the Allergy Report - The American Academic of Allergy, Asthma & Immunology - Diseases of the A

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Overview of Allergic Diseases:Diagnosis, Management, and Barriers to Care

IntroductionBackgroundPreventionDiagnostic TestingManagement of Allergic Diseases

Environmental Control Allergen ImmunotherapyPharmacologic Therapy Patient Education

Recommendations for Policy and Interventions

Volume 1

Diseases of the Atopic Diathesis

IntroductionRhinitisAsthmaAtopic DermatitisAssociated Disease: RhinosinusitisAssociated Disease: Chronic or Recurrent Otitis Media

Volume 2

Conditions That May Have anAllergic Component

IntroductionConjunctivitisUrticaria and AngioedemaContact DermatitisDrug ReactionsFood ReactionsInsect Sting ReactionsLatex ReactionsAnaphylactic and Anaphylactoid Reactions

Volume 3

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 AmericanAcademy of Allergy, Asthma & Immunology, Inc. (“AAAAI”) and, as to copyrightedworks of others which are contained herein, such other copyright owners. This work isprotected under U.S. copyright law and other international treaties and conventions.Except as stated herein, none of the material contained in this publication may becopied, reproduced, distributed, republished, downloaded, displayed, posted ortransmitted in any form or by any means, including, but not limited to, electronic,mechanical, photocopying, recording, or otherwise, without the prior writtenpermission of AAAAI or, as to copyrighted material of others, the copyright owner.Any inquiries regarding such permission should be directed to:

Ms. Amy StoneAmerican Academy of Allergy, Asthma & Immunology, Inc.611 East Wells StreetMilwaukee, WI 53202Phone: (414) 272-6071Fax: (414) 272-6070

Certain material in this publication is taken or derived from NIH Publication Nos. 97-4051 (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 Institutesof Health, National Heart, Lung and Blood Institute.

AAAAI gratefully acknowledges the assistance of the Academic ServicesConsortium, University of Rochester, in the preparation of this publication.

Permission is granted to display, copy, distribute and download the materials in thispublication for personal, non-commercial use only provided that such materials are notaltered or modified and AAAAI’s copyright notice is displayed thereon.

DISCLAIMER: This publication and the material and information contained herein havebeen produced for informational purposes as a service to members and the generalpublic and are provided “as is,” without warranty of any kind, either express orimplied, including, without limitation, implied warranties of merchantability and fitnessfor a particular purpose. AAAAI shall not be liable for direct, indirect, special,incidental or consequential damages related to the user’s decision to use thispublication or any material or information contained herein.

CONTENTS

Introduction ……………………………………………………………….…………. 13

Classification of Rhinitis ............................………………… ………………….. 21

Allergic Rhinitis……………………………………………………..……….. 22

Seasonal Allergic Rhinitis …………………………………………. 22Perennial Allergic Rhinitis …………………………………..…….. 22

Nonallergic Rhinitis ………………………………………...………………………. 23

Nonallergic Eosinophilic Rhinitis…………………………….…... 23Infectious Rhinitis…………………………………………...………. 23Idiopathic Nonallergic or Vasomotor Rhinitis………………….. 24Rhinitis Medicamentosa ………………………………..………….. 24Hormonal Rhinitis..……………………………………………….…. 24Anatomic Rhinitis ………………………………...……….………... 24

Natural History of Allergic Rhinitis ……………………………………..……….. 25

Allergic rhinitis often coexists with other allergic disorders….…….. 25

Allergic rhinitis and asthma often coexist....………….……….. 25Inflammatory components common to allergic rhinitisand asthma……………………………………………………………. 25Common symptoms of allergic rhinitis and theirmediators(chart)…………………………………………………….. 26Allergic rhinitis and rhinosinusitis frequently coexistand are definitely linked...………………………………..………... 27

Diagnosing the Patient with Allergic Rhinitis ………………………………….. 27

Medical History ..................……………………………… ……….……….. 27

Physical Examination ......................……………………………..……….. 28

Diagnostic Testing ......................…………………………….….………... 30

Nasal Smears..............…………………………………..…………... 30Imaging .............…………………………………………….………… 31

Considerations for Diagnosing Seasonal Allergic Rhinitis………….. 31

Rhinitis......……………………………………………… …….………. 21

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..........………………………………….…….………. 36Intranasal Corticosteroids.....…………………………..….. 36Oral Corticosteroids..........………………………………..... 36

Mast Cell Stabilizers ..........……………………………………..….. 38

Anticholinergics ……………………………………………………. 38

General pharmacologic management (chart)………………. …. 39

Stepwise approach to pharmacotherapy forseasonal allergic rhinitis (chart) ………………………………….. 40

Stepwise approach to pharmacotherapy forperennial allergic rhinitis (chart)……………………….….………. 41

Stepwise approach to pharmacotherapy forperennial 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/immunologyspecialist or otolaryngologic allergy specialist………………………... 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 is often associated with allergy……………………...…. 53

Rhinitis and asthma involve a common respiratorymucosa...........……………………………………..…………………. 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

Asthma .........……….……………………………..………………… 53

Two ways to use a peak flow meter for measuringPEF 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? ……………….………… 64Classifying asthma severity BEFORE treatment(chart) ……………………………………………..…………... 64Classifying asthma severity AFTER treatment...……..... 65

Patients with asthma may need additional tests to aid and/orconfirm 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 helpful...…..… 67

Measure PEF in the office .........………………….……….. 67

Measure PEF at home........………………..……………….. 68Cutpoints 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 controlmedications? ………………………………………………… 75

How do you help the patient regain control of his/herasthma?…………………………………………………..…… 75

When and how do you step down long-term controltherapy?..............…………………………………….………. 75

Reduce therapy gradually .............………………….…….. 76

What medications are used to treat asthma?...…….….. 77

Long-term Control Medications……………..……. 77Inhaled Corticosteroids ...………………….. 77Cromolyn Sodium/Nedocromil Sodium…. 78Leukotriene Modifiers .....…………….……. 78Long-acting Beta2 -agonists..………….….. 79Methylxanthines (theophylline)...... …...…. 80Oral Corticosteroids....………………………. 80

Quick-Relief Medications......…………………….… 81Short-acting Beta2 -agonists ……….…….. 81Oral Corticosteroids......…………….. …….. 81Anticholinergics (Ipratropium Bromide).... 81

Stepwise approach for managing infants and youngchildren (5 years of age) with acute or chronic asthma symptoms (chart) ................……….. …….…….. 82

Stepwise approach for managing asthma inpatients > 5 years of age with acute or chronicasthma symptoms (chart). ………………………………... 84

Medication Tables .........……………………….…….……… 86Long-Term Control Medications (charts)....….…. 87Quick-Relief Medications (charts) …………...…... 91New Medications (charts) ........……………………. 93

Types of inhalation devices for asthma medications(chart)………………………………………………………….. 94

Advantages of Using Spacers and Holding Chambers…96

Treat asthma exacerbations promptly andaggressively……….……………………..…………………… 97

Assessing the severity of an asthmaexacerbation.………………………………………….. 98

Risk factors for death from asthma.......……….... 98

Managing Asthma Exacerbations in the Home.... 99

rgent Care (Clinician’s Office or EmergencyDepartment) for Managing AsthmaExacerbations ……………………………...………… 100

Referral to an asthma specialist forconsultation or comanagement ..…………………..102

Special Considerations for Managing Asthma.…..….…. 103Managing Exercise-induced Bronchospasm(EIB).…………………………………………………... 103

Preventing “anticipated” episodes of asthmasymptoms (other than exercise) ………………………….. 104

Treating asthma symptoms due to upper viralrespiratory infections (URIs).…………………………….. 104

Treating the child with asthma.....……………….……… 105Children < 2 years ........……………….…………... 106Children between 3 and 5.....………………….….. 106For School-age children ...………………..……… 107Adolescents............………...……………….……... 107

The child’s schedule and giving asthmamedications………………………………..………………... 108

Asthma, inhaled corticosteroids, and linear growth.... 108Managing asthma in the elderly ....………. ……………. 109

Managing the pregnant patient with asthma……..…… 110

Managing bronchopulmonary aspergillosis in thepatient with asthma.………………………….....………… 111

Managing work-aggravated asthma and occupationalAsthma………………………………..……………………… 111

Some examples of compounds causing asthma(chart)……………………………………. ………………….. 112

Component 4. Educations for a Partnership inAsthma Care………………………………………………………… 113

Take a proactive approach to asthma education.….… 113What can you and your staff do in a singleasthma visit? .........……………………….………. 114Focus on what is doable to improve adherencewith asthma therapy ...…………………………… 114Education Recommendations (chart).……..….. 116Asthma Management Plan for Long-termControl and Exacerbations ..…………………….. 118Asthma and the School .....…………. …………... 119

Teachers, coaches, and school healthpersonnel need to know …….. ………….. 119How asthma friendly is your school? …. 120School Asthma Management Plan ……... 121

References .................………………………. ………………………….………... 123

Diagnosing the Patient with Atopic Dermatitis......…………… …………….. 135

Medical History ......................……………... ……………………………. 135

Distribution of lesions (figure) ..........…………………..………. 136

Ask the patient about what causes symptoms..….…………... 137

Physical Examination........………………………… …………………….. 137

Characteristics of atopic dermatitis lesions………………..…. 138

Distinguishing features of seborrheic and atopicdermatitis in infancy (chart) ............……………………….……. 140

Masqueraders of atopic dermatitis..…………………….………. 140

Diagnostic Testing ..........…………………………… ………….……….. 141

Elimination diets ...........…………………… …………………….. 141

Managing the Patient with Atopic Dermatitis.....………………..……………. 142

Atopic Dermatitis........……………….. ……... ………….………... 131

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

Corticosteroids.........................…………………….…….………. 145Topical Corticosteroids...........………………….……….. 145Topical Corticosteroids (charts) ..……………….……... 147

Oral Corticosteroids ..........………………….……………………. 149

Oral Antihistamines ..................………………………..………... 149

Tar preparations......…………………………... ………….………. 149

A Protocol for Treating Atopic Dermatitis……………..………. 150

Special Considerations for Treating Atopic Dermatitis..……. 150Antibiotics .......…………………………… ……………….. 150Antiviral Agents .......…………………………..…………... 151Antifungal Agents (topical or oral)………………..…….. 151

3. Evaluate for immunotherapy ............…………..……………………. 151

4. Education and regular follow-up are important...………….………. 151

Consultation/comanagement with an allergy/immunologyspecialist ..………………………………………………………….……….. 152

Referral to an allergy/immunology and/or dermatologyspecialist.…………………………………………... ………………………. 152

Tips for patients with Atopic Dermatitis ..……………….…….………. 153

References ....................................………………………… ………….………... 154

Classification of Rhinosinusitis ..................………………..…………………. 157

Acute Rhinosinusitis ....................................…………………..………………. 157

Associated Disease: Rhinosinusitis …………….………….…..157

Recurrent Acute Rhinosinusitis..........………………………………….. 157

Subacute (persisting acute) Rhinosinusitis .……………... …………. 157

Chronic Rhinosinusitis ................……………………………………….. 157Tips to distinguish chronic from acute rhinosinusitis .…..…. 158

Who is at risk for rhinosinusitis?...........………………………….……………. 159

Clinical and environmental factors that predispose anindividual to infectious rhinosinusitis (chart)..…. ……………..……. 159

Diagnosing the Patient with Rhinosinusitis ………………………...………... 160

Signs and Symptoms Associated with Rhinosinusitis .......………… 160

Differentiating acute infectious rhinosinusitis fromseasonal allergic rhinitis (chart) ..…………………..…………... 160

The signs and symptoms of rhinosinusitis may reveal which sinus is primarily affected .......…………………………. 161

Diagnostic Procedures ..............................…………………………….. 161

Imaging ....................................................……………………….. 161

Nasal Endoscopy ....................................……………………….. 162

Other diagnostic tests may be considered in somecircumstances ……………………………………………………… 162

Tips for diagnosing rhinosinusitis ....………………………….. 163

Managing the Patient with Infectious Rhinosinusitis ..……………………... 164

Palliative Treatment ....................................…………………………….. 164

Pharmacologic Management ....................……………………………... 164

Antibiotic Therapy..................................………………………… 164Intranasal Corticosteroids....................………………………… .165Decongestants ........................................……………………….. 165Oral Mucolytics ......................................………………………… 166

Surgery ............................................................………………………….. 166

Specific Considerations for Treating Rhinosinusitis..………………. 167

Acute Rhinosinusitis..............................………………………… 167Recurrent Acute Rhinosinusitis ........…………………………... 167Subacute (Persisting Acute Rhinosinusitis........……………... 167Chronic Infectious Rhinosinusitis ....…………………………... 168

Additional Management Considerations .……………………………... 168

Special Considerations for Treating Rhinosinusitis in Children….. 169

Consider referral to an allergy/immunology or an otolaryngologicallergy specialist for consultation and/or comanagement........….… 171

When is referral to an otolaryngologic allergy specialistpreferred?………………………………………………………….... 171

References ............................................................……………………………... 172

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 ........................................…………………………… 179

Managing the Patient with Otitis Media ......…………………………………… 179

Preventive Therapies ..................................……………………………. 179Therapeutic Treatments ............................……………………………... 180Referral to an allergy/immunology specialist or otolaryngologicallergy specialist ........................................................…………………. 180

References ............................................................……………………………... 181

Associated Disease: Recurrent or Chronic Otitis Media ..…………...….. 175

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

Glossary ....................……………………………… ………...…………………….. 185

Introduction i

T

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 InfectiousDiseases (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 isto ensure that a broad spectrum of healthcare providers learns about,understands, and implements clinical and best practice information fordiagnosing and managing patients with allergic diseases.

The Allergy Report represents the outcome of a first step of theinitiative: development of an evidence-based, practical and easy-to-access guide to allergic disorders to help family practice physicians,internists, pediatricians, nurse practitioners, school nurses, and otherswho manage or interact with patients with allergies. The Allergy Reportprovides guidance on the clinical management of allergic disorders,examines the barriers to effective care, and addresses future researchneeds for allergy mechanisms and clinical approaches to treatment.The Report is organized into three volumes. This Volume providesinformation on the diseases of atopic diathesis: rhinitis, asthma, andallergic dermatitis. It also includes sections on two commonlyassociated diseases: rhinosinusitis and recurrent or chronic otitis media.Volume 1 provides an overview of the allergic process, the principles incommon to the diagnosis and management of all allergic diseases, anddiscusses potential interventions for improving care for patients withallergic disorders. Volume 3 focuses on the conditions in which theremay be an allergic component, including: conjunctivitis, urticaria andangioedema, contact dermatitis, drug reactions, food reactions, insectsting reactions, latex reactions, and anaphylactic/anaphylactoid reactions.

Introduction ii

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

RhinitisAllergic rhinitis is the most common allergic disease in the U.S.affecting about 40 million people. It is associated with direct costs ofabout $4.5 billion annually and indirect costs that reflect approximately4 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 formanaging the allergic rhinitis patient. Specific medications are describedin terms of their effects on symptoms and potential impact on dailyactivities. For example, the older antihistamines are effective treatmentsbut in many patients cause drowsiness and/or loss of concentration andmay affect psychomotor performance. In these cases, the newer non-sedating antihistamines are appropriate therapeutic choices. There areother medications that have some sedating side effects, but less thanthe older antihistamines (hence, they are referred to as the “less-sedating antihistamines”). Stepwise protocols for treatment are givenfor both seasonal and perennial allergic rhinitis and nonallergic rhinitis.

AsthmaAsthma is a chronic inflammatory disease of the airways characterizedby airway obstruction which is at least partially reversible with orwithout medication, and increased bronchial responsiveness to avariety of stimuli. Asthma is often associated with allergy, and atopy isthe strongest identifiable predisposing factor for the development ofasthma. This section provides an overview of the diagnostic andtreatment recommendations for asthma based on the Expert PanelReport 2: Guidelines for the Diagnosis and Management of Asthma(EPR-2) published by the National Asthma Education and PreventionProgram (National Heart Lung and Blood Institute) in 1997.

Atopic DermatitisAtopic dermatitis is a chronic or recurrent atopic inflammatory skindisease that usually begins in the first few years of life. It is often theinitial clinical manifestation of an atopic predisposition, and oftenprecedes allergic rhinitis and asthma in children. Up to 15% of the

Introduction iii

population in the U.S. is affected by atopic dermatitis at some timeduring childhood, and the prevalence is increasing. Clinical criteriafor diagnosis are given including the morphology and distribution oflesions in relation to age and/or ethnicity, consideration ofappropriate diagnostic tests, and the distinguishing features ofcommon dermatoses of infancy that should be distinguished fromatopic dermatitis. Nonpharmacologic and pharmacologic approachesto treatment are included. The use of topical corticosteroids isdiscussed in detail.

Associated Disease: RhinosinusitisRhinosinusitis is an inflammation of the paranasal sinuses that occurswith rhinitis and is common in patients with perennial allergic andnonallergic 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 withrhinosinusitis are provided.

Associated Disease: Chronic or Recurrent Otitis MediaOtitis media is an acute or chronic inflammation of the middle earthat is often associated with allergic rhinitis, particularly in childrenover 3 years of age. Risk factors for otitis media, evaluation of thepatient, and preventative and therapeutic approaches to treatmentare discussed.

