend upon insect pollination (e.g., goldenrod, dandelions, and most flowers) rarely cause seasonal allergic rhinitis symptoms. Patients may show cross-reactivity to botanically related allergens.
Many of the allergenic substances of pollen grains are similar between plants from the same genus or family.
2
Rhinitis
nasal mucosa to one or more seasonal allergens. Symptoms occur, or are increased, during certain seasons. Symptoms are periodic, correlating with seasonal variation in aeroallergens. Characteristic symptoms include: o Watery rhinorrhea o Nasal congestion o Repetitive sneezing o Pruritus of the eyes, nose, ears, and throat o Watery eyes Nasal secretions usually contain eosinophils. Common allergens causing seasonal allergic rhinitis: o Grass pollens o Tree pollens o Weed pollens o Fungal (mold) spores
Perennial Allergic Rhinitis

Patients have an IgE-mediated reaction to allergens that
show little or no seasonal variation. Symptoms are intermittent or continuous throughout the year. Characteristic symptoms include: o Prominent and severe nasal blockage/congestion. o Postnasal drainage. Rhinorrhea and sneezing are less prominent than seasonal allergic rhinitis.
Seasonal pollen sensitivity may contribute to
exacerbations of rhinitis symptoms in patients with perennial allergic rhinitis. Common allergens causing perennial allergic rhinitis: o The most important causes of perennial allergic rhinitis are indoor inhaled allergens: House-dust mite Animal dander Cockroach Mold o Occupational allergens
Ingested food allergens rarely produce IgE-mediated rhinitis in adults without the involvement of other organs.
Nonallergic Rhinitis
Symptoms are similar to allergic rhinitis, but there is: o Usually no pruritus. o No evidence of allergic disease as determined by skin
testing or serum levels of IgE to specific allergens.
Patients with occupational perennial rhinitis have persistent symptoms which show a temporal association with workplace exposures.
Nonallergic Eosinophilic Rhinitis

Characterized by: o Marked nasal eosinophilia o Perennial symptoms of:
Sneezing Nasal obstruction Profuse watery rhinorrhea Nasal itching o Occasionally, loss of smell Coexistent eosinophilic inflammation of the paranasal sinuses and nasal polyps may be present. Patients with nonallergic asthma can also have nonallergic eosinophilic rhinitis. Some patients develop aspirin sensitivity.
Infectious Rhinitis
Usually caused by a virus. o Secondary bacterial rhinosinusitis is a common
complication.
Rhinitis
Characterized by discolored nasal secretions containing
neutrophils and, occasionally, bacteria. o Low grade fever is often present. Purulent discharge for > 5 days suggests bacterial rhinitis and/or rhinosinusitis.
Idiopathic Nonallergic or Vasomotor Rhinitis

Patients display nasal hyperresponsiveness to a variety
of nonspecific factors: o Chemical irritants o Strong smells o Environmental changes in: Humidity Temperature Barometric pressure There is no evidence of abnormal cellularity of nasal secretions. The mechanism has not been identified.
Rhinitis Medicamentosa Drugs producing rhinitis medicamentosa:

Topical decongestants
Patients experience drug-induced rhinitis. Topical nasal decongestant overuse is the most
common cause.
(most common) Antihypertensives Antipsychotics Oral contraceptives Cocaine
Hormonal Rhinitis
Patients experience rhinitis related to changes in
hormonal status. Symptoms may be associated with pregnancy, puberty, menses, and hypothyroidism. The characteristic symptoms are: o Nasal congestion o Rhinorrhea
Anatomic Rhinitis
Nasal septal deviation Adenoidal enlargement (children) Foreign body (especially in infants and young children) Choanal narrowing
4
Rhinitis
Natural History of Allergic Rhinitis

Allergic rhinitis is one of the most common allergic
diseases in the U.S. Onset is common in childhood, adolescence, and early adulthood. Symptoms often wane in older adults, but may develop or persist at any age. There is no apparent gender selectivity or predisposition for developing allergic rhinitis. Allergic rhinitis may contribute to other conditions, such as: o Sleep disorders o Fatigue o Learning problems
Allergic rhinitis is one of the most common allergic diseases in the U.S., affecting about 40 million people (including 19 million employed adults). Allergic rhinitis is associated with:
Direct costs
Allergic rhinitis often coexists with other allergic disorders.

Allergic rhinitis and asthma often coexist.
Some patients with allergic rhinitis report increased
approximating $4.5 billion/year.* 3.8 million lost work and school days annually.*
*
Rates vary between sources due to difficulty in assessing this common disorder. Source: Roundtable discussion. The health and economic impact of rhinitis. Am J Manag Care 1997: 3: S8-18.
asthma symptoms during the pollen season. Rhinitis and asthma involve a common respiratory mucosa. Inflammation is involved in the pathogenesis of both allergic rhinitis and asthma. o Allergic reactions in the nasal mucosa can potentially worsen asthmatic inflammatory processes in the lower airways.
Allergic rhinitis may contribute to:

Sleep disorders Fatigue Learning problems
Inflammatory components common to allergic rhinitis and asthma:

Inflammatory Cells Mast cells Eosinophils TH2 lymphocytes Inflammatory Mediators Histamine Leukotrienes Proinflammatory cytokines
Rhinitis
Inflammation in the nose may increase lower airway
The Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma (National Asthma Education and Prevention Program,1997) recommends intranasal corticosteroids for the treatment of chronic rhinitis in patients with persistent asthma. Antihistamines are not contraindicated for patients with asthma.
hyperresponsiveness. Possible mechanisms include: o Nasal allergic response altering bronchial responsiveness through naso-bronchial reflex. o Mouth breathing caused by nasal obstruction resulting in bronchospasm to cool, dry air. o Pulmonary aspiration of nasal contents. Clinical studies have shown that for some patients, treatment of allergic rhinitis with intranasal corticosteroids reduces asthma symptoms and bronchial hyperresponsiveness. o Treatment of upper airway diseases, alone, is not adequate treatment of asthma. Clinical studies of nonsedating antihistamines, decongestant combinations, and mildly sedating antihistamines showed improvement in pulmonary function and asthma symptoms in patients who had seasonal allergic rhinitis and asthma. o Antihistamines are not contraindicated for patients with asthma.
Common symptoms of allergic rhinitis and their mediators:

Symptoms Tickling Itchiness Nose rubbing Allergic salute Sneezing Nasal congestion Stuffy nose Mouth breathing Snoring Runny nose Post-nasal drip Throat clearing Histamine, leukotrienes Histamine, leukotrienes Histamine, leukotrienes, Bradykinin, platelet activating factor Mediators Histamine, prostaglandins
Rhinitis
Allergic rhinitis and rhinosinusitis frequently coexist and are definitely linked.
Sinusitis is rarely seen in the absence of rhinitis. Chronic rhinosinusitis may be associated with a similar
inflammatory process to that observed in allergic rhinitis. Nasal polyps are associated with chronic rhinosinusitis.
Allergic rhinitis may be associated with the development of other diseases due to common passageways.
Allergic Conjunctivitis Sinusitis
Otitis Media Allergic Rhinitis Asthma
Diagnosing the Patient with Allergic Rhinitis

Medical History
A detailed and accurate history is critical to the proper
diagnosis of allergic rhinitis and its successful treatment. Symptoms of allergic and nonallergic rhinitis are often similar. Ask the patient about specific symptoms and symptom patterns, including: o Onset o Progression o Severity
Rhinitis
Repetitive sneezing is a common symptom of seasonal allergic rhinitis.
o Duration o Relationship to seasons o Associated ocular, pharyngeal, and systemic
symptoms o Incidence of recurrent sinus or ear infections o Causal and exacerbating factors o Association with skin rashes (suggesting atopic dermatitis) o Association with asthma flare-ups o Relationship to drug use (medications and illicit drugs) o Relationship to GI symptoms (suggesting food allergy), especially in children Also ask about: o Personal and family histories of allergic disease (e.g., atopic dermatitis, asthma, colic in infancy) A negative family history does not rule out a diagnosis of allergic rhinitis. o Previous allergy testing o Medication use (prescription and nonprescription) o Facial and/or nasal trauma o Nasal surgery
Physical Examination
Examine the nose with high-illumination using a nasal speculum before and after topical decongestant administration.
The physical examination should focus on the nose,
eyes, throat, and ears, but should also include examination of the lungs and skin. Observe the patient for: o Mouth breathing. o Repeated nose wiggling, wiping, and pushing (allergic salute). o A nasal crease.
8
Rhinitis
o Allergic shiners a darkening of the infraorbital
skin resulting from venous dilation and indicative of chronic nasal congestion, particularly in children. o Related eye symptoms.
Repeated nose wiggling, wiping, and pushing (allergic salute) are common responses to the nasal itching associated with allergic rhinitis, particularly in children.
Reprinted from Fireman P . Allergic Rhinitis. In: Fireman P , Slavin R, (eds). Atlas of Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 146. By permission of the publisher Mosby.
Observe the patient for:

Mouth breathing Allergic salute Nasal crease Allergic shiners Related eye problems
Patients with chronic or repeated episodes of allergic rhinitis may have a nasal crease caused by continual upward rubbing of the nose to relieve itching.
Mouth breathing and allergic shiners, a darkening of the intraorbital skin related to chronic nasal congestion, are particularly common in children with allergic rhinitis.
Differential diagnoses of rhinitis include:

Allergic rhinitis Rhinitis medicamentosa Infectious rhinitis Anatomic obstruction Rhinosinusitis Nonallergic eosinophilic
Examine the nose with high illumination using a nasal
speculum before and after topical decongestant administration. Look for: o Pale blue and boggy nasal turbinates with a clear, watery discharge. o Inflamed/reddened mucosa. o Enlarged turbinates obstructing the nasal airway. o Nasal polyps which may appear as rounded, white, glistening masses resembling peeled grapes, commonly located within the middle meatus between the inferior and middle turbinates.
rhinitis Idiopathic nonallergic rhinitis

9
Rhinitis
Some patients with allergic rhinitis have systemic symptoms, including:

Weakness Malaise Irritability Fatigue Difficulty concentrating Decreased appetite
o Structural abnormalities, such as a deviated septum
or spur. o Character of drainage (clear or purulent, watery or thick). Examine the eyes for conjunctivitis (which may be subtle).
Symptoms of allergic conjunctivitis frequently accompany allergic rhinitis.

Reprinted from Wiley L, Arffa R, Fireman P . Alllergic Immunologic Ocular Diseases. In: Fireman P , Slavin R, (eds). Atlas of Allergies. 2nd ed. London: MosbyWolfe; 1996: 192. By permission of the publisher Mosby.
What suggests allergic rhinitis?

Itching of the nose,
throat, and eyes Clear, watery discharge Sneezing Pale, violaceous, swollen mucosa
Examine the pharynx for the presence and color of
posterior nasal drainage. Look at the appearance and size of tonsillar tissue, fullness of posterior soft palate, cobblestone appearance of posterior pharyngeal wall. Examine the ear with a pneumatic otoscope for: o Eustachian tube dysfunction o Dull, immobile tympanic membrane o Serous otitis o Excoriations Examine the lungs for wheezing. Examine the skin for evidence of atopic dermatitis.
Diagnostic Testing
The general principles of diagnostic testing are included in Volume 1: Diagnostic Testing, page 31. Specific tests used for diagnosing allergic rhinitis are included here.
Nasal Smears
Usually contain eosinophils in an allergic patient. Are useful in determining if chronic rhinitis has an
infectious origin (polymorphonuclear neutrophils). Do not differentiate allergic from nonallergic eosinophilic rhinitis.
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Rhinitis
Imaging
Radiographic imaging and computed tomography
(CT) are rarely used, except when chronic or recurrent rhinosinusitis is suspected as a complicating factor. Magnetic resonance imaging (MRI) provides better imaging of soft tissue than CT, but it is less suited to imaging the bony anatomy of this region.
Considerations for Diagnosing Seasonal Allergic Rhinitis

Itching of the nose is a prominent feature. o Itching of the ears, palate, or throat is commonly
Neither total serum IgE nor total circulating eosinophil counts are useful in diagnosing rhinitis, due to lack of sensitivity and specificity of these tests.
reported. During the pollen season, sneezing episodes may be aggravated by exposure to nonspecific stimuli (e.g., dust, air conditioning, tobacco smoke, strong odors). Sneezing episodes often cause tearing. Rhinorrhea is thin and clear, may be profuse and continuous, and usually contains eosinophils. In young children, the skin of the lower external nose and upper lip may become irritated and impetiginous. This is caused by: o Excessive and continual nasal discharge. o Rubbing and wiping. Nasal congestion caused by swollen turbinates is a common complaint and may: o Be the only presenting symptom, particularly in children. o Be intermittent at the onset of the pollen season. o Become more symptomatic as the pollen season progresses. o Disturb sleep, causing daytime fatigue, and impairing daily activities. Severe nasal obstruction can lead to blockage of the paranasal sinuses or eustachian tubes, causing sinus headache or earache. Senses of smell and taste may be altered. A nonproductive, hacking cough may develop due to posterior drainage of nasal secretions and irritation of the nasopharyngeal area. Asthma symptoms may worsen. Symptoms may correlate with the appearance and intensity of local pollens.
Rhinitis
11
Chronic nasal congestion may produce secondary complaints of:

A dry, irritated,
Symptoms may vary in occurrence and intensity in a
or sore throat Snoring Pain around the eyes Mouth breathing Frontal headaches Eustachian tube dysfunction Altered hearing, smell, and/or taste Sleep disturbance, with or without daytime fatigue
time-dependent fashion during the day or from season to season. Symptoms are often worse on arising in the morning even when the exposure occurred on the previous day (circadian pattern). Patients may not present with all symptoms.
Considerations for Diagnosing Perennial Allergic Rhinitis

Symptoms of perennial allergic rhinitis are very similar
to those of seasonal allergic rhinitis, although perennial is persistent, chronic, and generally less severe. The most common symptom is nasal congestion. o Sneezing, clear rhinorrhea, and nasopharyngeal and ocular itching occur less frequently in patients with perennial allergic rhinitis than seasonal allergic rhinitis. The perennial allergic rhinitis patient often complains of a persistent cold or chronic sinusitis.
Referral to an allergy/immunology or otolaryngologic allergy specialist for consultation and/or comanagement is recommended when there is:
A pattern of symptoms occurring
predominantly in relation to work. o Consider occupational rhinitis. Bilateral chronic nasal congestion with variable sneezing and discharge, but with significant olfactory disturbance. o Consider nasal polyps. Persistent rebound congestion resulting from overuse or abuse of intranasal decongestants. o Consider rhinitis medicamentosa. Continuous nasal congestion, particularly if unilateral, with bloodstained secretions. o Consider malignancy. A pattern of persistent symptoms that is not completely responsive to appropriate environmental control and medications. o Consider rhinosinusitis and/or noncompliance with therapeutic regimens.
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Rhinitis
Managing the Patient with Allergic Rhinitis

Four general principles of allergy management:
1 2
Avoid factors that cause symptoms. Use appropriate treatments.
3 4
Evaluate for immunotherapy. Educate and follow-up.
1 2
Avoid factors that cause symptoms.

The avoidance techniques and tips included in Volume 1: Prevention, page 21, are appropriate for the patient with allergic rhinitis.
Use appropriate treatments.

The goal of pharmacotherapy is to alleviate and prevent the patient's symptoms. Medications used to treat allergic rhinitis: o Antihistamines o Decongestants o Antihistamine-decongestant combinations o Corticosteroids o Mast cell stabilizers o Anticholinergics Palliative treatment may help. o Nasal lavage with warm salt water (with or without baking soda). o Inhalation of warm mist through the nose for 10 to 15 minutes, 2 to 4 times per day, may help.
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13
Antihistamines Antihistamines are the mainstay of pharmacotherapy for allergic rhinitis. Nonsedating antihistamines do not have the side effects associated with sedation caused by the older antihistamines (e.g., daytime somnolence, impaired performance).
The mainstay of pharmacotherapy for allergic rhinitis
is antihistamines. H1 -receptor antagonist activity o Blocks histamine-induced symptoms: Rhinorrhea Pruritus Sneezing o Has a rapid onset of action. o May reduce related symptoms in eyes and throat. Generally considered ineffective for treating nasal congestion. Older antihistamines have inherent sedating side effects. o May affect cognitive and motor functions even without obvious sedation. o Tolerance to the sedating side effects may occur to some extent. Using a sedating antihistamine at night and a nonsedating antihistamine during the day may still affect daytime functioning. o Nonsedating antihistamines are preferred. Topical (intranasal) antihistamines are effective. o Significant systemic absorption may occur, resulting in drowsiness. o May have bitter taste.
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Rhinitis
Decongestants
Sympathomimetic drugs. Relieve symptoms of nasal congestion or blockage by
constricting the capacitance vessels in the turbinates. Side effects of oral decongestants: o Nonselective vascular constriction resulting in hypertension o Restlessness o Agitation o Tremor o Insomnia o Headache o Dry mucous membranes o Urinary retention o Cardiovascular effects (e.g., palpitations, tachycardia, extrasystoles) o Exacerbation of thyrotoxicosis or glaucoma Topical (intranasal) decongestants act more rapidly and effectively than oral decongestants to relieve nasal congestion, and have fewer systemic side effects. A major side effect of topical decongestants is rhinitis medicamentosa. o A rebound phenomenon resulting in increased nasal congestion and edema. o Occurs after several repeated applications. o Limits use of topical decongestants. o Treat by: 1. Discontinuing nasal decongestants. 2. Starting nasal corticosteroids. 3. Using a short course of oral corticosteroids, if necessary.
Use oral decongestants with caution in patients with heart disease, high blood pressure, thyroid disease, diabetes, or difficulty in urination due to enlargement of the prostate gland. Limit use of topical decongestants to a maximum of 3 to 5 days to avoid rhinitis medicamentosa. Treating rhinitis medicamentosa due to topical decongestants
1. Discontinue nasal decongestants. 2. Start nasal corticosteroids. 3. Use a short course of oral corticosteroids, if necessary.
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15
Antihistamine-decongestant Combination Products

Effective in controlling rhinitis symptoms. o May be more effective than either product alone. In some patients, the stimulatory effect of the
decongestant may offset the sedative effect of a sedating antihistamine. o The other side effects of the older antihistamines may not be affected. o The combination of an oral decongestant with a nonsedating antihistamine may cause insomnia, but is preferred over sedating combinations.
Corticosteroids Corticosteroids are the most effective pharmacologic agents for treating allergic rhinitis.
The most effective pharmacologic agents for treating
allergic rhinitis. Treat the inflammatory component of the disease: o Reduce inflammatory cell infiltration in the superficial nasal mucosa. o Reduce endothelial and epithelial permeability. o Increase sympathetic vascular tone. o Decrease the response of mucous glands to cholinergic stimulation. o Reduce nasal hyperreactivity. Intranasal Corticosteroids The first line of therapy when obstruction is a major component of the patients rhinitis. Prophylactic use reduces: o Congestion o Sneezing o Rhinorrhea o Palatal pruritus o Cough Prophylactic use has variable effects on ocular symptoms. Times to onset and to maximum benefit are longer than with antihistamines. o Initial relief may be 4 to 12 hours after the first dose. o Maximum therapeutic benefit usually occurs within 2 weeks.
Intranasal corticosteroids are the first line of therapy when obstruction is a major component of the patients rhinitis.
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Rhinitis
Can be given concomitantly with antihistamines to
patients with continuous nasal symptoms and/or bothersome eye symptoms. Patients need to be instructed that to maintain effectiveness, this medication must be administered regularly, even in the absence of symptoms. o For maintenance therapy, taper to the lowest effective dose. Local side effects of intranasal corticosteroids include: o Stinging o Burning o Dryness o Sneezing o Epistaxis Some intranasal corticosteroids have been shown to cause a reduction in growth velocity when administered to children. o The relationship between short-term growth evaluations and long-term effects on growth is unclear. o These agents are safe and effective when used at recommended doses.
To maintain effectiveness, intranasal corticosteroids must be administered regularly, even in the absence of symptoms.
For maintenance
therapy, taper to the lowest effective dose.
For seasonal allergic rhinitis:

Start treatment 10 to 14 days before the
pollen season or at the onset of symptoms. Continue treatment for 2 to 3 weeks after the season to decrease nasal hyperreactivity that may persist after exposure to pollen has ended.
Oral Corticosteroids A short (3- to 7-day) course may be appropriate for some patients with severe symptoms or to gain control of symptom exacerbations. Prolonged systemic exposure can be avoided by a brief course of oral corticosteroids to achieve symptom control. o Maintain control with topical corticosteroids. Avoid depot parenteral corticosteroids.
A short (3- to 7-day) course of oral corticosteroids may be necessary:

For patients with severe
symptoms. To gain control of symptom exacerbations.

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17
Mast Cell Stabilizers

Mast cell stabilizer is the common terminology
Intranasal cromolyn sodium is a topical OTC nonsteroid anti-inflammatory agent which:

Blocks the early and late
nasal allergic responses. Relieves sneezing, rhinorrhea, nasal congestion, and pruritus. Has an excellent safety profile. May be used immediately prior to an anticipated exposure to prevent rhinitis symptoms.
referring to cromolyn-like agents. o The mechanism of action of cromolyn sodium remains uncertain and may not be related to mast cell stabilization. Intranasal cromolyn sodium is a topical OTC nonsteroid anti-inflammatory agent which: o Blocks both the early and late phase nasal allergic responses. o Relieves sneezing, rhinorrhea, nasal congestion, and nasal pruritus. It does not relieve ocular symptoms. o Has an excellent safety profile with few side effects. Most common side effects are sneezing and nasal burning. o Is effective for seasonal allergic rhinitis and perennial allergic rhinitis. Not as effective as nonsedating oral antihistamines or topical nasal corticosteroids. o May be used immediately prior to an anticipated exposure to prevent rhinitis symptoms. Preventive use is not as effective after symptoms have started.
Cromolyn Sodium is most effective when used prophylactically 4 to 6 times a day.

Start therapy early, relative to allergen exposure. Continue therapy throughout the exposure period. Observe full therapeutic effect usually within
2 weeks of starting treatment.
Anticholinergics
Ipratropium bromide provides relief from excessive
rhinorrhea not controlled by other medications. o Does not relieve nasal congestion, pruritus, or sneezing. o Not well absorbed from the nasal mucosa. o Common local side effects are dose-related: Nasal dryness Bloody nasal discharge
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Rhinitis
General pharmacologic management of allergic rhinitis:*

Agent Sneezing Itching Congestion Rhinorrhea Eye Symptoms
Oral antihistamines
++
++
+/
++
++
Nasal antihistamines
+/
Intranasal corticosteroids
++
++
++
++
Oral decongestants
Intranasal decongestants
++
Intranasal mast cell stabilizers
Topical anticholinergics
= provides no benefit
++
+/ = provides little or minimal benefit +

*
= provides modest benefit
++ = provides substantial benefit This table represents a consensus of the Task Forces opinion. Referral to and/or consultation with an allergy/immunology specialist is recommended.
Rhinitis
19
Stepwise approach to pharmacotherapy for seasonal allergic rhinitis:

Avoidance of allergic factors and irritants is the first step in the management of the patient with allergic rhinitis. Severity Intermittent symptoms Persistent mildto-moderate disease Consider referral to an allergy/ immunology specialist or otolaryngologic allergy specialist for consultation or comanagement. See page 27. None Daily Medication Quick-relief Medication
Oral nonsedating H1-antihistamine (with or without a decongestant combination). OR: Topical nasal corticosteroid (preferably start therapy 1 to 2 weeks before season and continue through season). CONSIDER: Topical nasal antihistamine; nasal cromolyn sodium for children. If there are prominent eye symptoms: topical ocular antihistamine with or without vasoconstrictor, topical ocular mast cell stabilizer, and/or topical ocular NSAID. Topical nasal corticosteroid (preferably start therapy 1 to 2 weeks before season and continue through season). AND: Oral nonsedating H1-antihistamine (with or without a decongestant combination). CONSIDER: Topical nasal antihistamine; nasal cromolyn sodium for children. AND, if needed: A short course (3- to 10-day) of oral corticosteroids. If there are prominent eye symptoms: topical ocular antihistamine with or without vasoconstrictor, topical ocular mast cell stabilizers, and/or topical ocular NSAIDS.
Rapid onset, oral, nonsedating H1antihistamine. OR Topical nasal antihistamine. CONSIDER: Nasal cromolyn sodium as a preventive measure before anticipated allergen exposures.
Severe disease Referral to an allergy/ immunology specialist or otolaryngologic allergy specialist for consultation or comanagement is recommended. See page 27.
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Rhinitis
w w
Stepwise approach to pharmacotherapy for perennial allergic rhinitis:

Avoidance of allergic factors and irritants is the first step in the management of the patient with allergic rhinitis. Severity Intermittent symptoms Persistent mild-tomoderate disease Consider referral to an allergy/ immunology specialist or otolaryngologic allergy specialist for consultation or comanagement. See page 27. Severe disease Referral to an allergy/ immunology specialist or otolaryngologic allergy specialist for consultation or comanagement is recommended. See page 27. None Daily Medication Quick-Relief Medication
Oral nonsedating H1-antihistamine (with or without a decongestant combination). AND/OR: Topical nasal corticosteroid. CONSIDER: Topical nasal antihistamine. Children should start with oral nonsedating H1-antihistamine or nasal cromolyn sodium.
Rapid onset, oral, nonsedating H1antihistamine. OR: Topical nasal antihistamine. CONSIDER: Nasal cromolyn sodium as a preventive measure before anticipated allergen exposures.
Topical nasal corticosteroid. AND: Oral nonsedating H1-antihistamine (with or without a decongestant combination). AND, if needed: A short course (3- to 10-day) of oral corticosteroid.
w w
Rhinitis
21
Stepwise approach to pharmacotherapy for perennial nonallergic rhinitis:

With little watery discharge 1. Advise avoidance of irritants. 2. Add daily topical nasal corticosteroid. 3. If treatment is ineffective after 1 month, consider:
A short course (3- to 10-day) of
With copius watery discharge 1. Advise avoidance of irritants. 2. Add daily topical nasal anticholinergic (ipratropium bromide). 3. If treatment is ineffective after 1 month, consider adding a topical nasal corticosteroid and consider referral to an allergy/immunology or otolaryngologic allergy specialist for further evaluation and/or comanagement.
oral corticosteroid.
Adding an oral decongestant. Referral to an allergy/immunology
or otolaryngologic allergy specialist for further evaluation and/or comanagement.
Medications to Treat Rhinitis

Oral nonsedating antihistamines:
Drug Name Generic Trade Desloratadine Fexofenadine hydrochloride Clarinex Allegra Capsules Allegra (30 mg) Allegra (60 mg) Allegra (180 mg) Loratadine Claritin Tablets Claritin Reditabs Claritin Syrup
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Rhinitis
Dose Adults 1 tablet (5mg) once daily. 1 capsule (60 mg) twice daily. Children 12 yr and older: same as adults. 12 yr and older: same as adults. 6-11 yrs of age. 1 tablet twice a day. 12 yr and older: same as adults. 12 yr and older: same as adults. 12 yr and older: same as adults. 6 through 11 yr: 1-2 teaspoons once daily. 2 through 5 yr: 1 teaspoon once daily.
1 tablet twice a day. 1 tablet once a day. 1 tablet (10 mg) once daily. 1 Reditab (10mg) once daily. 2 teaspoons (5mg/5ml) 1 time/day.
Oral less-sedating antihistamines:

Drug Name Generic Trade Cetirizine hydrochloride Zyrtec Tablets Zyrtec Syrup Dose Adults 1-2 (5-mg) tablets once daily or 1 (10-mg) tablet once daily. 1-2 teaspoons (5mg/5ml) once daily. Children 12 yr and older: same as adults. 6 through 11 yr: 1-2 teaspoons once daily. 2 through 5 yr: start with 0.5 teaspoon once daily; may increase to 1 teaspoon once daily or 0.5 teaspoon 2 times/day.
Oral less-sedating antihistamine-decongestant combinations:

Drug Name Generic Trade Cetirizine/ Pseudoephedrine HCl Zyrtec-D Dose Adults Children 1 tablet (5 mg/120 mg) 12 yr and older: same as adults. 2 times a day.
Oral nonsedating antihistamine-decongestant combinations:*

Drug Name Generic Trade Fexofenadine/ Pseudoephedrine HCl Loratadine/ Pseudoephedrine HCl Allegra-D Dose Adults 1 tablet (60 mg/ 120 mg) 2 times/day (q12 hr). 1 tablet (5 mg/ 120 mg) 2 times/day (q12 hr). 1 tablet (10 mg/ 240 mg) 1 time/day. Children 12 yr and older: same as adults. 12 yr and older: same as adults. 12 yr and older: same as adults.
Claritin-D 12 hour Claritin-D 24 hour
These medications should not be used with OTC decongestants or antihistamines, and should not be used by patients with urinary retention, narrow angle glaucoma, severe hypertension, or using MAO-inhibitors (within 14 days).
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23
Oral less-sedating antihistamine-decongestant combinations:*

Drug Name Generic Trade Acrivastine/ Pseudoephedrine HCl
*
Dose Adults Children 12 yr and older: same as adults.
Semprex-D 1 capsule (8 mg/ 60 mg), 4 times/day Capsules (every 4-6 hours).
These medications should not be used with OTC decongestants or antihistamines, and should not be used by patients with urinary retention, narrow angle glaucoma, severe hypertension, or using MAO-inhibitors (within 14 days).
Intranasal antihistamines:
Drug Name Generic Trade Azelastine hydrochloride Astelin Nasal Spray Dose Adults 2 sprays (137 mcg/ spray) in each nostril 2 times/day. Children 5-11 yrs of age: 1 spray in each nostril 2 times a day 12 yr and older: same as adults.
Intranasal mast cell stabilizers:

Drug Name Generic Trade Cromolyn sodium Nasalcrom Dose Adults One spray (5.2 mg/ spray) in each nostril 3-4 times/day (every 4-6 hrs); may increase up to 6 times/day. Children 6 yr and older: same as adults.
Intranasal anticholinergics:
Drug Name Generic Trade Ipratropium bromide Atrovent Nasal Spray 0.03% 0.06% Dose Adults 2 sprays (21 mcg/ spray ) in each nostril 2-3 times/day. 2 sprays (42 mcg/ spray) in each nostril 3-4 times/day. Children 6 yr and older: same as adults. 12 yr and older: same as adults.
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Rhinitis
Intranasal corticosteroids:
Drug Name Generic Trade
Beclomethasone dipropionate Beconase Inhalation Aerosol
Dose Adults
1 spray (42 mcg/ spray) in each nostril 2-4 times/ day.
Children
Beconase AQ Nasal Spray
Budesonide
Rhinocort Nasal Inhaler Nasarel Nasal Solution
Flunisolide
Fluticasone propionate
Flonase Nasal Spray Nasonex Nasal Spray
Mometasone furoate monohydrate Triamcinolone acetonide
Nasacort Nasal Inhaler
Nasacort AQ Nasal Spray
12 yr and older: same as adults. 6 to 12 yr: 1 spray in each nostril 2-3 times/day. 1-2 sprays (42 mcg/spray) 12 yr and older: same as adults. in each nostril 2 times/ day. 6 to 12 yr: 1 spray in each nostril 2 times/day. 2 sprays (32 mcg/ spray) 6 yr and older: same as adults. in each nostril 2 times/ day or 4 sprays in each nostril each morning. 2 sprays (25 mcg/ spray) 14 yr and older: same as adults. in each nostril 2 times/ day; may increase to 6 to 14 yr: 1 spray in 2 sprays in each nostril each nostril 3 times/day 3-4 times/day (maximum or 2 sprays in each of 8 sprays in each nostril nostril 2 times/day per day). (maximum of 4 sprays in each nostril per day). 4 yr and older: same as 2 sprays (50 mcg/spray) adults, but start with in each nostril 1 time/ 1 spray in each nostril day or 1 spray in each 1 time/day. nostril 2 times/day. 12 yr and older: same as 2 sprays (50 mcg/spray) adults. in each nostril 1 time/ day. 2 to 12 yr: 1 spray each nostril 1 time/day. 12 yr and older: same as 2 sprays (55 mcg/spray) adults. in each nostril 1 time/ day; may increase to 6 through 11 yr: 2 sprays in each nostril 2 sprays in each nostril 2 times/day or 1 spray in 1 time/day. each nostril 4 times/day. 12 yr and older: same as 2 sprays (55 mcg/spray) adults. in each nostril 1 time/ day. 6 to 12 yr: 1 spray in each nostril 1 time/; may increase to 2 sprays in each nostril 1 time/day.
NOTE: The FDA plans to eliminate the essential-use exemptions for steroid metered dose nasal inhalers on July 24, 2003. All CFC-containing nasally inhaled steroid products will be taken off the market.
Rhinitis
25
Evaluate for immunotherapy.

Clinical studies have demonstrated the
Immunotherapy should be administered under the direction of an allergy/immunology specialist or an otolaryngologic allergy specialist.
effectiveness of immunotherapy in treating symptoms of allergic rhinitis. Potent and standardized extracts are available for common allergens such as pollen, dander, and dust mites. Selection of allergen used in the extract is based on allergy testing and patients history. Considerations favoring the use of immunotherapy: o Long allergen season o Perennial symptoms o Poor response to, poor tolerance of, or unwillingness to use symptomatic medications o To prevent the worsening or development of asthma o Presence of chronic or recurrent rhinosinusitis o Presence of chronic or recurrent middle ear disease Administer under the direction of an allergy/ immunology specialist or an otolaryngologic allergy specialist.
Consider immunotherapy for allergic rhinitis when:

There is a long allergen season. The patient has perennial symptoms. The patient does not respond to, or does not
tolerate, medications. The patient cannot use, or is unwilling to use, medications. Developing, or worsening, asthma is possible. There is chronic or recurrent rhinosinusitis. There is chronic or recurrent middle ear disease.
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Rhinitis
Educate and follow-up.

The educational tips included in the Patient Education chapter of Volume 1 are appropriate for the patient with allergic rhinitis (see Volume 1: Patient Education, page 71).
Consultation/comanagement with an allergy/immunology specialist or otolaryngologic allergy specialist is recommended when:

Identification of allergens and/or other factors
causing symptoms is required (e.g., allergy testing). Rhinitis is inadequately controlled; for example: o Patient would benefit from additional education in allergen avoidance techniques. o Symptoms and/or medication side effects impair patient performance. o The patients quality of life is significantly affected (e.g., patient comfort and wellbeing, sleep disturbance, smell, taste). o Patient exhibits chronic or recurrent complications of rhinitis, or comorbid conditions, develop (e.g., rhinosinusitis, eustachian tube dysfunction, asthma). Repeated use of oral corticosteroids (more than 2 courses per year) is required to manage the patients rhinitis symptoms. The patient requires multiple medications for rhinitis over a prolonged period of time. The patient requires continued use of nasal corticosteroids for symptoms. Occupational rhinitis exists.
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27
Considerations for Special Populations

Managing the Child with Allergic Rhinitis
The diagnosis of allergic rhinitis is often missed in
In children, cognitive functioning and school performance may be impaired by allergic rhinitis symptoms and may be further impaired by sedating antihistamines.
Nonsedating
antihistamines can improve symptoms without negative effects on cognitive function.
children, especially those with: o Recurrent otitis media o Persistent middle ear effusion o Chronic or recurrent rhinosinusitis Early recognition of allergic rhinitis can lead to early treatment and reduce complications. Allergy tests can be done at any age and may yield important information. Allergic rhinitis is unusual in children under 3 years of age. Food allergy can cause allergic rhinitis in infants and children. There is evidence that symptoms of allergic rhinitis can impair cognitive functioning and school performance. o Further impairment may result from using sedating antihistamines. Children may be more susceptible to the side effects of sedating antihistamines. Long-term use of some intranasal corticosteroids may decrease growth rate in some children. o The clinical significance of this adverse effect on adult height has not been established. o Regular height measurements are advised for children using intranasal corticosteroids continuously. o Use at lowest effective dose when other treatments and therapeutic approaches have not been effective. In addition to the home, school and daycare environments must be evaluated for sources of allergen and/or irritant exposure.
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Rhinitis
Managing the Elderly Patient with Allergic Rhinitis

Allergy is a less common cause of perennial rhinitis in
individuals over 65 years of age. o Atrophic rhinitis is a cause of chronic, difficult-to-treat rhinitis in the older patient. o Consider drug-induced rhinitis from agents used to treat other diseases (e.g., reserpine, guanethidine, phentolamine, methyldopa, prazosin, chlorpromazine, ACE inhibitors). Decongestants may cause urinary retention in patients with prostatic hypertrophy. o Cardiac and CNS stimulation are also of concern. Sedating antihistamines may cause bladder disturbances or problems with visual accommodation. o The sedating effects may contribute to falls and fractures. o Nonsedating antihistamines are preferred.
Elderly patients may present with druginduced rhinitis from:

Reserpine Guanethidine Phentolamine Methyldopa Prazosin Chlorpromazine ACE inhibitors
Managing Allergic Rhinitis During Pregnancy

Intranasal cromolyn sodium is considered first-line
treatment. Antihistamine therapy should be considered in patients who do not respond to intranasal cromolyn sodium. o Chlorpheniramine and tripelennamine have a good safety record, but cause sedation. o Loratadine is the only nonsedating antihistamine with Pregnancy Category B. o Ceterizine is a partially sedating antihistamine with Pregnancy Category B. Intranasal corticosteroids may be considered as an alternative to oral medications or when intranasal cromolyn sodium is ineffective. o The agent with the most clinical experience is intranasal beclomethasone dipropionate. May help relieve nasal congestion after discontinuing a topical decongestant. Nasal congestion is common during the second half of pregnancy. o Pseudoephedrine may be considered to treat nasal congestion after the first trimester.
Intranasal cromolyn sodium is considered first-line treatment for allergic rhinitis during pregnancy. Nasal congestion is common during the second half of pregnancy. Consider:
Pseudoephedrine for
nasal congestion after the first trimester. Intranasal corticosteroids for nasal congestion after discontinuing a topical decongestant.
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29
References
Baraniuk JN. Pathogenesis of allergic rhinitis. J Allergy Clin Immunol 1997; 99: S763-772. Bernstein JA. Allergic rhinitis - helping patients lead an unrestricted life. Postgrad Med 1993; 93: 124-132. Bousquet J, Vignola AM, Campbell AM, Michel FB. Pathophysiology of allergic rhinitis. Int Arch Allergy Immunol 1996; 110: 207-218. Busse WW. Role of antihistamines in allergic disease. Ann Allergy 1994; 72: 371-375. Coates ML, Rembold CM, Farr BM. Does pseudoephedrine increase blood pressure in patients with controlled hypertension? J Fam Practice 1995; 40: 22-26. Corren J, Adinoff AD, Buchmeier AD, Irvin CG. Nasal beclomethasone prevents the seasonal increase in bronchial responsiveness in patients with allergic rhinitis and asthma. J Allergy Clin Immunol 1992; 90: 250-256. Corren J. Allergic rhinitis and asthma: how important is the link? J Allergy Clin Immunol 1997; 99: S781-786. Ferguson BJ. Allergic rhinitis - options for pharmacotherapy and immunotherapy. Postgrad Med 1997; 101: 117-120. Ferguson BJ. Allergic rhinitis - recognizing signs, symptoms, and triggering allergens. Postgrad Med 1997; 101: 110-116. Fireman P . Allergic rhinitis. In Fireman P , Slavin RG (eds). Atlas of Allergies, 2nd ed. London:Mosby-Wolfe, Times-Mirror 1996: 141-159. Fireman P . Otitis media and eustachian tube dysfunction: connection to allergic rhinitis. J Allergy Clin Immunol 1997; 99: S787-797. Grossman J. One airway, one disease. Chest 1997; 111: 511-516. Hogan MB, Grammer LC, Patterson R. Rhinitis. Ann Allergy 1994; 72: 293-300. Horak F. Seasonal allergic rhinitis - newer treatment approaches. Drugs 1993; 45: 518-527. International Rhinitis Management Working Group. International consensus report on the diagnosis and management of rhinitis. Allergy 1994; 19: S5-34. Jacobs RL, Freedman PM, Boswell RN. Nonallergic rhinitis with eosinophilia NARES) syndrome: clinical and immunologic presentation. J Allergy Clin Immunol 1981; 67: 253-262. Joint task force practice parameters on diagnosis and management of rhinitis. Ann Allergy Asthma Immunol 1998; 81: 463-518. Malone D, Lawson K, Smith D, Arrighi H, Battista C. A cost of illness study of allergic rhinitis in the United States. J Allergy Clin Immunol 1997; 99:22-27. Moneret-Vautrin DA, Shieh V, Wayoff M. Nonallergic rhinitis with eosinophilia syndrome (NARES) - a precursor of the triad. Ann Allergy 1990; 64: 513-518. Nathan RA. Changing strategies in the treatment of allergic rhinitis. Ann Allergy Asthma Immunol 1996; 77: 255-259. National Heart Lung and Blood Institute. National Asthma Education and Prevention Program. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. April 1997; NIH Publication 97-4051: 50. National Heart Lung and Blood Institute Report of the Working Group on Asthma and Pregnancy: Management of Asthma During Pregnancy. September 1993; NIH Publication 93-3279. Nelson HS. Allergic and nonallergic rhinitis. In: Kassirer JP , Greene HL (eds). Current Therapy in Adult Medicine, 4th ed. St. Louis: Mosby, 1997. Noble SL, Forbes RC, Woodbridge HB. Allergic rhinitis. Am Fam Physician 1995; 51: 837-846. Parikh A, Scadding GK. Seasonal allergic rhinitis. Br Med J 1997; 314: 1392-1395. Physicians Desk Reference. 53rd ed. Oradell, NJ: Medical Economics Company Inc.; 1999.
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Rhinitis
Reinberg A, Gervais P , Levi F, et al. Circadian and circannual rhythms of allergic rhinitis: an epidemiologic study involving chronobiologic methods. J Allergy Clin Immunol 1988; 81: 51-62. Ricketti AJ. Allergic rhinitis. In: Patterson R, Grammer LC, Greenberger PA (eds). Allergic Diseases - Diagnosis and Management, 5th ed. Philadelphia: Lippincott-Raven, 1997: 183-207. Round table discussion. The health and economic impact of rhinitis. Am J Man Care 1997; 3: S8-18. Rowe-Jones JM. The link between the nose and lung perennial rhinitis and asthma is it the same disease? Allergy 1997; 52: S20-28. Settipane GA, Chafee, FH. Nasal polyps in asthma and rhinitis. J Allergy Clin Immunol 1977; 59: 17-21. Smith LJ. Diagnosis and treatment of allergic rhinitis. Nurse Practitioner 1995; 20: 58-66. Spector SL. Overview of comorbid associations of allergic rhinitis. J Allergy Clin Immunol 1997; 99: S773-780. Storms W, Meltzer E, Nathan R, Selner J. The economic impact of allergic rhinitis. J Allergy Clin Immunol 1997; 99: S820-S824. Suonpaa J. Treatment of allergic rhinitis. Ann Med 1996; 28: 17-22. USPDI. Drug information for the healthcare professional. 18th ed. Rockville: USPC, 1998. Vuurman EF, VanVeggel LM, Uiterwijk MM, Leutner D, OHanlon JF. Seasonal allergic rhinitis and antihistamine effects on childrens learning. Ann Allergy 1993; 71: 121-6. Welsh PW, Stricker WE, Chu, CP , et al. Efficacy of beclomethasone nasal solution, flunisolide, and cromolyn in relieving symptoms of ragweed allergy. Mayo Clin Proc 1987; 62: 125-134.
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32
Asthma
sthma is a chronic inflammatory disease of the airways characterized by airway obstruction which is at least partially reversible with or without medication, and increased bronchial responsiveness to a variety of stimuli.
Asthma is a chronic inflammatory disease of the airways.
Asthma is often associated with allergy.

Risk factors for developing asthma include: o Sensitization to indoor allergens (e.g., house-dust
mites, animal danders, cockroaches). o Sensitization to outdoor allergens (e.g., Alternaria). o Early exposure to tobacco smoke. The allergic response in the airways may lead to increased airway inflammation and hyperresponsiveness.
Atopy is the strongest identifiable predisposing factor for the development of asthma.
Rhinitis and asthma involve a common respiratory mucosa.

Asthma is commonly associated with perennial and
seasonal rhinitis and rhinosinusitis. o Patients with allergic rhinitis may report increased asthma symptoms during the pollen season. Inflammation plays a key role in the pathogenesis of both allergic rhinitis and asthma. o Allergic reactions in the nasal mucosa may increase hyperresponsiveness of the lower airways in asthma. Treatment of upper respiratory tract symptoms is a potentially beneficial part of asthma management. o Intranasal corticosteroids can be used to treat chronic rhinitis for patients with persistent asthma. This may lead to asthma improvement. o Oral nonsedating antihistamines and antihistaminedecongestant combinations may improve asthma outcomes in some patients. Treatment of upper airway diseases, alone, is not adequate treatment of asthma.
Asthma is commonly associated with allergic rhinitis.

Rhinitis and asthma
involve a common respiratory mucosa. Treatment of rhinitis may improve asthma symptoms.
Asthma
33
Pathogenesis
Chronic inflammation in the airways may lead to airway wall remodeling, i.e., chronic structural changes that are unlikely to be reversible.
Inflammation in the The characteristic features of asthmatic inflammation are: Mast cell activation Inflammatory cell infiltration o Eosinophils o Airway macrophages o Neutrophils (particularly in sudden onset, fatal exacerbations) o Lymphocytes Edema Mucus hypersecretion Denudation and disruption of the bronchial epithelium Airway inflammation in asthma contributes to: o Airway hyperresponsiveness o Respiratory symptoms o Disease chronicity o Airflow limitation o Airway wall remodeling Collagen deposition beneath basement membrane Mucus gland hyperplasia Smooth muscle hypertrophy Vascular proliferation Loss of elastic fibers
airways and airway remodeling have been observed even in mild asthma.
34
Asthma
Progression to Airway Remodeling
Healthy Cells Mediators Actions
Acute
Mast cells Histamine, other inflammatory mediators
During an acute asthma attack, mast cells release inflammatory mediators, resulting in epithelial cell edema, muscle constriction, vascular leakage, and mucus hypersecretion.
Chronic
Eosinophils, lymphocytes Neuromechanisms, inflammatory mediators, cytokines
In chronic asthma, mast cells and eosinophils release inflammatory mediators. Epithelial cells are shed, resulting in exposed nerves. Epithelial cells start to lose their cilia, and increased numbers of glandular cells are observed. Changes include increased muscle mass, subbasement membrane collagen deposition, and vascular enlargement.
Remodeling
(permanent changes)
Myofibroblasts Growth factors

Remodeling can occur leading to permanent changes. Continued loss of epithelial cells, deposition of subbasement membrane collagen, and increased muscle mass are observed.
Asthma
35
Natural History
Asthma can develop at any time in life, even in the elderly, but the incidence is highest in childhood.
In children, asthma is Asthma is often first diagnosed in childhood. 50% to 80% of children with asthma develop asthma symptoms (coughing, wheezing, shortness of breath or rapid breathing, chest tightness) before 5 years of age. Factors associated with the onset of wheezing in children: o Smaller airways at birth and in early life. o Perinatal and childhood exposure to tobacco smoke. o Male gender. o Low birth weight. o A parent, particularly the mother, with atopy or asthma.
frequently found in association with atopy.
Risk factors for developing asthma:

Personal history of
Diagnosing the Patient with Asthma

In establishing a diagnosis of asthma, the clinician must determine that: Episodic symptoms of airflow obstruction are present: o Coughing o Wheezing o Shortness of breath or rapid breathing o Chest tightness Airflow limitation is at least partially reversible. Alternative diagnoses are excluded.
allergy. Family (particularly maternal) history of allergy or asthma. Passive tobacco smoke exposure during infancy and childhood. Sensitization to indoor allergens and Alternaria.
Key symptoms of asthma:

Coughing Wheezing Shortness of breath or rapid breathing Chest tightness
Associated symptoms in children:

Fatigue: The child may slow down, stop
playing, become easily irritated. Complaining: The young child may say that his/her chest hurts or feels funny. Avoidance: Older children may avoid certain activities (e.g., sports, sleepovers). Infants may show: o Rapid breathing o Grunting during sucking o Difficulty feeding
36
Asthma
Medical History
Are there episodic symptoms of: o Coughing? o Chest tightness? o Wheezing? o Short breath? Is there a pattern to the symptoms? Do they occur in
relation to certain: o Seasons? o Times of year? o Places (e.g., work, damp basements)? o Things (e.g., animals, smoke, scents)? o Times of day or night (e.g., awakening)? o Types of activities or exercise? What is the profile of a typical exacerbation? o Do chest colds last >10 days? How did the disease develop? o What was the age of onset of symptoms? o When was asthma first diagnosed? o Is there a family history of allergies? o Has the disease progressed (e.g., remitted, recurred)? o How has the patient managed his or her asthma (previously, presently)? o What was the patients response to treatment? Do precipitating and/or aggravating factors exist at home, work, school, and/or at daycare? Consider: o Upper respiratory infections (URI) o Environmental allergens (indoor and outdoor) o Exercise o Occupational activities o Environmental changes (e.g., weather, humidity) o Irritants (e.g., tobacco smoke, odors, pollutants) o Emotions o Drugs (e.g., ASA, NSAIDs) o Food and food additives (e.g., beer, wine [sulfites]) o Weather changes o Endocrine factors
Asthma
37
What is the impact of the disease on the patient (and
the family)? Consider: o Unscheduled care o Life-threatening exacerbations o Missed school/work/activities o Interference with sleep o Effects on: Growth Behavior Concentration and performance at work/in school Daily routines/activities Finances Are there factors that may interfere with adherence, such as: o School/childcare? o Workplace? o Patients (familys) level of education? o Substance abuse? What is the patients (and familys) perception of the disease? o Do they understand the disease and how it is treated? o Can they cope with the disease and its management? o Is support available or needed? o What are the economic resources? o Are there sociocultural beliefs that need to be considered?
38
Asthma
Focus on the upper
respiratory tract, chest, and skin. Findings that support the diagnosis of asthma: o Hyperexpansion of the thorax, especially in children. o Sounds of wheezing during normal breathing or during deep breathing. Wheezing during forced exhalation is not a reliable indicator of airflow limitation and may not be present. It may be produced by dynamic compression of the large airways. o Signs and symptoms of allergic rhinitis, rhinosinusitis, and nasal polyps. o Atopic dermatitis/eczema.
Physical examination of the patient with asthma may be normal.
Objective Measurements
If indicators from the
medical history and physical examination suggest asthma, then confirm the diagnosis with objective measures of pulmonary function. Spirometry (FEV1) before and 15 minutes after the patient inhales a short-acting bronchodilator is preferred. o Significant reversibility is indicated by an increase 12% (and, in adults, an increase of 200 mL) in FEV1 after inhaling a short-acting bronchodilator. o Consider the bronchodilator response even if spirometry is normal (i.e., 80% predicted normal). Correct technique, calibration methods, and maintenance of equipment are necessary to achieve consistently accurate test results. o Use equipment and techniques that meet the standards developed by the American Thoracic Society (1995).
Some patients may not be able to perform spirometry.

In this group, a trial with an
inhaled beta2-agonist and/or a short (3- to 10-day) course of oral corticosteroid may help aid and/or confirm the diagnosis.
In many patients with mild asthma, tests of lung function are normal. Office-based clinicians who care for asthma patients should have access to spirometry for diagnosis and for periodic monitoring.
Asthma
39
If the medical history and physical examination suggest asthma, confirm the diagnosis with objective measures of pulmonary function.
Spirometry (FEV1) before and 15 minutes
after the patient inhales a short-acting bronchodilator is preferred. Significant reversibility is indicated by an increase 12% (and, in adults, an increase of 200 mL) in FEV1 after inhaling a shortacting bronchodilator.
When is peak expiratory flow (PEF) used?

To diagnose asthma, spirometry is recommended
over peak expiratory flow (PEF) in the clinicians office because: o PEF is not as sensitive as FEV1 for diagnosing airflow obstruction. PEF is primarily a measurement of large airway function. o Peak flow meters are designed as monitoring, not diagnostic, tools. o Published PEF reference values vary widely and according to the brand of peak flow meter used. o Patient technique may vary over time. Peak flow measurements may be helpful in diagnosing asthma for patients who cannot perform spirometry or in patients who have normal spirometry at the time of examination.
Peak flow meter 40

Asthma
Monitoring PEF variability over 1 to 2 weeks is
recommended: o When patients have asthma symptoms, but normal spirometry, at the time of examination. o To assess disease severity. o To guide treatment or medication needs. PEF is generally lowest in the early morning hours (4 am to awakening) and highest in the afternoon (close to 4 pm).
To diagnose asthma, spirometry is recommended over peak expiratory flow (PEF) in the clinicians office because:
PEF is not as sensitive
Two ways to use the peak flow meter for measuring PEF variability:
1. Use only in the morning upon awakening BEFORE using a short-acting bronchodilator. OR 2. Use in the morning AND in the late afternoon or evening. The late afternoon or evening measurement may be done after the patient uses a shortacting bronchodilator. A greater then 20% difference between the morning and evening measurements suggests inadequately controlled asthma.
as FEV1 to diagnosis airflow obstruction. Peak flow meters are designed as monitoring, not diagnostic, tools. Published PEF reference values vary widely and according to the brand of peak flow meter used. Patient technique may vary over time.
Asthma
41
Differential Diagnosis
Recurrent episodes of coughing and wheezing (especially at night) are almost always due to asthma, in children and adults.
Masqueraders of asthma in children and adults:

Cause Upper airway diseases Both Rhinosinusitis (associated cough) Vocal cord dysfunction Children Nasal congestion (rhinitis, large adenoids) Adults
Enlarged lymph Large nodes or tumor airways obstruction Tracheal or bronchial stenosis or malacia Small Cystic fibrosis airways Heart disease obstruction Viral bronchiolitis Bronchopulmonary dysplasia
Chronic obstructive pulmonary disease Chronic bronchitis Bronchiectasis Congestive heart failure Pulmonary infiltration with eosinophilia Pulmonary embolism
Other causes
Recurrent cough not due to asthma Aspiration due to swallowing mechanism dysfunction Gastroesophageal reflux (GERD)
Cough secondary to medications (i.e., ACE inhibitors)
42
Asthma
Classification of Asthma Severity

Patients are classified as having mild intermittent or
mild, moderate, or severe persistent asthma based on the: o Severity, frequency, and duration of symptoms. o Level of airflow obstruction. o Extent to which the disease interferes with daily activities. For any patient with asthma, the severity of the disease can change over time. Any patient with asthma may have a severe exacerbation. o Classifying a patient as having mild asthma (either intermittent or persistent) does not rule out the possibility of a severe exacerbation. Patients with more than 2 episodes of asthma symptoms per week, or with evidence of airflow obstruction between symptom episodes, have persistent asthma.
Classification of asthma severity is based on the:

Severity, frequency, and
duration of symptoms. Degree of airflow obstruction. Extent to which the disease interferes with daily activities.
Severe
Asthma severity is a continuum. The severity may change over time.
Persistent asthma may
Moderate
Mild
Asthma severity is a continuum.
become more or less severe over time. Symptom exacerbations (asthma attacks) may be severe, regardless of the severity classification of the underlying asthma.
Asthma
43
How do you classify asthma severity?

1. Classifying asthma severity BEFORE treatment. The presence of one of the features of severity is sufficient to place a patient in that category. An individual should be assigned to the most severe grade in which any feature occurs. Those unable to perform lung function tests are classified by symptoms. Classification Asthma severity Clinical Features BEFORE Treatment Symptom severity Nighttime symptoms Lung function in patients who CAN use a spirometer or peak flow meter FEV1 or PEF 60% predicted Frequent PEF variability > 30% Short-acting beta2agonist use
Severe Persistent
Continual symptoms Limited physical activity Frequent exacerbations interfere with normal activities
q.i.d. use daily does NOT completely relieve symptoms
Moderate Persistent
Daily symptoms Exacerbations 2 times/ week; may last days; may affect activities Symptoms > 2 times/week but < 1 time/day Exacerbations may affect activities > 1 time/ week
FEV1 or PEF > 60% to < 80% predicted PEF variability > 30% FEV1 or PEF > 80% predicted PEF variability 20% to 30% FEV1 or PEF 80% predicted
Daily
Mild Persistent
> 2 time/ month
> 2 times/ week but < 1 time/ day
Mild Intermittent
Symptoms 2 times/week Asymptomatic and normal PEF between exacerbations Exacerbations brief (from a few hours to a few days); intensity may vary
2 times/ week
2 time/ month
PEF variability < 20%
44
Asthma
2. Classifying asthma severity AFTER optimal treatment is attained. The patients asthma severity can be classified according to the level of treatment needed to maintain control. For example: For mild intermittent asthma, no daily medication is needed. However, the use of a short-acting beta2-agonist more than 2 times per week may indicate the need to start long-term control therapy. For mild persistent asthma, one daily long-term control medication is necessary. For moderate persistent asthma, inhaled corticosteroids with or without additional long-term control medications are used. For severe persistent asthma, multiple long-term control medications are required, including high-dose inhaled corticosteroids and, if needed, oral corticosteroids.
All patients with asthma need a short-acting beta2agonist for acute symptoms, p.r.n.
The intensity of
Patients with asthma may need additional tests to aid and/or confirm the diagnosis.
The general principles of diagnostic testing are included in Volume 1: Diagnostic Testing, page 31. Specific diagnosis for Asthma is included here. Reasons for Additional Tests Patient has symptoms (coughing, wheezing, breathlessness, chest tightness), but spirometry is (near) normal Suggested Tests
Assess diurnal variation
treatment to relieve acute symptoms depends upon the severity of the exacerbation. Using a short-acting beta2-agonist daily, or increasing use, indicates the need for additional long-term control therapy (assuming compliance with therapy, no new exposures to causal factors, and no untreated rhinosinusitis, rhinitis, or gastroesophageal reflux).
Should the patient be skin-tested for allergy?

Many patients with
of PEF over 1 to 2 weeks Bronchoprovocation with histamine, methacholine, or exercise (if negative, may rule out asthma)
Nasal examination Allergy tests,
Suspect other factors are contributing to severity or asthma symptoms Symptoms suggest infection, large airway lesions, heart disease, or obstruction by foreign object Suspect coexisting chronic obstructive pulmonary disease or restrictive defect
gastroesophageal reflux tests, sinus radiography

Routine chest x-ray,
CAT scan
Additional pulmonary
function tests; diffusing capacity test
asthma are allergic, but allergy may not be recognized. Review the patients exposure to allergens. Skin-testing is recommended for patients with: o Persistent asthma who are exposed to perennial allergens. o Seasonal symptoms who are being considered for allergen immunotherapy. Consider referral to or consultation with an allergy/immunology specialist.
Asthma
45
The goals of therapy for the patient with asthma:

Prevent chronic and
Managing the Patient with Asthma

The four components of asthma management:
troublesome symptoms (e.g., coughing or breathlessness in the night, in the early morning, or after exertion). Maintain (near) normal pulmonary function. Maintain normal activity levels (including exercise and other physical activity). Prevent recurrent exacerbations of asthma, and minimize the need for emergency department visits or hospitalizations. Provide optimal pharmacotherapy, with minimal or no adverse effects. Meet the patients (and familys) expectations of, and satisfaction with, asthma care.
1 2
Measures of assessment and monitoring Control of factors contributing to asthma severity
3 4
Pharmacologic therapy Education for a partnership in asthma care
Component 1. Measures of Assessment and Monitoring

Once the initial diagnosis of asthma has been
confirmed, periodic assessments and ongoing monitoring are recommended. Monitor regularly: o Signs and symptoms of asthma o Pulmonary function o Occurrence of symptom exacerbations o Pharmacotherapy o Quality of life/functional status o Patients (and familys) satisfaction with therapy o Patients (and familys) understanding of asthma and its management Assess symptoms and clinical signs at each healthcare visit through appropriate questions and physical examination. o Detailed patient recall of symptoms changes over time. o Use a short (2- to 4-week) recall period. Review the patients medication(s) and dosage(s) regularly, including: o Adherence with treatment o Inhaler technique o Use of inhaled beta2-agonist o Frequency of oral corticosteroid burst therapy o Changes in dosage of long-term control medications o Medication side effects o Patient concerns
46
Asthma
Spirometry should be performed:

At the time of initial assessment. After treatment is initiated, and symptoms and PEF have
stabilized, to document attainment of (near) normal airway function. At least every 1 to 2 years to assess the maintenance of airway function. o Spirometry may be indicated more often than every year, depending on the patients asthma severity and response to management.
Peak expiratory flow monitoring may be helpful.