Comment on TerminologyThe Allergy Report represents the collaboration and team effort of22 organizations (see page vi). Eight drafts of the document weredeveloped, reviewed, and revised by some or all of the Task Forcebefore the final sign-off and endorsement. Several terms had differentdefinitions and/or interpretations by members of different groups.As a result, it was necessary for the Task Force to reach consensuson the following:

Allergy: In most of The Allergy Report, the term:

❑ “Allergen” refers to substances that can induce IgE antibodyresponses.

❑ “Allergy” refers to IgE antibody responses to allergens.

Introduction iv

❑ “Allergic disease” is the resulting clinical manifestations generatedby IgE antibody responses.

Allergens include generally harmless materials such as:

❑ Pollens ❑ Cockroaches

❑ Mold spores ❑ Foods

❑ Animal danders ❑ Latex

❑ House dust mites ❑ Insect venoms

❑ Penicillin and other drugs

In several places in The Report, the terms “allergy” and “allergic disease”are more broadly encompassing and include altered immunologicreactivity 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 thatare both IgE-mediated and non-IgE-mediated.

❑ Contact Dermatitis describes specific, non-IgE-mediated immune cellreactions (i.e., T-cell responses to contact antigens).

Another term that is frequently confused with “allergy” is “atopy.” Atopyrefers to the genetic tendency to develop the “classical” allergic diseases,namely, allergic rhinitis, asthma, and atopic dermatitis. Atopy is typicallyassociated with a genetically determined capacity to mount IgEresponses to common allergens, especially inhaled allergens and foodallergens. Recently, it has been shown that IgE responses to latex aremore frequent in atopic families, and thus, latex allergy may beconsidered an atopic disease. In contrast, IgE responses to insect venomand drugs are not more common in atopic families. Hence, thesedisorders are considered allergic, but not atopic, diseases.

Specialist: The Allergy Report identifies many clinical situations in whichreferral to a specialist is warranted. Specialists may include:

❑ Allergy/immunology specialists

❑ Dermatologists

❑ Infectious disease specialists

❑ Ophthalmologists

Introduction v

❑ Otolaryngologists

❑ Otolaryngologic allergy specialists

❑ Pulmonologists

In many cases, the type of specialist varies with the provider networkand the geography/community. For example, the Asthma section(page 82) uses the term “asthma specialist” in the same manner used bythe National Asthma Education and Prevention Program1 to refer to afellowship-trained allergist or pulmonologist or, occasionally, otherphysicians with experience in asthma management developed throughadditional training and experience. Similar complexities exist inidentifying specialists for management of such diseases as atopicdermatitis, rhinosinusitis, otitis media, conjunctivitis, urticaria andangioedema, and contact dermatitis. Therefore, consultation orcomanagement is recommended, as appropriate, with the type ofspecialist determined by the referring healthcare provider and takinginto account the patient’s health insurance coverage and the healthcareresources available in the community.

Allergies are the sixth leading cause of chronic disease in theUnited 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 causetime lost from work, school, and leisure activities and decreaseproductivity at work, in school, and at home; but they don’t have to!Learning what triggers allergies and understanding how to treat thediseases may make the difference between a chronic debilitatingillness and a productive, healthy lifestyle. To help healthcareprofessionals bridge the gap between current knowledge and practice,The Allergy Report presents basic recommendations for the diagnosisand management of allergic diseases. It is the hope of the Task Forceresponsible for developing The Allergy Report, and those who havereviewed it, that this initiative will improve healthcare and productivityfor patients with allergic diseases.

1 Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma: Clinical PracticeGuidelines. NIH Publication No. 97-4051, page 10.

AcknowledgementsThe Task Force acknowledges the support of Schering/Key, whichprovided an unrestricted educational grant for development,publication, and distribution of The Allergy Report.

ChairsHarold S. Nelson, M.D., FAAAAIAmerican Academy of Allergy, Asthma and ImmunologyNational Jewish Medical and Research CenterDenver, CO

Gary S. Rachelefsky, M.D., FAAAAIAmerican Academy of Allergy, Asthma and ImmunologyAllergy Research Foundation, Inc.University of California at Los AngelesLos Angeles, CA

Introduction vi

Task Force MembersJohn Bernick, M.D., Ph.D.American College of Occupationaland Environmental Medicine

A. Wesley Burks, M.D.American Academy of Pediatrics

Don Cui, PA-C, C.M.C.M.American Academy of PhysiciansAssistants

Mark Dykewicz, M.D., F.A.C.P.American College of PhysiciansAmerican Society of InternalMedicine

Ivor Emanuel, M.D.American Academy of OtolaryngicAllergy

John Georgitis, M.D., F.C.C.P.American College of Chest Physicians

Peter Gergen, M.D.Agency for Health Care Policy andResearch

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 ofAmerica

Joel Karlin, M.D.American Medical Association

Monica Kraft, M.D.American Thoracic Society

Barry Lampl, D.O.American Osteopathic College ofAllergy and Immunology

Outside ReviewersThe panel of content experts who reviewed the draft documentincluded: 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.

Doris Luckenbill, R.N., M.S.,C.R.N.P.National Association of SchoolNurses

Bryan Martin, D.O.American Osteopathic College ofAllergy and Immunology

Anne Muñoz-FurlongThe Food Allergy Network

Donna Nativio, Ph.D., C.R.N.P.,F.A.A.N.American College of NursePractitioners

Marshall Plaut, M.D.National Institute of Allergy andInfectious Diseases, NationalInstitutes of Health

Stephen Redd, M.D.Centers for Disease Control andPrevention

Daniel Rotrosen, M.D.National Institute of Allergy andInfectious Diseases, NationalInstitutes of Health

Nancy SanderAllergy and Asthma NetworkMothers of Asthmatics, Inc.

William Storms, M.D.American College of Allergy, Asthmaand Immunology

Karen Tietze, Pharm.D.American Pharmaceutical Association

Barbara Yawn, M.D.Specialist in Family Medicine

Introduction vii

1

Rhinitis

❑ Rhinitis is an inflammation of the mucousmembranes of the nose.

❑ The characteristic symptoms of rhinitis are:

♦ Sneezing

♦ Itching

♦ Nasal discharge

♦ Congestion

❑ Rhinitis can be allergic, nonallergic, or both.

❑ Rhinitis is often associated with other chronicconditions, including:

♦ Asthma

♦ Eustachian tube dysfunction and otitis media

♦ Rhinosinusitis

♦ Nasal polyposis

♦ Allergic conjunctivitis

♦ Atopic dermatitis

Rhinitis

Classification of RhinitisAllergic rhinitis:

❑ Seasonal allergic rhinitis❑ Perennial allergic rhinitis

Nonallergic rhinitis:

❑ Infectious rhinitis ❑ Idiopathic nonallergic or vasomotor rhinitis❑ Rhinitis medicamentosa❑ Hormonal rhinitis❑ Anatomical causes of rhinitis

Classification of Rhinitis

Rhinitis can beallergic, nonallergic,or both.

Rhinitis is oftenassociated with otherchronic conditions.The sameinflammatoryprocesses may affectthe mucosa of the:❑ Nasal passages

❑ Lower airways

❑ Sinuses

❑ Eustachian tube

Rhinitis withprolonged nasalinflammation andeustachian tubedysfunction can be a factor in thedevelopment of otitis media.

Rhinitis

Allergic Rhinitis❑ 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:♦ At lower allergen levels.♦ To nonspecific irritants.

2

Seasonal Allergic Rhinitis❑ Patients experience an IgE-mediated reaction of the

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:

♦ Watery rhinorrhea ♦ Nasal congestion♦ Repetitive sneezing♦ Pruritus of the eyes, nose, ears, and throat ♦ Watery eyes

❑ Nasal secretions usually contain eosinophils. ❑ Common allergens causing seasonal allergic rhinitis:

♦ Grass pollens♦ Tree pollens♦ Weed pollens♦ 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:

♦ Prominent and severe nasal blockage/congestion.♦ Postnasal drainage.

❑ Rhinorrhea and sneezing are less prominent thanseasonal allergic rhinitis.

Patients with allergicrhinitis are usuallysensitive tononspecific irritants(e.g., perfumes,tobacco smoke).❑ Repeated allergen

exposure primes thenasal mucosa resultingin hypersensitivity.

♦ Symptoms occur atlower allergen levels.

♦ Symptoms occur withnonspecific irritants.

Plants that dependupon insect pollination(e.g., goldenrod,dandelions, and mostflowers) rarely causeseasonal allergicrhinitis symptoms.

Patients may showcross-reactivity tobotanically relatedallergens. Many of the allergenicsubstances of pollen grainsare similar between plantsfrom the same genus orfamily.

3Rhinitis

❑ Seasonal pollen sensitivity may contribute toexacerbations of rhinitis symptoms in patients withperennial allergic rhinitis.

❑ Common allergens causing perennial allergic rhinitis:♦ The most important causes of perennial allergic

rhinitis are indoor inhaled allergens:⇒ House-dust mite⇒ Animal dander⇒ Cockroach ⇒ Mold

♦ Occupational allergens

Nonallergic Rhinitis❑ Symptoms are similar to allergic rhinitis, but there is:

♦ Usually no pruritus.♦ No evidence of allergic disease as determined by skin

testing or serum levels of IgE to specific allergens.

Nonallergic Eosinophilic Rhinitis ❑ Characterized by:

♦ Marked nasal eosinophilia♦ Perennial symptoms of:

⇒ Sneezing⇒ Nasal obstruction⇒ Profuse watery rhinorrhea⇒ Nasal itching

♦ 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.

♦ Secondary bacterial rhinosinusitis is a commoncomplication.

Ingested foodallergens rarelyproduce IgE-mediatedrhinitis in adultswithout theinvolvement of otherorgans.

Patients withoccupationalperennial rhinitishave persistentsymptoms which showa temporal associationwith workplaceexposures.

4 Rhinitis

❑ Characterized by discolored nasal secretions containingneutrophils and, occasionally, bacteria.♦ Low grade fever is often present.

❑ Purulent discharge for > 5 days suggests bacterialrhinitis and/or rhinosinusitis.

Idiopathic Nonallergic or VasomotorRhinitis❑ Patients display nasal hyperresponsiveness to a variety

of nonspecific factors:♦ Chemical irritants♦ Strong smells♦ Environmental changes in:

⇒ Humidity⇒ Temperature⇒ Barometric pressure

❑ There is no evidence of abnormal cellularity of nasalsecretions.

❑ The mechanism has not been identified.

Rhinitis Medicamentosa❑ Patients experience drug-induced rhinitis.❑ Topical nasal decongestant overuse is the most

common cause.

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:

♦ Nasal congestion♦ Rhinorrhea

Anatomic Rhinitis ❑ Nasal septal deviation❑ Adenoidal enlargement (children)❑ Foreign body (especially in infants and young children)❑ Choanal narrowing

Drugs producingrhinitismedicamentosa:❑ Topical decongestants

(most common)

❑ Antihypertensives

❑ Antipsychotics

❑ Oral contraceptives

❑ Cocaine

5Rhinitis

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: ♦ Sleep disorders♦ Fatigue♦ Learning problems

Allergic rhinitis often coexists withother allergic disorders.Allergic rhinitis and asthma often coexist.❑ Some patients with allergic rhinitis report increased

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.♦ Allergic reactions in the nasal mucosa can potentially

worsen asthmatic inflammatory processes in the lowerairways.

Inflammatory components common toallergic rhinitis and asthma:

Inflammatory Cells Inflammatory Mediators

Mast cells Histamine

Eosinophils Leukotrienes

TH2 lymphocytes Proinflammatory cytokines

Allergic rhinitis is oneof the most commonallergic diseases inthe U.S., affectingabout 40 millionpeople (including 19million employedadults). Allergicrhinitis is associatedwith: ❑ Direct costs

approximating $4.5billion/year.*

❑ 3.8 million lost workand school daysannually.*

*Rates vary between sourcesdue to difficulty in assessingthis common disorder.

Source: Roundtablediscussion. The healthand economic impact ofrhinitis. Am J Manag Care1997: 3: S8-18.

Allergic rhinitis maycontribute to: ❑ Sleep disorders

❑ Fatigue

❑ Learning problems

Symptoms Mediators

Tickling Histamine, prostaglandins

Itchiness

Nose rubbing

Allergic ‘salute’

Sneezing Histamine, leukotrienes

Nasal congestion Histamine, leukotrienes,

Stuffy nose Bradykinin, platelet

Mouth breathing

Snoring

Runny nose Histamine, leukotrienes

Post-nasal drip

Throat clearing

6 Rhinitis

❑ Inflammation in the nose may increase lower airwayhyperresponsiveness. Possible mechanisms include: ♦ Nasal allergic response altering bronchial

responsiveness through naso-bronchial reflex. ♦ Mouth breathing caused by nasal obstruction

resulting in bronchospasm to cool, dry air.♦ Pulmonary aspiration of nasal contents.

❑ Clinical studies have shown that for some patients,treatment of allergic rhinitis with intranasalcorticosteroids reduces asthma symptoms andbronchial hyperresponsiveness.♦ Treatment of upper airway diseases, alone, is not

adequate treatment of asthma.❑ Clinical studies of nonsedating antihistamines,

decongestant combinations, and mildly sedatingantihistamines showed improvement in pulmonaryfunction and asthma symptoms in patients who hadseasonal allergic rhinitis and asthma. ♦ Antihistamines are not contraindicated for patients

with asthma.

Common symptoms of allergic rhinitis andtheir mediators:

The Expert PanelReport 2: Guidelinesfor the Diagnosisand Management ofAsthma (NationalAsthma Educationand PreventionProgram,1997)recommendsintranasalcorticosteroids forthe treatment ofchronic rhinitis inpatients withpersistent asthma.

Antihistamines arenot contraindicatedfor patients withasthma.

activating factor

7Rhinitis

Allergic rhinitis and rhinosinusitisfrequently 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 allergicrhinitis.

❑ Nasal polyps are associated with chronic rhinosinusitis.

Allergic rhinitis may be associated with thedevelopment of other diseases due tocommon passageways.

AllergicConjunctivitis

Sinusitis

AllergicRhinitis

Otitis Media

Asthma

Diagnosing the Patient withAllergic RhinitisMedical 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:♦ Onset♦ Progression♦ Severity

8 Rhinitis

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

symptoms ♦ Incidence of recurrent sinus or ear infections♦ Causal and exacerbating factors ♦ Association with skin rashes (suggesting atopic

dermatitis)♦ Association with asthma flare-ups♦ Relationship to drug use (medications and illicit

drugs)♦ Relationship to GI symptoms (suggesting food

allergy), especially in children❑ Also ask about:

♦ 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. ♦ Previous allergy testing♦ Medication use (prescription and nonprescription)♦ Facial and/or nasal trauma♦ Nasal surgery

Physical Examination

❑ The physical examination should focus on the nose,eyes, throat, and ears, but should also includeexamination of the lungs and skin.

❑ Observe the patient for: ♦ Mouth breathing.♦ Repeated nose wiggling, wiping, and pushing

(allergic salute). ♦ A nasal crease.

Repetitive sneezing isa common symptom ofseasonal allergicrhinitis.

Examine the nose withhigh-illuminationusing a nasal speculumbefore and aftertopical decongestantadministration.

♦ “Allergic shiners” – a darkening of the infraorbitalskin resulting from venous dilation and indicative ofchronic nasal congestion, particularly in children.

♦ Related eye symptoms.

❑ Examine the nose with high illumination using a nasalspeculum before and after topical decongestantadministration. Look for:♦ Pale blue and boggy nasal turbinates with a clear,

watery discharge.♦ Inflamed/reddened mucosa.♦ Enlarged turbinates obstructing the nasal airway.♦ Nasal polyps which may appear as rounded, white,

glistening masses resembling peeled grapes,commonly located within the middle meatus betweenthe inferior and middle turbinates.

9Rhinitis

Repeated nose wiggling, wiping,and pushing (allergic salute) arecommon responses to the nasalitching associated with allergicrhinitis, particularly in children. Reprinted from Fireman P. AllergicRhinitis. In: Fireman P, Slavin R, (eds).Atlas of Allergies. 2nd ed. London:Mosby-Wolfe; 1996: 146. By permissionof the publisher Mosby.

Observe thepatient for: ❑ Mouth breathing

❑ Allergic salute

❑ Nasal crease

❑ Allergic shiners

❑ Related eye problems

Differential diagnosesof rhinitis include: ❑ Allergic rhinitis

❑ Rhinitis medicamentosa

❑ Infectious rhinitis

❑ Anatomic obstruction

❑ Rhinosinusitis

❑ Nonallergic eosinophilicrhinitis

❑ Idiopathic nonallergicrhinitis

Patients with chronic or repeatedepisodes of allergic rhinitis mayhave a nasal crease caused bycontinual upward rubbing of thenose to relieve itching. Reprinted from Fireman P. AllergicRhinitis. In: Fireman P, Slavin R, (eds).Atlas of Allergies. 2nd ed. London:Mosby-Wolfe; 1996: 146. By permissionof the publisher Mosby.

Mouth breathing and “allergicshiners,” a darkening of theintraorbital skin related tochronic nasal congestion, areparticularly common in childrenwith allergic rhinitis. Reprinted from Fireman P. AllergicRhinitis. In: Fireman P, Slavin R, (eds).Atlas of Allergies. 2nd ed. London:Mosby-Wolfe; 1996: 148. By permissionof the publisher Mosby.