Long-term daily PEF monitoring can help patients with
moderate-to-severe persistent asthma: o Evaluate responses to changes in therapy. o Detect early changes in disease severity that may require treatment. o Assess severity (for patients with poor perception of airflow obstruction). If long-term daily peak flow monitoring is not used, a short-term (2- to 3-week) period of peak flow monitoring is recommended to: o Evaluate responses to changes in chronic maintenance therapy. o Establish the individual patients personal best PEF. o Identify the temporal relationship between changes in PEF and exposure to environmental irritants or allergens.
To determine the patients personal best PEF:

Use the same peak flow
meter. Record PEF 2 times/day for 2 weeks. A burst of oral corticosteroid or a trial of high dose inhaled corticosteroid may be necessary.
Measure PEF in the office:

Before and 15 minutes after a short-acting beta2-agonist
to determine if response is adequate. To evaluate response to changes in chronic maintenance therapy. Before and after a short (3- to 10-day) course of oral corticosteroids. For evaluating response to treatment of an exacerbation.
Asthma
47
Using the peak flow meter requires effort and learned skill. Teach the patient (and family and caregivers):
How to use the peak
Measure PEF at home:

When perceptions of symptoms are unreliable. To determine when treatment needs to be increased or
flow meter. How to interpret peak flow measurements.
Two ways to use the peak flow meter for measuring PEF variability
1. Use only in the morning upon awakening BEFORE using a shortacting bronchodilator. OR 2. Use in the morning AND in the late afternoon or evening. The late afternoon or evening measurement may be done after the patient uses a shortacting bronchodilator. A greater than 20% difference between the morning and evening measurements suggests inadequately controlled asthma.
decreased. During an exacerbation, before and 15 minutes after bronchodilator to determine if response is adequate. To determine when to call the clinician and/or seek emergency care. To evaluate responses to changes in chronic maintenance therapy. Daily for 1 week before a regular office visit. Every morning and evening during a course of oral corticosteroids.
>80%
Green Zone: Good control! No asthma symptoms. Take medications as usual.
Yellow Zone: Caution!

Use a short-acting inhaled
50%-80%
beta2-agonist.
Check about changing
medications or increasing dose.
<50%
Red Zone: Medical alert! Use a short-acting inhaled beta2-agonist. Call doctor or go to emergency department.
Patients with moderate persistent or severe persistent asthma should have a peak flow meter at home, if feasible.
48
Asthma
Cutpoints for PEF monitoring: PEF 80% of the patients personal best before a shortacting bronchodilator may indicate a need for additional medication. PEF 50% of the patients personal best indicates a severe asthma exacerbation. Cutpoints are arbitrary, and should be tailored to the patients needs and PEF patterns.
To monitor quality of life/functional status, ask the patient (and/or caregiver) about:
Missed work or school due to asthma. Any reduction in usual activities
During periodic assessment and monitoring, it is critical to determine that the patient is using the appropriate pharmacotherapy for the level of disease severity. To evaluate the level of asthma control, ask about
1. Daytime symptoms (including wheeze, cough, chest tightness, or shortness of breath or rapid breathing). 2. Nocturnal awakening due to asthma symptoms. 3. Early morning symptoms. 4. Relationship of symptoms to exercise, respiratory infection, activities, environmental exposures. 5. Tolerance of exercise, cold air, physical activities. 6. Frequency of use of quick-relief medication.
(home/work/school/recreation/exercise). Disturbances in sleep due to asthma. Changes in caregiver activities due to a childs asthma. Monitor patient satisfaction with: Asthma control Quality of care Overall treatment plan Self-monitoring is important. Every patient with asthma should be taught to recognize symptom patterns that indicate inadequate asthma control. To monitor their disease, patients need to know: o How to use a peak flow meter. o Their warning signs of worsening disease. o How and when to seek emergency care.
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49
Tips for working within time constraints of the typical office visit:
Give the patient an assessment questionnaire
to complete in the waiting room. Have the patient come back to the office more frequently, especially at the beginning of treatment and after an exacerbation. Break the assessment and education needs into several components during these visits. Some could be completed at home, between visits. Train nurses or other office staff to teach MDI, DPI, and spacer/holding chamber techniques, use of the peak flow meter, and to answer questions and provide information. Consider using a home case-manager for follow-up assessments and education, if one is available through your HMO. Use videos and educational materials from outside sources. Suggest possible formal education programs and educational support groups. Refer to school nurse for monitoring and further education.
50
Asthma
Component 2. Controlling Factors Contributing to Asthma Severity

The first and most important step in controlling asthma
is to reduce exposure to causal factors. o Causal factors, sometimes referred to as triggers, provoke asthma symptoms (e.g., exercise, cold air). o Causal factors increase the underlying airway inflammation (e.g., allergens, viral respiratory infections, tobacco smoke, occupational exposures, air pollution). Patients with asthma at any level of severity should try to avoid environmental exposure to allergens to which they may be sensitive as well as to irritants such as tobacco smoke, wood smoke, air pollutants, and perfumes. Primary prevention of asthma (preventing initial development) may alter its course. See page 85. The avoidance techniques and tips included in Volume 1: Environmental control, page 43, are appropriate for the patient with asthma.
The most important step in controlling asthma is to reduce exposure to factors which exacerbate symptoms.
Allergens are common causal factors.

For patients with persistent asthma, the clinician should: o Identify allergen exposures. o Determine probable relationships to allergens by
pattern(s) of symptoms. o Determine sensitivity to indoor allergens to which the patient is exposed with skin-testing or in vitro measurements of serum IgE antibodies. o Assess the significance of positive tests in context of the patients medical history. Allergen immunotherapy may be considered for asthma patients when: o There is clear evidence of a relationship between symptoms and exposure to an unavoidable allergen to which the patient is sensitive. o Symptoms occur all year or during a major portion of the year. The addition of immunotherapy to pharmacologic therapy may be warranted when: o The medication is ineffective. o Multiple medications are required. o The patient or family is not accepting of medication. o The benefits of modifying the immune response are attractive to the patient.
Occupational exposures may increase asthma symptoms and/or precipitate asthma exacerbations (page 91).
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51
Common causal factors of asthma:

Environmental Factors
Animal dander
Recommendations for Reducing Exposure

Remove animal from house, or at minimum, keep animal
out of patients bedroom. Seal or cover with a filter, air ducts that lead to bedroom. Room air filters (HEPA-type). Dust mites Essential: Encase mattress, pillow, and boxsprings in an allergenimpermeable cover. Wash bedding weekly in hot water ( 130F). Reduce indoor humidity to < 50%. Desirable: Remove carpets from the bedroom, and carpets in other rooms that are laid on concrete. Minimize upholstered furniture.
Use poison bait or traps to control. Do not leave food or garbage exposed.
Cockroaches
Pollens and outdoor molds
Limit exposure during season by staying indoors with
windows closed, especially when pollen is elevated. (see Volume 1: Background, page 13) Use air conditioning.
Fix all water leaks. Clean moldy surfaces. Reduce indoor humidity to < 50%.
Indoor mold
Tobacco smoke
Advise patients and others in home to stop smoking or
smoke outside and away from the home; do not allow smoking in car. Discuss ways to reduce exposure to other sources of tobacco smoke. Indoor/outdoor pollutants and irritants
Discuss ways to reduce exposure to:
o Wood-burning stoves or fireplaces. o Unvented stoves or heaters. o Other irritants (e.g., perfumes, cleaners).
Dates and times of highest pollen counts differ geographically.

52
Asthma
Other Causal Factors

Rhinitis (allergic and nonallergic) Rhinosinusitis
Recommendations for Reducing Exposure

Optimize treatment of chronic rhinitis in patients with
persistent asthma.
Optimize treatment for chronic or recurrent rhinosinusitis. Use medical measures to promote drainage.
Respiratory infections Gastroesophageal reflux
Annual influenza vaccinations are recommended for patients
with persistent asthma who do not have severe systemic sensitivity to egg.
Patients with frequent heartburn or suspected GERD should:
o Avoid food and drink within 3 hours of retiring. o Avoid caffeine, alcohol, and chocolate. o Elevate the head of the bed 6 to 8-inches. o Pharmacologic therapy may be necessary.
Obstructive sleep apnea
Patients with symptoms of sleep apnea should:
o Consider weight reduction. o Treat rhinitis. o Consider intervention (e.g., CPAP).
Aspirin sensitivity
Counsel patients regarding the risks of aspirin as well as
other nonsteroidal anti-inflammatory drugs which may precipitate severe and even fatal asthma exacerbations in sensitive patients. Primary treatment is avoidance, though some patients demonstrate improvement with oral aspirin desensitization. Sulfite sensitivity
Patients with symptoms on exposure should avoid foods
processed with sulfites as preservatives, e.g.: o Processed potatoes o Shrimp o Dried fruit o Wine, beer Beta-blockers
Avoid beta-blockers, including eye drops. Always consider appropriate alternate agents.
Viral respiratory infection is the most common cause of asthma symptoms.

Exacerbations caused by viral respiratory infections may be intermittent yet severe. Annual flu shots are recommended for all patients with persistent asthma (who do not have severe systemic sensitivity to egg).
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53
Diagnosing and treating upper respiratory tract disease (rhinitis, rhinosinusitis) is an integral part of managing the patient with asthma.
Some patients are sensitive to changes in weather and humidity. Others are sensitive to pollens and environmental irritants (e.g., smog). Tell these patients to:
Check the weather forecast. Check the pollen count. Check the smog index. Keep a relatively constant temperature and
humidity in the house. Keep windows closed and air conditioning on when pollen, smog, and humidity are high.
Component 3. Pharmacologic Therapy

Asthma involves chronic airway inflammation.
Long-term control
A stepwise approach to treating asthma is recommended
therapy requires efforts to suppress asthmatic inflammation as well as to prevent episodes of asthma symptoms. All patients need to have a short-acting beta2-agonist to take as needed for acute symptoms.
to gain and maintain control of symptoms. Because asthma involves chronic airway inflammation, long-term control therapy requires efforts to suppress asthmatic inflammation as well as to prevent episodes of asthma symptoms. o The amount and frequency of medication is dictated by asthma severity and is directed toward suppressing airway inflammation. o When initiating therapy, take into account the needs and circumstances of the patient. o All patients need to have a short-acting beta2-agonist to take as needed for acute symptoms.
There are two approaches to initiating step-care therapy: Remember to:

Step down therapy
gradually when control is achieved. Monitor regularly to ensure that control is achieved and maintained.
1. Start therapy at a level higher than indicated by the patients initial severity. o Either add a short course of oral corticosteroids to inhaled corticosteroids, cromolyn sodium, nedocromil sodium, or other long-term control therapy, o Or use a higher dose of inhaled corticosteroids. This approach is preferred. OR 2. Start therapy at a level appropriate to the patients initial severity and gradually increase therapy if control is not achieved.
54
Asthma
When do you step up, or increase, long-term control medications? To regain control when the patient has: o Increased symptoms and/or nighttime or early morning awakenings due to symptoms. o Reduced ability to play, exercise, or participate in normal daily activities. o Daily or increasing use of short-acting beta2-agonists. o Gradual reduction in PEF (by about 20%). o Not met the goals of therapy. How do you help the patient regain control of his/her asthma? A short (3- to 10-day) course of oral corticosteroids may be needed to speed the resolution of moderate persistent or severe persistent exacerbations, or to re-establish control during a period of gradually deteriorating symptoms. If a short course of oral corticosteroids does not control symptoms, is effective for only a short time (i.e., < 2 weeks), or if the patient uses oral corticosteroids frequently, consider a step up, or increase, in the long-term control medication. o This can be achieved by increasing the dose of inhaled corticosteroid and/or adding long-term control therapy. When and how do you step down long-term control therapy? After starting daily long-term control medication, regular follow-up visits (at 1-to 6-month intervals) are essential. Monitor: o Symptoms, especially nighttime awakenings and activity levels. o Use of quick-relief medications. o Pulmonary function, preferably with spirometry. If asthma is controlled for 2 to 3 months, then gradually decrease the dose, frequency, or number of medications, and re-evaluate in 2 to 3 months. Most patients with persistent asthma require continued medication to suppress underlying airway inflammation. o Long-term control medications reduce the need for quick-relief medications and may prevent anticipated symptoms (e.g., from exercise, allergens, cold air).
Before stepping up therapy, review possible reasons for poor asthma control:
Adherence to
medication regimen Inhaler technique Environmental control Complicating factors (e.g., rhinosinusitis, allergic rhinitis) Psychosocial factors
Stepping up can be achieved by:

Increasing the inhaled
corticosteroid dose. Adding long-term control therapy.
Stepping down can be achieved by:

Lower doses Fewer doses Using a different
medication
Asthma
55
Always follow a decrease in therapy with close follow-up
in the clinic or by phone. o The patient should monitor asthma symptoms and PEF, and alert the doctor promptly if worsening occurs. Reduce therapy gradually. How much to reduce therapy is based on evaluation of the patients asthma severity and any special considerations. o Asthma can deteriorate at a highly variable rate and intensity. o For inhaled corticosteroids, some physicians suggest decreasing the dose by 25% every 2 to 3 months to the lowest possible dose to maintain control. o Carefully follow up.
Maintain the patient on the lowest dose of medication that controls asthma.
Patients with severe persistent asthma whose symptoms are not controlled on high doses of inhaled corticosteroids, long-acting bronchodilators, plus other long-term control medications (e.g., theophylline, leukotriene pathway modifiers) may need to use oral corticosteroids on a regular basis. For these patients: The aim of asthma therapy is to gain control promptly, and then step down to the lowest level of therapy that maintains control of asthma.
Use the lowest possible dose (single dose daily
or on alternate days). Monitor closely for corticosteroid adverse effects. Make persistent attempts to reduce use of oral corticosteroids when control of asthma is achieved. o High doses of inhaled corticosteroids are preferable because of fewer adverse effects. Consultation with an asthma specialist for comanagement is recommended.
56
Asthma
Remember the goals of therapy.

Prevent chronic and troublesome symptoms. Prevent exacerbations of symptoms. No acute asthma episodes requiring a doctor
visit, emergency room visit, or hospital stay. Maintain normal activity levels. Maintain normal pulmonary function. Minimal (ideally no) adverse effects from medication.
To keep medications at a minimum, use environmental control measures for:

Tobacco and/or wood
What medications are used to treat asthma?

Long-term Control Medications Long-term control medications are taken daily on a long-term basis to achieve and maintain control of persistent asthma. Inhaled Corticosteroids Most potent and effective long-term anti-inflammatory medications currently available. Broad action on the inflammatory process in the airways. Improve symptoms and pulmonary function. Reduce the need for quick-relief medications. Fewer side effects than oral corticosteroids. Local side effects: cough, dysphonia, oral thrush (candidiasis). Long-term use of very high doses of inhaled corticosteroids in adults may result in: o Osteoporosis, especially in post-menopausal women. o Increased intraocular pressure (older adults). o Cataracts (older adults). o The exact doses leading to these side effects are not known and may differ among patients and pharmacologic agents.
smoke. Allergens to which the patient is sensitive (e.g., dust mites, cockroaches, molds, animal dander). Other airborne irritants (e.g., fumes, odors).
Inhaled corticosteroids are the most potent and effective long-term anti-inflammatory medications currently available.
Inhaled corticosteroids
are extremely effective drugs and safe when used properly (i.e., at recommended doses and with a spacer/holding chamber). The potential risks of inhaled corticosteroids are well balanced by their benefits.
Asthma
57
Inhaled corticosteroids have been shown to cause a
reduction in growth velocity when administered to children. Poorly controlled asthma may delay growth. Children with asthma tend to have longer periods of reduced growth rates before puberty (males more than females). Growth rates are highly variable. Short-term evaluations may not be predictive of final attained adult height. Regular and accurate height measurements are advised every 3 to 4 months for all children and adolescents using these medications. Cromolyn Sodium/Nedocromil Sodium Nonsteroid anti-inflammatory agents. Alternative therapy to low doses of inhaled corticosteroids (especially in children) in mild persistent asthma. Cromolyn is no longer the preferred first-line treatment for mild persistent asthma in children. It has been replaced by low-dose inhaled corticosteroids. Nedocromil is no longer recommended for children under 5 years of age. Can be used on an as-needed basis to prevent symptoms from anticipated exposures (e.g., cold air, exercise, allergens). Reduce the need for quick-relief medications. Improve symptoms and pulmonary function. Good safety profiles. Nedocromil sodium may provide added benefit to inhaled corticosteroids. Leukotriene Modifiers Leukotriene receptor antagonists (e.g., montelukast, zafirlukast) block LTD4 receptors. 5-lipoxygenase inhibitors (e.g, zileuton) block synthesis of all leukotrienes. May be considered as alternative therapy to low doses of inhaled corticosteroids in mild persistent asthma, but the position of leukotriene modifiers in therapy has not been fully established.
58
Asthma
Improve symptoms and pulmonary function. Reduce the need for quick-relief medications. May provide added benefit to inhaled corticosteroids. Administered as tablets. Elevation of liver enzymes reported with zileuton;
monitoring is recommended. o Evaluate hepatic transaminases at initiation of and during therapy. o Serum ALT should be monitored: Before treatment. Once-a-month for the first 3 months. Every 2 to 3 months for the remainder of the year. Periodically thereafter for patients on long-term therapy. Absorption of zafirlukast is reduced by ingestion with food. Zileuton and zafirlukast have potential drug interactions, particularly with theophylline and warfarin. Have been associated with rare reports of Churg-Strauss vasculitis. Long-acting Beta2-agonists DO NOT REPLACE THE NEED FOR ANTI-INFLAMMATORY MEDICATIONS. Relax bronchial smooth muscle. Add-on therapy to anti-inflammatory medications for long-term control of symptoms, especially nighttime symptoms. Longer duration of action than short-acting beta2-agonists. Should not be used to treat acute symptoms or exacerbations. Reduce need for quick-relief medications. Continuous therapy may prevent exercise-induced bronchospasm. However, in some patients a diminished bronchoprotective effect may be observed with continuous therapy. The clinical significance is unclear.
Asthma
59
Methylxanthines (Theophylline) Alternative, but not preferred, monotherapy for persistent asthma. Monitoring is required to maintain serum levels between 5 and 15 mcg/mL. Absorption and bioavailability change with age, febrile viral illnesses, certain medications, and diet. Administration in early evening can provide control of nighttime symptoms. Adverse effects include nausea, insomnia, hyperactivity, cardiovascular effects, tremor. Oral Corticosteroids Broad anti-inflammatory effects. Long-term use is associated with systemic adverse effects. o Use lowest possible dose and/or alternate day dosing in severe persistant asthma.
60
Asthma
Quick-relief Medications
Quick-relief medications give prompt relief of bronchoconstriction and accompanying acute symptoms: Coughing, wheezing, shortness of breath or rapid breathing, chest tightness. Short-acting Beta2-agonists Relax bronchial smooth muscle, resulting in bronchodilation usually within 5 to 10 minutes of administration. Therapy of choice for relieving acute symptoms and preventing exercise-induced bronchospasm. Use more than 2 times per week, other than for prevention of exercise-induced asthma, is an indicator for initiating or increasing anti-inflammatory therapy. Increasing use indicates inadequate control of asthma and the need to intensify long-term control therapy. Oral Corticosteroids Broad anti-inflammatory effects. Use short (3- to 10-day) course to gain initial control and to speed resolution of moderate or severe exacerbations. o A course of 7 days or less is often sufficient. o Longer courses may be required to treat severe exacerbations. o Tapering dose is not necessary when used 10 days, unless warranted by disease severity. Single or twice daily dosing is preferred, if tolerated. Anticholinergics (Ipratropium Bromide) Possible additive benefit to inhaled beta2-agonists for acute exacerbations. Alternative for patients who cannot tolerate beta2agonists. Treatment of choice for bronchospasm in patients receiving beta-blockers.
Short-acting beta2agonists are the most effective medications for relieving acute bronchospasm. Increasing use of short-acting beta2agonists indicates inadequate control of asthma and the need to initiate or intensify long-term control therapy. Short-acting bronchodilators for URI:
Inhaled route is
preferred. With severe episodes, oral corticosteroids for 3 to 10 days may be necessary. For recurrent episodes (especially those requiring oral corticosteroids), consider starting or increasing the dose of daily anti-inflammatory medication.
Asthma
61
Stepwise approach for managing infants and young children (5 years of age and younger) with acute or chronic asthma symptoms:
Classify Severity: Clinical Features Before Treatment or Adequate Control Symptoms/Day Symptoms/Night Medications Required To Maintain Long-Term Control
Daily Medications
Preferred treatment:
Step
4 3
Continual Frequent
Severe persistant
High-dose inhaled corticosteroids And Long-acting inhaled beta2-agonists And (if needed) Corticosteroid tablets or syrup long term (2 mg/kg/day, generally do not exceed 60 mg per day). (Make repeat attempts to reduce systemic steroids and maintain control with high-dose inhaled corticosteroids.)
Preferred treatment:
Step
Daily > 1 night/week
Moderate persistant
Step
2 1
> 2/week but < 1x/day > 2 nights/month
Mild persistant 2 days/week 2 nights/month
Low-dose inhaled corticosteroids and long-acting inhaled beta2-agonists. OR Medium-dose inhaled corticosteroids. Alternative treatment: Low-dose inhaled corticosteroids and either leukotriene receptor antagonist or theophylline. If needed (particularly in patients with recurring severe exacerbations) Preferred treatment: Medium-dose inhaled corticosteroids and long-acting beta2-agonists Alternative treatment: Medium-dose inhaled corticosteroids and either leukotriene receptor antagonist or theophylline. Preferred treatment: Low-dose inhaled corticosteroids (with nebulizer or MDI with holding chamber with or without face mask or DPI) Alternative treatments (listed alphabetically): Cromolyn (nebulizer is preferred; or MDI with holding chamber) OR leukotriene receptor antagonist. No daily medication needed.
Step
Mild intermittent Step Down Review treatment every 1 to 6 months; a gradual stepwise reduction in treatment may be possible. Step Up If control is not maintained, consider step up. First, review patient medication technique, adherence, and environmental control (avoidance of allergens and/or other factors that contribute to asthma severity).
Source: NAEPP Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma Update on Selected Topics 2002, www.nhlbi.nih.gov.
62
Asthma
Quick Relief for all patients 5 years of age and younger with acute asthma symptoms Bronchodilator as needed for symptoms. Intensity of
treatment will depend upon severity of exacerbation.
Preferred treatment: Short-acting inhaled beta2-agonists by nebulizer or face mask and space/holding chamber Alternative treatment: Oral beta2-agonist
With viral respiratory infection

Bronchodilator q 4-6 hours up to 24 hours (longer with physician consult); in general, repeat no more than once every 6 weeks Consider systemic corticosteroid if exacerbation is severe or patient has history of previous severe exacerbations
Use of short-acting beta2-agonists > 2 times week in intermittent

asthma (daily, or increasing use in persistent asthma) may indicate the need to initiate (increase long-term control therapy.
Further explanation of information in asthma stepchart on page 62: Step 2:

For children younger than 5 years of age, recommendations are based on extrapolation of studies in older children. Preferred are low-dose inhaled corticosteroids, with nebulizer, dry powder inhaler, or metered-dose inhaled with holding chamber, with or without a facemask. Alternative, but not preferred, therapies include (in alphabetical order) cromolyn (nebulizer is preferred over MDI with holding chamber), or LTRA.
Step 3:
Recommendations for treating infants and young children at step 3 (moderate persistent asthma) are based on extrapolation from studies in older children and adults and expert opinion. Until sufficient data in children are available, there are two options for preferred therapy in Step 3 care: either low- dose inhaled corticosteroids plus long-acting inhaled beta agonists (Evidence B extrapolation from adult studies) OR increasing the dose of inhaled corticosteroids within the medium dose range (Evidence D). However, combination therapy is preferred over use of high doses of inhaled corticosteroids to avoid the potential for adverse effects in this younger population. Alternative, but less effective approaches are adding leukotriene modifiers or theophylline to low-dose inhaled corticosteroids. Regardless of which form of adjunctive therapy is selected, once control is achieved for 2 to 3 months, therapy should be stepped down if possible.
Step 4:
High-dose inhaled corticosteroids plus inhaled long-acting beta2agonists. And If needed, add systemic corticosteroid.
Asthma
62A
For exacerbations triggered by viral URIs, use shortacting bronchodilator q4- to 6-hr, as needed, up to 24 hr (longer with physician consult). If exacerbations occur more frequently than every 6 wk, consider prophylactic anti-inflammatory therapy (Steps 2 or 3). Consider oral corticosteroids (3- to 10-day): o If the exacerbation is severe. o At the onset of a viral respiratory infection in a child with a history of previous severe exacerbations. The Stepwise Approach presents guidelines to assist clinical decision-making. Asthma is highly variable. Clinicians should tailor specific medication plans to the needs and circumstances of the child and family. Gain control as quickly as possible. Start treatment with either: o Aggressive therapy (e.g., a course of oral corticosteroid or a higher dose of inhaled corticosteroid); OR o A level appropriate to the childs initial severity, and step up if necessary. THEN gradually decrease treatment to the least medication necessary to maintain control. A rescue course of oral corticosteroid may be needed at any time and step. In general, use of a short-acting beta2-agonist on a daily basis indicates the need for additional long-term control therapy. Some children with intermittent asthma experience severe and life-threatening exacerbations separated by long periods of normal lung function and no symptoms. This may be especially common with exacerbations provoked by respiratory infections. A short course of oral corticosteroid is recommended. At each step, children (and their families) should control their environment to avoid causal factors that make their asthma worse (e.g., allergens, irritants). This requires specific diagnosis and patient education. Consultation with an asthma specialist is recommended for children with moderate or severe persistent asthma in this age group. Consultation should be considered for all children with mild persistent asthma. It is important to remember that there are very few studies on asthma therapy for infants.
Maintain the child on the lowest dose of medication that controls asthma. To keep medications to a minimum, use environmental control measures for:
Tobacco and/or wood
smoke. Allergens to which the child is sensitive (e.g., dust-mites, cockroaches, molds, animal danders). Other airborne irritants (e.g. fumes, odors).
Goals of therapy:
Minimal (ideally NO)
symptoms during the day or at night. Minimal (ideally NO) asthma episodes. Minimal use (<1x/day) of short-acting beta2-agonist. PEF 80% of personal best, if used. Minimal (ideally NO) adverse effects from medications. NORMAL ACTIVITIES.
Asthma
63
Stepwise approach for managing asthma in adults and children older than 5 years of age with acute or chronic asthma symptoms:
Classify Severity: Clinical Features Before Treatment or Adequate Control
Symptoms/Day Symptoms/Night PEF of FEV-1 PEF Variability 60% > 30%
Medications Required To Maintain Long-Term Control
Daily Medications Preferred treatment: High-dose inhaled corticosteroids And Long-acting inhaled beta2-agonists And (if needed). Corticosteroid tablets or syrup long term (2 mg/kg/day, generally do not exceed 60 mg per day). (Make repeat attempts to reduce systemic steroids and maintain control with high-dose inhaled corticosteroids.) Preferred treatment: Low-to-medium dose inhaled corticosteroids and long-acting inhaled beta2-agonists. Alternative treatment (listed alphabetically): Increase inhaled corticosteroids within the medium-dose range. OR Low-to-medium dose inhaled corticosteroids and either leukotriene modifier or theophylline. If needed (particularly in patients with recurring severe exacerbations): Preferred treatment: Increase inhaled corticosteroids within medium-dose range and add long-acting beta2agonists. Alternative treatment (listed alphabetically): Increase inhaled corticosteroids within mediumdose range and add either leukotriene receptor antagonist or theophylline. Preferred treatment: Low-dose inhaled corticosteroids. Alternative treatment (listed alphabetically): Cromolyn, leukotriene modifier, nedocromil OR sustained release theophylline to serum concentration of 5-15 mcg/mL. No daily medication needed. Severe exacerbations may occur, separated by long periods of normal lung function and no symptoms. A course of systemic corticosteroids is recommended.
Step
4 3
Continual Frequent
Severe persistant
Step
Daily> > 1 night/week
60% - < 80% > 30%
Moderate persistant
Step
2 1
> 2/week but < 1/day > 2 nights/month
80% 20-30%
Mild persistant
Step
2 days/week 2 nights/month
80% < 20%
Mild intermittent Step Down

Review treatment every 1 to 6 months; a gradual stepwise reduction in treatment may be possible.
Step Up
If control is not maintained, consider step up. First, review patient medication technique, adherence, and environmental control (avoidance of allergens and/or other factors that contribute to asthma severity).
Source: NAEPP Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma Update on Selected Topics 2002, www.nhlbi.nih.gov.
64
Asthma
Quick Relief for all patients adults and children older than 5 years with acute asthma symptoms Short-acting bronchodilator: 2-4 puffs shortacting inhaled beta2-agonists as needed for symptoms. Intensity of treatment will depend on severity of exacerbation; up to 3 treatments at 20-minute intervals or a single nebulizer treatment as needed. Course of systemic corticosteroids may be needed. Use of short-acting beta2-agonists > 2 times a week in intermittent asthma (daily, or increasing use in persistent asthma) may indicate the need to initiate (increase long-term control therapy. Stepwise approach for managing asthma in patients > 5 years of age with acute or chronic asthma symptoms. Further explanation of information in asthma stepchart on page 64: Step 2: For children 5 years of age and older, the preferred therapy is inhaled corticosteroids (low dose). Alternative therapies (listed alphabetically because there are no data to enable rank) include cromolyn, LTRAs, nedocromil, or sustained-release theophylline. Step 3: Preferred therapy: Low-medium dose inhaled corticosteroids plus long acting inhaled beta2-agonists. Alternative therapy: medium-dose inhaled corticosteroids or low-medium dose inhaled corticosteroids plus leukotriene modifier, or lowmedium dose inhaled corticosteroids plus theophylline. Step 4: High-dose inhaled corticosteroids plus inhaled longacting beta2-agonists. And If needed, add systemic corticosteroid.
Asthma
64A
For exacerbations triggered by viral URIs, use short-acting bronchodilator q2- to 4-hr, as needed, up to 24 hr (longer with physician consult). If exacerbations occur more frequently than every 6 wk, consider prophylactic antiinflammatory therapy (Steps 2 or 3). Consider oral corticosteroids (3- to 10-day): o If the exacerbation is severe. o At the onset of a viral respiratory infection in a patient with a history of previous severe exacerbations.
Maintain the patient on the lowest dose of medication that controls asthma. To keep medications to a minimum, use environmental control measures for:
Tobacco and/or wood
The Stepwise Approach presents guidelines to assist clinical decision-making. Asthma is highly variable. Clinicians should tailor specific medication plans to the needs and circumstances of the patient (and family). Gain control as quickly as possible. Start treatment with either: o Aggressive therapy (e.g., a course of oral corticosteroid or a higher dose of inhaled corticosteroid); OR o A level appropriate to the patients initial severity, and step up if necessary. THEN gradually decrease treatment to the least medication necessary to maintain control. A rescue course of oral corticosteroid may be needed at any time and step. In general, use of a short-acting beta2-agonist on a daily basis indicates the need for additional long-term control therapy. Some patients with intermittent asthma experience severe and life-threatening exacerbations separated by long periods of normal lung function and no symptoms. This may be especially common with exacerbations provoked by respiratory infections. A short course of oral corticosteroid is recommended. At each step, patients (and their families) should control their environment to avoid causal factors that make their asthma worse (e.g., allergens, irritants). This requires specific diagnosis and patient education. Referral to an asthma specialist for consultation or comanagement is recommended if there are difficulties achieving or maintaining control of asthma or if the patient requires Step 4 care. Referral may be considered if the patient requires Step 3 care.
smoke. Allergens to which the patient is sensitive (e.g., dust-mites, cockroaches, molds, animal danders). Other airborne irritants (e.g. fumes, odors).
Goals of therapy:
Minimal (ideally NO)
symptoms during the day or at night. Minimal (ideally NO) asthma episodes. Minimal use (<1x/day) of short-acting beta2-agonist. PEF 80% of personal best, if used. Minimal (ideally NO) adverse effects from medications. NORMAL ACTIVITIES.
Asthma
65
66
Asthma
Medications to Treat Patients with Asthma in the United States

The most important determinant of appropriate dosing is the clinicians judgment of the patients response to therapy. The clinician must monitor several clinical parameters to assess both efficacy and adverse effects, and adjust the dose accordingly. The Stepwise Approach to therapy emphasizes that once control of asthma is achieved, the dose of medication should be carefully titrated to the minimum dose required to maintain control.
Charts on pages 67-73 reflect information from National Heart Lung and Blood Institute. National Asthma Education and Prevention Program. Expert panel report 2: guidelines for the diagnosis and management of asthma. April 1997: NIH Publication 97-4051; American Academy of Allergy, Asthma and Immunology. Pediatric asthma promoting best practice: Guide for managing asthma in children, 1999; and the Physicians Desk Reference, 53rd ed. Oradell, NJ; Medical Economics Company, Inc., 1999.
Long-Term Control Medications

Inhaled corticosteroids Generic name Brand name(s)
Beclomethasone dipropionate Beclovent,Vanceril Vanceril-DS
Dosage form(s)
low
MDI:42 mcg/puff MDI:84 mcg/puff
2-8 puffs/day 1-4 puffs/day
Dose1
medium high2
8-16 puffs/day > 16 puffs/day 4-8 puffs/day > 8 puffs/day max: 0.84 mg/ day adults, 0.42 mg/day children 4 puffs/day 8 puffs/day max: 1.6 mg/ day adults, 0.8 mg/day children 2.0 mg/day
Potential adverse effects and therapeutic issues

FOR ALL INHALED CORTICOSTEROIDS: Cough, dysphonia, moniliasis; high doses may have systemic effects although studies are not conclusive and clinical significance is not clear. Monitoring growth is recommended when used in children. The potential risks of inhaled corticosteroids are well balanced by their benefits. To minimize local and systemic adverse events, use MDI with a spacer/holder chamber.
Budesonide
Pulmicort Turbuhaler Pulmicort Respules AeroBid, AeroBid-M Flovent
DPI:
200 mcg/puff
2 puffs/day
Budesonide
Nebulizing suspension MDI:250 mcg/puff
.50 mg/day
1.0 mg/day
Flunisolide
2-3 puffs/day
4-5 puffs/day
> 5 puffs/day max: 2 mg/ day adults, 1 mg/day children > 4 puffs/day > 2 puffs/day max: 0.88 mg/ day adults > 4 puffs/day > 2 puffs/day max: 1 mg/ day adults, 0.2 mg/ day children > 12 puffs/day max: 1.6 mg/ day adults, 1.2 mg/day children
Fluticasone propionate
MDI:44 mcg/puff 110 mcg/puff 220 mcg/puff DPI: 50 mcg/puff 100 mcg/puff 250 mcg/puff
2-4 puffs/day 2-4 puffs/day 1-2 puffs/day
4-10 puffs/day 2-4 puffs/day 1-2 puffs/day 2-4 puffs/day 1-2 puffs/day
Flovent Rotadisk
Triamcinolone acetonide
Asthma
1 2
Azmacort
MDI:100 mcg/puff
4-8 puffs/day
8-12 puffs/day
These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient. Max dose represents aggragate dose and can vary depending on previous therapy.
67
68

Cromolyn sodium/Nedocromil sodium Generic name Brand name(s) Dosage form(s)
Cromolyn sodium Intal MDI: 1 mg/puff Nebulizer solution: 20 mg/ampule
Asthma
Dose1
1-2 puffs, 10-15 min before exercise 1-2 puffs, t.i.d.-q.i.d. 1 ampule, t.i.d.-q.i.d.

Therapeutic response to cromolyn and nedocromil often occurs within 2 wk, but a 4- to 6-wk trial may be needed to determine maximum benefit. Dose of cromolyn MDI (1 mg/puff) may be inadequate to affect airway hyperresponsiveness. Nebulizer delivery (20 mg/ ampule) may be preferred for some patients. Safety is the primary advantage of these agents. Unpleasant taste for some patients.
Nedocromil sodium
Tilade
MDI: 1.75 mg/puff
1-2 puffs, 30 min before exercise 1-2 puffs, b.i.d.-q.i.d.
Leukotriene modifiers Generic name Brand name(s)

Montelukast Singulair
Dosage form(s)
Tablet: 5 mg, chewable, for ages 6 through 14 yr; 10 mg for ages 15 yr and older Tablet: 20 mg, for ages 12 yr and older; 10 mg, for ages 7 through 11yrs. Tablet: 600 mg, for ages 12 yr and older
Dose1
1 tablet in evening
2
Zafirlukast
Accolate
Drug interactions (warfarin); increases 1 tablet, b.i.d. prothrombin time.2 Take 1 hour before or 2 hours after meals 1 tablet, q.i.d. Possible elevation of liver enzymes requires monitoring; drug interactions (warfarin, theophylline).2
Zileuton
Zyflo
1 These 2
doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient. Data about adverse effects in patients are limited. Increased clinical experience and further study in a wide range of patients are needed to determine those patients most likely to benefit from leukotriene modifiers and to establish a more specific role for these medications in asthma therapy.

Usual Dosages for Long-Term-Control Medications Medication Dosage form Adult Dose Child Dose*
Inhaled Corticosteroids (See Estimated Comparative Daily for inhaled corticosteroids.) Systemic Corticosteroids (Applies to all three corticosteroids)
Methylprednisolone Prednisolone Prednisone 2, 4, 8, 16, 32 mg tablets 5 mg tablets, 5 mg/ 5 cc, 15 mg/ 5 cc 1, 2.5, 5, 10, 20, 50 mg tablets; 5 mg/cc, 5 mg/5 cc 7.5-60 mg daily in a single dose in a.m. or qod as needed for control Short-course burst to achieve control: 40-60 mg per day as single or 2 divided doses for 310 days 2 puffs q 12 hours 1 blister q 12 hours 1 capsule q 12 hours 0.25-2 mg/kg daily in single dose in a.m. or qod as needed for control Short-course burst: 1-2 mg/kg/day, maximum 60 mg/day for 3-10 days
Long-Acting Inhaled Beta2-Agonists (Should not be used for symptom relief or for exacerbations. Use with inhaled corticosteroids.)
Salmeterol Formoterol MDI 21 mcg/puff DPI 50 mcg/blister DPI 12 mcg/single-use capsule DPI 100, 250, or 500 mcg/50 mcg MDI 1 mg/puff Nebulizer 20 mg/ampule MDI 1.75 mg/puff 4 or 5 mg chewable tablet 10 mg tablet 10 or 20 mg tablet 300 or 600 mg tablet Liquids, sustained-release tablets, and capsules 1-2 puffs q 12 hours 1 blister q 12 hours 1 capsule q 12 hours
Combined Medication Fluticasone/Salmeterol Cromolyn and Nedocromil Cromolyn

Nedocromil
1 inhalation bid; dose depends on 1 inhalation bid; dose depends on severity of asthma severity of asthma 2-4 puffs tid-qid 1 ampule tid-qid 2-4 puffs bid-qid 10 mg qhs 40 mg daily (20 mg tablet bid) 2,400 mg daily (give tablets qid) Starting dose 10 mg/kg day up to 300 mg max; usual max 800 mg/day 1-2 puffs tid-qid 1 ampule tid-qid 1-2 puffs bid-qid 4 mg qhs (2-5 yrs) 5 mg qhs (6-14 yrs) 10 mg qhs (> 14 yrs) 20 mg daily (7-11 yrs) (10 mg tablet bid) Starting dose 10 mg/kg/day; usual max: < 1 year of age: 0.2 (age in weeks) + 5 = mg/kg/day 1 year of age: 16 mg/kg/day
Leukotriene Modifiers
Montelukast Zafirlukast Zileuron Theophylline
Asthma
Methylxanthines (Serum monitoring is important [serum concentration of 5-15 mcg/mL at steady state]).
* Children 5 years of age
68A
68B
Asthma

Estimated Comparative Daily Dosages for Inhaled Corticosteroids: Drug
Beclomethasone CFC 42 or 84 mcg/puff Beclomethasone HFA 40 or 80 mcg/puff Budesonide DPI 200 mcg/inhalation Budesonide Nebulizing suspension Flunisolide 250 mcg/puff Fluticasone MDI: 44, 110, or 220 mcg/puff DPI: 50, 100, or 250 mcg/ inhalation Triamcinolone acetonide 100 mcg/puff
* Children 12 years of age
Low Daily Dose Adult Child*

168-504 mcg 80-240 mcg 200-600 mcg 84-336 mcg 80-160 mcg 200-400 mcg 0.5 mg 5001,000 mcg 88-264 mcg 100-300 mcg 400-1,000 mcg 500-750 mcg 88-176 mcg 100-200 mcg 400-800 mcg
Medium Daily Dose Adult Child*

504-840 mcg 240-480 mcg 600-1,200 mcg 336-672 mcg 160-320 mcg 400-800 mcg 1.0 mg 1,0002,000 mcg 264-660 mcg 300-600 mcg 1,0002,000 mcg 1, 0001,250 mcg 176-440 mcg 200-400 mcg 8001,200 mcg
High Daily Dose Adult Child*

> 840 mcg > 480 mcg > 1,200 mcg > 672 mcg > 320 mcg > 800 mcg 2.0 mg > 2,000 mcg > 660 mcg > 600 mcg > 2,000 mcg > 1,250 mcg > 440 mcg > 400 mcg > 1,200 mcg

Long-acting bronchodilators Generic name Brand name(s)
Formoterol Foradil
Dosage form(s)
DPI (12 mcg) (Single-use capsule)
Dose1
1 capsule every 12 hours

Tachycardia, tremor. The clinical relevance of
potential diminished bronchoprotective effect is uncertain. DO NOT USE in place of anti-inflammatory therapy! Tachycardia, tremor. The clinical relevance of potential diminished bronchoprotective effect is uncertain. DO NOT USE in place of anti-inflammatory therapy!
Salmeterol
Serevent
MDI: 21 mcg/puff DPI: 50 mcg/blister
2 puffs, 30-60 min before exercise 1-2 puffs, q12 hr 1 blister, q12 hr 0.3-0.6 mg/kg/day, not to exceed 4-8 mg/day, q12 hr Starting dose: 10 mg/kg/day Maximal dose: < 1 yr3: (0.2 x age in wks) + 5=mg/kg/day Maximal dose: 1 yr: 16 mg/kg/day, not to exceed the adult maximum (800 mg/day)
Sustainedrelease albuterol Theophylline2
Volmax Proventil Repetabs Aerolate-III Aerolate-JR Aerolate-SR Choledyl-SA Elixophyllin Quibron-T Quibron-T/SR Slo-b.i.d. Slo-Phyllin Theo-24 Theochron Theo-Dur Theolair Theolair-SR T-Phyl Uni-Dur Uniphyl
Tablet: 4, 8 mg Tablet: 4 mg Capsules, tablets
Tachycardia, tremor, irritability Tachycardia, nausea, vomiting, headache, CNS

stimulation.
Monitoring serum levels (5-15 mcg/mL) is

essential to ensure therapeutic, but not toxic, doses are achieved. Serum levels may be affected by numerous factors (diet, febrile illness, other medications).
These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient. Sustained-release theophylline may be considered an alternative, but not preferred, long-term control medication when issues arise related to cost, adherence, or ability to use inhaled medications. Sustained release theophylline may have particular risks of adverse effects in infants, who frequently have febrile illnesses which increase theophylline levels. Consider theophylline for infants only if serum levels will be carefully monitored.
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Asthma

Combined long-term control medications Generic name
Fluticasone plus salmeterol
Brand name
Advair TM
Dosage form
100/50 250/50 500/50
Dose
One inhalation twice daily

Side effects of fluticasone and
salmeterol separately
Oral corticosteroids Generic name

Methylprednisolone
Brand name(s) Dosage form(s)

Medrol Tablet: 2, 4, 8, 16, 24, 32 mg
Dose1
0.25-2 mg/kg daily in single dose or q.o.d. as needed for control Short-course (3- to 10-day) burst: 1-2 mg/kg/day (max: 60 mg/day) 0.25-2 mg/kg daily in single dose or q.o.d. as needed for control Short-course (3- to 10-day) burst, 1-2 mg/kg/day (max: 60 mg/day) 0.25-2 mg/kg daily in single dose or q.o.d. as needed for control Short-course (3- to 10-day) burst, 1-2 mg/kg/day (max: 60 mg/day)

FOR ALL ORAL CORTICOSTEROIDS: Long-term use is associated with
systemic effects. Use lowest effective dose either daily or on alternate days (which may lessen adrenal suppression). Short courses or bursts are effective for establishing control when initiating therapy or during a period of gradual deterioration. See page 72.
Prednisolone Prelone Pediapred
Tablet: 5 mg Liquid: 15 mg/5 mL Liquid: 5 mg/5 mL
Prednisone
Prednisone Deltasone Orasone Liquid Pred Prednisone IntensolTM
Tablet: 1, 2.5, 5, 10, 20, 25, 50 mg Liquid: 5 mg/5 mL Liquid: 5 mg/mL
These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient.
Quick-Relief Medications
Short-acting inhaled beta2-agonists Generic name Brand name(s)
Albuterol
Airet Proventil Ventolin
Dosage form(s)
MDI: 90 mcg/puff Nebulizer solution: 5 mg/mL (0.5%); 0.083% (unit dose2) containing 2.5 mg MDI: 90 mcg/puff DPI: 200 mcg/capsule MDI3: 370 mcg/puff Nebulizer solution: 2 mg/1ml (0.2%)
Dose1
1-2 puffs, 15 min before exercise FOR ALL SHORT-ACTING 2 puffs, t.i.d.-q.i.d., prn BETA2-AGONISTS: 0.05 mg/kg (minimum: 1.25 mg; maximum: 2.5 mg) Tremor, tachycardia, headache.
Proventil-HFA Ventolin Rotacaps
1-2 puffs, 15 min before exercise 2 puffs, t.i.d.-q.i.d., prn 1 capsule, 15 min before exercise 1 capsule t.i.d.-q.i.d., prn 1-2 puffs, 15 min before exercise 2 puffs, t.i.d.-q.i.d., prn 10-15min administration; 8 mg max intermittent; 14mg max continuous 0.63 mg q 4-6 hr. for maintenance 1.25 mg q 4-6 hr. for acute bronchospasm and for patients unresponsive to lower dose 1-2 puffs, t.i.d.-q.i.d., prn 1-2 puffs, t.i.d.-q.i.d., prn
Bitolterol
Tornalate
NOTE: Increasing use of short-acting beta-agonists, use of > 1 canister/month, or lack of expected effect indicates inadequate asthma control. See doctor to increase or add long-term control mediction(s).
Levalbuterol
Xopenex
Nebulizer solution: Unit dose vials: 0.63 mg/ 3 mL 1.25 mg/ 3 mL MDI: 200 mcg/puff MDI: 200 mcg/puff
Pirbuterol Terbutaline
1
Maxair Brethaire
The doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient. Do not use partial unit dose. Also available as a nebulizer solution (2 mg/mL = 0.2%), but a childrens dose has not been established.
2 3
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71
72
Quick-Relief Medications
Oral corticosteroids Generic name Brand name(s)
Methyl prednisolone Medrol
Asthma
Dosage form(s)
Tablet: 2, 4, 8, 16, 24, 32 mg
Dose1
Short-course (3- to 10-day) burst: 1-2 mg/kg/day (max: 60 mg/day)2 Short-course course (3- to 10-day) burst: 1-2 mg/kg/day (max: 60 mg/day)2 Short-course course (3- to 10-day) burst: 1-2 mg/kg/day (max: 60 mg/day)2

FOR ALL ORAL CORTICOSTEROIDS: Short courses or bursts are effective for establishing control when initiating therapy or during a period of gradual deterioration. Short-term therapy should continue until patient achieves 80% PEF personal best, or until symptoms resolve (usually 3- to 10-day, but may take longer). There is no evidence that tapering the dose following improvement prevents relapse.
Prednisolone
Prelone Pediapred Prednisone Deltasone Orasone Liquid Pred Prednisone IntensolTM
Tablet: 5 mg Liquid: 15 mg/5 mL Liquid: 5 mg/5 mL Tablet: 1, 2.5, 5, 10, 20, 25, 50 mg Liquid: 5 mg/5mL Liquid: 5mg/mL
Prednisone
Anticholinergics Generic name Brand name(s)

Ipratropium bromide Atrovent
Dosage form(s)
MDI: 18 mcg/puff Nebulizer solution: 0.5 mg/2.5mL (0.02%)
Dose1
1-2 puffs every 6 hours 0.5 mg every 6 hours

Dry mouth, avoid contact with eyes. May provide additive effect(s) to short-acting beta2-agonist.
These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient. 2 A course of 7 days or less is usually sufficient. In some cases, the exacerbation may require up to 10 days of treatment.
New Medications (Not available in U.S. at time of writing but pending approval by FDA) Long-term Control Medications
Inhaled Corticosteroids Generic name Brand name(s) Dosage form(s)
Low
Dose1
Medium High
Mometasone furoate
Asmanex
DPI: 200 mcg/puff DPI: 400 mcg/puff
200 mg, q.d. 400 mg, q.d. 400 mg, b.i.d. FOR ALL INHALED CORTICOSTEROIDS: Cough, dysphonia, moniliasis; high doses may have systemic effects although studies are not conclusive and clinical significance is not clear. Monitoring growth is recommended when used in children. The potential risks of inhaled steroids are well balanced by their benefits. To minimize local and systemic adverse events, use a spacer/holding chamber.
These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs and circumstances of the patient.
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Types of inhalation devices for asthma medications:

Device/Medications Metered-dose inhaler (MDI) Beta2-agonists Corticosteroids Cromolyn sodium Nedocromil sodium Anticholinergics Age1 Comments
Adults: A spacer/holding chamber may be Spacer/holding chamber helpful if patient has recommended for difficulty coordinating patients having difficulty inhalation and with inhalation. triggering a puff. technique; recommended routinely for patients on corticosteroids. Children: 5 years: spacer/holding chamber recommended. <5 years: spacer/holding chamber with facemask recommended.
Breath-actuated MDI Beta2-agonists Dry-powder inhaler (DPI) Beta2-agonists Corticosteroids Nebulizer Beta2-agonists Cromolyn sodium Anticholinergics
Children >12 yr and adults Children 4 yr and adults
Some patients have
difficulty triggering a puff while inhaling.

Dose delivered may
differ from the MDI for some medications. Can be effort dependent
Useful for infants, very
Patients of any age who cannot use an MDI with spacer/holding chamber with or without facemask.
young children, elderly patients, and any patient with a moderate to severe asthma episode (although, MDI with spacer/holding chamber may be as effective).
These ages are suggested as guides for making clinical decisions. The clinician must use his/her own judgment to tailor treatment to the specific needs and circumstances of the patient.
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Asthma
Types of inhalation devices: Choose medications and delivery devices according to the patients ability to use them.
MDI
MDI with Spacer
Breath-actuated MDI
Nebulizer without facemask
Nebulizer with facemask
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75
Common side effects of MDIs All MDIs:

o Reflex cough o Bronchospasm Corticosteroid MDIs: o Oral candidiasis
Advantages of Using Spacers and Holding Chambers

Used with MDIs (not DPIs) because some patients have
(thrush) o Dysphonia
a difficult time inhaling while pressing the inhaler to trigger a puff. o Simple tubes do not take care of this problem! Decrease oropharyngeal deposition. Reduce possible side effects, particularly with inhaled corticosteroids.
Using a DPI avoids the problem of coordinating inhalation and activation.

DPIs cannot be used
Using an MDI with a spacer/holding chamber may be easier than using an MDI alone.
Trigger one puff from MDI into spacer/holding
with a spacer or holding chamber.
In the near future inhaled asthma medications will be administered as:

Non-chlorofluorocarbon-
chamber for each inhalation. Some patients (particularly young children) may prefer using an MDI with spacer/holding chamber and facemask. If a facemask is used, allow 3 to 5 inhalations for each puff triggered from the MDI.
(non-CFC-) propelled devices (e.g., HFA-134a) Dry powder inhaler devices Nebulized solutions This is due to the worldwide ban on CFCs to prevent further atmospheric ozone depletion.
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Asthma
Treat asthma exacerbations promptly and aggressively.

All patients with asthma need an inhaled short-acting
beta2-agonist for exacerbations. Give the patient and/or caregiver(s) a written, easy-to-understand action plan to manage exacerbations. Include: o The early signs of worsening asthma. o What medications to use and how to use them. o Specific instructions for when to contact the clinician or emergency room. A short (3- to 10-day) course of oral corticosteroid may be needed to speed the resolution of exacerbations, or to re-establish control during a period of gradually deteriorating symptoms. Exacerbations of asthma symptoms (coughing, wheezing, shortness of breath or rapid breathing, chest tightness) with viral respiratory infections are common, and need to be treated appropriately with adequate doses of short-acting beta2-agonists and, in some cases, oral corticosteroids. Moderate or severe exacerbations may require treatment at the clinicians office or emergency room. o Pulse oximetry is recommended to follow oxygen saturation. o Use oxygen to relieve hypoxemia. o Monitor the response to therapy with serial measurements of FEV1 or PEF.
All offices that treat acute exacerbations of asthma should be prepared for emergency airway management, and should have available:
A peak flow meter A power-driven nebulizer An oximeter Oxygen A crash cart with: o Epinephrine o Antihistamines o Intravenous catheters o Bag-mask-valve devices
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Assessing the severity of an asthma exacerbation: Look at the patient for signs of distress: Shortness of breath or rapid breathing Inability to speak Increased respiratory rate Use of accessory muscles with retractions Wheezing: o In mild exacerbations, wheezing is evident on expiration. o As the severity of the exacerbation increases, both inspiratory and expiratory wheezing may be present. o During a severe exacerbation, the chest may be silent. Decreased PEF Agitation Cyanosis
Risk factors for death from asthma:

Past history of sudden severe exacerbations. Prior intubation for asthma. Prior admission to intensive care unit for asthma. 2 hospitalizations for asthma in past 12 months. 3 emergency care visits for asthma in past
12 months. Hospitalization or emergency care visit for asthma in past month. Use of > 2 canisters/month of inhaled short-acting beta2-agonist. Current chronic use of oral corticosteroids. Difficulty perceiving airflow obstruction or its severity. Low socioeconomic status and urban residence. Illicit drug use. Serious psychiatric disease or psychosocial problems. Allergic sensitivity to outdoor mold.
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Asthma
Managing Asthma Exacerbations in the Home

Assess Severity
Measure PEF: < 50% predicted or personal best suggests severe exacerbation. Note signs and symptoms: degree of cough, breathlessness, wheeze, chest tightness correlate imperfectly with severity. Accessory muscle use and retractions (sucking in of chest) suggest severe exacerbation.
w
Initial Treatment
Inhaled short-acting beta2-agonist: up to 3 treatments of 2 to 4 puffs by MDI every 20 min, or 1 nebulizer treatment.
w
Response to treatment: Exacerbation PEF (predicted or personal best) Wheezing or shortness of breath Continued treatment Good Mild > 80% Incomplete Moderate 50% to 80% Poor Severe < 50%
None
Persistent
Marked
Continue inhaled short-acting beta2agonist every 3 to 4 hr- for 24 to 48 hr. For patients on inhaled corticosteroids, double dose for 7 to 10 days. Contact clinician.
Continue inhaled short-acting beta2agonist. Add oral corticosteroid.
Repeat beta2agonist immediately. Add oral corticosteroid.
Follow-up
Contact clinician in same day.
If distress is severe and patient is nonresponsive,

CALL HEALTHCARE PROVIDER IMMEDIATELY, AND PROCEED TO ER OR URGENT CARE CENTER. CONSIDER CALLING AMBULANCE OR 911.
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Urgent Care (Clinicians Office or Emergency Department) for Managing Asthma Exacerbations
Nebulized short-acting beta2-agonist and supplemental oxygen should be available in a physicians office. However, serious exacerbations require close observation, frequent treatment, and repetitive measurement of lung functions. Most severe exacerbations require prompt transfer to emergency department.
Initial Assessment
History, physical examination, including: auscultation, use of accessory muscles, retractions (sucking in of chest), heart rate, respiratory rate, FEV1 or PEF, O2 saturation, and other tests as indicated.
w
Response to initial treatment: FEV1 or PEF > 50% < 50% (severe exacerbation) Nebulized high dose with anticholinergic every 20 min, or continuous, for 1 hr. To 90% saturation. Impending/actual respiratory arrest Nebulized high dose with anticholinergic.
Inhaled beta2agonist
By MDI or nebulizer, up to 3x in first hr.
O2
To 90% saturation.
Intubation and mechanical ventilation with 100% O2. i.v.
Corticosteroid
Oral, if no immediate response or if patient recently used oral corticosteroid.
Oral
Admit to ICU.
w
Repeat assessment (symptoms, physical, O2 saturation, other tests as needed).
w
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Asthma
Urgent Care for Managing Asthma Exacerbations (cont.)