10 Rhinitis

Diagnostic TestingThe general principles of diagnostic testing are included inVolume 1: Diagnostic Testing, page 31. Specific tests usedfor 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.

Some patients withallergic rhinitis havesystemic symptoms,including:❑ Weakness

❑ Malaise

❑ Irritability

❑ Fatigue

❑ Difficulty concentrating

❑ Decreased appetite

What suggests allergicrhinitis?❑ Itching of the nose,

throat, and eyes

❑ Clear, watery discharge

❑ Sneezing

❑ Pale, violaceous, swollenmucosa

♦ Structural abnormalities, such as a deviated septumor spur.

♦ Character of drainage (clear or purulent, wateryor thick).

❑ Examine the eyes for conjunctivitis (which may besubtle).

❑ Examine the pharynx for the presence and color ofposterior nasal drainage.

❑ Look at the appearance and size of tonsillar tissue,fullness of posterior soft palate, cobblestoneappearance of posterior pharyngeal wall.

❑ Examine the ear with a pneumatic otoscope for: ♦ Eustachian tube dysfunction♦ Dull, immobile tympanic membrane ♦ Serous otitis ♦ Excoriations

❑ Examine the lungs for wheezing.❑ Examine the skin for evidence of atopic dermatitis.

Symptoms of allergic conjunctivitisfrequently accompany allergic rhinitis. Reprinted from Wiley L, Arffa R, Fireman P. AlllergicImmunologic Ocular Diseases. In: Fireman P, SlavinR, (eds). Atlas of Allergies. 2nd ed. London: Mosby-Wolfe; 1996: 192. By permission of the publisherMosby.

11Rhinitis

Considerations for DiagnosingSeasonal Allergic Rhinitis❑ Itching of the nose is a prominent feature.

♦ Itching of the ears, palate, or throat is commonlyreported.

❑ During the pollen season, sneezing episodes may beaggravated 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:♦ Excessive and continual nasal discharge.♦ Rubbing and wiping.

❑ Nasal congestion caused by swollen turbinates is acommon complaint and may:♦ Be the only presenting symptom, particularly in

children. ♦ Be intermittent at the onset of the pollen season.♦ Become more symptomatic as the pollen season

progresses. ♦ Disturb sleep, causing daytime fatigue, and impairing

daily activities.❑ Severe nasal obstruction can lead to blockage of the

paranasal sinuses or eustachian tubes, causing sinusheadache 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 ofthe nasopharyngeal area.

❑ Asthma symptoms may worsen.❑ Symptoms may correlate with the appearance and

intensity of local pollens.

Imaging❑ Radiographic imaging and computed tomography

(CT) are rarely used, except when chronic or recurrentrhinosinusitis is suspected as a complicating factor.

❑ Magnetic resonance imaging (MRI) provides betterimaging of soft tissue than CT, but it is less suitedto imaging the bony anatomy of this region.

Neither totalserum IgE nor totalcirculating eosinophilcounts are useful indiagnosing rhinitis,due to lack ofsensitivity andspecificity of thesetests.

12 Rhinitis

❑ Symptoms may vary in occurrence and intensity in atime-dependent fashion during the day or from seasonto season.

❑ Symptoms are often worse on arising in the morningeven when the exposure occurred on the previous day(circadian pattern).

❑ Patients may not present with all symptoms.

Considerations for DiagnosingPerennial Allergic Rhinitis❑ Symptoms of perennial allergic rhinitis are very similar

to those of seasonal allergic rhinitis, although perennialis persistent, chronic, and generally less severe.

❑ The most common symptom is nasal congestion.♦ Sneezing, clear rhinorrhea, and nasopharyngeal and

ocular itching occur less frequently in patients withperennial allergic rhinitis than seasonal allergicrhinitis.

❑ The perennial allergic rhinitis patient often complains ofa “persistent cold” or “chronic sinusitis.”

Referral to an allergy/immunology orotolaryngologic allergy specialist forconsultation and/or comanagement isrecommended when there is:❑ A pattern of symptoms occurring

predominantly in relation to work.♦ Consider occupational rhinitis.

❑ Bilateral chronic nasal congestion withvariable sneezing and discharge, but withsignificant olfactory disturbance.♦ Consider nasal polyps.

❑ Persistent rebound congestion resulting fromoveruse or abuse of intranasal decongestants.♦ Consider rhinitis medicamentosa.

❑ Continuous nasal congestion, particularly if unilateral, with bloodstained secretions.♦ Consider malignancy.

❑ A pattern of persistent symptoms that is notcompletely responsive to appropriateenvironmental control and medications.♦ Consider rhinosinusitis and/or

noncompliance with therapeutic regimens.

Chronic nasalcongestion mayproduce secondarycomplaints of:❑ A dry, irritated,

or sore throat

❑ Snoring

❑ Pain around the eyes

❑ Mouth breathing

❑ Frontal headaches

❑ Eustachian tubedysfunction

❑ Altered hearing, smell,and/or taste

❑ Sleep disturbance, withor without daytimefatigue

13Rhinitis

Avoid factors that cause symptoms.

Use appropriate treatments.

1 Evaluate for immunotherapy.

Educate and follow-up.2

34

Managing the Patient with AllergicRhinitisFour general principles of allergymanagement:

Avoid factors that cause symptoms.The avoidance techniques and tips included inVolume 1: Prevention, page 21, are appropriate forthe patient with allergic rhinitis.

Use appropriate treatments.The goal of pharmacotherapy is to alleviate andprevent the patient's symptoms. ❑ Medications used to treat allergic rhinitis:

♦ Antihistamines♦ Decongestants ♦ Antihistamine-decongestant combinations♦ Corticosteroids♦ Mast cell stabilizers♦ Anticholinergics

❑ Palliative treatment may help.♦ Nasal lavage with warm salt water

(with or without baking soda).♦ Inhalation of warm mist through the nose for

10 to 15 minutes, 2 to 4 times per day, may help.

2

1

14 Rhinitis

Antihistamines❑ The mainstay of pharmacotherapy for allergic rhinitis

is antihistamines.❑ H1 -receptor antagonist activity

♦ Blocks histamine-induced symptoms:⇒ Rhinorrhea⇒ Pruritus⇒ Sneezing

♦ Has a rapid onset of action.♦ May reduce related symptoms in eyes and throat.

❑ Generally considered ineffective for treating nasalcongestion.

❑ Older antihistamines have inherent sedating side effects.♦ May affect cognitive and motor functions even without

obvious sedation.♦ Tolerance to the sedating side effects may occur to

some extent. ⇒ Using a sedating antihistamine at night and a

nonsedating antihistamine during the day maystill affect daytime functioning.

♦ Nonsedating antihistamines are preferred.❑ Topical (intranasal) antihistamines are effective.

♦ Significant systemic absorption may occur, resultingin drowsiness.

♦ May have bitter taste.

Antihistamines are the mainstay ofpharmacotherapy forallergic rhinitis.

Nonsedatingantihistamines do nothave the side effectsassociated withsedation caused by theolder antihistamines(e.g., daytimesomnolence, impairedperformance).

15Rhinitis

Decongestants❑ Sympathomimetic drugs.❑ Relieve symptoms of nasal congestion or blockage by

constricting the capacitance vessels in the turbinates.❑ Side effects of oral decongestants:

♦ Nonselective vascular constriction resulting inhypertension

♦ Restlessness♦ Agitation♦ Tremor♦ Insomnia ♦ Headache ♦ Dry mucous membranes♦ Urinary retention♦ Cardiovascular effects (e.g., palpitations, tachycardia,

extrasystoles)♦ Exacerbation of thyrotoxicosis or glaucoma

❑ Topical (intranasal) decongestants act more rapidly andeffectively than oral decongestants to relieve nasalcongestion, and have fewer systemic side effects.

❑ A major side effect of topical decongestants is rhinitismedicamentosa.♦ A “rebound phenomenon” resulting in increased

nasal congestion and edema.♦ Occurs after several repeated applications. ♦ Limits use of topical decongestants. ♦ Treat by:

1. Discontinuing nasal decongestants.2. Starting nasal corticosteroids.3. Using a short course of oral corticosteroids,

if necessary.

Use oraldecongestants withcaution in patientswith heart disease,high blood pressure,thyroid disease,diabetes, or difficultyin urination due toenlargement of theprostate gland.

Limit use of topicaldecongestants to amaximum of 3 to 5days to avoid rhinitismedicamentosa.

Treating rhinitismedicamentosa dueto topicaldecongestants1. Discontinue nasal

decongestants.

2. Start nasalcorticosteroids.

3. Use a short course oforal corticosteroids,if necessary.

16 Rhinitis

Antihistamine-decongestant CombinationProducts❑ Effective in controlling rhinitis symptoms.

♦ May be more effective than either product alone.❑ In some patients, the stimulatory effect of the

decongestant may offset the sedative effect of a sedatingantihistamine.♦ The other side effects of the older antihistamines may

not be affected.♦ The combination of an oral decongestant with a

nonsedating antihistamine may cause insomnia, but ispreferred over sedating combinations.

Corticosteroids❑ The most effective pharmacologic agents for treating

allergic rhinitis. ❑ Treat the inflammatory component of the disease:

♦ Reduce inflammatory cell infiltration in the superficialnasal mucosa.

♦ Reduce endothelial and epithelial permeability.♦ Increase sympathetic vascular tone. ♦ Decrease the response of mucous glands to

cholinergic stimulation.♦ Reduce nasal hyperreactivity.

Intranasal Corticosteroids

❑ The first line of therapy when obstruction is a majorcomponent of the patient’s rhinitis.

❑ Prophylactic use reduces:♦ Congestion♦ Sneezing♦ Rhinorrhea♦ Palatal pruritus♦ Cough

❑ Prophylactic use has variable effects on ocularsymptoms.

❑ Times to onset and to maximum benefit are longer than with antihistamines. ♦ Initial relief may be 4 to 12 hours after the first dose.♦ Maximum therapeutic benefit usually occurs within

2 weeks.

Corticosteroids arethe most effectivepharmacologic agentsfor treating allergicrhinitis.

Intranasalcorticosteroidsare the first lineof therapy whenobstruction is amajor componentof the patient’srhinitis.

17Rhinitis

To maintaineffectiveness,intranasalcorticosteroids mustbe administeredregularly, even in theabsence of symptoms. ❑ For maintenance

therapy, taper to thelowest effective dose.

A short (3- to 7-day)course of oralcorticosteroids may benecessary:❑ For patients with severe

symptoms.

❑ To gain control ofsymptom exacerbations.

❑ Can be given concomitantly with antihistamines topatients with continuous nasal symptoms and/orbothersome eye symptoms.

❑ Patients need to be instructed that to maintaineffectiveness, this medication must be administeredregularly, even in the absence of symptoms.♦ For maintenance therapy, taper to the lowest effective

dose.❑ Local side effects of intranasal corticosteroids include:

♦ Stinging♦ Burning ♦ Dryness ♦ Sneezing♦ Epistaxis

❑ Some intranasal corticosteroids have been shown tocause a reduction in growth velocity when administeredto children.♦ The relationship between short-term growth

evaluations and long-term effects on growth isunclear.

♦ These agents are safe and effective when used atrecommended doses.

Oral Corticosteroids

❑ A short (3- to 7-day) course may be appropriate forsome patients with severe symptoms or to gain controlof symptom exacerbations.

❑ Prolonged systemic exposure can be avoided by a briefcourse of oral corticosteroids to achieve symptomcontrol.♦ Maintain control with topical corticosteroids.

❑ Avoid depot parenteral corticosteroids.

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 hyperreactivitythat may persist after exposure to pollenhas ended.

Mast Cell Stabilizers ❑ Mast cell stabilizer is the common terminology

referring to cromolyn-like agents. ♦ The mechanism of action of cromolyn sodium

remains uncertain and may not be related to mast cellstabilization.

❑ Intranasal cromolyn sodium is a topical OTC nonsteroidanti-inflammatory agent which: ♦ Blocks both the early and late phase nasal allergic

responses.♦ Relieves sneezing, rhinorrhea, nasal congestion, and

nasal pruritus.⇒ It does not relieve ocular symptoms.

♦ Has an excellent safety profile with few side effects.⇒ Most common side effects are sneezing and nasal

burning.♦ Is effective for seasonal allergic rhinitis and perennial

allergic rhinitis.⇒ Not as effective as nonsedating oral antihistamines

or topical nasal corticosteroids.♦ May be used immediately prior to an anticipated

exposure to prevent rhinitis symptoms.⇒ Preventive use is not as effective after symptoms

have started.

Anticholinergics ❑ Ipratropium bromide provides relief from excessive

rhinorrhea not controlled by other medications.♦ Does not relieve nasal congestion, pruritus, or

sneezing. ♦ Not well absorbed from the nasal mucosa.♦ Common local side effects are dose-related:

⇒ Nasal dryness ⇒ Bloody nasal discharge

Intranasal cromolynsodium is a topicalOTC nonsteroid anti-inflammatoryagent which: ❑ Blocks the early and late

nasal allergic responses.

❑ Relieves sneezing,rhinorrhea, nasalcongestion, and pruritus.

❑ Has an excellent safetyprofile.

❑ May be used immediatelyprior to an anticipatedexposure to preventrhinitis symptoms.

Cromolyn Sodium is most effective whenused 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.

18 Rhinitis

Agent

Oral antihistamines ++

– = provides no benefit

+/– = provides little or minimal benefit

+ = provides modest benefit

++ = provides substantial benefit*This table represents a consensus of the Task Force’s opinion. Referral to and/or consultation with anallergy/immunology specialist is recommended.

General pharmacologic management of allergic rhinitis:*

Sneezing Itching Congestion Rhinorrhea EyeSymptoms

++ +++/– ++

Nasal antihistamines ++ ++/– –

Intranasalcorticosteroids ++++ ++++ +

Oral decongestants –– –+ –

Intranasaldecongestants –– –++ –

Intranasal mastcell stabilizers ++ ++ –

Topical anticholinergics –– ++– –

19Rhinitis

Severity

Intermittentsymptoms

Stepwise approach to pharmacotherapy for seasonal allergicrhinitis:Avoidance of allergic factors and irritants is the first step in the management of thepatient with allergic rhinitis.

Daily Medication Quick-reliefMedication

None

Persistent mild-to-moderatedisease

Consider referral to an allergy/immunologyspecialist orotolaryngologicallergy specialist forconsultation orcomanagement.See page 27.

Oral nonsedating H1-antihistamine (with orwithout a decongestant combination).

OR:

Topical nasal corticosteroid (preferably starttherapy 1 to 2 weeks before season andcontinue through season).

CONSIDER:

Topical nasal antihistamine; nasal cromolynsodium for children.

If there are prominent eye symptoms:topical ocular antihistamine with or withoutvasoconstrictor, topical ocular mast cellstabilizer, and/or topical ocular NSAID.

Rapid onset,oral, non-sedating H1-antihistamine.

OR

Topical nasalantihistamine.

CONSIDER:Nasalcromolynsodium as apreventivemeasurebeforeanticipatedallergenexposures.

Severe diseaseReferral to anallergy/immunologyspecialist orotolaryngologicallergy specialistfor consultation orcomanagementis recommended.See page 27.

Topical nasal corticosteroid (preferably starttherapy 1 to 2 weeks before season andcontinue through season).

AND:


CONSIDER:

Topical nasal antihistamine; nasal cromolynsodium for children.

AND, if needed:

A short course (3- to 10-day) of oralcorticosteroids.

If there are prominent eye symptoms:topical ocular antihistamine with or withoutvasoconstrictor, topical ocular mast cellstabilizers, and/or topical ocular NSAIDS. ▼

▼

20 Rhinitis

21Rhinitis

Stepwise approach to pharmacotherapy for perennial allergicrhinitis:Avoidance of allergic factors and irritants is the first step in the management of thepatient with allergic rhinitis.

Severity

Intermittentsymptoms

Daily Medication Quick-ReliefMedication

None

Persistentmild-to-moderate disease

Consider referral to an allergy/immunologyspecialist orotolaryngologicallergy specialist for consultationor comanagement.See page 27.

Oral nonsedating H1-antihistamine (withor without a decongestant combination).

AND/OR:

Topical nasal corticosteroid.

CONSIDER:

Topical nasal antihistamine.

Children should start with oral nonsedatingH1-antihistamine or nasal cromolyn sodium.

Rapid onset,oral, non-sedating H1-antihistamine.

OR:

Topical nasalantihistamine.

CONSIDER:Nasalcromolynsodium as apreventivemeasurebeforeanticipatedallergenexposures.

Severe disease

Referral to anallergy/immunologyspecialist orotolaryngologicallergy specialist forconsultationor comanagementis recommended.See page 27.

Topical nasal corticosteroid.

AND:


AND, if needed:

A short course (3- to 10-day) of oralcorticosteroid.

▼

▼

With little watery discharge

1. Advise avoidance of irritants.

2. Add daily topical nasalcorticosteroid.

3. If treatment is ineffective after1 month, consider:

♦ A short course (3- to 10-day) oforal corticosteroid.

♦ Adding an oral decongestant.

♦ Referral to an allergy/immunologyor otolaryngologic allergy specialistfor further evaluation and/orcomanagement.

With copius watery discharge

1. Advise avoidance of irritants.

2. Add daily topical nasalanticholinergic (ipratropiumbromide).

3. If treatment is ineffective after1 month, consider adding a topicalnasal corticosteroid and considerreferral to an allergy/immunology orotolaryngologic allergy specialist forfurther evaluation and/orcomanagement.

22 Rhinitis

Stepwise approach to pharmacotherapy for perennialnonallergic rhinitis:

Medications to Treat RhinitisOral nonsedating antihistamines:

Drug NameGeneric Trade

Desloratadine

Fexofenadinehydrochloride

Loratadine

DoseAdults Children

Clarinex®

Allegra®

Capsules

Allegra®

(30 mg)

Allegra®

(60 mg)

Allegra®

(180 mg)

Claritin®

Tablets

Claritin®

Reditabs

Claritin®

Syrup

1 tablet (5mg) oncedaily.

1 capsule (60 mg)twice daily.

1 tablet twice a day.

1 tablet once a day.

1 tablet (10 mg) oncedaily.

1 Reditab (10mg)once daily.

2 teaspoons(5mg/5ml) 1 time/day.

12 yr and older: sameas adults.


6-11 yrs of age.




6 through 11 yr: 1-2teaspoons once daily.

2 through 5 yr: 1teaspoon once daily.

1 tablet twice a day.

23Rhinitis

Oral less-sedating antihistamines:


Cetirizinehydrochloride

DoseAdults Children

Zyrtec®

Tablets

Zyrtec®

Syrup

1-2 (5-mg) tabletsonce daily or 1 (10-mg) tablet once daily.

1-2 teaspoons(5mg/5ml) once daily.

12 yr and older: same as adults.

6 through 11 yr: 1-2teaspoons once daily.

2 through 5 yr: startwith 0.5 teaspoononce daily; mayincrease to 1 teaspoononce daily or 0.5teaspoon 2 times/day.

Oral less-sedating antihistamine-decongestant combinations:


Cetirizine/PseudoephedrineHCl

DoseAdults Children

Zyrtec-D® 1 tablet (5 mg/120 mg)2 times a day.


Oral nonsedating antihistamine-decongestant combinations:*


Fexofenadine/PseudoephedrineHCl

Loratadine/PseudoephedrineHCl

DoseAdults Children

Allegra-D®

Claritin-D®

12 hour

Claritin-D®

24 hour

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.




*These medications should not be used with OTC decongestants or antihistamines, and should not be used bypatients with urinary retention, narrow angle glaucoma, severe hypertension, or using MAO-inhibitors (within14 days).

24 Rhinitis

Intranasal antihistamines:


Azelastinehydrochloride

DoseAdults Children

Astelin® NasalSpray

2 sprays (137 mcg/spray) in each nostril2 times/day.

5-11 yrs of age: 1 spray in each nostril2 times a day


Intranasal anticholinergics:


Ipratropiumbromide

DoseAdults Children

Atrovent®

Nasal Spray0.03%

0.06%

2 sprays (21 mcg/spray ) in each nostril2-3 times/day.

2 sprays (42 mcg/spray) in each nostril3-4 times/day.



Intranasal mast cell stabilizers:


Cromolynsodium

DoseAdults Children

Nasalcrom® One spray (5.2 mg/spray) in each nostril3-4 times/day (every4-6 hrs); may increaseup to 6 times/day.


Oral less-sedating antihistamine-decongestant combinations:*


Acrivastine/PseudoephedrineHCl

DoseAdults Children

Semprex-D®

Capsules1 capsule (8 mg/60 mg), 4 times/day(every 4-6 hours).


*These medications should not be used with OTC decongestants or antihistamines, and should not be used bypatients with urinary retention, narrow angle glaucoma, severe hypertension, or using MAO-inhibitors (within14 days).

Intranasal corticosteroids:


Beclomethasonedipropionate

Budesonide

Flunisolide

Fluticasonepropionate

Mometasonefuroatemonohydrate

Triamcinoloneacetonide

DoseAdults Children

Beconase®

InhalationAerosol

Beconase AQ®

Nasal Spray

Rhinocort®

Nasal Inhaler

Nasarel®

Nasal Solution

Flonase®

Nasal Spray

Nasonex®

Nasal Spray

Nasacort® NasalInhaler

Nasacort® AQNasal Spray

1 spray (42 mcg/ spray)in each nostril 2-4 times/day.

1-2 sprays (42 mcg/spray)in each nostril 2 times/day.

2 sprays (32 mcg/ spray)in each nostril 2 times/day or 4 sprays in eachnostril each morning.2 sprays (25 mcg/ spray)in each nostril 2 times/day; may increase to 2 sprays in each nostril 3-4 times/day (maximumof 8 sprays in each nostrilper day).

2 sprays (50 mcg/spray)in each nostril 1 time/day or 1 spray in eachnostril 2 times/day.2 sprays (50 mcg/spray)in each nostril 1 time/day.

2 sprays (55 mcg/spray)in each nostril 1 time/day; may increase to 2 sprays in each nostril 2 times/day or 1 spray ineach nostril 4 times/day.2 sprays (55 mcg/spray)in each nostril 1 time/day.

12 yr and older: same asadults.6 to 12 yr: 1 spray in eachnostril 2-3 times/day.12 yr and older: same asadults.6 to 12 yr: 1 spray ineach nostril 2 times/day.

6 yr and older: same asadults.

14 yr and older: same asadults.6 to 14 yr: 1 spray ineach nostril 3 times/dayor 2 sprays in eachnostril 2 times/day (maximum of 4 sprays in each nostril per day).4 yr and older: same asadults, but start with 1 spray in each nostril 1 time/day.12 yr and older: same asadults.2 to 12 yr: 1 spray eachnostril 1 time/day. 12 yr and older: same asadults.6 through 11 yr: 2 sprays in each nostril 1 time/day.

12 yr and older: same asadults.6 to 12 yr: 1 spray in eachnostril 1 time/; may increase to 2 sprays ineach nostril 1 time/day.

25Rhinitis

NOTE: The FDA plans to eliminate the essential-use exemptions for steroid metered dose nasal inhalers on July24, 2003. All CFC-containing nasally inhaled steroid products will be taken off the market.

Evaluate for immunotherapy.❑ Clinical studies have demonstrated the

effectiveness of immunotherapy in treatingsymptoms of allergic rhinitis.

❑ Potent and standardized extracts are available forcommon allergens such as pollen, dander, anddust mites.

❑ Selection of allergen used in the extract is basedon allergy testing and patient’s history.

❑ Considerations favoring the use of immunotherapy:♦ Long allergen season♦ Perennial symptoms♦ Poor response to, poor tolerance of, or

unwillingness to use symptomatic medications♦ To prevent the worsening or development of

asthma♦ Presence of chronic or recurrent rhinosinusitis♦ Presence of chronic or recurrent middle ear

disease❑ Administer under the direction of an allergy/

immunology specialist or an otolaryngologicallergy specialist.

Consider immunotherapy for allergicrhinitis 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.

26 Rhinitis

3

Immunotherapyshould beadministered underthe direction of anallergy/immunologyspecialist or anotolaryngologicallergy specialist.

❑ Identification of allergens and/or other factorscausing symptoms is required (e.g., allergytesting).

❑ Rhinitis is inadequately controlled; forexample:♦ Patient would benefit from additional

education in allergen avoidance techniques.♦ Symptoms and/or medication side effects

impair patient performance.♦ The patient’s quality of life is significantly

affected (e.g., patient comfort and well-being, sleep disturbance, smell, taste).

♦ Patient exhibits chronic or recurrentcomplications of rhinitis, or comorbidconditions, develop (e.g., rhinosinusitis,eustachian tube dysfunction, asthma).

❑ Repeated use of oral corticosteroids (morethan 2 courses per year) is required tomanage the patient’s rhinitis symptoms.

❑ The patient requires multiple medications forrhinitis over a prolonged period of time.

❑ The patient requires continued use of nasalcorticosteroids for symptoms.

❑ Occupational rhinitis exists.

Educate and follow-up. The educational tips included in the PatientEducation chapter of Volume 1 are appropriate forthe patient with allergic rhinitis (see Volume 1:Patient Education, page 71).

4

27Rhinitis

Consultation/comanagement with anallergy/immunology specialist orotolaryngologic allergy specialist isrecommended when:

Considerations for SpecialPopulationsManaging the Child with AllergicRhinitis ❑ The diagnosis of allergic rhinitis is often missed in

children, especially those with:♦ Recurrent otitis media♦ Persistent middle ear effusion♦ Chronic or recurrent rhinosinusitis

❑ Early recognition of allergic rhinitis can lead to earlytreatment and reduce complications.

❑ Allergy tests can be done at any age and may yieldimportant information.

❑ Allergic rhinitis is unusual in children under 3 yearsof age.

❑ Food allergy can cause allergic rhinitis in infants andchildren.

❑ There is evidence that symptoms of allergic rhinitis canimpair cognitive functioning and school performance.♦ 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.♦ The clinical significance of this adverse effect on adult

height has not been established.♦ Regular height measurements are advised for children

using intranasal corticosteroids continuously.♦ 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 allergenand/or irritant exposure.

In children, cognitivefunctioning andschool performancemay be impaired byallergic rhinitissymptoms and maybe further impairedby sedatingantihistamines. ❑ Nonsedating

antihistamines canimprove symptomswithout negative effectson cognitive function.

28 Rhinitis

Managing the Elderly Patient withAllergic Rhinitis❑ Allergy is a less common cause of perennial rhinitis in

individuals over 65 years of age.♦ Atrophic rhinitis is a cause of chronic, difficult-to-treat

rhinitis in the older patient.♦ 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 patientswith prostatic hypertrophy.♦ Cardiac and CNS stimulation are also of concern.

❑ Sedating antihistamines may cause bladder disturbancesor problems with visual accommodation.♦ The sedating effects may contribute to falls and

fractures.♦ Nonsedating antihistamines are preferred.

Managing Allergic Rhinitis DuringPregnancy ❑ Intranasal cromolyn sodium is considered first-line

treatment.❑ Antihistamine therapy should be considered in patients

who do not respond to intranasal cromolyn sodium.♦ Chlorpheniramine and tripelennamine have a good

safety record, but cause sedation.♦ Loratadine is the only nonsedating antihistamine with

Pregnancy Category B. ♦ Ceterizine is a partially sedating antihistamine with

Pregnancy Category B. ❑ Intranasal corticosteroids may be considered as an

alternative to oral medications or when intranasalcromolyn sodium is ineffective.♦ 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.♦ Pseudoephedrine may be considered to treat nasal

congestion after the first trimester.

29Rhinitis

Elderly patients maypresent with drug-induced rhinitis from: ❑ Reserpine

❑ Guanethidine

❑ Phentolamine

❑ Methyldopa

❑ Prazosin

❑ Chlorpromazine

❑ ACE inhibitors

Intranasal cromolynsodium is consideredfirst-line treatmentfor allergic rhinitisduring pregnancy.

Nasal congestion iscommon during thesecond half ofpregnancy. Consider:❑ Pseudoephedrine for

nasal congestion afterthe first trimester.

❑ Intranasalcorticosteroids for nasalcongestion afterdiscontinuing a topicaldecongestant.

Rhinitis

Baraniuk JN. Pathogenesis of allergicrhinitis. J Allergy Clin Immunol 1997; 99:S763-772.

Bernstein JA. Allergic rhinitis - helpingpatients lead an unrestricted life. PostgradMed 1993; 93: 124-132.

Bousquet J, Vignola AM, Campbell AM,Michel FB. Pathophysiology of allergicrhinitis. Int Arch Allergy Immunol 1996;110: 207-218.

Busse WW. Role of antihistamines in allergicdisease. Ann Allergy 1994; 72: 371-375.

Coates ML, Rembold CM, Farr BM. Doespseudoephedrine increase blood pressure inpatients with controlled hypertension?J Fam Practice 1995; 40: 22-26.

Corren J, Adinoff AD, Buchmeier AD, IrvinCG. Nasal beclomethasone prevents theseasonal increase in bronchialresponsiveness in patients with allergicrhinitis and asthma. J Allergy Clin Immunol1992; 90: 250-256.

Corren J. Allergic rhinitis and asthma:how important is the link? J Allergy ClinImmunol 1997; 99: S781-786.

Ferguson BJ. Allergic rhinitis - options forpharmacotherapy and immunotherapy.Postgrad Med 1997; 101: 117-120.

Ferguson BJ. Allergic rhinitis - recognizingsigns, 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 tubedysfunction: 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 - newertreatment approaches. Drugs 1993; 45:518-527.

International Rhinitis Management WorkingGroup. International consensus report onthe diagnosis and management of rhinitis.Allergy 1994; 19: S5-34.

Jacobs RL, Freedman PM, Boswell RN.Nonallergic rhinitis with eosinophiliaNARES) syndrome: clinical andimmunologic presentation. J Allergy ClinImmunol 1981; 67: 253-262.

Joint task force practice parameters ondiagnosis and management of rhinitis. AnnAllergy Asthma Immunol 1998; 81: 463-518.

Malone D, Lawson K, Smith D, Arrighi H,Battista C. A cost of illness study of allergicrhinitis in the United States. J Allergy ClinImmunol 1997; 99:22-27.

Moneret-Vautrin DA, Shieh V, Wayoff M.Nonallergic rhinitis with eosinophiliasyndrome (NARES) - a precursor of thetriad. Ann Allergy 1990; 64: 513-518.

Nathan RA. Changing strategies in thetreatment of allergic rhinitis. Ann AllergyAsthma Immunol 1996; 77: 255-259.

National Heart Lung and Blood Institute.National Asthma Education and PreventionProgram. Expert Panel Report 2: Guidelinesfor the Diagnosis and Management ofAsthma. April 1997; NIH Publication97-4051: 50.

National Heart Lung and Blood InstituteReport of the Working Group on Asthmaand Pregnancy: Management of AsthmaDuring Pregnancy. September 1993;NIH Publication 93-3279.

Nelson HS. Allergic and nonallergic rhinitis.In: Kassirer JP, Greene HL (eds). CurrentTherapy 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 allergicrhinitis. Br Med J 1997; 314: 1392-1395.

Physician’s Desk Reference. 53rd ed.Oradell, NJ: Medical Economics Company Inc.; 1999.

References

30

Reinberg A, Gervais P, Levi F, et al.Circadian and circannual rhythms ofallergic rhinitis: an epidemiologic studyinvolving 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 andManagement, 5th ed. Philadelphia:Lippincott-Raven, 1997: 183-207.

Round table discussion. The health andeconomic impact of rhinitis. Am J ManCare 1997; 3: S8-18.

Rowe-Jones JM. The link between the noseand lung perennial rhinitis and asthma –is it the same disease? Allergy 1997; 52:S20-28.

Settipane GA, Chafee, FH. Nasal polyps inasthma and rhinitis. J Allergy Clin Immunol1977; 59: 17-21.

Smith LJ. Diagnosis and treatment ofallergic rhinitis. Nurse Practitioner 1995;20: 58-66.

Spector SL. Overview of comorbidassociations 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 healthcareprofessional. 18th ed. Rockville: USPC,1998.

Vuurman EF, VanVeggel LM, Uiterwijk MM,Leutner D, O’Hanlon JF. Seasonal allergicrhinitis and antihistamine effects onchildren’s learning. Ann Allergy 1993; 71:121-6.

Welsh PW, Stricker WE, Chu, CP, et al.Efficacy of beclomethasone nasal solution,flunisolide, and cromolyn in relievingsymptoms of ragweed allergy. Mayo ClinProc 1987; 62: 125-134.

31Rhinitis

33

Asthma

sthma is a chronic inflammatory disease of theairways characterized by airway obstruction

which is at least partially reversible with or withoutmedication, and increased bronchial responsivenessto a variety of stimuli.

Asthma is often associated with allergy. ❑ Risk factors for developing asthma include:

♦ Sensitization to indoor allergens (e.g., house-dustmites, animal danders, cockroaches).

♦ Sensitization to outdoor allergens (e.g., Alternaria). ♦ Early exposure to tobacco smoke.

❑ The allergic response in the airways may lead toincreased airway inflammation andhyperresponsiveness.

Rhinitis and asthma involve a commonrespiratory mucosa.❑ Asthma is commonly associated with perennial and

seasonal rhinitis and rhinosinusitis.♦ 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.♦ 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.♦ Intranasal corticosteroids can be used to treat chronic

rhinitis for patients with persistent asthma. This maylead to asthma improvement.

♦ Oral nonsedating antihistamines and antihistamine-decongestant combinations may improve asthmaoutcomes in some patients.⇒ Treatment of upper airway diseases, alone, is not

adequate treatment of asthma.

Asthma

A Asthma is a chronicinflammatory diseaseof the airways.

Atopy is thestrongest identifiablepredisposing factorfor the developmentof asthma.

Asthma is commonlyassociated withallergic rhinitis. ❑ Rhinitis and asthma

involve a commonrespiratory mucosa.

❑ Treatment of rhinitismay improve asthmasymptoms.