Repeat assessment after 1 hour
w
Severity of Exacerbation FEV1 or PEF (predicted or personal best) Physical exam Moderate 50 to 80% Severe < 50%
Improvement evident; moderate Sx.
No improvement; severe Sx at rest; accessory muscle use; retractions; highrisk patient. Inhaled short-acting beta2-agonist with anticholinergic hourly or continuous; systemic corticosteroid; O2.
CONTINUE TREATMENT
Inhaled short-acting beta2-agonist every 60 min; systemic corticosteroid.
Continue treatment 1 to 3 hr, if there is improvement. Response to treatment: FEV1 or PEF (predicted or personal best) Physical exam Good 70% Incomplete 50% but < 70% Mild-tomoderate Sx. Poor < 50%
Normal; response sustained 60 min after treatment; no distress. Discharge home with: x Inhaled beta2-agonist x Oral corticosteroid x Patient education Review medications Review/initiate action plan Recommend close medical follow-up
Severe Sx; drowsiness; confusion; PCO2 42 mmHg. Admit to ICU.
Follow-up
Individualized decision re: hospital admission.
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Referral to an asthma specialist for consultation or comanagement is recommended when:

The patient has had a life-threatening asthma
exacerbation. The patient is unresponsive, or poorly responsive, to therapy. Signs and symptoms are atypical or there are concerns with the differential diagnosis. Other conditions complicate persistent or difficult-to-control asthma or its diagnosis (e.g., difficult-to-control allergic rhinitis, rhinosinusitis). Additional diagnostic testing is indicated (e.g., allergy testing to identify possible allergic factors). The patient/parents/caregivers require additional education and guidance on therapy or allergen avoidance. The patient is being considered for immunotherapy. The patient has severe persistent asthma. The patient requires continuous therapy with oral corticosteroids or high-dose inhaled corticosteroids, or has required more than two bursts of oral corticosteroids in the past year. The patient is under 3 years of age and requires Step 3 or Step 4 care. The patient requires confirmation of a history that suggests that an occupational or environmental inhalant or ingested substance is contributing to or provoking asthma. The patient is not achieving the goals of therapy, see page 46.
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Special Considerations for Managing Asthma

Managing exercise-induced bronchospasm (EIB): Exercise-induced bronchospasm (EIB) is caused by a loss of heat, water, or both from the airways during exercise due to increased ventilation and inhalation of cool, dry air relative to the air within the lungs. EIB usually begins during exercise and peaks 5 to 10 minutes after stopping exercise. Exercise may be the only cause of asthma for some patients. o These patients should be monitored regularly because EIB is often a marker of inadequate asthma management. Symptoms may spontaneously resolve within 1 hour after exercise. A warm-up period before exercise may help. If asthma symptoms occur regularly with usual activities or exercise, increasing (or adding) daily long-term control medication(s) may be warranted. Appropriate long-term control therapy, especially with anti-inflammatory medications, may help reduce exerciseinduced symptoms.
Exercise-induced symptoms should be anticipated in ALL patients with asthma. Teachers and coaches need to be notified if a child has exerciseinduced symptoms. They should be told that the child can participate in activities, but may need inhaled medication before the activity.
Treatment for Minutes before Prevents exercise-induced exercise to take symptoms for asthma: approximately: medication: Short-acting inhaled beta2agonist (2 to 4 puffs) Cromolyn sodium or nedocromil sodium (2 to 4 puffs) 5 to 30 (best taken just before exercising) 5 to 30 (best taken just before exercising) 2 to 3 hours
1 to 2 hours
Long-acting At least 30 inhaled beta2agonist (2 puffs for MDI, 1 puff for DPI)
10 to 12 hours with intermittent use (with continuous use, protective effect lasts for less than 8 hours) Up to 24 hours, depending on medication
Asthma
Leukotriene modifier
At least 120
83
Preventing anticipated episodes of asthma symptoms (other than exercise): When the patient understands and recognizes the aggravating factors that increase asthma symptoms, it is possible to prevent or at least minimize episodes of symptoms due to anticipated exposures to the factor. For anticipated Treat with: symptoms upon exposure to:
Managing the patient with seasonal symptoms:

Start or increase daily
Cold (dry) air
Short-acting inhaled beta2-
long-term control therapy 2 to 4 weeks before the season. Gradually decrease (or stop) daily longterm control therapy 2 to 4 weeks after season. If symptoms are associated with seasonal allergic rhinitis or seasonal exacerbations of perennial allergic rhinitis, treat allergic rhinitis symptoms aggressively.
agonist; cromolyn sodium; or nedocromil sodium shortly (5 to 30 minutes) before going out in the cold. Cover nose and mouth with a scarf on cold or windy days. Allergens (e.g., animal dander, pollens)
Cromolyn sodium or
nedocromil sodium shortly (5 to 30 minutes) before an anticipated exposure. Regular use of a long-term control medication may reduce the likelihood of allergeninduced symptoms.
Exacerbations of asthma symptoms (coughing, wheezing, difficulty breathing, chest tightness) are common with viral and other respiratory infections.
Treating asthma symptoms due to viral upper respiratory infections (URIs): Patient should begin regular PEF monitoring at URI onset. For mild symptoms not associated with a decline in peak flow rate, a short-acting inhaled beta2-agonist (every 4 to 6 hours for 24 hours, longer with clinician consult) may be sufficient to control the symptoms. o For recurrent URIs, when this therapy needs to be repeated more frequently than every 6 weeks, a seasonal increase in (or starting) long-term control therapy (usually cromolyn sodium for young children; inhaled corticosteroids for other patients) may be necessary.
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Asthma
For symptoms associated with a decline in PEF into the
yellow zone (per the patients action plan), use a shortacting inhaled beta2-agonist, consider doubling the inhaled corticosteroid dose for 7 to 10 days. o If patient does not respond or PEF decreases into the red zone, add a short (3- to 10-day) course of oral corticosteroid. If the patient has a history of severe recurrent exacerbations with URIs, consider initiating a short (3- to 10-day) course of oral corticosteroid at the first sign of URI. Treating the child with asthma: Administering asthma medications to infants and children can be challenging. Medications to treat asthma in children may be given by inhalation or orally (as tablets or liquids). o The inhaled route is generally preferred because: Higher concentrations can be delivered more effectively to the airways. Systemic side effects are avoided or minimized. The onset of action of short-acting beta2-agonists is substantially shorter when inhaled. Dosages reaching the airway vary considerably depending on the route of administration (and the device(s) used for inhaled medications). The ability of individual children to use different devices for inhaled medications may vary considerably.
Appropriate long-term control therapy during the viral respiratory season may reduce the frequency and severity of virus-induced symptoms.
Using an MDI with a spacer/holding chamber may be easier than using an MDI alone.
Trigger one puff from
Primary prevention of asthma (preventing initial development) may alter its course.
Minimize exposure to dust mites, tobacco
MDI into spacer/holding chamber for each inhalation. Some young children may be able to use an MDI with spacer/ holding chamber and facemask. o If a facemask is used, allow 3 to 5 inhalations for each puff triggered from the MDI.
smoke, animal dander, cockroach allergens. o Exposure to high levels of dust mite and tobacco smoke are associated with an increased incidence of asthma among infants. Prolonged breast-feeding and avoiding the early introduction of allergenic foods may reduce eczema and food sensitization (see Volume 3: Food Reactions, page 69), but have not been shown to reduce the prevalence of asthma.
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Asthma
How do you give medication to infants and young children?

Use a metered dose
inhaler with a spacer/holding chamber plus a facemask. Use a nebulizer. Use a liquid. Liquid albuterol does not have as rapid an onset of action as inhaled albuterol, a consideration for treating exacerbations.
Many children have multiple caregivers. All homes and caregivers should have medications, devices, and a management plan for how and when to use them.
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Asthma
Children < 2 Years Early management of wheezing may alter the course of asthma. However, infants can be difficult to manage. Referral to a pediatric asthma specialist for consultation or comanagement should be considered for children being given daily medication. Carefully monitor the response to medication: o Treat the wheeze for 4 to 8 weeks. o If there is no clear response, stop treatment. o Consider alternate therapy or an alternate diagnosis if the child is not growing and developing normally, eating normally and gaining weight, or sleeping. Diet is usually not a factor for the wheezing child. o When there are reactions after ingesting food, the most common causes are milk, peanuts, soy, wheat, eggs. Reducing exposure to viral respiratory infections may be important for the difficult-to-manage wheezer. Nebulizer therapy with facemask may be preferred for administering cromolyn sodium and for short-acting beta2-agonists during exacerbations. Short-acting beta2-agonists are available as liquids, but: o The onset of action is slower than when given by inhalation (approximately 30 minutes for the liquid as compared to several minutes for inhalation). o Adverse effects (e.g., tremor, irritability) are more likely. Drugs administered by MDI may be given using a spacer/holding chamber and facemask. o The administered dose will be variable and may require extra dosing. o Actuate one dose at a time in the device. o Inhaled corticosteroids by MDI should always be given with a spacer/holding chamber. Children Between 3 and 5 Years Inhaled medications are preferred. Some children can use an MDI and spacer/holding chamber. If the desired therapeutic effects are not achieved, or if the child cannot use an MDI with spacer/holding chamber, a nebulizer or MDI plus spacer/holding chamber with facemask may be required.
Consultation with an asthma specialist is
recommended for children with moderate and severe persistent asthma. A consult may be considered for children with mild persistent asthma.
Viral upper respiratory infections are a key precipitating factor of asthma symptoms in young children.
School-age Children Inhaled medications are preferred. MDIs, DPIs, and nebulizers may be used. o The child should be able to produce the necessary effort and coordination needed for the specific device. All inhaled corticosteroids by MDI should be used with a spacer/holding chamber. Some children carry their short-acting beta2-agonist MDI without a spacer/holding chamber. This is acceptable if the child has demonstrated good technique. Consultation with an asthma specialist is recommended for children with moderate and severe persistent asthma. A consult may be considered for young children with mild persistent asthma. Adolescents LISTEN to the patient! Find out his/her expectations and goals. Find out what the adolescent is willing to do, and then work out a management plan together.
Working with teenagers can be challenging. They may:

View treatment as
infringing on their independence. Fail to recognize the danger of poorly controlled asthma. Respond best to peers and to peer idols. Using known personalities who themselves have asthma and using teen support groups can be very effective. Parents need to stay involved.
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87
Special concerns of the adolescent include:

Effects of medications on
Ask the adolescent about smoking, exposure to tobacco
appearance (height, weight, acne), ability to exercise, menses. Taking medications in public. Peer pressure.
smoke, and possible drug use. Encourage exercise and physical activity. Asthma should not be an excuse for not participating in physical education or sports. Develop an asthma management plan that will allow them to participate in any activity that they wish. Make it easy to take medications before exercise. Consider symptoms related to hobbies and workplace exposures. Consider nonadherence if the teen is not doing well. The childs schedule and giving asthma medications: Provide an action plan for handling exacerbations, including the clinicians recommendation regarding selfadministration of medication and plans to ensure prompt, reliable access to medications. If possible, schedule long-term control medications so that they are not taken at school, even if this results in uneven dosing intervals. However, some children benefit from close supervision of therapy. For these children, giving medication at school, under the supervision of a school health professional, is recommended. It may be helpful for some younger children to have a compressor-driven nebulizer available at their school or daycare facility. Asthma, inhaled corticosteroids, and linear growth. A reduction in growth velocity in children or adolescents may occur as a result of inadequate control of chronic diseases such as asthma or from the use of corticosteroids of treatment. Overall, however, the available cumulative data in children suggest that, although low-to-medium doses of inhaled corticosteroids may have the potential of decreasing growth velocity, the effects are small, nonprogressive, and may be reversible. When high doses of inhaled corticosteroids are necessary to achieve satisfactory asthma control, the use of adjunctive long-term control therapy should be instituted to reduce the dose of inhaled corticosteroids and thus minimize possible dose-related long-term effects on growth. Physicians should monitor the growth of children and adolescents taking corticosteroids by any route and weigh the benefits of corticosteroid therapy and asthma control against the possibility of growth suppression or delay if a childs or an adolescents growth appears slowed.
Reliable, prompt access to asthma medication is essential during the day.

The child, caregivers,
teachers, and school nurses should understand this. Older children should be allowed to carry and selfadminister quick-relief medications, with clinician and parent approval.
Poorly controlled asthma may delay growth.
The potential risks of inhaled corticosteroids are well-balanced by their benefits.
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Managing asthma in the elderly: Because of the high prevalence of other obstructive lung diseases (e.g., chronic bronchitis, emphysema) among the elderly, it is important to determine the extent of reversible airflow obstruction. o Evaluate carefully. The precise cause of severe airflow obstruction can be difficult to identify in older patients. o A 2- to 3-week trial of therapy with oral corticosteroids can help detect the presence of significant reversibility of airway disease. Long-term control asthma medication can then be offered. Medication side effects may be increased in the elderly patient. o Airway response to bronchodilators may change with age, although this is not clearly established. o Older patients, especially those with pre-existing ischemic heart disease, may be more sensitive to beta2-agonist side effects, including tremor and tachycardia. o Theophylline clearance is reduced in the elderly patient, causing increased blood levels of theophylline. Age is an independent risk factor for developing life-threatening events from iatrogenic chronic theophylline overdose. There is increased potential for drug interactions due to the increased use of medications in this age group. o Interactions are of concern between theophylline and certain drugs including: Antibiotics (e.g., ciprofloxacin, erythromycin) H2-antagonists (e.g., cimetidine) Oral contraceptives Theophylline and epinephrine may exacerbate underlying heart conditions. Oral corticosteroids can provoke confusion, agitation, and changes in glucose metabolism. Very high doses of inhaled corticosteroids may be associated with a dose-dependent reduction in bone mineral content. o Elderly patients may be at greater risk due to preexisting osteoporosis, changes in estrogen levels affecting calcium utilization, and a sedentary lifestyle.
Medication side effects may be increased in the elderly patient, and may require a change in the asthma medication plan. Inadequately controlling asthma may unnecessarily limit the patients mobility and activities. Medications to treat other diseases may exacerbate asthma; adjustments may need to be made. Consider:
Aspirin and
nonsteroidal anti-inflammatory agents for treating arthritis. Nonselective betablockers for treating hypertension and/or arrhythmias. Beta-blockers found in some eye drops used to treat glaucoma.
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For more information on asthma in older patients, see the National Asthma Education Prevention Program Working Group Report: Considerations for Diagnosing and Managing Asthma in the Elderly (NHLBI 1996).
o Concurrent treatment with calcium supplements
and vitamin D, and estrogen replacement when appropriate, are recommended. At very high doses, inhaled corticosteroids may increase the risk of cataracts and may increase intraocular pressure.
Older patients may be at greater risk for bone loss due to corticosteroid therapy.
Before starting treatment, evaluate risk with
Poorly controlled asthma during pregnancy increases the risk of:

Perinatal mortality Prematurity Low birth weight
bone densitometry for patients using moderate to high doses. Consider regular risk assessments every 12 to 18 months during treatment. The benefits of this approach have not been evaluated in clinical trials.
All long-term control medications and short-acting inhaled beta2-agonists appear to be safe in pregnancy. For more information on asthma and pregnancy, see Executive Summary: Management of Asthma During Pregnancy (NHLBI 1992).
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Managing the pregnant patient with asthma: Poorly controlled asthma during pregnancy can result in increased perinatal mortality, increased prematurity, and low birth weight. Maintaining sufficient lung function and blood oxygenation to ensure adequate oxygen supply to the fetus is essential. For most medications used to treat asthma and rhinitis, there are little data to suggest an increased risk to the fetus. Treating asthma is paramount. All long-term control medications and short-acting inhaled beta2-agonists appear to be safe in pregnancy. Medications with some possibility of risk to the fetus include: o Decongestants (other than pseudoephedrine) o Antibiotics (tetracycline, sulfonamides, and ciprofloxacin) o Live virus vaccines o Iodides o Brompheniramine o Epinephrine
Managing bronchopulmonary aspergillosis in the patient with asthma: Patients with asthma are susceptible to colonization by fungi, especially bronchopulmonary aspergillosis. Aspergillosis causes an immune reaction that is accompanied by: o Pulmonary infiltrate o Peripheral eosinophilia o Rise in total serum IgE o Worsening asthma Treat with prolonged (many months) and tapering prednisone. If aspergillosis is suspected or confirmed, referral to an asthma specialist is indicated. Managing work-aggravated asthma and occupational asthma: Occupational asthma is suggested by a correlation between asthma symptoms and the workplace. o Occupational exposures may increase asthma symptoms and/or precipitate asthma exacerbations (i.e., work-aggravated asthma). Diagnosis of occupational asthma depends on history, physical examination, and spirometry, correlated with an assessment of the workplace environment. o Peak flow monitoring may be helpful in some cases. o Occupational asthma is suggested by a correlation between asthma symptoms and work, with improvement when away from work for several days. o The patient may fail to recognize the work relationship because symptoms often begin several hours after exposure. o Objective documentation of changes in airway function with workplace exposure is important in establishing the diagnosis. Early recognition and control of exposures are important in occupational-induced asthma because the likelihood of complete resolution of symptoms decreases with time of continuous exposure.
Patients with asthma are susceptible to colonization by fungi, especially bronchopulmonary aspergillosis.
Asthma symptoms that improve when away from work suggest occupational asthma.
Some tips for managing workaggravated and occupational asthma:

Work with onsite
healthcare providers and/or managers/ supervisors. Discuss avoidance, ventilation, respiratory protection, a smoke-free environment. Minimize (ideally, avoid completely) exposure to aggravating agent(s).
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Some examples of compounds causing occupational asthma:

Allergen Animals Arthropods Shellfish and fish Wood and vegetable products Enzymes Pharmaceuticals Amines Anhydrides Diisocyanates Fluxes Metals and metal salts Occupation Farmers; laboratory personnel Farmers; laboratory personnel Shellfish farmers and processors Carpenters; woodworkers; grain handlers; bakers; food process workers; printers Bakers; detergent industry workers; nurses; pharmaceutical employees; plastics workers Pharmaceutical workers; pharmacists Shellac, rubber, lacquer handlers; photographers; solderers; fur dyers; chemists; chemical manufacturers Paint, plastic, plastics, electronics, epoxy resin, chemical manufacturers Polyurethane, plastics, varnish, foam, foundry, rubber manufacturers; spray painters Electronics workers; metal joiners Pot room, hard metal, electroplating workers; printers; tanners; diamond polishers; platinum refiners; hard metal grinders; solderers; locksmiths Chemical, reactive dye, resin, plastics, glove manufacturers; meat wrappers; chemical packaging; refrigeration, textile industry, healthcare workers; hairdressers
Other chemicals
Newman L. Occupational Asthma. Clinics in Chest Medicine. 1995; 16:621-636.
Occupational exposures may increase asthma symptoms and/or precipitate asthma exacerbations
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Component 4. Education for a Partnership in Asthma Care

Take a proactive approach to asthma education. Form a partnership with the patient (and family).
The educational tips included in the Patient Education chapter of Volume 1 are appropriate for the patient with asthma (see Volume 1: Patient Education, page 71). Below find suggestions specific to the patient with asthma. Provide sufficient information. Start educating at the time of diagnosis, and continue at every clinic visit. Adopt a team approach. Have all healthcare team members and office staff reinforce the educational messages. Regularly teach and review: o Basic asthma facts. o Roles of medications. o Device and monitoring skills. o Environmental control measures. o When and how to take rescue actions. Provide written action plans for managing exacerbations.
To take medications correctly, patients with asthma (and their families and caregivers) need education.
Education is time-
consuming, but will improve adherence with therapy.
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Be aware of cultural differences, e.g.:

In some Latino
populations, asthma is viewed as a cold illness, amenable to hot treatments. Suggest that asthma medications be taken with hot tea, hot water, or broth. In some Asian populations, oral medications are preferred.
What can you and your staff do in a single asthma visit? Document the patients (and familys) concerns. Review the medications: How often are you using your long-term control medicine? your quick-relief medicine? Review self-management skills: Show me how you use your inhaler. your peak flow meter. Repeat the important messages: Asthma can be controlled. Our goal is for you to participate in whatever activities youd like. Help with problem solving: What makes it easier for you to remember to take your medications? to avoid your causal or aggravating factors? Focus on what is doable to improve adherence with asthma therapy. Keep therapy simple. o Limit medications. o Limit doses. o Meet the patients schedule. Establish priorities. Write an action plan. Enlist family and peer support.
Open and unrestricted communication (with the patient, family, caregiver) is essential to successful asthma management.
Encourage the patient to
discuss any concerns and expectations. Resolution of anxiety is an important treatment goal and will increase adherence to all aspects of the treatment plan.
Maintain a partnership with the patient (and family). At each visit:

Demonstrate, review, and evaluate correct
inhaler/spacer/holding chamber technique. Ask the patient about concerns to be addressed. Review short-term goals agreed upon at the last visit. Review the daily self-management plan and the action plan. Continue teaching the basic educational messages for asthma. Provide new educational materials for review.
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Provide clear and accurate information about asthma.

Asthma is a physical illness, not an emotional one. Asthma is a chronic disease, not just episodic
or acute. Medication for asthma is NOT addictive. Medication for asthma remains effective with long-term use. Prescription medications should be used to treat asthma, not over-the-counter medications. Patients with asthma should see their physician on a regular basis, when symptom-free as well as when symptoms occur.
Over-the-counter MDIs should be avoided because they:

Are not as effective
as prescription short-acting inhaled beta2-agonists. May have side effects at lower doses. May unnecessarily delay seeking medical care.
All patients with persistent asthma should have 2 asthma care plans:
A DAILY MANAGEMENT PLAN describing
regular medications and measures to keep asthma under control. AN ACTION PLAN describing actions to take when asthma worsens, including: o What medications to take. o When to contact the clinician and/or when to go to the emergency room.
All patients with asthma need an inhaled shortacting beta2-agonist for prompt relief of symptoms.
Give patient and/or caregiver(s) a written easy-to-understand management plan describing how to manage exacerbations, what medications to use, and how to use them.
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Some examples of delivery of asthma education by clinicians during patient care visits*:
Recommendations for initial visit:
Assessment questions focus on: concerns, goals of therapy, quality of life, expectations Teach information in simple language Teach and demonstrate skills
What worries you most about your asthma? What do you want to accomplish at this visit? What do you want to be able to do that you cant do now because of your asthma? What do you expect from treatment? What medicines have you tried? What other questions do you have for me today?
What is asthma? A chronic lung disease. The airways are very sensitive. They become inflamed and narrow; breathing becomes difficult. Two types of medicines are needed: Long-term control: medicines that prevent symptoms, often by reducing inflammation. Quick-relief: short-acting bronchodilator relaxes muscles around airways. Bring all medicines to every appointment. When to seek medical advice. Provide appropriate telephone number.
Inhaler technique (see page 93) and spacer/holding chamber. Check performance. Self-monitoring skills tied to action plan: Recognize intensity and frequency of asthma symptoms. Review the signs of deterioration and the need to re-evaluate therapy: o Waking at night with asthma. o Increased medication use. o Decreased activity tolerance. Use of an asthma management plan (see page 98).
Recommendations for first follow-up visit (2 to 4 weeks or sooner as needed):

Ask relevant questions from previous visit and also ask: What medicines are you taking? How and when are you taking them? What problems have you had using your medicines? Please show me how you use your inhaled medicines?
*
Use of two types of medicines. Remind patient to bring all medicines and the peak flow meter to every appointment for review. Self-evaluation of progress in asthma control using symptoms and peak flow as a guide.
Use of an asthma management plan (see page 98). Review and adjust as needed. Peak flow monitoring (see pages 40 to 41) and daily diary recording. Correct inhaler and spacer/holding chamber technique.
Taken from the Practical Guide for the Diagnosis and Management of Asthma, based on the Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma.
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Recommendations for second follow-up visit:

Assessment questions focus on: concerns, goals of therapy, quality of life, expectations
Teach information in simple language
Teach and demonstrate skills
Ask relevant questions from previous visits and also ask: Have you noticed anything in your home, work, or school that makes your asthma worse? Describe for me how you know when to call your doctor or go to the hospital for asthma care. What questions do you have about the action plan? Can we make it easier? Are your medicines causing you any problems?
Relevant environmental control/avoidance strategies (see page 51). How to identify and control home, work, or school exposures that can cause or worsen asthma. How to avoid cigarette smoke (active and passive). Review all medicines and review and interpret peak flow and symptom scores from daily diary.
Inhaler/spacer/holding chamber technique. Peak flow monitoring technique. Review use of action plan. Confirm that patient knows what to do if asthma gets worse.
Recommendations for all subsequent visits:

Ask relevant questions from previous visits and also ask: Have you tried to control things that make your asthma worse? Please show how you use your inhaled medicines. Review and reinforce all: Educational messages. Environmental control strategies at home, work, or school. Medicines. Review and interpret peak flow and symptom scores from daily diary. Inhaler/spacer/holding chamber technique. Peak flow monitoring technique. Review use of action plan. Confirm that patient knows what to do if asthma gets worse. Periodically review and adjust written action plan.
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Sample Asthma Management Plan for Long-Term Control and for Treating Asthma Exacerbations
GREEN ZONE: Doing well
No cough, wheeze, chest tightness or shortness of breath during the day or night Can do usual activities And, if a peak-flow meter is used, Peak flow: more than (80% or more of my best peak flow) My best peak flow is: Before exercise
Take these long-term control medicines each day (include anti-inflammatory): Medicine When to take it How much to take
2 or
4 puffs
5 to 30 minutes before exercise
YELLOW ZONE: Asthma is getting worse
FIRST
Add Quick-Relief medicine and keep taking your GREEN ZONE medicine:
(short-acting beta2-agonist)
Cough, wheeze, chest tightness or shortness of breath, OR SECOND Waking at night due to asthma, OR Can do some, but not all, usual activities OR Peak flow: to (50% of my best peak flow)
If your symptoms (and peak flow, if used) return to GREEN ZONE after 1 hour of above treatment: Take the quick-relief medicine every 4 hours for 1 to 2 days. Double the dose of your inhaled corticosteroid for (7-10) days. If your symptoms (and peak flow, if used) do not return to GREEN ZONE after 1 hour of above treatment: Take: 2 or 4 puffs or Nebulizer
(short-acting beta2-agonist) (oral corticosteroid)
Add: Call the doctor before/ within
mg per day for (3-10) days. hours after taking the oral corticosteroid. 2 or 4 puffs or mg. Nebulizer
RED ZONE: Medical Alert!

Very short breath, OR Quick-relief medicines have not helped, OR Cannot do usual activities, OR Symptoms are same or get worse after 24 hours in Yellow Zone OR Peak flow: to (< 50% of my best peak flow) DANGER SIGNS. Trouble walking and talking due to shortness of breath Lips or fingernails are blue
Take this medicine:

(short-acting beta2-agonist) (oral corticosteroid)
Then call your doctor NOW. Go to the hospital or You are still in the red zone after 15 minutes AND You have not reached your doctor.
call for an ambulance if:
Take 4 or 6 puffs of your quick-relief medicine AND Go to the hospital or call for an ambulance (
) NOW!
Asthma and the School

Since school is the childs home away from home, it is one of the most important environments to safeguard. The clinician should work closely with school personnel to help them understand asthma, its impact, and how to meet the special needs of children with asthma. Teachers, coaches, and school health personnel need to know: The early warning signs of an asthma episode. How to treat an asthma episode, including: o What medications are used. o How the medications are used. o When to contact the clinician or emergency room. What medications the student uses. o Common side effects of asthma medications that warrant communication with the parents and/or clinician: nervousness, nausea, drowsiness, jitteriness, hyperactivity. How to help the child with asthma follow his/her management plan at school. o What causal and aggravating factors are associated with the students asthma. o How the student premedicates to prevent exerciseinduced symptoms (and symptoms from other anticipated exposures; e.g., allergens, cold air). o How to minimize exposure to causal and aggravating factors (e.g., allergens, strong odors) in the classroom and school environment that can worsen the students asthma. Whether the student has clinician and parent approval to carry and use his/her inhaler(s). Phone numbers for the clinician, the parents, and the emergency room. How to use devices to deliver asthma medications, spacers/holding chambers. How to use a peak flow meter (if appropriate).
The child with asthma can function normally at school. Be aware of common school problems faced by the student with asthma:
Absences due to asthma
symptoms or to doctor visits. Avoidance of school or activities. Not taking medications because it is bothersome to go to the health office. Side effects that interfere with performance or concentration.
Students with asthma need to have prompt and easy access to their medications. They should be permitted to carry and use their medication, with physician and parent approval. Some schools do not have full-time nurses. The action plan must be understandable for use by health aides or office personnel.
Give the school an action plan. Include:

The early warning signs of an asthma episode. What medications the student uses and how
they are taken. When to contact the clinician or emergency room.

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How asthma-friendly is your school?