34 Asthma

PathogenesisThe characteristic features of asthmatic inflammation are:❑ Mast cell activation❑ Inflammatory cell infiltration

♦ Eosinophils♦ Airway macrophages♦ Neutrophils (particularly in sudden onset, fatal

exacerbations)♦ Lymphocytes

❑ Edema❑ Mucus hypersecretion❑ Denudation and disruption of the bronchial epithelium❑ Airway inflammation in asthma contributes to:

♦ Airway hyperresponsiveness♦ Respiratory symptoms ♦ Disease chronicity♦ Airflow limitation♦ Airway wall remodeling

⇒ Collagen deposition beneath basement membrane⇒ Mucus gland hyperplasia⇒ Smooth muscle hypertrophy⇒ Vascular proliferation⇒ Loss of elastic fibers

Chronic inflammationin the airways maylead to airway wall“remodeling,” i.e.,chronic structuralchanges that areunlikely to bereversible. ❑ Inflammation in the

airways and airwayremodeling have beenobserved even in mildasthma.

35A

sthma

Progression to Airway Remodeling

Healthy Acute Chronic Remodeling(permanent changes)

Cells

Actions

MediatorsHistamine,

other inflammatorymediators

Neuromechanisms,inflammatory mediators,

cytokinesGrowth factors

During an acute asthmaattack, mast cells releaseinflammatory mediators,resulting in epithelial celledema, muscleconstriction, vascularleakage, and mucushypersecretion.

In chronic asthma, mast cells andeosinophils release inflammatorymediators. Epithelial cells areshed, resulting in exposednerves. Epithelial cells start tolose their cilia, and increasednumbers of glandular cells areobserved. Changes includeincreased muscle mass, sub-basement membrane collagendeposition, and vascularenlargement.

Remodeling can occurleading to permanentchanges. Continued lossof epithelial cells,deposition of sub-basement membranecollagen, and increasedmuscle mass are observed.

MyofibroblastsEosinophils,

lymphocytesMast cells

36 Asthma

Natural HistoryAsthma is often first diagnosed in childhood.❑ 50% to 80% of children with asthma develop asthma

symptoms (coughing, wheezing, shortness of breath orrapid breathing, chest tightness) before 5 years of age.

❑ Factors associated with the onset of wheezing in children:♦ Smaller airways at birth and in early life.♦ Perinatal and childhood exposure to tobacco smoke.♦ Male gender.♦ Low birth weight.♦ A parent, particularly the mother, with atopy or asthma.

Diagnosing the Patient with AsthmaIn establishing a diagnosis of asthma, the clinician mustdetermine that:❑ Episodic symptoms of airflow obstruction are present:

♦ Coughing♦ Wheezing♦ Shortness of breath or rapid breathing♦ Chest tightness

❑ Airflow limitation is at least partially reversible.❑ Alternative diagnoses are excluded.

Asthma can develop atany time in life, evenin the elderly, but theincidence is highest inchildhood. ❑ In children, asthma is

frequently found inassociation with atopy.

Risk factors fordeveloping asthma:❑ Personal history of

allergy.❑ Family (particularly

maternal) history ofallergy or asthma.

❑ Passive tobacco smokeexposure during infancyand childhood.

❑ Sensitization to indoorallergens 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:

♦ Rapid breathing♦ Grunting during sucking♦ Difficulty feeding

37Asthma

Medical History❑ Are there episodic symptoms of:

♦ Coughing?♦ Chest tightness? ♦ Wheezing?♦ Short breath?

❑ Is there a pattern to the symptoms? Do they occur inrelation to certain:♦ Seasons?♦ Times of year?♦ Places (e.g., work, damp basements)?♦ Things (e.g., animals, smoke, scents)?♦ Times of day or night (e.g., awakening)?♦ Types of activities or exercise?

❑ What is the profile of a typical exacerbation?♦ Do chest colds last >10 days?

❑ How did the disease develop? ♦ What was the age of onset of symptoms?♦ When was asthma first diagnosed?♦ Is there a family history of allergies?♦ Has the disease progressed (e.g., remitted, recurred)?♦ How has the patient managed his or her asthma

(previously, presently)? ♦ What was the patient’s response to treatment?

❑ Do precipitating and/or aggravating factors exist athome, work, school, and/or at daycare? Consider:♦ Upper respiratory infections (URI)♦ Environmental allergens (indoor and outdoor)♦ Exercise♦ Occupational activities♦ Environmental changes (e.g., weather, humidity)♦ Irritants (e.g., tobacco smoke, odors, pollutants)♦ Emotions♦ Drugs (e.g., ASA, NSAIDs)♦ Food and food additives (e.g., beer, wine [sulfites])♦ Weather changes♦ Endocrine factors

38 Asthma

❑ What is the impact of the disease on the patient (andthe family)? Consider:♦ Unscheduled care♦ Life-threatening exacerbations♦ Missed school/work/activities♦ Interference with sleep♦ 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:♦ School/childcare? ♦ Workplace?♦ Patient’s (family’s) level of education? ♦ Substance abuse?

❑ What is the patient’s (and family’s) perceptionof the disease? ♦ Do they understand the disease and how it is treated?♦ Can they cope with the disease and its management? ♦ Is support available or needed?♦ What are the economic resources?♦ Are there sociocultural beliefs that need to be

considered?

39Asthma

Objective Measurements❑ If indicators from the

medical history andphysical examinationsuggest asthma, thenconfirm the diagnosiswith objectivemeasures ofpulmonary function.

❑ Spirometry (FEV1)before and 15 minutesafter the patientinhales a short-acting bronchodilator is preferred.♦ Significant reversibility is indicated by an increase

≥ 12% (and, in adults, an increase of 200 mL) in FEV1after inhaling a short-acting bronchodilator.

♦ Consider the bronchodilator response even ifspirometry is normal (i.e., ≥ 80% predicted normal).

❑ Correct technique, calibration methods, andmaintenance of equipment are necessary to achieveconsistently accurate test results. ♦ Use equipment and techniques that meet the

standards developed by the American ThoracicSociety (1995).

Physical examinationof the patient withasthma may be normal.

Some patients may notbe able to performspirometry.❑ In this group, a trial with an

inhaled beta2-agonist and/ora short (3- to 10-day)course of oral corticosteroidmay help aid and/orconfirm the diagnosis.

In many patients withmild asthma, tests oflung function arenormal.

Office-based clinicianswho care for asthmapatients should haveaccess to spirometryfor diagnosis and forperiodic monitoring.

Physical Examination❑ Focus on the upper

respiratory tract, chest, andskin.

❑ Findings that support thediagnosis of asthma:♦ Hyperexpansion of the

thorax, especially inchildren.

♦ Sounds of wheezingduring normal breathingor during deep breathing. ⇒ Wheezing during forced exhalation is not a reliable

indicator of airflow limitation and may not bepresent. It may be produced by dynamiccompression of the large airways.

♦ Signs and symptoms of allergic rhinitis, rhinosinusitis,and nasal polyps.

♦ Atopic dermatitis/eczema.

40 Asthma

If the medical history and physicalexamination suggest asthma, confirmthe diagnosis with objective measuresof pulmonary function. ❑ Spirometry (FEV1) before and 15 minutes

after the patient inhales a short-actingbronchodilator is preferred.

❑ Significant reversibility is indicated by anincrease ≥ 12% (and, in adults, an increaseof 200 mL) in FEV1 after inhaling a short-acting bronchodilator.

When is peak expiratory flow (PEF) used?❑ To diagnose asthma, spirometry is recommended

over peak expiratory flow (PEF) in the clinician’s officebecause:♦ PEF is not as sensitive as FEV1 for diagnosing airflow

obstruction. ⇒ PEF is primarily a measurement of large airway

function. ♦ 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.

❑ Peak flow measurements may be helpful in diagnosingasthma for patients who cannot perform spirometry orin patients who have normal spirometry at the time ofexamination.

Peak flow meter

41Asthma

❑ Monitoring PEF variability over 1 to 2 weeks isrecommended:♦ When patients have asthma symptoms, but normal

spirometry, at the time of examination. ♦ To assess disease severity.♦ 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 isrecommended overpeak expiratory flow(PEF) in theclinician’s officebecause:❑ PEF is not as sensitive

as FEV1 to diagnosisairflow obstruction.

❑ Peak flow meters aredesigned as monitoring,not diagnostic, tools.

❑ Published PEF referencevalues vary widely andaccording to the brandof peak flow meterused.

❑ Patient technique mayvary over time.

Two ways to use the peak flow meterfor 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 afternoonor evening.

❑ The late afternoon or evening measurementmay be done after the patient uses a short-acting bronchodilator.

❑ A greater then 20% difference between themorning and evening measurements suggestsinadequately controlled asthma.

42 Asthma

Masqueraders of asthma in children and adults:

Upperairwaydiseases

❑ Rhinosinusitis(associated cough)

❑ Vocal corddysfunction

❑ Nasal congestion(rhinitis, largeadenoids)

Largeairwaysobstruction

❑ Enlarged lymphnodes or tumor

❑ Tracheal orbronchial stenosisor malacia

❑ Chronicobstructivepulmonary disease

❑ Chronic bronchitis

❑ Bronchiectasis

Smallairwaysobstruction

❑ Cystic fibrosis

❑ Heart disease

❑ Congestive heartfailure

❑ Pulmonaryinfiltration witheosinophilia

❑ Pulmonaryembolism

❑ Viral bronchiolitis

❑ Broncho-pulmonarydysplasia

Othercauses

❑ Recurrent coughnot due to asthma

❑ Aspiration due toswallowingmechanismdysfunction

❑ Gastroesophagealreflux (GERD)

❑ Cough secondaryto medications(i.e., ACEinhibitors)

Cause Both Children Adults

Recurrent episodes of coughing and wheezing(especially at night) are almost always due to asthma,in children and adults.

Differential Diagnosis

43Asthma

Mild

Moderate

Severe

Asthma severity is a continuum.

Classification of Asthma Severity❑ Patients are classified as having mild intermittent or

mild, moderate, or severe persistent asthma based onthe:♦ Severity, frequency, and duration of symptoms. ♦ Level of airflow obstruction.♦ 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.♦ Classifying a patient as having “mild asthma” (either

intermittent or persistent) does not rule out thepossibility of a severe exacerbation.

❑ Patients with more than 2 episodes of asthma symptomsper week, or with evidence of airflow obstructionbetween symptom episodes, have persistent asthma.

Classification ofasthma severity isbased on the:❑ Severity, frequency, and

duration of symptoms. ❑ Degree of airflow

obstruction.❑ Extent to which the

disease interferes withdaily activities.

Asthma severity is acontinuum. The severity may change over time.❑ Persistent asthma may

become more or lesssevere over time.

❑ Symptom exacerbations(“asthma attacks”) maybe severe, regardless ofthe severity classificationof the underlying asthma.

44 Asthma

SeverePersistent

❑ Continualsymptoms

❑ Limited physicalactivity

❑ Frequent exacerbationsinterfere withnormal activities

Classification Clinical Features BEFORE Treatment

❑ FEV1 orPEF ≤ 60%predicted

❑ PEF variability> 30%

q.i.d. use dailydoes NOTcompletelyrelievesymptomsFrequent

ModeratePersistent

❑ Daily symptoms

❑ Exacerbations≥ 2 times/ week; maylast days; mayaffect activities

❑ FEV1 or PEF> 60% to < 80%predicted

❑ PEF variability> 30%

Daily > 1 time/week

MildPersistent

❑ Symptoms > 2times/week but< 1 time/day

❑ Exacerbationsmay affectactivities

❑ FEV1 or PEF> 80%predicted

❑ PEF variability20% to 30%

> 2 times/week but< 1 time/day

> 2 time/month

MildIntermittent

❑ Symptoms ≤ 2times/week

❑ Asymptomaticand normalPEF betweenexacerbations

❑ Exacerbationsbrief (from a fewhours to a fewdays); intensitymay vary

❑ FEV1 or PEF≥ 80%predicted

❑ PEF variability< 20%

≤ 2 times/week

≤ 2 time/month

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 shouldbe assigned to the most severe grade in which any feature occurs. Those unable toperform lung function tests are classified by symptoms.

Asthmaseverity

Symptomseverity

Nighttimesymptoms

Lung function in patients who CAN use aspirometer orpeak flow meter

Short-actingbeta2-agonist use

45Asthma

2. Classifying asthma severity AFTER optimaltreatment is attained. The patient’s asthma severitycan be classified according to the level of treatmentneeded to maintain control. For example:

❑ For mild intermittent asthma, no daily medication isneeded. However, the use of a short-acting beta2-agonistmore than 2 times per week may indicate the need tostart long-term control therapy.

❑ For mild persistent asthma, one daily long-termcontrol medication is necessary.

❑ For moderate persistent asthma, inhaledcorticosteroids with or without additional long-termcontrol medications are used.

❑ For severe persistent asthma, multiple long-termcontrol medications are required, including high-doseinhaled corticosteroids and, if needed, oralcorticosteroids.

Patients with asthma may need additionaltests to aid and/or confirm the diagnosis.The general principles of diagnostic testing are included inVolume 1: Diagnostic Testing, page 31. Specific diagnosisfor Asthma is included here.

Patient has symptoms(coughing, wheezing,breathlessness, chesttightness), but spirometryis (near) normal

❑ Assess diurnal variationof PEF over 1 to 2 weeks

❑ Bronchoprovocationwith histamine,methacholine, orexercise (if negative, may rule out asthma)

Suspect other factors arecontributing to severity orasthma symptoms

❑ Nasal examination❑ Allergy tests,

gastroesophageal refluxtests, sinus radiography

Symptoms suggestinfection, large airwaylesions, heart disease, orobstruction by foreignobject

❑ Routine chest x-ray,CAT scan

Suspect coexisting chronicobstructive pulmonarydisease or restrictivedefect

❑ Additional pulmonaryfunction tests; diffusingcapacity test

Reasons forAdditional Tests

Suggested Tests

All patients withasthma need a short-acting beta2-agonist for acutesymptoms, p.r.n. ❑ The intensity of

treatment to relieveacute symptomsdepends upon theseverity of theexacerbation.

❑ Using a short-actingbeta2-agonist daily, orincreasing use, indicatesthe need for additionallong-term control therapy(assuming compliancewith therapy, no newexposures to causalfactors, and no untreatedrhinosinusitis, rhinitis, orgastroesophageal reflux).

Should the patient beskin-tested for allergy?❑ Many patients with

asthma are allergic,but allergy may not berecognized.

❑ Review the patient’sexposure to allergens.

❑ Skin-testing isrecommended forpatients with: ♦ Persistent asthma who

are exposed toperennial allergens.

♦ Seasonal symptomswho are beingconsidered for allergenimmunotherapy.

❑ Consider referral to orconsultation with anallergy/immunologyspecialist.

46 Asthma

Component 1. Measures of Assessmentand Monitoring ❑ Once the initial diagnosis of asthma has been

confirmed, periodic assessments and ongoingmonitoring are recommended.

❑ Monitor regularly:♦ Signs and symptoms of asthma♦ Pulmonary function♦ Occurrence of symptom exacerbations♦ Pharmacotherapy♦ Quality of life/functional status♦ Patient’s (and family’s) satisfaction with therapy♦ Patient’s (and family’s) understanding of asthma and

its management❑ Assess symptoms and clinical signs at each healthcare

visit through appropriate questions and physicalexamination. ♦ Detailed patient recall of symptoms changes over

time. ♦ Use a short (2- to 4-week) recall period.

❑ Review the patient’s medication(s) and dosage(s)regularly, including: ♦ Adherence with treatment♦ Inhaler technique♦ Use of inhaled beta2-agonist♦ Frequency of oral corticosteroid “burst” therapy♦ Changes in dosage of long-term control medications♦ Medication side effects♦ Patient concerns

The goals of therapyfor the patient withasthma:❑ Prevent chronic and

troublesome symptoms(e.g., coughing orbreathlessness in thenight, in the earlymorning, or afterexertion).

❑ Maintain (near)“normal” pulmonaryfunction.

❑ Maintain normal activitylevels (includingexercise and otherphysical activity).

❑ Prevent recurrentexacerbations ofasthma, and minimizethe need for emergencydepartment visits orhospitalizations.

❑ Provide optimalpharmacotherapy, withminimal or no adverseeffects.

❑ Meet the patient’s (andfamily’s) expectationsof, and satisfaction with,asthma care.

Measures ofassessmentand monitoring

Control of factorscontributingto asthma severity

1 Pharmacologictherapy

Education for apartnershipin asthma care2

34

Managing the Patient with AsthmaThe four components of asthmamanagement:

47Asthma

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 ofairway function. ♦ Spirometry may be indicated more often than every

year, depending on the patient’s asthma severity andresponse to management.

Peak expiratory flow monitoring maybe helpful.❑ Long-term daily PEF monitoring can help patients with

moderate-to-severe persistent asthma:♦ Evaluate responses to changes in therapy.♦ Detect early changes in disease severity that may

require treatment.♦ 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 flowmonitoring is recommended to:♦ Evaluate responses to changes in chronic

maintenance therapy. ♦ Establish the individual patient’s personal best PEF.♦ Identify the temporal relationship between changes

in PEF and exposure to environmental irritants orallergens.

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.

To determine thepatient’s personalbest PEF:❑ Use the same peak flow

meter.❑ Record PEF 2 times/day

for 2 weeks.❑ A burst of oral

corticosteroid or a trialof high dose inhaledcorticosteroid may benecessary.

48 Asthma

Measure PEF at home:❑ When perceptions of symptoms are unreliable.❑ To determine when treatment needs to be increased or

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.

Using the peak flowmeter requires effortand learned skill.Teach the patient (and family andcaregivers):❑ How to use the peak

flow meter.❑ How to interpret peak

flow measurements.