Children with asthma need proper support at school to keep their asthma under control and to be fully active. Use the questions below to find out how well the school assists children with asthma: 1. Is the school free of tobacco smoke all of the time, including during schoolsponsored events? 2. Does the school maintain good indoor air quality? Does it reduce or eliminate allergens and irritants that can make asthma worse? Allergens and irritants include pets with fur or feathers, molds, dust mites (for example, in carpets and upholstery), cockroaches, and strong odors or fumes from such products as pesticides, paint, perfumes, and cleaning chemicals. 3. Is there a school nurse in the school all day, every day? If not, is a nurse regularly available to the school to help write plans and give guidance for students with asthma about medicines, physical education, and field trips? 4. Can children take medicines at school as recommended by their doctor and parents? May children carry their own asthma medicines? 5. Does the school have an emergency plan for taking care of a child with a severe asthma episode (attack)? Is it made clear what to do? Who to call? When to call? 6. Does someone teach school staff about asthma, asthma mangement plans, and asthma medicines? Does someone teach all students about asthma and how to help a classmate who has it? 7. Do students have good options for fully and safely participating in physical education class and recess? (For example, do students have access to their medicine before exercise? Can they choose modified or alternative activities when medically necessary?) If the answer to any question is no, students may be facing obstacles to asthma control. Asthma out of control can hinder a students attendance, participation, and progress in school. School staff, health professionals, and parents can work together to remove obstacles and to promote students health and education.
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School Asthma Management Plan

Student Asthma Action Card
Name: Teacher: Parent/Guardian Parent/Guardian Name: Address: Name: Grade: Room: Ph (H): Ph (W): Ph (H): Ph (W):
Name Relationship Relationship Phone Phone
Age:
ID Photo
Emergency Phone Contact #1: Emergency Phone Contact #2:

Name
Physician Student Sees for Asthma: Other Physician:
Ph: Ph:
Daily Asthma Management Plan

Identify the things which start an asthma episode (check each that applies to the student).
Exercise Respiratory infections Change in temperature Animals Comments:
Strong odors or fumes Chalk dust Carpets in the room Pollens
Other
Food Molds
Control of School Environment

(List any environmental control measures, premedications, and/or dietary restrictions that the student needs to prevent an asthma episode.)
Peak Flow Monitoring

Personal Best Peak Flow Number: Monitoring Times:
Daily Medication Plan

Name
Amount
When to Use
1. 2. 3. 4.
*
Developed by the Asthma and Allergy Foundation of America (AAFA); Endorsed by National Asthma Education and Prevention Program (NAEPP)
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School Asthma Management Plan (continued) Emergency Plan

Emergency action is necessary when the student has symptoms such as or has a peak flow reading of Steps to take during an asthma episode: 1. Give medications as listed below. 2. Have student return to classroom if 3. Contact parent if 4. Seek emergency medical care if the student has any of the following: No improvement 15-20 minutes after initial treatment with medication and a relative cannot be reached. Peak flow of . .
Hard time breathing: Chest and neck are pulled in with breathing. Child is hunched over. Child is struggling to breathe. Trouble walking or talking. Stops playing and cant start activity again. Lips or fingernails are gray or blue. Emergency Asthma Medications
Name Amount
IF THIS HAPPENS, GET EMERGENCY HELP NOW!
When to Use
1. 2. 3. 4. Comments/Special Instructions
For Inhaled Medications I have instructed (name) in the proper way to use his/her medications. It is my professional opinion that he/she should be allowed to carry and use that medication by him/herself. It is my opinion that by him/herself. should not carry his/her inhaled medication
Physician Signature Parent Signature Date Date
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Holt PG. Early acquisition of sensitization in childhood asthma. Pediatr Pulmonol 1995; 11: 44-46. Hopkin J. The rise of asthma and atopy. Quart J Med 1998; 91: 169-170. Hu FB, Persky V, Flay BR, Zelli A, Cooksey J, Richardson J. Prevalence of asthma and wheezing in public schools children: association with maternal smoking during pregnancy. Ann Allergy Asthma Immunol 1997; 79: 80-87. Ingram JM, Sporik R, Rose G, et al. Quantitative assessment of exposure to dog (Can f1) and cat (Fel d1) allergens: Relation to sensitization and asthma among children living in Los Alamos, New Mexico. J Allergy Clin Immunol 1995; 96: 449-456. James JM, Bernhisel-Broadbent J, Sampson HA. Respiratory reactions provoked by double-blind food challenges in children. Am J Respir Crit Care Med 1994; 149: 59-64. Jenkins MA, Hopper JL, Bowes G, et al. Factors in childhood as predictors of asthma in adult life. BMJ 1994; 309: 90-93. Joos GF, Germonpre PR, Kips JC, Peleman RA, Pauwels RA. Sensory neuropeptides and the human lower airways: present state future directions. Eur Respir J 1994; 7: 1161-1171. Kang BC, Johnson J, Veres-Thorner C. Atopic profile of inner-city asthma with a cooperative analysis on the cockroachsensitive and ragweed-sensitive subgroups. J Allergy Clin Immunol 1993; 92: 802-811. Kattan M, Mitchell H, Eggleston P , et al. Characteristics of inner-city children with asthma: the National Cooperative Inner-City Asthma Study. Pediatr Pulmonol 1997; 24: 253-262. Kay J, Mortimer MJ, Jaron AG. Do both paternal and maternal smoking influence the prevalence of childhood asthma? A study into the prevalence of asthma in children and the effects of parental smoking. J Asthma 1995; 32: 47-55. Kelloway JS, Wyatt RA, Adlis SA. Comparison of patients compliance with prescribed oral and inhaled asthma medications. Arch Intern Med 1994; 154: 1349-1352.
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Kemp T, Pearce N, Fitzharris P , et al. Is infant immunization a risk factor for childhood asthma or allergy? Epidemiology 1997; 91: 45-55. Kesten S, Szalai J, Dzyngel B. Air quality and the frequency of emergency room visits for asthma. Ann Allergy Clin Immunol 1995; 74: 269-273. Klucka CV, Ownby DR, Green J, Zoratti E. Cat shedding of Fel d1 is not reduced by washings, Allerper-C spray, or acepromazine. J Allergy Clin Immunol 1995; 95: 1164-1171. Koenig JQ, Larson TV, Hanley QS, et al. Pulmonary function changes in children associated with fine particulate matter. Environmental Research 1993; 63: 26-38. Krahn M. Issues in the cost-effectiveness of asthma education. Chest 1994; 106; S264-269. Kroegel C, Virchow JC Jr., Luttmann W, Walker C, Warner JA. Pulmonary immune cells in health and disease: the eosinophil leucocyte. Eur Respir J 1994; 7: 519-543. Kropfelder L, Winkestein M. A case management approach to pediatric asthma. Ped Nursing 1996; 22: 291-295. Kuehr J, Frisher T Meinert R, et al. Sensitization to mite allergens is a risk factor for early and late onset of asthma and for persistence of asthmatic signs in children. J Allergy Clin Immunol 1995; 95: 655-662. Kumar A, Busse W. Airway inflammation in asthma. Scientific Am Sci Med 1995: 38-47. Laitinen A, Laitinen LA. Airway morphology: Epithelium/basement membrane. Am J Respir Crit Care Med 1994; 150: S14-17. Lang DM, Sherman MS, Polansky M. Guidelines and realities of asthma management. The Philadelphia Story. Arch Intern Med 1997; 157: 1193-1200. Lieu TA, Quesenberry CP , Capra AM, et al. Outpatient management practices associated with reduced risk of pediatric asthma hospitalization and emergency department visits. Pediatrics 1997; 100: 334-341. Litner TJ, Brame KA. The effects of season, climate and air conditioning on the prevalence of Dermtophagoides mite allergens in household dust. J Allergy Clin Immunol 1993; 91: 862-867. 106
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Lozano P , Fishman P , VonKorff M, Hecht J. Healthcare utilization and cost among children with asthma who were enrolled in a health maintenance organization. Pediatrics 1997; 99: 757-764. Mahr TA, Evans R. Allergist influence on asthma care. Ann Allergy 1993; 71: 115-120. Martinez FD. Viral infections and the development of asthma. Am J Respir Crit Care Med 1995; 151: 1644-1647. Martinez FD. Complexities of the genetics of asthma. Am J Respir Crit Care Med 1997; 156: S117-122. Mellins RB, Zimmerman B, Clark NM. Patient compliance. Are we wasting our time and dont know it? Am Rev Respir Dis 1992; 146: 1376-7. Moore R, Khan A, Burton F. Long-acting inhaled beta2-agaonists in asthma therapy. Chest 1998; 113: 1095-1108. Mullins J, White J, Davies BH. Circadian periodicity of grass pollen. Ann Allergy 1986; 57: 371-374. Munzenberger PJ. Improving adherence in patients with asthma. Am Pharmacy 1993; NS33: 32-36. National Heart Lung and Blood Institute. National Asthma Education and Prevention Program. Expert panel report 2: guidelines for the diagnosis and management of asthma. April 1997: NIH Pudlication 97-4051. National Heart Lung and Blood Institute Report of the Working Group on Asthma and Pregnancy: Management of Asthma During Pregnancy. September 1993; NIH Publication 93-3279. Nelson HS, Fernandez-Caldas E. Prevalence of house-dust mites in the rocky mountain states. Ann Allergy Asthma Immunol 1995; 75: 337-339. Nelson HS, Hirsch SR, Ohman JL, et al. Recommendations for the use of residential air cleaning devices in the treatment of allergic respiratory diseases. J Allergy Clin Immunol 1988; 82: 661-669.
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110
Atopic Dermatitis
Atopic dermatitis is a chronic or recurrent atopic
inflammatory skin disease that:

o Generally begins in the first few years of life. o May be the initial clinical manifestation of an
Atopic dermatitis is sometimes referred to as the itch that rashes. Atopic dermatitis may be the initial clinical manifestation of an allergic predisposition, usually preceding allergic rhinitis and asthma.
More than 50% of
allergic predisposition, usually preceding allergic rhinitis and asthma.

The etiology of atopic dermatitis is generally
unknown.
o There is a high frequency of elevated serum IgE
levels, but the exact role of IgE in the pathogenesis of atopic dermatitis is not clear.
o Approximately 85% of atopic dermatitis patients
have elevated IgE levels with positive immediate skin tests.

In some patients, particularly young children,
allergy to food or aeroallergens contributes to the disease.

Atopic dermatitis may present at any age, but
usually has an onset in childhood.

o Approximately 50% of patients develop symptoms
atopic dermatitis patients develop asthma. Approximately 75% of atopic dermatitis patients develop allergic rhinitis.
in the first year of life.

o Another 30% develop symptoms between the
ages of 1 and 5 years.

The characteristic symptoms of atopic dermatitis
The prevalence of atopic dermatitis in children is increasing.

Up to 10% to 15% of the
are intense pruritus and skin reactivity.

o Scratching may be intermittent during the day. o Scratching is usually worse in the early evening
population are affected by atopic dermatitis during childhood.
and at night.
Disruption of normal sleep patterns is
common.
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111
Atopic dermatitis involves a complex inflammatory process associated with local activation of lymphocytes, monocytes/macrophages, eosinophils, and mast cells.
Causal Factors
Foods Environment Pathogens Temperature Stress
+ IgE +
Atopic Individual
w
Inflammatory Cells and Mediators Mast cell derived:
Histamine Leukotrienes
Eosinophil derived:
Leukotrienes Major Basic Proteins Peptides
w
Inflammation Pruritis Acute Dermatitis Chronic Dermatitis
Certain foods may exacerbate rashes in some
patients, particularly children. (See Volume 3: Food Reactions, page 69)

o Skin testing and oral challenges may be necessary
to confirm allergies.
o Common foods causing symptoms include eggs,
peanuts, and milk.

Eliminating these foods may ameliorate
symptoms in allergic patients.

112
Atopic Dermatitis
Some patients develop symptoms when exposed to
aeroallergens, especially house dust mites and animal danders.

o Avoiding aeroallergens may improve symptoms in
sensitive patients.
Ocular complications associated with atopic
dermatitis:
o Atopic keratoconjunctivitis, frequently associated
with eyelid dermatitis and blepharitis.

o Keratoconus from persistent rubbing of the eyes.
Characteristic symptoms of atopic dermatitis are intense pruritus and skin reactivity. o Scratching may be intermittent during the day. o Scratching is usually worse in the early evening and at night. o Disruption of normal sleep patterns is common.
Flaring atopic dermatitis with severe pruritus and multiple excoriations.

Photo provided by Anthony Gaspari, M.D., University of Rochester.
Atopic Dermatitis
113
Patients with atopic dermatitis often develop
recurrent bacterial, fungal, and viral skin infections, which may lead to difficulty in controlling the disease.
o Decreased cellular immunity and increased skin
hyperactivity is related to susceptibility of skin to infections.

o Secondary skin infection is common in all age
groups.
o Common bacterial infections include
staphylococci and streptococci.

Bacterial infection is suggested by: Honey-colored crusting Extensive serous weeping Folliculitis Pyoderma
o Fungal infections include Trichophyton rubrum
and Pityrosporum ovale.

o Viral infections include herpes simplex, warts,
and molluscum contagiosum.
Infantile eczema complicated by eczema herpeticum in gluteal cleft.

Altered barrier function, especially during acute
episodes of atopic dermatitis increases:

o Transepidermal water loss. o Absorption of medicaments, allergens, and
irritants.
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Atopic Dermatitis
Diagnosing the Patient with Atopic Dermatitis

Medical History
A detailed and accurate history is critical to the proper
diagnosis of atopic dermatitis and its successful treatment. Consider: o Assessment of the pruritic nature of the skin rash. o Age of onset. o Family history of allergic diseases. o Distribution and characteristics of the skin rash. Pattern and duration of symptoms: o Chronicity o Relapsing nature o Seasonal variation Assessment of casual factors: o Environmental exposures o Food hypersensitivity Presence of other allergic diseases, particularly: o Asthma o Rhinitis o Conjunctivitis Presence of other conditions: o Eye complications o Ichthyosis cluster Dry skin Keratosis pilaris (rough hair follicles) Follicular prominences Hyperlinear palms Icthyosis vulgaris
Adult atopic dermatitis with ichthyosis vulgaris skin changes.
Patients with atopic dermatitis often have concomitant medical problems, particularly asthma, allergic rhinitis, and conjunctivitis.
Atopic Dermatitis
115
Distribution of lesions of atopic dermatitis in older children and adults:
Older Children
Adults
Patient Infants Older children; adults
Distribution Facial and Extensor surfaces Flexural
Characteristics Exudative (oozing, weeping) Lichenified (dry)
During severe exacerbations, the lesions may become more generalized.

116
Atopic Dermatitis
Ask the patient about what causes symptoms, such as:

Allergens o Environmental allergens (e.g., pollens, dogs,
cats, dust mites) o Foods o Personal care products o Medications Chemical irritants o Acids, alkali o Solvents o Plastics o Smoke Physical irritants o Scratchy clothing o Occlusive clothing o Scratching or vigorous scrubbing o Extremes of environmental temperature or humidity Sweating Extreme dryness o Hot water Internal changes o Infection o Emotional stress o Hormonal changes associated with menstruation or pregnancy
Evaluate the morphology and distribution of skin
lesions. Assess potential complications related to chronic corticosteroid therapy (e.g., striae or skin atrophy). Realize that acute, subacute, and/or chronic lesions are commonly seen in atopic dermatitis. Look for evidence of a skin infection.
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117
Characteristics of atopic dermatitis lesions:

Acute lesions/eczema o Intensely pruritic o Erythematous papules and vesicles over
erythematous skin o Frequently associated with extensive excoriations and erosions o Accompanied by a serous exudate Subacute lesions o Erythema o Excoriation o Scaling Chronic lesions o Thickened skin plaques o Fibrotic papules (lichen simplex chronicus) o Accentuated skin markings (lichenification)
Chronic dry lichenified dermatitis in child with atopic dermatitis.

The morphology and distribution of lesions change
with age and/or ethnicity. o Infants and young children: Erythematous lesions. Scaling eruptions on scalp, face, ears, trunk and extensor surfaces.
Hand dermatitis in a 5-year old with atopic dermatitis.
118
Atopic Dermatitis
o Older children and adults:
Popliteal and antecubital fossae, neck, intragluteal creases, wrists, ankles.
Flexural eczema in teenager with secondary impetigo.

African-Americans: o Erythema (redness) may be difficult to appreciate
because of underlying pigmentation. o Pigment changes (hyper- or hypo-pigmentation) may be prominent.

Chronic atopic dermatitis may be associated with pigment changes in AfricanAmericans.
Reprinted from Fireman P . Atopic Dermatitis. In: Fireman P , Slavin R, (eds.) Atlas of Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 241. By permission of the publisher Mosby.
Common dermatoses of infancy should be differentiated
from atopic dermatitis: o Seborrheic dermatitis o Diaper dermatitis o Diaper dermatitis with Candida
This exudative dermatitis (eczema) is typical with infantile atopic dermatitis.
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119
Distinguishing features of seborrheic and atopic dermatitis in infancy:

Feature Seborrheic Dermatitis Usually none Usually under 2 months Scalp; face and neck; any flexures, especially genitoanal; in older child, eyebrows, eyelids Erythema with greasy, yellowish scales; sharply demarcated flexural lesions Minimal Eosinophilia absent; negative skin tests Usually clear in 3 to 4 weeks, up to 2 months; no associated defects Normal Atopic Dermatitis History of atopic disease Usually over 2 months Cheeks, forehead, scalp, extensor surfaces of limbs (flexural involvement in older patients) Erythema, papules, vesicles; no scales (may be crusted); tapering edges; fine scaly appearance Severe (a hallmark of disease) Eosinophilia; positive skin tests, elevated IgE Prolonged course; high incidence of associated allergic rhinitis and asthma White dermatographism
Common clinical features of atopic dermatitis:

Pruritus Facial and extensor
Family history Age of onset Distribution
involvement in infants and children Flexural lichenification in adults Chronic or chronically relapsing dermatitis Personal or family history of atopic disease
Source: Hanifin JM, Rajka G. Acta Derm Venerol 1980; 92: 44-47.
Lesions
Pruritus Laboratory
Common dermatoses of infancy should be differentiated from atopic dermatitis:

Seborrheic dermatitis Diaper dermatitis Diaper dermatitis with
Prognosis
Skin reactivity
Candida
Masqueraders of atopic dermatitis:

Seborrheic dermatitis Contact dermatitis (allergic or irritant) Scabies Nummular eczema Hyper-IgE syndrome Wiskott Aldrich syndrome Cutaneous T-cell lymphoma (in adults)
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Atopic Dermatitis
Diagnostic Testing
Skin tests or in vitro tests for specific allergens must be
interpreted cautiously. o Skin tests have a high rate of false-positive (i.e., clinically insignificant) results. o Consultation with an allergy/immunology specialist is recommended. The use of a basic elimination diet may be helpful in assessing the role of food allergy.
Elimination diets:
Should be supervised by an allergy/immunology
specialist. Are therapeutic trials: o Used only for a limited period of time (10 to 14 days)? o Monitored for outcomes closely? Blinded oral challenges may be useful in identifying food allergens. o Oral food challenges should be supervised by an allergy/immunology specialist. For more information, see Volume 3: Food Reactions, page 77.
Food-sensitive patients who respond to the basic elimination diet should be referred to an allergy/immunology specialist in a timely manner.
Elimination diets are therapeutic trials and should be supervised by an allergy/immunology specialist.
They may fail if the patient: Does not receive adequate education before starting. o The family/caregiver(s) should also receive education. Does not adhere to the diet. Is allergic to other foods which were not eliminated. Has a coexisting disease that masks a beneficial response. Has an incorrect diagnosis of atopic dermatitis.
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121
Targeted elimination diet: Food-sensitive patients who respond to targeted food elimination diets should:
Continue the diet. Avoid overzealous
Foods eliminated based on results from specific
restriction of nonimplicated foods. Have weight (and height) monitored regularly. Be re-evaluated or every 4 to 6 months. Consider seeing a dietitian for education and help in managing their diet.
IgE tests (e.g., skin tests or in vitro tests) or from a suggestive history given by patient and/or parent. o Positive skin tests or in vitro tests for specific allergens must be interpreted cautiously. Consultation with an allergy/immunology specialist is recommended. Oral challenges may be useful to confirm food allergy.
Managing the Patient with Atopic Dermatitis

Four general principles of allergy management:
Goals of treatment for atopic dermatitis:

Relieve symptoms. Reduce cutaneous
1 2
Avoid factors that cause symptoms. Use appropriate medications.
3 4
Evaluate for immunotherapy. Educate and follow-up.
inflammation. Enhance skin hydration. Remove flare factors (e.g., infections, exposure to irritants).
Avoid factors that cause symptoms.

Avoiding causal factors can decrease symptoms, prevent exacerbations, and reduce the need for medications.
All patients should: o Avoid common irritants (e.g., some soaps, detergents,
Nonpharmacologic theraphy is important for treating atopic dermatitis.
chemicals, abrasive or heavy clothing, extremes of temperature and humidity). o Keep fingernails trimmed short to minimize skin trauma from scratching. o Cover hands when sleeping (e.g., cotton gloves, socks). o Control emotional stress which can exacerbate pruritus and dermatitis.
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Atopic Dermatitis
Food sensitive patients who respond to targeted food
elimination diets should: o Continue the diet. o Avoid overzealous restriction of nonimplicated foods. o Have weight (and height) monitored regularly. o Be re-evaluated every 4 to 6 months. o Consider seeing a dietitian for education and help in managing their diet. o Use vitamin and mineral supplements, if needed.
Long-term trial elimination diets should be avoided.

Regular monitoring of
weight and height (in children) is essential.
Avoiding causal factors can:

Prevent exacerbations. Reduce the need for
Help the patient learn how to reduce emotional stress.

Patients may respond to stress with increased
medications. Decrease symptoms.
itching and scratching. Psychological evaluation or counseling should be considered for patients who have difficulty with emotional or psychological problems that aggravate symptoms.
Dust mite elimination may be helpful for some patients with atopic dermatitis.
Skin care is important for palliation of symptoms.

The patient should: o Hydrate the skin with proper use of emollients or
topical hydrating agents. o Avoid skin care products containing perfumes and dyes (e.g., bubble baths, bath oils, alcohol-containing baby wipes). o Rinse clothing thoroughly after washing to remove detergent and soap residue. o Avoid fabric softeners (liquids and dryer sheets). o Wear soft cotton clothing next to the skin. o Avoid irritating fabrics (e.g., wool, nylon).
Patients with atopic dermatitis may be especially sensitive about their appearance.
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123
o Take daily baths (showers are permissible for patients
with mild disease). Superfatted, unscented soap or soap substitutes are recommended. Follow by hydrating the skin with a bland emollient while skin is still damp. Some patients need to avoid excessive bathing. o Avoid products containing urea, lactic acid, or other alpha-hydroxy acids if skin is inflamed. o Use a humidifier, if needed, for dry skin during winter months. Natural sunlight can be beneficial for patients with atopic dermatitis, but caution the patient about: o Sunburn and other potential adverse effects of sunlight. o Exacerbation of symptoms by high heat and humidity. Phototherapy with ultraviolet A and/or B or PUVA (psoralen plus ultraviolet A) may be helpful for adolescents and adults with chronic recalcitrant disease. o Consider administration under the direction of a dermatologist.
Localized hydration by wet dressings may be helpful.

Recommended for severely affected or
chronically involved areas of dermatitis refractory to conventional skin care. Physiologic saline or Domeboros solution (i.e., calcium acetate, aluminum sulfate astringent) may be helpful for exudative and/or crusted localized areas of infection. May decrease itching and exudation. Must be closely monitored by the healthcare provider. Overuse can chill or macerate the skin, resulting in secondary infection.
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Use appropriate medications to alleviate and prevent the patient's symptoms.
Corticosteroids
Topical Corticosteroids Topical corticosteroid preparations, due to their antiinflammatory actions, are the key treatment for lesions associated with atopic dermatitis. Use in conjunction with emollients to help promote hydration of the epidermis. When using a topical corticosteroid: o Use the least potent agent that gives control. o Switch to a less potent agent when control is achieved. o Remember that certain areas (face, genitalia, axillae) are especially susceptible to local side effects. o Avoid using agents in Groups I through III on children under 14 years of age. Topical corticosteroids may: o Interfere with wound healing. o Mask infection. o Exacerbate infection. Local side effects of topical corticosteroid therapy: Atrophy Burning Contact dermatitis Hypopigmentation Irritation Itching Striae Perioral dermatitis Purpura Rosaceaform dermatitis Telangiectasia
Medications used to treat Atomic Dermatitis:

Corticosteroids Antihistamines Antibiotics Antiviral agents
General considerations for using a topical corticosteroid:

For total body treatment
start with Groups IV or V. May use Group VII or diluted Group VI on face. For spot (exacerbation) treatments, use Groups IV or V. If the patient fails to respond, refer to a specialist for consultation and/or comanagement.
Systemic side effects with topical corticosteroids are rare, but may include: Adrenal suppression Cataracts Growth retardation Iatrogenic Cushings Syndrome Increased intraocular pressure
Side effects are directly related to the potency rating of the corticosteroid and the extent of use.
Use of topical corticosteroids with an occlusive dressing may facilitate absorption and increase the potential for side effects. Consultation with a specialist is recommended.
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125
Some suggestions for using topical corticosteroids:

Advise the patient to apply the topical
corticosteroid: After bathing in tepid water to hydrate the skin and help remove crusts. Before nonmedicated emollients. Only to inflamed pruritic areas (not to areas that are dry, but not inflamed). Ointment-based preparations are more lubricating than creams, and are preferable on chronic lichenified areas. Creams may be tolerated better than ointments, especially in hot, humid weather. Lotions and creams can be suitable for scalp dermatitis depending on age of patient. Use with caution in young children. Consider referral to a specialist. Reserve the more potent corticosteroids for initial treatment of nonfacial, nonskinfold areas. Switch to less potent agents after several days. Once symptoms are in remission, an emollient alone may be sufficient for many patients. Avoid occlusive dressings with topical corticosteroids because of the potential risk of increased absorption and/or skin infection.
Topical Immunosuppressants
Adults
Elidel 1% cream (pimecrolimus) Protopic 0.03% ointment 0.1% ointment (tacrolimus) apply 2 times a day apply 2 times a day either dose
Children
>2 yrs of age apply 2 times a day >2 yrs of age apply 0.03% ointment 2 times a day
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Atopic Dermatitis
Topical corticosteroids with potency rankings based on vasoconstrictor assays:

Group VII: Least Potent
Hydrocortisone hydrochloride 1.0%, 2.5% (cream, lotion, ointment) Hydrocortisone acetate 1.0%, 2.5% (cream, lotion, ointment) Pramoxine hydrochloride 1.0% (cream, lotion, ointment)
Group VI
Alclometasone dipropionate 0.05% (cream, ointment) Betamethasone valerate 0.1% (lotion) Desonide 0.05% (cream) Fluocinolone acetonide 0.01% (cream, solution)
Group V
Betamethasone dipropionate 0.05% (lotion) Betamethasone valerate 0.1% (cream) Fluocinolone acetonide 0.025% (cream) Fluticasone propionate 0.05% (cream) Flurandrenolide 0.05% (cream) Hydrocortisone valerate 0.2% (cream) Prednicarbate 0.1% (cream)
Group IV
Hydrocortisone valerate 0.2% (ointment) Flurandrenolide 0.05% (ointment) Fluocinolone acetonide 0.025% (ointment) Mometasone furoate 0.1% (cream) Triamcinolone acetonide 0.1% (cream)
Least Potent
Group III Group II
Use after consultation with specialist
Moderately Potent
Group I: Most Potent

Most likely to cause side effects. Use only for short periods of time and on areas that are lichenified. DO NOT USE on face, diaper area, genitalia, axillae. Use after consultation with specialist.
Amcinonide 0.1% (cream, lotion) Betamethasone dipropionate 0.05% (cream) Betamethasone valerate 0.1% (ointment) Desoximetasone 0.05% (cream) Diflorasone diacetate 0.05% (cream) Fluocinonide 0.05% (cream) Halcinonide 0.1% (ointment, solution) Triamcinolone acetonide 0.1% (ointment)
Amcinonide 0.1% (ointment) Betamethasone dipropionate 0.05% (ointment) Desoximetasone 0.05% (gel) Fluocinonide 0.05% (gel, ointment, solution) Halcinonide 0.1% (cream) Mometasone furoate 0.1% (ointment)
Betamethasone dipropionate 0.05% augmented (cream, ointment) Clobetasol propionate 0.05% (cream, ointment) Halobetasol propionate 0.05% (cream, ointment)
Moderately Potent
Group VII agents are least likely to cause long-term side effects. Group I agents are most likely to cause long-term side effects.
Most Potent
w
Atopic Dermatitis
w
127
Commonly used topical corticosteroids:

Brand name Aclovate Aristocort Cordran Cutivate

Generic name Alclometasone diproprionate Triamcinolone acetonide Flurandrenolide Fluticasone propionate Amcinonide Betamethasone diproprionate Betamethasone diproprionate Mometasone furoate Diflorisone diacetate Halcinonide Hydrocortisone Triamcinolone acetonide Fluocinonide Hydrocortisone butyrate
Group VI III, IV , VI IV ,V III, V II, III I, II III II, IV II, III II, III VII IV ,V , VI II, III V VI II, III II, III VII I IV ,V , VI I II, III V , VI I III, V ,V V
Cyclocort
Diprolene Elocon Halog

Diprosone Florone

Hytone Lidex
Kenalog Locoid
Locortan Maxiflor Maxlvate
Flumethasone plvolate Diflorasone diacetate Betamethasone diproprionate
Pramosone Psorcon Synalar

Hydrocortisone acetate, pramoxine HCL Difiorasone discatate Fluocinolone acetonide Clobetasol propionate Desoximetason Desonide Halobetasol propionate Betamethasone valerate Hydrocortisone valerate
Temovate Topicort
Tridesilon Valisone
*
Ultravate

Westcort
Cream (0.05%) approved for atopic dermatitis in infants 3 months of age or older.
Stoughton RB. Vasocanstrictor assay-specific applications. In: MaibachHI, Surber G (eds). Topical Steroids. Basel, Switzerland: Darger 1992: 42-53.
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Atopic Dermatitis
Oral Corticosteroids
Reserve for only extremely severe exacerbations. Use a short course of oral corticosteroids. Abstain from using long-term. Patients usually experience a short rebound period in their
symptoms after discontinuing oral corticosteroids. Avoid use in children, if possible.
Typical daily prednisone dosage schedule for moderate flare:

Adults: 0.5 to 1 mg/kg, tapering over 3 to 10 days depending on severity. Children: 0.5 to 1 mg/kg, tapering over 3 to 5 days depending on severity. Avoid recurrent use of oral corticosteroids. If patient is nonresponsive following the course of corticosteroid, consider referral to an allergy/immunology or dermatology specialist.
Oral Antihistamines
Should be used to control pruritus, especially at night. Older agents, such as hydroxyzine are highly effective, but are
associated with increased sedation. Use as single dose before bedtime (1 to 2 mg/kg, up to 75 mg). Newer nonsedating (or less-sedating) antihistamines should be considered when sedation or impairment of performance or cognitive function is an issue. Dosages of the nonsedating antihistamines are generally higher than required for allergic rhinitis.
Tar Preparations
Can play a role in atopic dermatitis therapy as an alternative
or adjunct to topical corticosteroids. Were used extensively in the past. Are often beneficial for scalp treatment (i.e., shampoos). Are useful for chronic lichenified atopic dermatitis. Have side effects including folliculitis and occasional photosensitivity. Are messy and stain clothing and skin (reversibly).
Topical immunosuppressants
Protopic (tacrolimus) - 0.03% and 0.1% ointment macrolide dervative inhibits t-lymphocyte activation improvement with 2 weeks of use apply 2 times a day avoid wetting skin before or after use 0.03% ointment for children 2-15 years of age Elidel 1% cream (pimecrolimus) macrolataim derivative inhibits T-lymphocyte activation improvement with 15 days of use apply 2 times a day use in children older than 2 years of age
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A Protocol for Treating Atopic Dermatitis

First-line therapy: Hydration of skin Avoidance of causal factors (i.e., environmental control of allergens/irritants) Topical corticosteroids in conjunction with oral antihistamines Treating prolonged and/or severe symptoms: Explore family, personal, and environmental factors, and compliance. Basic elimination diet (when suggested by history, especially for children under 5 years old). Targeted elimination diet (under specialist consultation). Course of oral corticosteroids: o Prednisone (0.5 to 1.0 mg/kg) with tapering over 2 to 3 weeks. Consider referral for consultation and/or comanagement with specialist.
Special Considerations for Treating Atopic Dermatitis

Antibiotics Indicated when the patient has a secondary bacterial infection. Macrolide antibiotics (e.g., erythromycin) are usually beneficial. For patients with macrolide-resistant Staphylococcus aureus, a penicillinase-resistant penicillin (dicloxacillin, oxacillin, or cloxacillin) maybe preferred. First-generation cephalosporins (cephalexin, cefadroxil) are effective against both staphylococci and streptococci.
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Atopic Dermatitis
Antiviral Agents Systemic acyclovir is recommended for superinfection with herpes simplex virus (eczema herpeticum). Severe infection may be life threatening. Consider referral to an allergy/immunology or dermatology specialist. Antifungal Agents (topical or oral) Antifungal treatment may improve atopic dermatitis in dermatophyte-infected patients.
Evalute for immunotherapy.