Two ways to use thepeak flow meter formeasuring PEFvariability1. Use only in the morning

upon awakeningBEFORE using a short-acting bronchodilator.

OR

2. Use in the morning ANDin the late afternoon orevening.

❑ The late afternoon orevening measurementmay be done after thepatient uses a short-acting bronchodilator.

❑ A greater than 20%difference between themorning and eveningmeasurements suggestsinadequately controlledasthma.

Patients withmoderate persistentor severe persistentasthma should have apeak flow meter athome, if feasible.

>80%

50%-80%

<50%

Green Zone: Good control!❑ No asthma symptoms.❑ Take medications as usual.

Yellow Zone: Caution!❑ Use a short-acting inhaled

beta2-agonist.❑ Check about changing

medications or increasing dose.

Red Zone: Medical alert!❑ Use a short-acting inhaled

beta2-agonist.❑ Call doctor or go to emergency

department.

49Asthma

During periodicassessment andmonitoring, it iscritical to determinethat the patient isusing the appropriatepharmacotherapy forthe level of diseaseseverity.

To evaluate the levelof asthma control, askabout1. Daytime symptoms

(including wheeze,cough, chest tightness,or shortness of breathor rapid breathing).

2. Nocturnal awakeningdue to asthmasymptoms.

3. Early morningsymptoms.

4. Relationship ofsymptoms to exercise,respiratory infection,activities, environmentalexposures.

5. Tolerance of exercise,cold air, physicalactivities.

6. Frequency of use ofquick-relief medication.

Cutpoints for PEF monitoring:

❑ PEF ≤ 80% of the patient’s personal best before a short-acting bronchodilator may indicate a need for additionalmedication.

❑ PEF ≤ 50% of the patient’s personal best indicates asevere asthma exacerbation.

❑ Cutpoints are arbitrary, and should be tailored to thepatient’s 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

(home/work/school/recreation/exercise).❑ Disturbances in sleep due to asthma.❑ Changes in caregiver activities due to a child’s 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 inadequateasthma control.

❑ To monitor their disease, patients need to know:♦ How to use a peak flow meter.♦ Their warning signs of worsening disease.♦ How and when to seek emergency care.

50 Asthma

Tips for working within timeconstraints 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 oftreatment and after an exacerbation.

❑ Break the assessment and education needs intoseveral components during these visits. Somecould 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 answerquestions and provide information.

❑ Consider using a home case-manager forfollow-up assessments and education, if one is available through your HMO.

❑ Use videos and educational materials fromoutside sources.

❑ Suggest possible formal education programsand educational support groups.

❑ Refer to school nurse for monitoring andfurther education.

Component 2. Controlling FactorsContributing to Asthma Severity❑ The first and most important step in controlling asthma

is to reduce exposure to causal factors.♦ Causal factors, sometimes referred to as “triggers,”

provoke asthma symptoms (e.g., exercise, cold air).♦ Causal factors increase the underlying airway

inflammation (e.g., allergens, viral respiratoryinfections, tobacco smoke, occupational exposures,air pollution).

❑ Patients with asthma at any level of severity should try toavoid environmental exposure to allergens to which theymay be sensitive as well as to irritants such as tobaccosmoke, wood smoke, air pollutants, and perfumes.

❑ Primary prevention of asthma (preventing initialdevelopment) may alter its course. See page 85.

❑ The avoidance techniques and tips included inVolume 1: Environmental control, page 43, areappropriate for the patient with asthma.

Allergens are common causal factors.❑ For patients with persistent asthma, the clinician should:

♦ Identify allergen exposures.♦ Determine probable relationships to allergens by

pattern(s) of symptoms.♦ Determine sensitivity to indoor allergens to which the

patient is exposed with skin-testing or in vitromeasurements of serum IgE antibodies.

♦ Assess the significance of positive tests in context ofthe patient’s medical history.

❑ Allergen immunotherapy may be considered for asthmapatients when:♦ There is clear evidence of a relationship between

symptoms and exposure to an unavoidable allergen towhich the patient is sensitive.

♦ Symptoms occur all year or during a major portion ofthe year.

❑ The addition of immunotherapy to pharmacologictherapy may be warranted when: ♦ The medication is ineffective. ♦ Multiple medications are required. ♦ The patient or family is not accepting of medication.♦ The benefits of modifying the immune response are

attractive to the patient.51Asthma

The most importantstep in controllingasthma is to reduceexposure to factorswhich exacerbatesymptoms.

Occupationalexposures mayincrease asthmasymptoms and/orprecipitate asthmaexacerbations (page 91).

Common causal factors of asthma:

EnvironmentalFactors

❑ Remove animal from house, or at minimum, keep animalout of patient’s bedroom.

❑ Seal or cover with a filter, air ducts that lead to bedroom.

❑ Room air filters (HEPA-type).

Animal dander

Essential:

❑ Encase mattress, pillow, and boxsprings in an allergen-impermeable cover.

❑ Wash bedding weekly in hot water (≥ 130ºF).

❑ Reduce indoor humidity to < 50%.

Desirable:

❑ Remove carpets from the bedroom, and carpets in otherrooms that are laid on concrete.

❑ Minimize upholstered furniture.

Dust mites

❑ Use poison bait or traps to control.

❑ Do not leave food or garbage exposed.

Cockroaches

❑ Limit exposure during season by staying indoors withwindows closed, especially when pollen is elevated. (see Volume 1: Background, page 13)

❑ Use air conditioning.

Pollens and outdoormolds

❑ Fix all water leaks.

❑ Clean moldy surfaces.

❑ Reduce indoor humidity to < 50%.

Indoor mold

❑ Advise patients and others in home to stop smoking orsmoke outside and away from the home; do not allowsmoking in car.

❑ Discuss ways to reduce exposure to other sources oftobacco smoke.

Tobacco smoke

❑ Discuss ways to reduce exposure to:

♦ Wood-burning stoves or fireplaces.

♦ Unvented stoves or heaters.

♦ Other irritants (e.g., perfumes, cleaners).

Indoor/outdoorpollutants and irritants

Dates and times of highest pollencounts differ geographically.

52 Asthma

Recommendations for Reducing Exposure

Other CausalFactors

❑ Optimize treatment of chronic rhinitis in patients withpersistent asthma.

Rhinitis (allergic andnonallergic)

❑ Optimize treatment for chronic or recurrent rhinosinusitis.

❑ Use medical measures to promote drainage.

Rhinosinusitis

❑ Annual influenza vaccinations are recommended for patientswith persistent asthma who do not have severe systemicsensitivity to egg.

Respiratoryinfections

❑ Patients with frequent heartburn or suspected GERD should:

♦ Avoid food and drink within 3 hours of retiring.

♦ Avoid caffeine, alcohol, and chocolate.

♦ Elevate the head of the bed 6 to 8-inches.

♦ Pharmacologic therapy may be necessary.

Gastroesophagealreflux

❑ Patients with symptoms of sleep apnea should:

♦ Consider weight reduction.

♦ Treat rhinitis.

♦ Consider intervention (e.g., CPAP).

Obstructive sleepapnea

❑ Counsel patients regarding the risks of aspirin as well asother nonsteroidal anti-inflammatory drugs which mayprecipitate severe and even fatal asthma exacerbations insensitive patients.

❑ Primary treatment is avoidance, though some patientsdemonstrate improvement with oral aspirin desensitization.

Aspirin sensitivity

❑ Patients with symptoms on exposure should avoid foodsprocessed with sulfites as preservatives, e.g.:

♦ Processed potatoes ♦ Shrimp

♦ Dried fruit ♦ Wine, beer

Sulfite sensitivity

❑ Avoid beta-blockers, including eye drops.

❑ Always consider appropriate alternate agents.

Beta-blockers

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).

53Asthma

Recommendations for Reducing Exposure

Some patients are sensitive to changesin weather and humidity. Others aresensitive to pollens and environmentalirritants (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❑ A stepwise approach to treating asthma is recommended

to gain and maintain control of symptoms.❑ Because asthma involves chronic airway inflammation,

long-term control therapy requires efforts to suppressasthmatic inflammation as well as to prevent episodes ofasthma symptoms. ♦ The amount and frequency of medication is dictated by

asthma severity and is directed toward suppressingairway inflammation.

♦ When initiating therapy, take into account the needsand circumstances of the patient.

♦ All patients need to have a short-acting beta2-agonist totake as needed for acute symptoms.

There are two approaches to initiatingstep-care therapy:1. Start therapy at a level higher than indicated by the

patient’s initial severity.♦ Either add a short course of oral corticosteroids to

inhaled corticosteroids, cromolyn sodium, nedocromilsodium, or other long-term control therapy,

♦ Or use a higher dose of inhaled corticosteroids. Thisapproach is preferred.

OR2. Start therapy at a level appropriate to the patient’s initial

severity and gradually increase therapy if control is notachieved.

54 Asthma

Diagnosing andtreating upperrespiratory tractdisease (rhinitis,rhinosinusitis) is anintegral part ofmanaging the patientwith asthma.

Asthma involveschronic airwayinflammation.❑ Long-term control

therapy requires effortsto suppress asthmaticinflammation as well asto prevent episodes ofasthma symptoms.

❑ All patients need tohave a short-actingbeta2-agonist to takeas needed for acutesymptoms.

Remember to:❑ Step down therapy

gradually when controlis achieved.

❑ Monitor regularly toensure that control isachieved andmaintained.

When do you step up, or increase, long-termcontrol medications?

❑ To regain control when the patient has:♦ Increased symptoms and/or nighttime or early

morning awakenings due to symptoms.♦ Reduced ability to play, exercise, or participate in

normal daily activities.♦ Daily or increasing use of short-acting beta2-agonists.♦ Gradual reduction in PEF (by about 20%).♦ Not met the goals of therapy.

How do you help the patient regain control ofhis/her asthma?

❑ A short (3- to 10-day) course of oral corticosteroids may be needed to speed the resolution of moderatepersistent or severe persistent exacerbations, or to re-establish control during a period of graduallydeteriorating 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 oralcorticosteroids frequently, consider a step up, orincrease, in the long-term control medication.♦ This can be achieved by increasing the dose of

inhaled corticosteroid and/or adding long-termcontrol therapy.

When and how do you step down long-term controltherapy?

❑ After starting daily long-term control medication,regular follow-up visits (at 1-to 6-month intervals) areessential. Monitor:♦ Symptoms, especially nighttime awakenings and

activity levels.♦ Use of quick-relief medications.♦ Pulmonary function, preferably with spirometry.

❑ If asthma is controlled for 2 to 3 months, then graduallydecrease the dose, frequency, or number ofmedications, and re-evaluate in 2 to 3 months.

❑ Most patients with persistent asthma require continuedmedication to suppress underlying airway inflammation.♦ Long-term control medications reduce the need for

quick-relief medications and may prevent anticipatedsymptoms (e.g., from exercise, allergens, cold air).

55Asthma

Before stepping uptherapy, reviewpossible reasons forpoor asthma control: ❑ Adherence to

medication regimen❑ Inhaler technique❑ Environmental control❑ Complicating factors

(e.g., rhinosinusitis,allergic rhinitis)

❑ Psychosocial factors

Stepping up can beachieved by:❑ Increasing the inhaled

corticosteroid dose.❑ Adding long-term

control therapy.

Stepping down can beachieved by:❑ Lower doses❑ Fewer doses❑ Using a different

medication

❑ Always follow a decrease in therapy with close follow-upin the clinic or by phone.♦ The patient should monitor asthma symptoms

and PEF, and alert the doctor promptly ifworsening occurs.

Reduce therapy gradually.

❑ How much to reduce therapy is based on evaluation ofthe patient’s asthma severity and any specialconsiderations.♦ Asthma can deteriorate at a highly variable rate and

intensity.♦ For inhaled corticosteroids, some physicians suggest

decreasing the dose by 25% every 2 to 3 months tothe lowest possible dose to maintain control.

♦ Carefully follow up.

Patients with severe persistent asthmawhose symptoms are not controlled onhigh doses of inhaled corticosteroids,long-acting bronchodilators, plus otherlong-term control medications (e.g.,theophylline, leukotriene pathwaymodifiers) may need to use oralcorticosteroids on a regular basis. Forthese patients: ❑ 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 isachieved. ♦ High doses of inhaled corticosteroids are

preferable because of fewer adverse effects.❑ Consultation with an asthma specialist for

comanagement is recommended.

56 Asthma

Maintain the patienton the lowest doseof medication thatcontrols asthma.

The aim of asthmatherapy is to gaincontrol promptly, andthen “step down” tothe lowest level oftherapy that maintainscontrol of 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.

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 ofpersistent 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:♦ Osteoporosis, especially in post-menopausal women.♦ Increased intraocular pressure (older adults).♦ Cataracts (older adults).♦ The exact doses leading to these side effects are not

known and may differ among patients andpharmacologic agents.

57Asthma

To keep medicationsat a minimum, useenvironmental controlmeasures for:❑ Tobacco and/or wood

smoke.❑ Allergens to which the

patient is sensitive(e.g., dust mites,cockroaches, molds,animal dander).

❑ Other airborne irritants(e.g., fumes, odors).

Inhaledcorticosteroids are themost potent andeffective long-term anti-inflammatorymedications currentlyavailable.❑ Inhaled corticosteroids

are extremely effectivedrugs and safe when used properly (i.e., atrecommended dosesand with aspacer/holdingchamber).

❑ The potential risks ofinhaled corticosteroids are well balanced bytheir benefits.

58 Asthma

❑ Inhaled corticosteroids have been shown to cause areduction in growth velocity when administered tochildren.♦ Poorly controlled asthma may delay growth.♦ Children with asthma tend to have longer periods of

reduced growth rates before puberty (males morethan females).

♦ Growth rates are highly variable. Short-termevaluations may not be predictive of final attainedadult height.

♦ Regular and accurate height measurements areadvised every 3 to 4 months for all children andadolescents using these medications.

Cromolyn Sodium/Nedocromil Sodium❑ Nonsteroid anti-inflammatory agents.❑ Alternative therapy to low doses of inhaled

corticosteroids (especially in children) in mildpersistent asthma.

❑ Cromolyn is no longer the preferred first-line treatmentfor mild persistent asthma in children. It has beenreplaced by low-dose inhaled corticosteroids.Nedocromil is no longer recommended for childrenunder 5 years of age.

❑ Can be used on an as-needed basis to preventsymptoms 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, butthe position of leukotriene modifiers in therapy has notbeen fully established.

❑ 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. ♦ Evaluate hepatic transaminases at initiation of and

during therapy.♦ 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, especiallynighttime 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 diminishedbronchoprotective effect may be observed withcontinuous therapy. The clinical significance is unclear.

59Asthma

60 Asthma

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.

♦ Use lowest possible dose and/or alternate day dosingin severe persistant asthma.

61Asthma

Short-acting beta2-agonists are the mosteffective medicationsfor relieving acutebronchospasm.

Increasing use ofshort-acting beta2-agonists indicatesinadequate control ofasthma and the needto initiate or intensifylong-term controltherapy.

Short-actingbronchodilators forURI:❑ Inhaled route is

preferred. ❑ With severe episodes,

oral corticosteroids for3 to 10 days may benecessary.

❑ For recurrent episodes(especially thoserequiring oralcorticosteroids),consider starting orincreasing the dose ofdaily anti-inflammatorymedication.

Quick-relief MedicationsQuick-relief medications give prompt relief ofbronchoconstriction 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 indicatorfor initiating or increasing anti-inflammatory therapy.

❑ Increasing use indicates inadequate control of asthmaand 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 severeexacerbations.♦ A course of 7 days or less is often sufficient. ♦ Longer courses may be required to treat severe

exacerbations.♦ 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 beta2-

agonists.❑ Treatment of choice for bronchospasm in patients

receiving beta-blockers.

62 Asthma

Step Down Step Up

Review treatment every 1 to 6 months; a gradualstepwise reduction in treatment may be possible.

If control is not maintained, consider step up.First, review patient medication technique,adherence, and environmental control(avoidance of allergens and/or other factors thatcontribute to asthma severity).

Symptoms/DaySymptoms/Night Daily Medications

Classify Severity: Clinical Medications Required To MaintainFeatures Before Treatment or Long-Term ControlAdequate Control

ContinualFrequent

Stepwise approach for managing infants and young children (5 yearsof age and younger) with acute or chronic asthma symptoms:

❑ 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 steroidsand maintain control with high-dose inhaledcorticosteroids.)

Daily> 1 night/week

> 2/week but < 1x/day> 2 nights/month

Mild persistant

Step2 ❑ Preferred treatment:– Low-dose inhaled corticosteroids (with nebulizer or

MDI with holding chamber with or without face maskor DPI)

❑ Alternative treatments (listed alphabetically):– Cromolyn (nebulizer is preferred; or MDI with holding

chamber) OR leukotriene receptor antagonist.≤ 2 days/week≤ 2 nights/month

Mild inter-mittent

Step1 ❑ No daily medication needed.

Moderatepersistant

Step3

Severe persistant

Step4

❑ Preferred treatment:– Low-dose inhaled corticosteroids and long-acting

inhaled beta2-agonists.OR

– Medium-dose inhaled corticosteroids.❑ Alternative treatment:

– Low-dose inhaled corticosteroids and eitherleukotriene receptor antagonist or theophylline.

If needed (particularly in patients with recurring severeexacerbations)❑ Preferred treatment:

– Medium-dose inhaled corticosteroids and long-actingbeta2-agonists

❑ Alternative treatment:– Medium-dose inhaled corticosteroids and either

leukotriene receptor antagonist or theophylline.

Source: NAEPP Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma – Update on SelectedTopics 2002, www.nhlbi.nih.gov.

62AAsthma

Quick Relief for all patients 5 years of age andyounger with acute asthma symptoms

❑ Bronchodilator as needed for symptoms. Intensity oftreatment 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 orpatient has history of previous severe exacerbations

❑ Use of short-acting beta2-agonists > 2 times week in intermittentasthma (daily, or increasing use in persistent asthma) may indicatethe need to initiate (increase long-term control therapy.

Further explanation of information in asthma step-chart on page 62:

❑ Step 2:♦ For children younger than 5 years of age, recommendations are

based on extrapolation of studies in older children. Preferred arelow-dose inhaled corticosteroids, with nebulizer, dry powderinhaler, or metered-dose inhaled with holding chamber, with orwithout a facemask. Alternative, but not preferred, therapiesinclude (in alphabetical order) cromolyn (nebulizer is preferredover 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 fromstudies in older children and adults and expert opinion. Untilsufficient data in children are available, there are two options forpreferred therapy in Step 3 care: either low- dose inhaledcorticosteroids plus long-acting inhaled beta agonists (Evidence Bextrapolation from adult studies) OR increasing the dose ofinhaled corticosteroids within the medium dose range (EvidenceD). However, combination therapy is preferred over use of highdoses of inhaled corticosteroids to avoid the potential for adverseeffects in this younger population. Alternative, but less effectiveapproaches are adding leukotriene modifiers or theophylline tolow-dose inhaled corticosteroids. Regardless of which form ofadjunctive therapy is selected, once control is achieved for 2 to 3months, therapy should be stepped down if possible.

❑ Step 4:♦ High-dose inhaled corticosteroids plus inhaled long-acting beta2-

agonists.

And

If needed, add systemic corticosteroid.

The Stepwise Approach presents guidelines toassist clinical decision-making. Asthma is highlyvariable. Clinicians should tailor specific medication plansto the needs and circumstances of the child and family.❑ Gain control as quickly as possible. Start treatment

with either:♦ Aggressive therapy (e.g., a course of oral

corticosteroid or a higher dose of inhaledcorticosteroid); OR

♦ A level appropriate to the child’s initial severity,and step up if necessary.

THEN gradually decrease treatment to the leastmedication 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-termcontrol therapy.

❑ Some children with intermittent asthma experiencesevere and life-threatening exacerbations separated bylong periods of normal lung function and no symptoms.This may be especially common with exacerbationsprovoked by respiratory infections. A short course oforal corticosteroid is recommended.

❑ At each step, children (and their families) shouldcontrol their environment to avoid causal factors thatmake their asthma worse (e.g., allergens, irritants). Thisrequires specific diagnosis and patient education.

❑ Consultation with an asthma specialist is recommendedfor children with moderate or severe persistent asthmain this age group. Consultation should be consideredfor all children with mild persistent asthma.

❑ It is important to remember that there are very fewstudies on asthma therapy for infants.

Maintain the childon the lowest doseof medication thatcontrols asthma.

To keep medicationsto a minimum, useenvironmental controlmeasures 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 theday or at night.

❑ Minimal (ideally NO)asthma episodes.

❑ Minimal use (<1x/day)of short-acting beta2-agonist.

❑ PEF ≥ 80% of personalbest, if used.

❑ Minimal (ideally NO)adverse effects frommedications.

❑ NORMAL ACTIVITIES.

63Asthma

For exacerbations triggered by viral URIs, use short-acting bronchodilator q4- to 6-hr, as needed, up to24 hr (longer with physician consult).❑ If exacerbations occur more frequently than every

6 wk, consider prophylactic anti-inflammatorytherapy (Steps 2 or 3).

❑ Consider oral corticosteroids (3- to 10-day):♦ If the exacerbation is severe.♦ At the onset of a viral respiratory infection in

a child with a history of previous severeexacerbations.

64 Asthma

Stepwise approach for managing asthma in adults and children olderthan 5 years of age with acute or chronic asthma symptoms:

Symptoms/Day PEF of FEV-1Symptoms/Night PEF Variability Daily Medications

Classify Severity: Clinical Medications Required To MaintainFeatures Before Treatment or Long-Term ControlAdequate Control

ContinualFrequent

❑ 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 perday). (Make repeat attempts to reduce systemicsteroids and maintain control with high-doseinhaled corticosteroids.)

Daily>> 1 night/week

> 2/week but < 1/day> 2 nights/month

Mild persistant

Step2 ❑ Preferred treatment:– Low-dose inhaled corticosteroids.

❑ Alternative treatment (listed alphabetically):– Cromolyn, leukotriene modifier, nedocromil OR

sustained release theophylline to serumconcentration of 5-15 mcg/mL.

≤ 2 days/week≤ 2 nights/month

≤ 60%> 30%

60% - < 80%> 30%

≥ 80%20-30%

≥ 80%< 20%

Mild inter-mittent

Step1 ❑ No daily medication needed.❑ Severe exacerbations may occur, separated by long

periods of normal lung function and no symptoms. Acourse of systemic corticosteroids is recommended.

Moderatepersistant

Step3

Severe persistant

Step4

❑ Preferred treatment:– Low-to-medium dose inhaled corticosteroids

and long-acting inhaled beta2-agonists.❑ Alternative treatment (listed alphabetically):

– Increase inhaled corticosteroids within themedium-dose range.OR

– Low-to-medium dose inhaled corticosteroids andeither leukotriene modifier or theophylline.

If needed (particularly in patients with recurring severeexacerbations):❑ Preferred treatment:

– Increase inhaled corticosteroids withinmedium-dose range and add long-acting beta2-agonists.

❑ Alternative treatment (listed alphabetically):– Increase inhaled corticosteroids within medium-

dose range and add either leukotriene receptorantagonist or theophylline.

Source: NAEPP Expert Panel Report: Guidelines for the Diagnosis and Management of Asthma – Update on SelectedTopics 2002, www.nhlbi.nih.gov.

Step Down Step Up

Review treatment every 1 to 6 months; a gradualstepwise reduction in treatment may be possible.

If control is not maintained, consider step up. First,review patient medication technique, adherence, andenvironmental control (avoidance of allergens and/orother factors that contribute to asthma severity).

64AAsthma

Quick Relief for all patients – adults and childrenolder than 5 years – with acute asthma symptoms

❑ Short-acting bronchodilator: 2-4 puffs short-acting inhaled beta2-agonists as needed forsymptoms.

❑ Intensity of treatment will depend on severity ofexacerbation; up to 3 treatments at 20-minuteintervals or a single nebulizer treatment asneeded. Course of systemic corticosteroids maybe needed.

❑ Use of short-acting beta2-agonists > 2 times aweek in intermittent asthma (daily, or increasinguse in persistent asthma) may indicate the needto initiate (increase long-term control therapy.

Stepwise approach for managing asthma in patients> 5 years of age with acute or chronic asthmasymptoms.

Further explanation of information in asthma step-chart on page 64:

❑ Step 2:

♦ For children 5 years of age and older, the preferredtherapy is inhaled corticosteroids (low dose).Alternative therapies (listed alphabetically becausethere are no data to enable rank) include cromolyn,LTRAs, nedocromil, or sustained-release theophylline.

❑ Step 3:

♦ Preferred therapy: Low-medium dose inhaledcorticosteroids plus long acting inhaled beta2-agonists.

♦ Alternative therapy: medium-dose inhaledcorticosteroids or low-medium dose inhaledcorticosteroids plus leukotriene modifier, or low-medium dose inhaled corticosteroids plustheophylline.

❑ Step 4:

♦ High-dose inhaled corticosteroids plus inhaled long-acting beta2-agonists.

AndIf needed, add systemic corticosteroid.

The Stepwise Approach presents guidelines to assistclinical decision-making. Asthma is highly variable.Clinicians should tailor specific medication plans to theneeds and circumstances of the patient (and family).❑ Gain control as quickly as possible. Start treatment

with either:♦ Aggressive therapy (e.g., a course of oral

corticosteroid or a higher dose of inhaledcorticosteroid); OR

♦ A level appropriate to the patient’s initial severity,and step up if necessary.

THEN gradually decrease treatment to the leastmedication 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-termcontrol therapy.

❑ Some patients with intermittent asthma experiencesevere and life-threatening exacerbations separated bylong periods of normal lung function and no symptoms.This may be especially common with exacerbationsprovoked by respiratory infections. A short course oforal corticosteroid is recommended.

❑ At each step, patients (and their families) shouldcontrol their environment to avoid causal factors thatmake their asthma worse (e.g., allergens, irritants). Thisrequires specific diagnosis and patient education.

❑ Referral to an asthma specialist for consultation orcomanagement is recommended if there are difficultiesachieving or maintaining control of asthma or if thepatient requires Step 4 care. Referral may be consideredif the patient requires Step 3 care.

Maintain the patienton the lowest doseof medication thatcontrols asthma.

To keep medicationsto a minimum, useenvironmental controlmeasures for:❑ Tobacco and/or wood

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 theday or at night.

❑ Minimal (ideally NO)asthma episodes.

❑ Minimal use (<1x/day)of short-acting beta2-agonist.

❑ PEF ≥ 80% of personalbest, if used.

❑ Minimal (ideally NO)adverse effects frommedications.

❑ NORMAL ACTIVITIES.

65Asthma

For exacerbations triggered by viral URIs, useshort-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 anti-inflammatory therapy (Steps 2 or 3).

❑ Consider oral corticosteroids (3- to 10-day):♦ If the exacerbation is severe.♦ At the onset of a viral respiratory infection in a

patient with a history of previous severeexacerbations.

66A

sthma

The most important determinant of appropriate dosing is the clinician’s judgment of the patient’s response to therapy.The clinician must monitor several clinical parameters to assess both efficacy and adverse effects, and adjust the doseaccordingly.The Stepwise Approach to therapy emphasizes that once control of asthma is achieved, the dose of medication shouldbe carefully titrated to the minimum dose required to maintain control.

Medications to Treat Patients with Asthma in the United States

Charts on pages 67-73 reflect information from National Heart Lung and Blood Institute. National Asthma Education and Prevention Program. Expertpanel report 2: guidelines for the diagnosis and management of asthma. April 1997: NIH Publication 97-4051; American Academy of Allergy, Asthma andImmunology. Pediatric asthma promoting best practice: Guide for managing asthma in children, 1999; and the Physician’s Desk Reference, 53rd ed. Oradell,NJ; Medical Economics Company, Inc., 1999.

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1 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 circumstancesof the patient.

2 Max dose represents aggragate dose and can vary depending on previous therapy.

Long-Term Control MedicationsInhaled corticosteroids

Dosage form(s)Brand name(s)

Beclovent®,Vanceril®

Vanceril-DS®

Generic nameDose1 Potential adverse effects

and therapeutic issues

Beclomethasonedipropionate

MDI:42 mcg/puffMDI:84 mcg/puff

2-8 puffs/day1-4 puffs/day

FOR ALL INHALEDCORTICOSTEROIDS:

❑ Cough, dysphonia,moniliasis; high doses mayhave systemic effectsalthough studies are notconclusive and clinical significance is not clear.

❑ Monitoring growth isrecommended when usedin children.

❑ The potential risks ofinhaled corticosteroids arewell balanced by theirbenefits.

❑ To minimize local andsystemic adverse events,use MDI with aspacer/holder chamber.

low medium high2

8-16 puffs/day4-8 puffs/day

> 16 puffs/day> 8 puffs/daymax: 0.84 mg/ dayadults, 0.42mg/day children

PulmicortTurbuhaler®

Budesonide DPI: 200 mcg/puff 8 puffs/daymax: 1.6 mg/ dayadults, 0.8mg/day children

AeroBid®,AeroBid-M®

Flunisolide MDI:250 mcg/puff

2 puffs/day 4 puffs/day

PulmicortRespules™

Budesonide Nebulizing suspension .50 mg/day 1.0 mg/day 2.0 mg/day

> 5 puffs/daymax: 2 mg/ dayadults, 1 mg/daychildren

Flovent®Fluticasonepropionate

MDI:44 mcg/puff110 mcg/puff220 mcg/puff

DPI: 50 mcg/puff100 mcg/puff250 mcg/puff

4-5 puffs/day

Azmacort®Triamcinoloneacetonide

MDI:100 mcg/puff 4-8 puffs/day 8-12 puffs/day > 12 puffs/daymax: 1.6 mg/ dayadults, 1.2 mg/daychildren

2-3 puffs/day

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

—> 4 puffs/day> 2 puffs/daymax: 0.88 mg/ dayadults

—

> 4 puffs/day> 2 puffs/daymax: 1 mg/ dayadults, 0.2 mg/day children

Flovent®

Rotadisk®

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sthma


Singulair®

Accolate®

Zyflo®

Generic name Dose1 Potential adverse effectsand therapeutic issues

Montelukast

Zafirlukast

Zileuton

Tablet: 5 mg, chewable, forages 6 through 14 yr; 10 mgfor ages 15 yr and older

Tablet: 20 mg, for ages 12yr and older; 10 mg, forages 7 through 11yrs.

Tablet: 600 mg, for ages 12yr and older

1 tablet in evening

1 tablet, b.i.d.Take 1 hourbefore or 2hours after meals

1 tablet, q.i.d.

❑ 2

❑ Drug interactions (warfarin); increasesprothrombin time.2

❑ Possible elevation of liver enzymes requiresmonitoring; drug interactions (warfarin,theophylline).2

Leukotriene modifiers

1 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 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.

Long-Term Control MedicationsCromolyn sodium/Nedocromil sodium


Intal®


Cromolyn sodium

MDI: 1 mg/puffNebulizer solution: 20 mg/ampule

1-2 puffs, 10-15 minbefore exercise1-2 puffs, t.i.d.-q.i.d.1 ampule, t.i.d.-q.i.d.

❑ Therapeutic response to cromolyn andnedocromil often occurs within 2 wk, but a4- to 6-wk trial may be needed to determinemaximum benefit.

❑ Dose of cromolyn MDI (1 mg/puff) may beinadequate to affect airway hyper-responsiveness. Nebulizer delivery (20 mg/ampule) may be preferred for some patients.

❑ Safety is the primary advantage of these agents.

Tilade®Nedocromilsodium

MDI: 1.75 mg/puff 1-2 puffs, 30 minbefore exercise1-2 puffs, b.i.d.-q.i.d.

❑ Unpleasant taste for some patients.

68AA

sthma

Long-Term Control MedicationsUsual Dosages for Long-Term-Control Medications

Adult DoseDosage form

2, 4, 8, 16, 32 mg tablets5 mg tablets,5 mg/ 5 cc, 15 mg/ 5 cc1, 2.5, 5, 10, 20, 50 mg tablets;5 mg/cc, 5 mg/5 cc

MDI 21 mcg/puffDPI 50 mcg/blister DPI 12 mcg/single-use capsule

DPI 100, 250, or 500 mcg/50 mcg

MDI 1 mg/puffNebulizer 20 mg/ampuleMDI 1.75 mg/puff

4 or 5 mg chewable tablet10 mg tablet

10 or 20 mg tablet300 or 600 mg tablet

Liquids, sustained-release tablets,and capsules

Medication Child Dose*

MethylprednisolonePrednisolone

Prednisone

Salmeterol

Formoterol

Fluticasone/Salmeterol

Cromolyn

Nedocromil

Montelukast

ZafirlukastZileuron

Theophylline

❑ 7.5-60 mg daily in a single dosein a.m. or qod as needed forcontrol

❑ Short-course “burst” to achievecontrol: 40-60 mg per day assingle or 2 divided doses for 3-10 days

2 puffs q 12 hours1 blister q 12 hours1 capsule q 12 hours

1 inhalation bid; dose depends onseverity of asthma

2-4 puffs tid-qid1 ampule tid-qid2-4 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 to300 mg max; usual max 800mg/day

❑ 0.25-2 mg/kg daily in singledose in a.m. or qod as neededfor control

❑ Short-course “burst”: 1-2 mg/kg/day, maximum 60 mg/day for 3-10 days

1-2 puffs q 12 hours1 blister q 12 hours1 capsule q 12 hours

1 inhalation bid; dose depends onseverity of asthma

1-2 puffs tid-qid1 ampule tid-qid1-2 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 mgtablet bid)

Starting dose 10 mg/kg/day; usualmax:< 1 year of age: 0.2 (age in weeks)+ 5 = mg/kg/day≥ 1 year of age: 16 mg/kg/day

Inhaled Corticosteroids (See Estimated Comparative Daily for inhaled corticosteroids.)Systemic Corticosteroids (Applies to all three corticosteroids)

Long-Acting Inhaled Beta2-Agonists (Should not be used for symptom relief or for exacerbations. Use with inhaled corticosteroids.)

Combined Medication

Cromolyn and Nedocromil

Leukotriene Modifiers

Methylxanthines (Serum monitoring is important [serum concentration of 5-15 mcg/mL at steady state]).