Allergen immunotherapy is not indicated for the treatment of atopic dermatitis.
Well-controlled studies are still required to determine the role of allergen immunotherapy in the treatment of atopic dermatitis.
Allergen immunotherapy is not indicated for the
treatment of atopic dermatitis. Well-controlled studies are still required to determine the role of allergen immunotherapy in the treatment of atopic dermatitis. Allergen immunotherapy may be indicated for accompanying allergic rhinitis or asthma.
The educational tips included in Volume 1: Patient Education, page 71, are appropriate for the patient with atopic dermatitis.
Education and regular follow-up are important.
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Consultation and/or comanagement with an allergy/immunology specialist for assistance in diagnosis and management is recommended for:
Skin tests Targeted elimination diets Identification of causal factors Test interpretation DBPCFC (double-blind, placebo-controlled,
food challenge)
Referral to an allergy/immunology and/or dermatology specialist is recommended for:

Consider referral for patients with:
Coexisting asthma,
Patients failing to respond to treatment with
allergic rhinitis, or allergic conjunctivitis Impaired quality of life (lost work days, lost school days, sleep disturbance) Poorly controlled pruritus Psychosocial complications
topical corticosteroids or antihistamines Complications Severe or persistent disease: o Patient requiring long-term or frequent use of potent topical corticosteroids (e.g., Groups < III, see pages 127) o 20% general skin involvement or 10% skin involvement affecting eyelids, hands, intertriginous areas, and not responsive to first-line therapy o Hospitalized patient o Recurrent infections o Erythroderma or extensive exfoliation Assistance with diagnosis and management Patient education
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Atopic Dermatitis
Tips for Patients with Atopic Dermatitis

DO:
Use soaps that are not drying. Use tepid (not hot) water for bathing, for no more than
3 to 5 minutes. Wear open-weave, loose-fitting cotton or cotton blend garments. Wash new clothing before wearing. Use liquid, not powdered, laundry detergent. Use minimal fabric softener and a second rinse cycle when laundering clothes and bedding. Use air conditioning during hot weather. Minimize exposure to allergens and irritants that cause symptoms. Use nonirritating sunscreens before sun exposure. Keep fingernails trimmed short. Sleep with cotton socks on feet, cotton gloves on hands.
DONT:
Use drying soaps, chemicals, or solvents on skin. Use astringents or skin products containing alcohol. Wear abrasive or heavy clothing. Stay out in extremely hot or cold, or wet or dry
environments. Get sunburned. Use sunscreens with irritating ingredients. Participate in sports that cause intense perspiration and physical contact. Bathe too frequently. Scrub skin excessively. Use anything more abrasive than a damp washcloth while bathing. Scrub skin with brushes or use a buff-puff.
REMEMBER THAT:
Sun exposure is beneficial, but sweating may cause
itching. o Avoid sunscreens containing irritating ingredients. Swimming may be good, but shower immediately after to rinse off chlorine. o Apply skin lubricant.
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References
Boguniewicz m, Leung DYM. Atopic Dermatitis. In Middleton E, Reed CE, Ellis EF, et al (eds). Allergy Principles and Practice, St Louis, MO: Mosby, 5th edition 1998: 1123-1134. Brehler R, Hildebrand A, Luger TA. Recent developments in the treatment of atopic eczema. J Am Acad Dermatol 1997; 36: 983-994. Cooper KD. Atopic dermatitis: recent trends in pathogenesis and therapy. J Invest Dermatol 1994; 102: 128-137. David TJ, Patel L, Ewing CI, Stanton RHJ. Dietary regimens for atopic dermatitis in childhood. J Royal Soc Med 1997; 90: S9-14. Finlay AY. Measurement of disease activity and outcome in atopic dermatitis. Br J Dermatol 1996; 135: 509-515. Fireman P . Atopic Dermatitis. In: Fireman P , Slavin R, (eds). Atlas of Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 233-248. Friedmann PS, Tan BB, Musaba E, Strickland I. Pathogenesis and management of atopic dermatitis. Clin Exp Allergy 1995; 25: 799-806. Graham-Brown R. Managing adults with atopic dermatitis. Dermatologic Clinics 1996; 14: 531-537. Halbert AR, Weston WL, Morelli JG. Atopic dermatitis: is it an allergic disease? J Am Acad Dermatol 1995; 33: 1008-1018. Hanifin JM, Klas PA. The spectrum of cutaneous patch-test reactions in patients with atopic dermatitis. Clin Rev Allergy Immunol 1996; 14: 225-240. Hannuksela M, Kalimo K, Lammintausta K, et al. Dose ranging study: cetirizine in the treatment of atopic dermatitis in adults. Ann Allergy 1993; 70: 127-133. Li JT, Bernstein IL, Berger WE, et al. Disease management of atopic dermatitis: A practice parameter. Ann Allergy Asthma Immunol 1997; 79: 197-204. Landow K. Atopic dermatitis: current concepts support old therapies and spur new ones. Postgrad Med 1997; 101: 101-118. Leung DYM. Atopic dermatitis: immunobiology and treatment with immune modulators. Clin Exp Immunol 1997; 107: S25-30. Leung DYM. Atopic dermatitis: the skin as a window into the pathogenesis of chronic allergic diseases. J Allergy Clin Immunol 1995; 96: 302-318. Linna O, Kokkonen J, Lahtela P , et al. Ten-year prognosis for generalized infantile eczema. Act Paediatr 1992; 81: 1013-1016. Przybilla B, Eberlein-Konig B, Rueff F. Practical management of atopic eczema. The Lancet 1994; 343: 1342-1346. Resnick SD, Hornung R, Konrad TR. A comparison of dermatologists and generalists: management of childhood atopic dermatitis. Arch Dermatol 1996; 132: 1047-1052. Reynolds NJ. Recent advances in atopic dermatitis. J Royal College Physicians London 1997; 31: 241-245. Ring J, Brockow K, Abeck D. The therapeutic concept of "patient management" in atopic eczema. Allergy 1996; 51: 206-215. Romeo SP . Atopic dermatitis: the itch that rashes. Ped Nursing 1995; 21: 157-163. Roth HL. Atopic dermatitis. In: Conn HF. Conns current therapy. Philadelphia, 1998: 836-837. Rothe MJ, Grant-Kels JM. Atopic dermatitis: an update. J Am Acad Dermatol 1996; 35: 1-13. Sampson HA. Food sensitivity and the pathogenesis of atopic dermatitis. J Royal Soc Med 1997; 90: S2-8. Sampson HA. The immunopathogenic role of food hypersensitivity in atopic dermatitis. Acta Derm Venerol 1992; 176: 34-37. Seymour JL, Keswick BH, Hanifin JM, et al. Clinical effects of diaper types on the skin of normal infants and infants with atopic dermatitis. J Am Acad Dermatol 1987; 17: 988-997.
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Schultz Larsen F. the epidemiology of atopic dermatitis. Monograph Allergy 1993; 31: 9-28. Singleton JK. Pediatric dermatoses: three common skin disruptions in infancy. Nurse Practitioner 1997; 22: 32-50. Stoughton RB. Vasoconstrictor assayspecific applications. In: Maibach HI, Surber C, (eds.) Topical Steroids. Basel, Switzerland: Darger 1992: 42-53. Williams HC. On the definition and epidemiology of atopic dermatitis. Dermatol Clinics 1995; 13: 649-657. Working Group on Atopic Dermatitis. Disease management of atopic dermatitis: a practice parameter. Ann Allergy Asthma Immunol 1997; 79: 197-211.
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136
hinosinusitis is an inflammation of the paranasal sinuses that occurs with rhinitis. It: Rarely occurs in the absence of nasal inflammation. Is common in patients with perennial rhinitis.
Rhinosinusitis:
Rarely occurs in the
Classification of Rhinosinusitis
Acute Rhinosinusitis
Is a common infection. Lasts for up to 3 weeks. Often follows a viral upper respiratory infection (URI). o If URI symptoms worsen after 5 days, or persist after
absence of nasal inflammation. Frequently occurs in patients with perennial rhinitis.
7 days, then acute rhinosinusitis should be suspected. o The incidence of acute, infectious rhinosinusitis may increase with seasonal allergic rhinitis. o Some young children may develop an acute episode with high fever, purulent nasal discharge, and toxicity.
Acute rhinosinusitis is a common infection that often follows a viral upper respiratory infection. Consider acute rhinosinusitis if URI symptoms:
Worsen after 5 days
Recurrent Acute Rhinosinusitis

Four or more episodes of acute rhinosinusitis per year
separated by at least 8 weeks of symptom-free intervals.
or Persist after 7 days
Subacute (Persisting Acute) Rhinosinusitis

Lasts between 3 weeks and 3 months.
Chronic Rhinosinusitis
Is a complex of symptoms associated with: o Inflammation of the sinuses characterized by
persistent symptoms of acute rhinosinusitis lasting longer than 3 months. o A lack of response to treatment. o A positive imaging study. May have superimposed bouts of acute rhinosinusitis.
Associated Associated Disease: Disease: Rhinosinusitis Rhinosinusitis
137
Common causes: o Infection (i.e., infectious rhinosinusitis) o Mechanical obstruction o Obstruction due to an allergic process o Primary eosinophilic inflammation of nasal and sinus
Eosinophilic inflammation of the sinuses may be associated with asthma and rhinitis (allergic or nonallergic) and should be distinguished from rhinosinusitis of an infectious or obstructive nature.
mucosa Rare cases may be due to: o An immunologic reaction to a fungal agent. o A fungal infection (e.g., Aspergillus). Invasive fungal infections are more likely to occur in: Geographic areas with high humidity. Diabetes mellitus patients. More than 50% of moderate to severe asthmatics have chronic rhinosinusitis. o In the asthma patient, the eosinophilic inflammation often involves the sinuses as well as the nose and bronchi. o Clinical evidence of infection is often absent, except during acute purulent episodes.
Tips to distinguish chronic from acute rhinosinusitis:

The symptoms of chronic rhinosinusitis may be
less severe than those of acute rhinosinusitis, but may persist for months to years. The primary complaint of chronic rhinosinusitis is usually nasal obstruction or discharge. Chronic cough (particularly during the night or upon awakening in the morning) is often a presenting symptom of chronic rhinosinusitis. o In children, it may be the only symptom.
138
Who is at risk for rhinosinusitis?

Clinical and environmental factors that predispose an individual to infectious rhinosinusitis:
Local More common Upper respiratory infection (usually viral) Allergic rhinitis Nonallergic rhinitis Less common Overuse of topical decongestants Hypertrophied adenoids* Deviated nasal septum Concha bullosa Malformed uncinate process Prominent ethmoid bulla Nasal polyps Tumors Foreign bodies* Swimming and diving* Cigarette smoke Cocaine abuse Barotrauma Dental diseases GERD
*
Systemic Immunodeficiency (IgG or IgA)* Cystic fibrosis* Bronchiectasis Immotile cilia syndrome* Wegeners granulomatosis Acquired immunodeficiency syndrome* Immunosuppressive therapy Kartageners syndrome
Particularly apply to children.
139
Diagnosing the Patient with Rhinosinusitis

In general, the diagnosis of rhinosinusitis is made by
the constellation of symptoms plus confirmatory physical findings. Treatment is initiated on a presumptive basis.
Signs and Symptoms Associated with Rhinosinusitis

Major
Facial pain and/or pressure Facial fullness Nasal obstruction/blockage Nasal discharge/purulence o Discolored postnasal drip Hyposmia/anosmia Cough
* *
Minor
Headache Halitosis
*
Fever Fatigue
* *
Dental pain
Ear fullness/pain/pressure
More common in adults.
Differentiating acute infectious rhinosinusitis from seasonal allergic rhinitis:

Acute Rhinosinusitis Seasonal Allergic Rhinitis Itchy, runny nose Paroxysmal sneezing Thin, watery nasal discharge Seasonal symptoms
Allergic rhinitis should always be suspected, evaluated, and treated.
Nasal obstruction/ congestion Pressure with pain Thick, discolored nasal discharge Fever Cough
140
Ethmoid sinus Sphenoid sinus
Frontal sinus Maxillary sinus
The signs and symptoms of rhinosinusitis may reveal which sinus is primarily affected.
Sinus Maxillary Ethmoid Key Signs and Symptoms Toothache or pain over cheekbone Medial canthal pain or pressure Periorbital headache Frontal Sphenoid Severe frontal headache Frontal tenderness Severe headache with multiple locations or occipital area
Diagnostic Procedures
Imaging
Imaging is used when the patient has failed to respond
to adequate pharmacotherapy (e.g., chronic rhinosinusitis). Types of imaging used for chronic or recurrent acute rhinosinusitis: o Coronal computerized tomography (CT) scan o Sinus x-rays
141
Limited Screening Coronal CT Scan Can identify involved sinuses: o Maxillary o Frontal o Ethmoid o Sphenoid Is not optimal for evaluation of ostiomeatal complex. Extensive Coronal CT Scan Use when: o Defining pathological changes in the paranasal sinuses. o Surgical intervention is being considered. o Complications are suspected. o Diagnosis is in question. Plain Sinus X-rays No longer considered a useful diagnostic modality in recurrent or chronic rhinosinusitis in adults. May still be used in some areas that do not have screening CT scans. A Waters x-ray may suffice for acute rhinosinusitis. o Is an adequate screening procedure in children.
Nasal Endoscopy
Helps to: o Pinpoint the source of purulence within the middle
meatus. o Identify anatomic abnormalities. o Guide nasal cultures from the ostiomeatal complex.
Other diagnostic tests may be considered in some circumstances:

Identification of allergens to which the patient is
sensitive o Tests for specific IgE Mucociliary clearance measurements Nasal airway assessment
142
Tips for diagnosing rhinosinusitis:

Failure of symptoms to resolve after a typical
URI is an important clinical clue to the diagnosis of acute rhinosinusitis. o Symptoms may be indolent and smoldering. o Symptoms may not be considered important by the patient. Nasal discharge and post-nasal drip may turn from clear to yellow or green. o Diagnosis is supported by visual confirmation of purulent discharge from the area of the sinus ostia. Low-grade fever may develop or persist. Frontal head discomfort and facial pain is often worse on bending over or straining. Fever is usually not a finding for patients with chronic rhinosinusitis. The physical may be normal.
Rhinosinusitis is a common cause of asthma exacerbations.

Consider rhinosinusitis
for asthma exacerbations that do not respond to aggressive treatment.
Some acute episodes need aggressive treatment:

Acute frontal (or sphenoid) rhinosinusitis
is a potential medical emergency. o Severe neurologic complications can occur. Acute ethmoid rhinosinusitis can progress to subperiosteal abscess formation. Development of acute visual symptoms may indicate spread of infection to structures near the optic nerve. o Requires immediate evaluation by an otolaryngologist and/or ophthalmologist. Perinasal cellulitis can lead to cavernous sinus thrombosis. o Follow carefully. Referral to an otolaryngologic allergy specialist is recommended.
143
Managing the Patient with Infectious Rhinosinusitis

Management goals:
Control infection. Reduce tissue edema. Facilitate drainage. Maintain patency of
Management of rhinosinusitis includes: o Using appropriate medications. o Palliative measures. o Surgery, when aggressive medical management
has failed.
ostia. Break pathological cycle leading to chronic rhinosinusitis.
Palliative Treatment
Nasal lavage with warm salt water (with or without
baking soda). Inhalation of warm mist through the nose for 10 to 15 minutes, 3 to 4 times per day, may help.
Pharmacologic Management
Antibiotic Therapy
Before selecting antibiotic therapy for the treatment of
Common bacterial pathogens in acute rhinosinusitis:

Streptococcus
rhinosinusitis, consider: o Local sensitivity patterns. o Potential for resistance. Common bacterial pathogens in acute rhinosinusitis: o Streptococcus pneumoniae o Haemophilus influenzae o Moraxella catarrhalis (primarily in children) o Streptococcal species Initial choice of antibiotic for an isolated episode of acute rhinosinusitis: Amoxicillin or trimethoprim/sulfamethoxazole (TMP/SMX) in adults and erythromycin ethylsuccinate/sulfisoxazole acetyl in children, may be effective, inexpensive, and well tolerated. o Erythromycin and ceflacor are generally not effective in the treatment of rhinosinusitis. o CDC estimates that 25% of S. pneumoniae infections are resistant to TMP/SMX. Significant resistance is also seen with cefixime. o Resistance to amoxicillin and cefaclor are common. Local sensitivity patterns that are associated with high prevalence of resistance may justify the use of other antibiotics. Assess response to treatment after 3 to 5 days, and change antibiotic if needed.
pneumoniae Haemophilus influenzae Moraxella catarrhalis (primarily in children) Streptococcal species
144
Choice of antibiotic for repeated episodes of acute or recurrent rhinosinusitis: The choice of antibiotic depends on the: Suspected bacteria Local sensitivity patterns Patients allergy history Consider: Amoxicillin/clavulanate potassium (Augmentin ) Azithromycin (Zithromax ) Cefdinir (Omnicef ) Cefpodoxime proxetil (Vantin ) Cefprozil (Cefzil ) Ceftibuten (Cedax ) Ceftizoxime (Cefizox ) Cefuroxime axetil (Ceftin ) Clarithromycin (Biaxin ) Levofloxacin (Levaquin ) Loracarbef (Lorabid ) Gatefloxacin (Tequin ) Cross-allergenicity can exist between penicillin and cephalosporin.
Intranasal Corticosteroids
Indicated to treat allergic and nonallergic rhinitis and
nasal polyps. Useful maintenance therapy for chronic rhinosinusitis. Should not be used long-term for acute rhinosinusitis. Consider for patient with recurrent rhinosinusitis.
Use intranasal corticosteroids for the patient with:

Chronic rhinosinusitis. Recurrent
rhinosinusitis.
Decongestants
Oral and topical decongestants may be beneficial
for symptoms. Topical agents should be used with caution because of problems associated with prolonged use: Rebound vasodilation Congestion Rhinitis medicamentosa
Avoid prolonged use of topical decongestants.
145
Oral Mucolytics
May help to: o Thin discharge o Promote drainage o Assist resolution Clinical effectiveness is uncertain.
Surgery
Consider surgery when appropriate medical management of rhinosinusitis has failed.
Surgery for chronic or recurrent acute rhinosinusitis is
generally reserved for patients for whom appropriate aggressive medical management has failed. The goals of surgery are to: o Reduce recurrences of rhinosinusitis. o Remove obstruction(s) to sinus drainage (e.g., anatomical abnormalities, polyps). o Alleviate acute complications Indications for surgery: o Bilateral extensive and massive obstructive nasal polyposis with complications. o Complications of adult rhinosinusitis, including: Potts puffy tumor Brain abscess Meningitis o Complications of childhood rhinosinusitis (e.g., meningitis). o Chronic adult rhinosinusitis with mucocele or mucopyocele formation. o Invasive or allergic fungal rhinosinusitis. o Tumor(s) of nasal cavity and paranasal sinuses. o Cerebrospinal fluid rhinorrhea.
146
When should surgery be considered?

Persistently opacified maxillary sinus requiring
therapeutic or diagnostic intervention. Complications from adenoidal enlargement (e.g., sleep disturbance, eustachian tube dysfunction, rhinosinusitis). Nasal septal deviation and/or other nasal anatomical abnormalities (e.g., concha bullosa). Difficult-to-control asthma and the presence of chronic rhinosinusitis. Presence of chronic infectious rhinosinusitis. Subperiosteal orbital abscess.
Specific Considerations for Treating Rhinosinusitis

Acute Rhinosinusitis
Length of treatment is typically 10 to 14 days. o Patient should be symptom-free for 7 days. o Treatment for up to 21 days is sometimes necessary.
For recurrent acute rhinosinusitis, consider referral to an allergy/ immunology or an otolaryngologic allergy specialist for the:
Adult who has had
Recurrent Acute Rhinosinusitis

Length of treatment is typically 10 to 14 days. o Patient should be symptom-free for 7 days. o Treatment for up to 21 days is sometimes necessary. Recurrent acute rhinosinusitis is a more common
more than 4 episodes in 12 months. Child who has had 3 or more episodes in 6 months, or 5 or more episodes in 12 months.
problem in children. Long-term use of intranasal corticosteroids may be helpful. Consider referral to an allergy/immunology or an otolaryngologic allergy specialist: o For an adult who has had more than 4 episodes in 12 months. o For a child who has had 3 or more episodes in 6 months, or 5 or more episodes in 12 months.
Acute, recurrent acute, and subacute (persisting acute) rhinosinusitis are typically treated for 10 to 14 days.
Patient should be
symptom-free for 7 days. Treatment for up to 21 days is sometimes necessary.
Subacute (Persisting Acute) Rhinosinusitis

Treat like recurrent acute rhinosinusitis.
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Chronic Infectious Rhinosinusitis Chronic infectious rhinosinusitis may need up to 6 weeks of antibiotic treatment. Consider:
Topical intranasal
If unresponsive, broaden antibiotic coverage. o In adults, consider:
corticosteroids. A short course of oral corticosteroids, unless contraindicated. Nasal irrigation with bulb pik. Referral to an allergy/immunology or an otolaryngologic allergy specialist if symptoms do not improve.
Ciprofloxacin (no anaerobic coverage) Levofloxacin Adding metronidazole to cover anaerobic organisms o In children consider: Clindamycin Adding metronidazole to cover anaerobic organisms Treat for up to 4 to 6 weeks. o If symptoms do not improve, consider referral to an allergy/immunology or an otolaryngologic allergy specialist. Consider topical intranasal corticosteroids. o A short course of oral corticosteroids may be helpful, unless contraindicated. Have patient use nasal irrigation with bulb pik.
Four general principles for managing allergic diseases

1. Avoid factors that cause symptoms. 2. Use appropriate medications. 3. Evaluate for immunotheropy. 4. Educate and follow-up.
Additional Management Considerations for the Allergic Rhinosinusitis Patient

Treat concomitant rhinitis. Determine allergens to which the patient is sensitive. Educate the patient about allergen and irritant
avoidance techniques and general self-management skills. Consider immunotherapy. Referral to an allergy/immunology or an otolaryngologic allergy specialist is recommended.
Managing allergic rhinitis can improve rhinosinusitis and asthma symptoms.
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More than 50% of moderate to severe asthmatics have chronic rhinosinusitis.

In the asthma patient, the eosinophilic
inflammation often involves the sinuses as well as the nose and bronchi. Clinical evidence of infection is often absent, except during acute purulent episodes.
In asthmatic patients with appropriate symptoms or who are not responding to therapy, consider a superimposed acute rhinosinusitis infection.
Upper airway symptoms
Aspirin and NSAID sensitivities are common in adult nonallergic rhinosinusitis patients, especially those who have nasal polyps.
This is referred to as Samter s Triad. Primary treatment is avoidance of aspirin and NSAID products, though some patients demonstrate improvement with oral aspirin desensitization.
may not be reported by the patient. Treatment of infectious rhinosinusitis frequently improves asthma symptoms.
Special Considerations for Treating Rhinosinusitis in Children

The diagnosis of rhinosinusitis is often missed in
children. o Children may be diagnosed with concurrent otitis media, but not treated long enough to cure the sinus component of the infection. This can result in subacute disease. Rhinosinusitis is a common reason for asthma exacerbations. o May be a silent reason for exacerbations that respond poorly to aggressive therapy, including oral corticosteroids.
The diagnosis of rhinosinusitis is often missed in children.
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The most common symptoms of rhinosinusitis in children are:

Cough Rhinorrhea
The most common symptoms of rhinosinusitis in
It is relatively uncommon for children to complain of:

Sinus pressure Headache Facial pain Tooth pain
children are: o Cough o Rhinorrhea It is relatively uncommon to hear complaints of: o Sinus pressure o Headache o Facial pain o Tooth pain Rhinosinusitis may be a manifestation of immunodeficiency. o Consider referral for a thorough immune evaluation for patients with recalcitrant disease. o Patients with immunodeficiency are less likely to have an optimal response to surgical intervention. Rhinosinusitis with nasal polyposis indicates evaluation for cystic fibrosis. Other risk factors include structural and environmental considerations: o Adenoid hyperplasia o Swimming/diving o Passive tobacco smoke exposure Long-term use of intranasal corticosteroids may be helpful in children with recurrent rhinosinusitis. o Patients should be seen at frequent (3 to 6 months) intervals for: Evaluation of the nasal mucosa. Assessment of growth rate. o Dosage should be tapered to the least amount that is effective.
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Consider referral to an allergy/ immunology or an otolaryngologic allergy specialist for consultation and/or comanagement when:
The condition or its treatment interferes with
the patients performance causing significant loss of school or work on a chronic or recurrent basis. The patients quality of life is significantly affected despite treatment. There are complications of rhinosinusitis. The condition becomes chronic, persists for several months, or recurs 3 to 4 times per year, despite treatment. There is need for allergy or immunologic testing. There is need for complex pharmacology, such as with antibiotic allergies or resistant pathogens. Allergic fungal rhinosinusitis is present.
When is referral to an otolaryngologic allergy specialist preferred?

When anatomical defects exist which obstruct
the sinus outflow track, including the ostiomeatal complex and adenoidal tissues, and are thought to be contributing to recurrent or chronic rhinosinusitis. When nasal polyps obstruct the sinus drainage and persist despite appropriate medical treatment. For biopsy of the nasal mucosa to rule out granulomatous disease, neoplasms, ciliary dyskinesia, or fungal infections. When maxillary antral puncture is required for diagnosis and/or treatment. For recurrent rhinosinusitis associated with middle ear disease. If adenoidectomy is being considered.
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References
Anand VK, Osguthorpe JD, Rice D. Surgical management of adult rhinosinusitis. Otolaryngol Head Neck Surg 1997; 117: S50-52. Arjmand EM, Lusk RP . Management of recurrent and chronic sinusitis in children. Am J Otolaryngol 1995; 16: 367-382. Bernstein DI. Nasal polyposis, sinusitis, and nonallergic rhinitis. In Patterson R, Grammer LC, Greenberger PA (eds). Allergic Diseases, 5th ed. Philadelphia: Lippincott-Raven, 1997: 425-437. Cook PR, Nishioka GJ. Allergic rhinosinusitis in the pediatric population. Otolaryngol Clin North Am 1996; 29: 39-56. Corey JP , Delsupehe KG, Ferguson BJ. Allergic fungal sinusitis: allergic, infectious, or both? Otolaryngol Head Neck Surg 1995; 113: 110-119. Davidson TM, Hudgins PA, Kennedy DW. Wholl benefit from endoscopic sinus surgery? Patient Care, June 1996: 178-196. Derebery MJ. Otolaryngic allergy. Otolaryngol Clin North Am 1993; 26: 593-611. deShazo RD, Swain RE. Diagnostic criteria for allergic fungal sinusitis. J Allergy Clin Immunol 1995; 96: 24-35. Dohlman AW. Role of antibiotic and non-antibiotic therapy in the treatment of sinusitis with an allergic basis. Clin Exp Allergy 1994; 24: 1094-1097. Ferguson B. Acute and chronic sinusitis. Postgrad Med. 1995: 9745-9757. Ferguson BJ, Bensimhon D. Whats causing your patients rhinosinusitis? J Respir Dis 1997; 18: 321-334. Gungor A, Corey JP . Pediatric sinusitis: a literature review with emphasis on the role of allergy. Otolaryngol Head Neck Surg 1997; 116: 4-15. Joint task force on practice parameters. Parameters for the diagnosis and management of sinusitis. J Allergy Clin Immunol 1998; 102: S107-144. Kaliner MA. Allergy care in the next millennium: guidelines for the specialty. J Allergy Clin Immunol 1997; 99: 729-734. Kaliner MA. Human Host defense and sinusitis. In: Gershen ME, Incaudo GA (eds). Diseases of the sinuses. New Jersey: Humana Press. 1996: 53-60. Kaliner MA. Medical management of sinusitis. Am J Med Sci 1998; 316: 21-28. Kaliner MA, Osguthorpe JD, Fireman P , et al. Sinusitis: bench to bedside. J Allergy Clin Immunol 1997; 99: S829-848. Karlsson G, Holmberg K. Does allergic rhinitis predispose to sinusitis? Acta Otolaryngol (Stockh) 1994; 515: S26-29. Mackay IS, Durham SR. The classification and diagnosis of rhinitis. In: Kay AB (ed). Allergy and Allergic Diseases. Vol 2. Malden, MA: Blackwell Science Ltd 1997; 1293-1299. Lanza DC, Kennedy DW. Adult rhinosinusitis defined. Otolaryngol Head Neck Surg 1997; 117: S1-7. Mabry RL. Allergic and infective rhinosinusitis: differential diagnosis and interrelationship. Otolaryngol Head Neck Surg 1994; 111: 335-339. McNally PA, White MV, Kaliner MA. Sinusitis in an allergists office: analysis of 200 consecutive cases. Allergy Asthma Proceedings 1997; 18: 169-175. Nelson HS. Diagnosis and management of severe asthma in the adult. In: Szefler SJ, Leung DY (eds.) Severe asthma pathogenesis and clinical management. New York: Marcel Dekker, 1996: 397-419. Parsons DS. Chronic sinusitis: a medical or surgical disease ? Otolaryngol Clin North Am 1996; 29: 1-9. Parsons DS, Wald ER. Otitis media and sinusitis: similar diseases. Otolaryngol Clin North Am 1996; 29: 11-25. Reuler J, Lucas L, Kumar K. Sinusitis: a review for generalists. West J Med 1995; 163: 40-48.
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Rowe-Jones JM. The link between the nose and lung, perennial rhinitis and asthma is it the same disease? Allergy 1997; 52: S20-28. Senior BA, Kennedy DW. Management of sinusitis in the asthmatic patient. Ann Allergy Asthma Immunol 1996; 77: 6-19. Shapiro GG, Rachelefsky GS. Introduction and definition of sinusitis. J Allergy Clin Immunol 1992; 90: 417-418. Slavin RG. Nasal polyps and sinusitis. J Am Med Assoc 1997; 278: 1849-1854. Spector S. Overview of comorbid associations of allergic rhinitis. J Allergy Clin Immunol 1997; 99: S773-780. Weinberg EA, Brodsky L, Brody A, Pizzuto M, Stiner H. Clinical classification as a guide to treatment of sinusitis in children. Laryngoscope 1997; 107: 241-246.
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titis media can be an acute or chronic inflammation of the middle ear.
The patient may experience recurrent acute
episodes (recurrent otitis media).

May be attributed to eustachian tube dysfunction
Otitis media is the most common childhood disease requiring physician care. Otitis media is classified as:
Acute otitis media Recurrent acute otitis
and accumulation of serous or purulent fluid in the middle ear cavity.

Most commonly occurs in infants and children
younger than 4 years, but can occur at any age.

Often associated with rhinitis. May be of infectious and/or allergic causation. It may be: o Acute o Recurrent acute o With effusion o Chronic with effusion
media Otitis media with effusion Chronic otitis media with effusion
Characteristic Signs and Symptoms

The earliest signs of acute otitis media are ear pain and
discomfort. o The patient may be irritable. o The child may pull on the affected ear. o Infant may fail to feed. Snoring, mouth-breathing, or nasal obstruction may suggest adenoidal obstruction. Hearing loss may or may not be present. Nonspecific signs associated with otitis media: o Fever o Anorexia o Headache o Vomiting o Apathy o Diarrhea
Children with persistent otitis media with effusion or recurrent otitis media often experience a conductive hearing loss with the potential for defects in speech and language development and school performance.
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Natural History of Otitis Media

Risk factors for otitis media:
Viral upper respiratory infection Allergic rhinitis Eustachian tube dysfunction Cigarette smoke exposure Age (< 1 yr) Race (American Indians) Sinusitis Cilia dysfunction Male sex Immunodeficiency Fall/winter season Genetic predisposition Daycare Siblings Adenoidal enlargement Cleft palate
Allergy plays a role in recurrent or chronic otitis media. o As many as 50% of children older than 3 years with
As many as 50% of children older than 3 years with chronic otitis media have confirmed allergic rhinitis.
chronic otitis media have confirmed allergic rhinitis. o Eustachian tube dysfunction is a key contributing factor to acute otitis media. An underlying eustachian tube dysfunction may be present in some infants and young children. Tubal function becomes further compromised in the presence of allergic rhinitis. o Eustachian tube dysfunction is common in infants and younger children because: The eustachian tube has less cartilage support. The eustachian tube is less angulated. The tensor veli palatini muscle is less efficient. o Interactions between viruses and allergens and their respective immune/inflammatory responses may predispose to development of otitis media.
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Eustachian tube dysfunction, middle ear negative pressure, and/or nasal inflammation (e.g., allergy, URI) can contribute to otitis media development.
Adult Child
Orientation, short length, and patency of child's eustachian tube causes decreased protective function.
2 3
Nasal secretions enter middle ear through eustachian tube.
Eustachian tube dysfunction, a key contributing factor to otitis media, is common in infants and younger children because:
The eustachian tube has
Secretions create obstruction, causing inflammation and dysfunction.
less cartilage support. The eustachian tube is less angulated. The tensor veli palatini muscle is less efficient.
Diagnosing the Patient with Otitis Media

A detailed medical history and physical examination
using a pneumatic otoscope are usually sufficient to establish the diagnosis. Consider: o Duration of symptoms o When symptoms occur o Previous history of and treatment for ear disease o Family history of atopic disease o Presence of associated allergic disease (e.g., allergic rhinitis) o Environmental history to identify allergic or irritant causal factors o Information on the other risk factors such as: Daycare Bottle feeding while lying down Smoking in household
Recurrent otitis media or otitis media with effusion:

3 episodes in
6 months or 4 episodes in 12 months
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Evaluate for underlying factors prior to initiating
preventative treatments: o Allergy o Rhinosinusitis o Hypertrophic adenoids o Immunodeficiency o Food intolerance reaction Based on anecdotal evidence Requires further clinical investigation
History and physical examination using a pneumatic otoscope are usually sufficient to establish the diagnosis of otitis media.
Normal tympanic membrane.

Reprinted from Bull TR. Examination of the ear. In: Bull TR (ed). Color atlas of ENT diagnosis. London: Year Book Medical Publishers, Inc; 1974: 12-13. By permission of publisher Mosby.
Acute otitis media.

Reprinted from Bull TR. The tympanic membrane and middle ear. In: Bull TR (ed). Color atlas of ENT diagnosis. London: Year Book Medical Publishers, Inc; 1974: 92-93. By permission of publisher Mosby.
Otitis media with effusion.

158
Does the patient need further allergy evaluation? Consider whether:

There is a personal or family history of allergy
(e.g., rhinitis, asthma, atopic dermatitis). Sneezing, rhinorrhea, and nasal congestion are prominent and present year-round or seasonally. o Interfere with normal activities. o Improve with antiallergy medications (e.g., antihistamines, intranasal cromolyn sodium, intranasal corticosteroids). The patient is exposed to allergens (e.g., cat, dog, dust mites, pollens). The nasal mucosa appears pale and boggy.
Managing the Patient with Otitis Media

Preventive Therapies
Use to treat recurrent otitis media o Prophylactic antibiotic o Tympanostomy tube insertion with or without
adenoidectomy
A flanged Teflon tube (grommet) may be used to prevent middle ear fluid recurrence.
Four general principles of allergy management

1. Avoid factors that cause symptoms. 2. Use appropriate medications. 3. Evaluate for immunotherapy. 4. Educate and follow-up.
Inserted tube ventilates the middle ear.

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Therapeutic Treatments
Early treatment of otitis media is important.
Children with persistent otitis media with effusion or recurrent otitis media often experience conductive hearing loss with the potential for speech defects affecting: Language development School performance
When otitis media is associated with allergic rhinitis,
When otitis media is associated with allergic rhinitis, control of allergic rhinitis frequently results in the resolution of otitis media.
control of allergic rhinitis frequently results in the resolution of otitis media. If associated allergic rhinitis is documented, intensive allergy therapy is indicated. Consider: o Allergen avoidance o Antihistamine therapy o Intranasal corticosteroids and/or occasional short courses of oral corticosteroids may be useful for reducing inflammation and eustachian tube obstruction o Intranasal cromolyn sodium o Allergen immunotherapy Decongestants are widely used to treat the associated eustachian tube dysfunction, but their clinical efficacy has not been established.
Otitis media is multifactorial in nature. The best therapeutic results for chronic or complicated problems are often obtained when the patient is managed by a coordinated effort involving the primary care provider, otolaryngologic allergy specialist and/or allergy/immunology specialist.
Consider referral to an allergy/ immunology specialist or otolaryngologic allergy specialist for consultation or comanagement, particularly for chronic or complicated cases.
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References
Bernstein JM. The role of IgE-mediated hypersensitivity in the development of otitis media with effusion: a review. Otolaryngol Head Neck Surg 1993; 109: 611-20. Bernstein JM, Doyle WJ. Role of IgEmediated hypersensitivity in otitis media with effusion: pathophysiologic considerations. Ann Otol Rhinol Laryngol 1994; 103: 15-19. Bernstein JM. Role of allergy in Eustachian tube blockage and otitis media with effusion: a review. Otolaryngol Head Neck Surg 1996; 114: 562-568. Bluestone CD, Klein JO. Otitis media, atelectasis, and eustachian tube dysfunction. In: Bluestone CD, Stool SE, Scheetz MD (eds). Pediatric Otolaryngology, Vol 1. Philadelphia: WB Saunders, 1990: 320-386. Fireman P . Otitis media. In: Kay AB (ed). Allergy and Allergic Diseases, Vol 2. Oxford: Blackwell Science. 1997: 1632-1644. Fireman P . Otitis media and Eustachian tube dysfunction: connection to allergic rhinitis. J Allergy Clin Immunol 1997; 99: S787-797. Fireman P . Otitis media and its relation to allergic rhinitis. Allergy Asthma Proc 1997; 18: 135-143. Lieberman PL, Blaiss MS. Allergic diseases of the eye and ear. In: Patterson R, Grammer LC, Greenberger PA (eds). Allergic Diseases - Diagnosis and Management, 5th ed. Philadelphia: Lippincott-Raven, 1997; 223-251. Mattucci KF, Greenfield BJ. Middle ear effusion: allergy relationships. ENT 1995; 74: 752-758. Parsons DS, Wald ER. Otitis media and sinusitis: similar diseases. Otolaryngol Clin North Am 1996; 29: 11-25. Skoner DP , Casselbrant ML. Otitis media. In Middleton E, Reed CE, Ellis EF, et al (eds). Allergy Principles and Practice, 5th ed. St. Louis, MO: Mosby 1998: 1036-1049. Spector SL. Overview of comorbid associations of allergic rhinitis. J Allergy Clin Immunol 1997; 99: S773-780. Wald ER. Otitis media. In: Conn HF. Conns current therapy. Philadelphia, 1998: 208-210.
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Resource Organizations
Contact the organizations listed below for information and helpful ideas.
Allergy and Asthma Network/ Mothers of Asthmatics, Inc. 2751 Prosperity Ave., Suite 150 Fairfax, VA 22030 Phone: (800) 878-4403 www.aanma.org American Academy of Allergy, Asthma and Immunology 611 East Wells Street Milwaukee, WI 53202 (800) 822-ASMA or (414) 272-6071 www.aaaai.org American Academy of Pediatrics 141 Northwest Point Boulevard Elk Grove Village, IL 60007-1098 (800) 433-9016 or (847) 228-5005 www.aap.org American Association for Respiratory Care 11030 Ables Lane Dallas, TX 75229 (972) 243-2272 www.aarc.org American College of Allergy, Asthma and Immunology 85 West Algonquin Road, Suite 550 Arlington Heights, IL 60005 (800) 842-7777 or (847) 427-1200 www.acaai.org The American Lung Association For the affiliate nearest you, call (800) LUNG USA www.lungusa.org Asthma and Allergy Foundation of America 1125 Fifteenth St, N.W ., Suite 502 Washington, DC 20005 Phone: (800) 7-ASTHMA www.aafa.org Centers for Disease Control and Prevention 1600 Clifton Rd. Atlanta, GA 30333 (800) 311-3435 The Food Allergy Network 10400 Eaton Pl., Suite 107 Fairfax, VA 22030 Phone: 1-800-929-4040 www.foodallergy.org Healthy Kids: The Key to Basics Educational Planning for Students with Chronic Health Conditions 79 Elmore Street Newton, MA 02459-1137 (617) 965-9637 E-mail: erg-hk@juno.com Immune Deficiency Foundation 25 W . Chesapeake Ave., Suite 206 Towson, MD 21204 Phone: (800) 296-4433 www.primaryimmune.org National Heart, Lung and Blood Institute (National Asthma Education and Prevention Program) P .O. Box 30105 Bethesda, MD 20824 Phone: (301) 251-1222 www.nhlbi.nih.org National Institute of Allergy and Infectious Diseases Building 31, Room 7A-50 National Institutes of Health Bethesda, MD 20892 Phone: (301) 496-5717 www.niaid.nih.gov
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U.S. Department of Education Office for Civil Rights, Customer Service Team Mary E. Switzer Building 330 C Street, S.W . Washington, DC 20202-1328 (800) 421-3481 or (202) 205-5413 www.ed.gov/offices/OCR U.S. Environmental Protection Agency Indoor Environments Division 401 M Street, S.W . (6604J) Washington, DC 20460 (202) 233-9370 Indoor Air Quality Information Clearinghouse (800) 438-4318 www.epa.gov/iaq
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Glossary
AAAAI: American Academy of Allergy, Asthma and Immunology. Airway wall remodeling: structural changes that are unlikely to be reversible, resulting from continued inflammation observed in chronic asthma. Permanent changes include continued loss of epithelial cells, deposition of subbasement membrane collagen, and increased muscle mass and blood vessels. Allergen immunotherapy (allergy vaccine therapy): a form of long-term therapy consisting of repeated, controlled administration of specific allergens to patients with IgE-mediated conditions to reduce disease severity from natural exposure to these allergens. Allergen: the source of an allergy-producing substance, the allergy-producing substance itself, or one or more of the specific proteins that make up the substance and provoke the immune response, including IgE antibodies. They are often common, usually harmless substances such as pollen, mold spores, animal dander, dust, foods, insect venoms, and drugs. Allergic diseases: represent the clinical manifestations of adverse immune responses (including IgE responses), following repeated contact with usually harmless substances such as pollen, mold spores, animal dander, dust, foods, insect venoms, and drugs; include diseases of the atopic diathesis as well as diseases which may have an allergic component. Allergy: an acquired potential to develop immunologically mediated adverse reactions to normally innocuous substances upon re-exposure to the sensitizing allergen (including IgE antibody responses to allergens), causing the release of inflammatory mediators. Anaphylactoid reaction: an immediate systemic reaction that mimics anaphylaxis but is not an IgE-mediated response. Anaphylaxis: is the most severe form of allergic reaction. It is a rapid, immune-mediated, systemic reaction to allergens to which the patient has been previously exposed. It has many etiologies, resulting from immune-mediated (i.e., IgE-mediated) rapid release of potent mediators from tissue mast cells and peripheral blood basophils. The reaction occurs rapidly and often dramatically, and is usually unanticipated. Signs and symptoms arise systemically and may include faintness, syncope, severe difficulty breathing, and throat closing. Symptoms generally start within 15 to 30 minutes from exposure to allergen, occasionally begin after 1 hour, and rarely occur hours later. Other reactions (i.e., anaphylactoid reactions) can mimic anaphylaxis. Anaphylaxis is always a medical emergency! See also exercise-induced anaphylaxis, anaphylactoid reaction, and idiopathic anaphylactic/anaphylactiod reactions.
Glossary
165
Angioedema: swelling in the deep cutaneous layer, but the skin may appear normal. Antihistamines: drugs that inhibit allergy symptoms by blocking the actions of histamine at the H1 receptor. Older sedating antihistamines cause drowsiness and/or loss of concentration and may affect psychomotor performance. Nonsedating antihistamines have poor penetration of the CNS, resulting in no sedative or psychomotor adverse effects. Asthma: is a chronic inflammatory disease of the airways characterized by airway obstruction, which is at least partially reversible with or without medication, and manifests increased bronchial responsiveness to a variety of stimuli. Atopic dermatitis: is a chronic or recurrent atopic inflammatory skin disease that usually begins in the first few years of life. It is often the initial clinical manifestation of an atopic predisposition, with many children later developing asthma and/or allergic rhinitis. Atopy: the genetic tendency to develop the classical allergic diseases, namely, allergic rhinitis, asthma, and atopic dermatitis. Atopy is typically associated with a genetically determined capacity to mount IgE responses to common allergens, especially inhaled allergens and food allergens. Beta2-agonists: drugs that are used in the treatment of asthma for short-acting quick relief, long-term 12-hour control, and for preventing exercise-induced bronchospasm. The bronchial smooth muscle relaxes in response to beta2adrenergic receptor stimulation. Chlorofluorocarbon (CFC): propellant used in MDIs to deliver inhaled asthma medications. Other propellants (HFA-134) will be replacing CFCs in the future because CFCs deplete the ozone layer. Conjunctivitis: a group of ocular disorders that result in inflammation of the conjunctiva. May be of allergic or nonallergic origin. Contact dermatitis: refers to a broad range of reactions resulting from the direct contact of an exogenous agent (allergen or irritant) with the surface of the skin. Corticosteroids: medications related to cortisone with anti-inflammatory effects useful in many allergic conditions. Newer preparations for lung, nasal, and skin use minimize risk for side effects. Cromolyn sodium/Nedocromil sodium: are topical nonsteroid antiinflammatory agents. DBPCFC: double-blind, placebo-controlled food challenge. Considered the gold standard for diagnosing food allergies.
166
Glossary
Decongestants: are sympathomimetic drugs that relieve symptoms of nasal congestion or blockage by constricting the capacitance vessels in the turbinates. Desensitization: a medical procedure utilized to reduce or eliminate sensitivity to certain drugs. Desensitization for IgE-mediated drug reactions is achieved by administering progressive doses of the drug until a full therapeutic dose is clinically tolerated. Indicated for patients with established drug allergy where no substitute for the responsible drug is available and treatment is essential. Desensitization for non-IgE-mediated drug reactions is successful for aspirin and NSAIDs. Domeboros solution: calcium acetate, aluminum sulfate astringent used to dry oozing dermatitis. Dry-powder inhaler (DPI): delivery mechanism without propellant for inhaled asthma medications that are in powdered form. Early phase reaction (immediate hypersensitivity reaction): an immunological reaction that occurs within minutes of subsequent exposure of the IgE antibody to the allergen in sensitized individuals. With repeat exposure of allergen, multiple IgE-FcR-complexes are cross-linked resulting in immediate hypersensitivity reactions (i.e., mast cells degranulate releasing histamine, leukotrienes, cytokines, and proteases). Eczema: is an inflammatory disease of the skin with lesions that can be erythematous, edematous, papular, crusting, lichenified, scaling, itching, burning, and sometimes skin discoloration can occur. Elimination diet: a restricted diet used for food allergy for a limited period of time (10 to 14 days) to evaluate the patient. Specific foods may be eliminated (e.g., targeted elimination diet) or basic/severe elimination diet protocols may be utilized in more complicated situations. Epicutaneous (patch) testing: a form of allergy skin testing that identifies or confirms suspected T-cell-mediated, delayed hypersensitivity, contact allergens in contact eczematous dermatitis. Exercise-induced anaphylactic/anaphylactoid reactions: a generalized reaction with initial symptoms of fatigue, diffuse warmth, pruritus, erythema, urticaria, and/or wheezing occurring during or immediately following exercise. Reactions may be associated with prior ingestion of food and/or analgesics. Exercise-induced bronchospasm (EIB): Smooth muscle contraction in the lungs caused by a loss of heat, water, or both from the airways during exercise due to increased ventilation and inhalation of cool, dry air relative to the air within the lungs. FDA: Food and Drug Administration.
Glossary
167
Food allergy: a group of disorders characterized by immunologic responses to specific food proteins. Any food may cause a food allergic reaction. The prevalence is greatest in the fist few years of life and declines over the first decade. Hepa-filters: high efficiency particulate air filter. Idiopathic anaphylactic/anaphylactoid reactions: a generalized reaction that is diagnosed by exclusion when neither a causative allergen nor physical factor can be identified. Immediate local reaction: describes an insect sting reaction and is sometimes referred to as the normal reaction. Presents as pain, erythema, itching, and swelling at the sting site. It is a transient response that usually disappears within several hours. In vitro: refers to a lab test (e.g., ELISA) to diagnose allergens that a person is sensitized to. Ipratropium bromide: used as adjunct therapy to bronchodilators in the treatment of acute asthma exacerbations. Affects are primarily due to anticholinergic action on bronchial smooth muscle. Also used to control rhinorrhea in a patient with nonallergic rhinitis. Large local reaction: describes an insect sting reaction that displays extensive swelling and erythema, extending from the sting site over a large area and often involves most of an extremity. Swelling often peaks within 48 hours and may last as long as 7 to 10 days. Occasionally, fatigue, low-grade fever, and nausea accompany the reaction. Late phase reaction: an immunological reaction that begins 2 to 4 hours following exposure to allergen and can last for 24 hours before subsiding. Inflammatory leukocytes (e.g., neutrophils, basophils, eosinophils) are involved but the late response is primarily mediated by eosinophils in atopic individuals. These inflammatory cells release cytokines and chemokines during the response. Latex allergy: an allergic response to the proteins in natural latex rubber or to the additives used in processing latex. Leukotriene modifiers: a group of drugs that may be used as long-term control medications for the treatment of mild persistent asthma. May be considered as alternative therapy to low doses of inhaled corticosteroids in mild persistent asthma, but the position of leukotriene modifiers in therapy has not been fully established.
168
Glossary
Long-term control medications: drugs that are taken daily on a long-term basis to achieve and maintain control of persistent asthma. Examples include inhaled corticosteroids, long-acting bronchodilators (e.g., beta2-agonists), plus other long-term control medications (e.g., methylxanthines [theophylline], leukotriene pathway modifiers). Mast cell stabilizer: a group of drugs that exhibit anti-inflammatory properties (e.g., cromolyn sodium, nedocromil sodium). The mechanism of action of these drugs remains uncertain. Metered-dose inhaler (MDI): propellant-driven delivery mechanism for inhalation of asthma medications. MMR: measles, mumps, and rubella vaccine. NIAID: National Institute of Allergy and Infectious Diseases. Nonallergic (or irritant) reaction: reactions that do not involve the immune system but can be important cofactors for developing allergic reactions. Oral allergy syndrome: a self-limiting condition associated with the ingestion of fresh fruits and vegetables that does not display symptoms of throat closing; appears to be a cross sensitivity to pollens that the individual is allergic to. Otitis media: an acute or chronic inflammation of the middle ear. Patch testing: see epicutaneous (patch) testing. Peak expiratory flow (PEF): a measurement of pulmonary function that is not as sensitive as FEV1 for diagnosing airflow obstruction; primarily a measurement of large airway function. Peak flow meters are designed as monitoring, not diagnostic, tools. Prick/puncture test: are a test used to confirm hypersensitivity to a wide variety of allergens, the most convenient and specific method for detecting IgE antibodies. Primary prevention: focuses on blocking sensitization and development of IgE-mediated response. Quick-relief medications: a group of drugs that give prompt relief of bronchoconstriction and accompanying acute asthma symptoms: coughing, wheezing, shortness of breath or rapid breathing, chest tightness. Examples including short acting beta2-agonists and anticholinergics.
Glossary
169
Rhinitis: inflammation of the mucous membranes of the nose with symptoms of sneezing, itching, nasal discharge, and congestion. The etiology can be allergic, nonallergic, or both. Seasonal allergic rhinitis is an IgE-mediated reaction of the nasal mucosa to one or more seasonal allergens. Perennial allergic rhinitis is an IgE-mediated reaction to allergens that show little or no seasonal variation. It is persistent, chronic, and generally less severe than seasonal. Rhinosinusitis: is an inflammation of the paranasal sinuses that occurs with rhinitis. It rarely appears in the absence of nasal inflammation, commonly occurring in patients with perennial allergic and nonallergic rhinitis and in patients with moderate to severe asthma. Acute rhinosinusitis is a common infection that lasts for up to 3 weeks and often follows a viral upper respiratory tract infection. Suspect if symptoms worsen after 5 days or persist after 7 days. Recurrent acute rhinosinusitis is characterized by four or more episodes of acute rhinosinusitis per year separated by at least 8 weeks of symptom-free intervals. Subacute (persisting acute) rhinosinusitis lasts between 3 weeks and 3 months. Chronic rhinosinusitis is a complex of symptoms associated with inflammation of the sinuses characterized by persistent symptoms of acute rhinosinusitis lasting longer than 3 months, a lack of response to treatment, and a positive imaging study. Secondary prevention: attempts to block the expression of the disease, despite sensitization. Short-acting beta2-agonists: a group of drugs that relax bronchial smooth muscle, resulting in bronchodilation usually within 5 to 10 minutes of administration. They are most effective medication for relieving acute bronchospasm, and are the therapy of choice for relieving acute symptoms and preventing exercise-induced bronchospasm. Using more than two times per week, other than for prevention of exercise-induced asthma, is an indicator for initiating or increasing anti-inflammatory therapy. Increasing use indicates inadequate control of asthma and the need to intensify long-term control therapy. Specialist: use of specialists in this document may include: Allergy/immunology specialists Dermatologists Infectious disease specialists Ophthalmologists Otolaryngologic allergy specialists Otolaryngologists Pulmonologists In many cases, the type of specialist varies with the provider network and the geography/community. For example, the Asthma section (Volume 2) uses the term asthma specialist in the same manner used by the National Asthma
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Education and Prevention Program1 to refer to a fellowship-trained allergist or pulmonologist or, occasionally, other physicians with experience in asthma management developed through additional training and experience. Similar complexities exist in identifying specialists for management of such diseases as atopic dermatitis, rhinosinusitis, otitis media, conjunctivitis, urticaria and angioedema, and contact dermatitis. Therefore, consultation or comanagement is recommended, as appropriate, with the type of specialist determined by the referring healthcare provider and taking into account the patients health insurance coverage and the healthcare resources available in the community. Spirometry (FEV1): pulmonary measurements made with a spirometer to evaluate airway obstruction, and if so, whether it is reversible with a bronchodilator. It is mandatory to diagnose and characterize asthma severity. Targeted elimination diet: an elimination diet with foods eliminated based on results from specific IgE tests (e.g., skin tests or in vitro tests) or from a suggestive history given by patient and/or parent. Tertiary prevention: targets the control of factors that increase symptoms. Theophylline: a drug with long-term control properties for asthma. It displays bronchodilation, respiratory stimulation, and may attenuate airway hyperreactivity. Treating through: continuing drug treatment in the presence of a suspected allergic reaction to the drug. Urticaria: a skin disease that occurs in the dermis, is characterized by pruritic, erythematous, and cutaneous elevations (i.e., rash) that blanch with pressure, indicating the presence of dilated blood vessels and edema in the dermis. Individual lesions last less than 24 hrs. Acute urticaria is a self-limited disorder that usually lasts for a few days. Chronic urticaria lasts longer than 6 weeks.
Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma: Clinical Practice Guidelines. NIH Publication No. 97-4051, page 10.
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Overview of Allergic Diseases:

Recommendations for Policy and Interventions Volume 2

Diseases of the Atopic Diathesis

Conditions That May Have an Allergic Component

Atopic Dermatitis.......... ... ....

Associated Disease: Rhinosinusitis ....157

157 157 157 158 159

161 161 161 162

162 163 164

Surgery .............................................................. 166

167 167 167 167 168 168 169

171 172 175

Resource Organizations ................................. 183

Glossary .................... ..... 185

The Allergy Report

Overview of Sections of Volume 2: Diseases of the Atopic Diatheses Rhinitis

Associated Disease: Rhinosinusitis

Associated Disease: Chronic or Recurrent Otitis Media

Allergic disease is the resulting clinical manifestations generated

Otolaryngologists Otolaryngologic allergy specialists Pulmonologists

Task Force Members

membranes of the nose.

Seasonal Allergic Rhinitis

Perennial Allergic Rhinitis

Seasonal pollen sensitivity may contribute to

testing or serum levels of IgE to specific allergens.

Nonallergic Eosinophilic Rhinitis

Characterized by discolored nasal secretions containing

Idiopathic Nonallergic or Vasomotor Rhinitis

Rhinitis Medicamentosa Drugs producing rhinitis medicamentosa:

(most common) Antihypertensives Antipsychotics Oral contraceptives Cocaine

Natural History of Allergic Rhinitis

Allergic rhinitis often coexists with other allergic disorders.

Allergic rhinitis may contribute to:

Inflammatory components common to allergic rhinitis and asthma:

Inflammation in the nose may increase lower airway

Common symptoms of allergic rhinitis and their mediators:

Otitis Media Allergic Rhinitis Asthma

Diagnosing the Patient with Allergic Rhinitis

Repetitive sneezing is a common symptom of seasonal allergic rhinitis.

o Duration o Relationship to seasons o Associated ocular, pharyngeal, and systemic

The physical examination should focus on the nose,

o Allergic shiners a darkening of the infraorbital

Observe the patient for:

Differential diagnoses of rhinitis include:

Examine the nose with high illumination using a nasal

rhinitis Idiopathic nonallergic rhinitis

Some patients with allergic rhinitis have systemic symptoms, including:

o Structural abnormalities, such as a deviated septum

Symptoms of allergic conjunctivitis frequently accompany allergic rhinitis.

What suggests allergic rhinitis?

Examine the pharynx for the presence and color of

Considerations for Diagnosing Seasonal Allergic Rhinitis

Chronic nasal congestion may produce secondary complaints of:

Symptoms may vary in occurrence and intensity in a

Considerations for Diagnosing Perennial Allergic Rhinitis

Managing the Patient with Allergic Rhinitis

Avoid factors that cause symptoms. Use appropriate treatments.

Evaluate for immunotherapy. Educate and follow-up.

Avoid factors that cause symptoms.

Use appropriate treatments.

Antihistamine-decongestant Combination Products