* Children ≤ 5 years of age

68BA

sthma Long-Term Control Medications

Estimated Comparative Daily Dosages for Inhaled Corticosteroids:

Medium Daily DoseAdult Child*

Low Daily DoseAdult Child*

168-504 mcg 84-336 mcg

80-240 mcg 80-160 mcg

200-600 mcg 200-400 mcg

0.5 mg

500- 500-750 mcg1,000 mcg88-264 mcg 88-176 mcg

100-300 mcg 100-200 mcg

400-1,000 mcg 400-800 mcg

DrugHigh Daily Dose

Adult Child*

Beclomethasone CFC42 or 84 mcg/puffBeclomethasone HFA40 or 80 mcg/puffBudesonide DPI200 mcg/inhalationBudesonideNebulizing suspensionFlunisolide250 mcg/puffFluticasoneMDI: 44, 110, or 220 mcg/puffDPI: 50, 100, or 250 mcg/inhalationTriamcinolone acetonide100 mcg/puff

504-840 mcg 336-672 mcg

240-480 mcg 160-320 mcg

600-1,200 mcg 400-800 mcg

1.0 mg

1,000- 1, 000- 2,000 mcg 1,250 mcg264-660 mcg 176-440 mcg

300-600 mcg 200-400 mcg

1,000- 800-2,000 mcg 1,200 mcg

> 840 mcg > 672 mcg

> 480 mcg > 320 mcg

> 1,200 mcg > 800 mcg

2.0 mg

> 2,000 mcg > 1,250 mcg

> 660 mcg > 440 mcg

> 600 mcg > 400 mcg

> 2,000 mcg > 1,200 mcg

* Children ≤ 12 years of age

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Foradil®

Serevent®

Volmax®

ProventilRepetabs®

Aerolate®-IIIAerolate®-JRAerolate®-SRCholedyl®-SAElixophyllin®

Quibron®-TQuibron®-T/SRSlo-b.i.d.®

Slo-Phyllin®

Theo-24®

Theochron®

Theo-Dur®

Theolair®

Theolair®-SRT-Phyl®

Uni-Dur®

Uniphyl®


Formoterol

Salmeterol

Sustained-release albuterol

Theophylline2

DPI (12 mcg)(Single-use capsule)

MDI: 21 mcg/puffDPI: 50 mcg/blister

Tablet: 4, 8 mgTablet: 4 mg

Capsules, tablets

1 capsule every 12hours

2 puffs, 30-60 minbefore exercise1-2 puffs, q12 hr1 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, notto exceed theadult maximum(800 mg/day)

❑ Tachycardia, tremor. The clinical relevance ofpotential diminished bronchoprotective effectis uncertain. DO NOT USE in place of anti-inflammatory therapy!

❑ Tachycardia, tremor. The clinical relevance ofpotential diminished bronchoprotective effectis uncertain. DO NOT USE in place of anti-inflammatory therapy!

❑ Tachycardia, tremor, irritability

❑ Tachycardia, nausea, vomiting, headache, CNSstimulation.

❑ Monitoring serum levels (5-15 mcg/mL) isessential to ensure therapeutic, but not toxic,doses are achieved.

❑ Serum levels may be affected by numerousfactors (diet, febrile illness, other medications).

Long-Term Control MedicationsLong-acting bronchodilators

1 These doses are suggested as guides for making clinical decisions. The clinician must use his/her judgment to tailor treatment to the specific needs andcircumstances of the patient.

2 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.

3 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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0.25-2 mg/kg daily in singledose or q.o.d. as needed forcontrolShort-course (3- to10-day) “burst:” 1-2mg/kg/day (max: 60mg/day)

0.25-2 mg/kg daily in singledose or q.o.d. as needed forcontrolShort-course (3- to 10-day) “burst,” 1-2mg/kg/day (max: 60mg/day)

0.25-2 mg/kg daily in single dose or q.o.d. as needed for controlShort-course (3- to 10-day) “burst,” 1-2 mg/kg/day (max: 60 mg/day)


Medrol®

Prelone®

Pediapred®

PrednisoneDeltasone®

Orasone®

Liquid Pred®

PrednisoneIntensolTM


Methylprednisolone

Prednisolone

Prednisone

Tablet: 2, 4, 8,16, 24, 32 mg

Tablet: 5 mgLiquid: 15 mg/5 mLLiquid: 5 mg/5 mL

Tablet: 1, 2.5, 5,10, 20, 25, 50 mg

Liquid: 5 mg/5 mL

Liquid: 5 mg/mL

FOR ALL ORAL CORTICOSTEROIDS:

❑ Long-term use is associated with systemic effects. Use lowest effectivedose either daily or on alternatedays (which may lessen adrenalsuppression).

❑ Short courses or “bursts” areeffective for establishing controlwhen initiating therapy or during a period of gradual deterioration. See page 72.

Oral corticosteroids

1 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.

One inhalation twice daily

Dosage formBrand name

Advair TM

Generic name Dose Potential adverse effectsand therapeutic issues

Fluticasone plussalmeterol

100/50250/50500/50

❑ Side effects of fluticasone andsalmeterol separately

Long-Term Control Medications Combined long-term control medications

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Airet®

Proventil®

Ventolin®

Proventil®-HFA

Ventolin®

Rotacaps

Tornalate®

Xopenex®

Maxair®

Brethaire®


Albuterol

Bitolterol

Levalbuterol

Pirbuterol

Terbutaline

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%)

Nebulizer solution: Unit dose vials:0.63 mg/ 3 mL 1.25 mg/ 3 mL

MDI: 200 mcg/puff

MDI: 200 mcg/puff

1-2 puffs, 15 min before exercise2 puffs, t.i.d.-q.i.d., prn0.05 mg/kg (minimum: 1.25 mg; maximum: 2.5 mg)

1-2 puffs, 15 min before exercise2 puffs, t.i.d.-q.i.d., prn

1 capsule, 15 min before exercise1 capsule t.i.d.-q.i.d., prn

1-2 puffs, 15 min before exercise2 puffs, t.i.d.-q.i.d., prn10-15min administration; 8 mg maxintermittent; 14mg max continuous

0.63 mg q 4-6 hr. for maintenance1.25 mg q 4-6 hr. for acute bronchospasm and for patientsunresponsive to lower dose

1-2 puffs, t.i.d.-q.i.d., prn

1-2 puffs, t.i.d.-q.i.d., prn

FOR ALL SHORT-ACTING BETA2-AGONISTS:

❑ Tremor, tachycardia, headache.

NOTE: Increasing use of short-acting beta-agonists, use of > 1canister/month, or lack of expectedeffect indicates inadequate asthmacontrol. See doctor to increase oradd long-term control mediction(s).

Quick-Relief MedicationsShort-acting inhaled beta2-agonists

1 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.

2 Do not use partial unit dose.3 Also available as a nebulizer solution (2 mg/mL = 0.2%), but a children’s dose has not been established.

72A

sthma


Atrovent®


Ipratropiumbromide

MDI: 18 mcg/puffNebulizer solution: 0.5 mg/2.5mL (0.02%)

1-2 puffs every 6 hours0.5 mg every 6 hours

Dry mouth, avoid contactwith eyes. May provide additive effect(s) to short-acting beta2-agonist.


2 A course of 7 days or less is usually sufficient. In some cases, the exacerbation may require up to 10 days of treatment.

Anticholinergics

Dosage form(s)Brand name(s)Generic name Dose1 Potential adverse effectsand therapeutic issues

Methyl prednisolone

Prednisolone

Prednisone

Tablet: 2, 4, 8, 16, 24, 32 mg

Tablet: 5 mgLiquid: 15 mg/5 mLLiquid: 5 mg/5 mL

Tablet: 1, 2.5, 5,10, 20, 25, 50 mg

Liquid: 5 mg/5mL

Liquid: 5mg/mL

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 controlwhen initiating therapy or duringa period of gradual deterioration.

❑ Short-term therapy should continue until patient achieves80% PEF personal best, or untilsymptoms resolve (usually 3- to10-day, but may take longer).There is no evidence thattapering the dose followingimprovement prevents relapse.

Quick-Relief MedicationsOral corticosteroids

Medrol®

Prelone®

Pediapred®

PrednisoneDeltasone®

Orasone®

Liquid Pred®

PrednisoneIntensolTM

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sthma

New Medications (Not available in U.S. at time of writing but pending approval by FDA)

Long-term Control Medications

Inhaled Corticosteroids



Asmanex™


Mometasonefuroate

DPI: 200 mcg/puffDPI: 400 mcg/puff

FOR ALL INHALEDCORTICOSTEROIDS:

Cough, dysphonia, moniliasis; highdoses may have systemic effectsalthough studies are not conclusiveand clinical significance is not clear.

Monitoring growth is recommendedwhen used in children.

The potential risks of inhaledsteroids are well balanced by theirbenefits.

To minimize local and systemicadverse events, use a spacer/holdingchamber.

High

400 mg, b.i.d.

Medium

400 mg, q.d.

Low

200 mg, q.d.

74 Asthma

Types of inhalation devices for asthma medications:

Metered-dose inhaler(MDI)

Beta2-agonistsCorticosteroidsCromolyn sodiumNedocromil sodiumAnticholinergics

Device/Medications Age1 Comments

Adults:Spacer/holding chamberrecommended forpatients having difficultywith inhalation.technique; recommendedroutinely for patients oncorticosteroids.

Children:≥ 5 years: spacer/holdingchamber recommended.<5 years: spacer/holdingchamber with facemaskrecommended.

❑ A spacer/holdingchamber may behelpful if patient hasdifficulty coordinatinginhalation andtriggering a puff.

Breath-actuated MDI

Beta2-agonistsChildren >12 yrand adults

❑ Some patients havedifficulty triggeringa puff while inhaling.

Dry-powderinhaler (DPI)

Beta2-agonistsCorticosteroids

Children ≥ 4 yr and adults

❑ Dose delivered maydiffer from the MDI forsome medications.

❑ Can be effort dependent

Nebulizer

Beta2-agonistsCromolyn sodiumAnticholinergics

Patients of any agewho cannot use anMDI with spacer/holdingchamber with or withoutfacemask.

❑ Useful for infants, veryyoung children, elderly patients, andany patient with amoderate to severeasthma episode(although, MDI withspacer/holdingchamber may be aseffective).

1These ages are suggested as guides for making clinical decisions. The clinician must use his/her own judgmentto tailor treatment to the specific needs and circumstances of the patient.

Types of inhalation devices:

Choose medicationsand delivery devicesaccording to thepatient’s ability to use them.

75Asthma

MDI MDI with Spacer

Breath-actuated MDI

Nebulizer withoutfacemask

Nebulizer withfacemask

76 Asthma

Common sideeffects of MDIs ❑ All MDIs:

♦ Reflex cough♦ Bronchospasm

❑ Corticosteroid MDIs:♦ Oral candidiasis

(thrush)♦ Dysphonia

Using a DPI avoids the problem ofcoordinatinginhalation andactivation.❑ DPIs cannot be used

with a spacer or holdingchamber.

In the near futureinhaled asthmamedications will beadministered as: ❑ Non-chlorofluorocarbon-

(non-CFC-) propelleddevices (e.g., HFA-134a)

❑ Dry powder inhalerdevices

❑ Nebulized solutionsThis is due to theworldwide ban on CFCsto prevent furtheratmospheric ozonedepletion.

Advantages of Using Spacersand Holding Chambers❑ Used with MDIs (not DPIs) because some patients have

a difficult time inhaling while pressing the inhaler totrigger a puff. ♦ Simple tubes do not take care of this problem!

❑ Decrease oropharyngeal deposition.❑ Reduce possible side effects, particularly with inhaled

corticosteroids.

Using an MDI with a spacer/holdingchamber may be easier than using an MDI alone.❑ Trigger one puff from MDI into spacer/holding

chamber for each inhalation.❑ Some patients (particularly young children)

may prefer using an MDI with spacer/holdingchamber and facemask.

❑ If a facemask is used, allow 3 to 5 inhalationsfor each puff triggered from the MDI.

77Asthma

Treat asthma exacerbations promptly andaggressively.❑ 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:♦ The early signs of worsening asthma.♦ What medications to use and how to use them.♦ 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, orto re-establish control during a period of graduallydeteriorating symptoms.

❑ Exacerbations of asthma symptoms (coughing,wheezing, shortness of breath or rapid breathing, chesttightness) with viral respiratory infections are common,and need to be treated appropriately with adequatedoses of short-acting beta2-agonists and, in some cases,oral corticosteroids.

❑ Moderate or severe exacerbations may requiretreatment at the clinician’s office or emergency room.♦ Pulse oximetry is recommended to follow oxygen

saturation.♦ Use oxygen to relieve hypoxemia.♦ Monitor the response to therapy with serial

measurements of FEV1 or PEF.

All offices that treat acute exacerbationsof asthma should be prepared foremergency airway management, andshould have available:❑ A peak flow meter❑ A power-driven nebulizer❑ An oximeter❑ Oxygen❑ A crash cart with:

♦ Epinephrine♦ Antihistamines♦ Intravenous catheters♦ Bag-mask-valve devices

78 Asthma

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.

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:

♦ In mild exacerbations, wheezing is evident onexpiration.

♦ As the severity of the exacerbation increases, bothinspiratory and expiratory wheezing may be present.

♦ During a severe exacerbation, the chest may be“silent.”

❑ Decreased PEF❑ Agitation❑ Cyanosis

79Asthma

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 andretractions (sucking in of chest) suggest severe exacerbation.

Initial Treatment

Inhaled short-acting beta2-agonist: up to 3 treatments of 2 to 4puffs by MDI every 20 min, or 1 nebulizer treatment.

Managing Asthma Exacerbations in the Home

Response totreatment: Good Incomplete Poor

Exacerbation Mild Moderate SeverePEF (predicted > 80% 50% to 80% < 50% or personalbest)

Wheezing or None Persistent Markedshortness of breath

Continued Continue inhaled Continue inhaled Repeat beta2-treatment short-acting beta2- short-acting beta2- agonist

agonist every 3 to 4 agonist. Add oral immediately.hr- for 24 to 48 hr. corticosteroid. Add oral For patients on corticosteroid.inhaled cortico-steroids, doubledose for 7 to 10 days.

Follow-up Contact clinician. Contact clinician If distress isin same day. severe and

patient isnonresponsive,CALL HEALTHCAREPROVIDERIMMEDIATELY, AND PROCEED TO ER OR URGENTCARE CENTER.CONSIDERCALLING AMBULANCEOR 911.

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80 Asthma

Urgent Care (Clinician’s Office or Emergency Department)for Managing Asthma Exacerbations

Nebulized short-acting beta2-agonist and supplemental oxygen should be available in aphysician’s office. However, serious exacerbations require close observation, frequenttreatment, and repetitive measurement of lung functions. Most severe exacerbationsrequire 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, andother tests as indicated.

Repeat assessment (symptoms, physical, O2 saturation,other tests as needed).

Response to initial treatment:

FEV1 or PEF > 50% < 50% Impending/actual(severe respiratoryexacerbation) arrest

Inhaled beta2- By MDI or Nebulized high Nebulized highagonist nebulizer, up dose with anti- dose with

to 3x in first hr. cholinergic anticholinergic.every 20 min,or continuous,for 1 hr.

O2 To ≥ 90% To ≥ 90% Intubation andsaturation. saturation. mechanical

ventilation with100% O2.

Corticosteroid Oral, if no Oral i.v. immediate response or if patient recently used oralcorticosteroid.

Admit to ICU.

▼

▼

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81Asthma

Urgent Care for Managing Asthma Exacerbations (cont.)

Repeat assessment after 1 hour

Severity of Exacerbation Moderate Severe

FEV1 or PEF 50 to 80% < 50%(predicted orpersonal best)

Physical exam Improvement evident; No improvement;moderate Sx. severe Sx at rest;

accessory muscle use;retractions; high-risk patient.

CONTINUETREATMENT

Continue treatment 1 to 3 hr, if there is improvement.

Response to treatment: Good Incomplete Poor

FEV1 or PEF ≥ 70% ≥ 50% < 50%(predicted or but < 70%personal best)

Physical exam Normal; response Mild-to- Severe Sx; sustained ≥ 60 min moderate Sx. drowsiness;after treatment; confusion;no distress. PCO2

≥ 42 mmHg.

Follow-up Discharge home Individualized Admit to ICU.with: decision◆ Inhaled beta2-agonist re: hospital ◆ Oral corticosteroid admission.◆ Patient education

⇒ Review medications

⇒ Review/initiate action plan

⇒ Recommend close medical follow-up

▼

Inhaled short-acting Inhaled short-actingbeta2-agonist every 60 min; beta2-agonist withsystemic corticosteroid. anticholinergic hourly

or continuous; systemiccorticosteroid; O2.

82 Asthma

Referral to an asthma specialist forconsultation or comanagement isrecommended 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 allergicfactors).

❑ The patient/parents/caregivers requireadditional education and guidance on therapyor allergen avoidance.

❑ The patient is being considered forimmunotherapy.

❑ The patient has severe persistent asthma.❑ The patient requires continuous therapy with

oral corticosteroids or high-dose inhaledcorticosteroids, or has required more than twobursts of oral corticosteroids in the past year.

❑ The patient is under 3 years of age and requiresStep 3 or Step 4 care.

❑ The patient requires confirmation of a historythat suggests that an occupational orenvironmental inhalant or ingested substance iscontributing to or provoking asthma.

❑ The patient is not achieving the goals oftherapy, see page 46.

83Asthma

Special Considerations for Managing AsthmaManaging exercise-induced bronchospasm (EIB):❑ Exercise-induced bronchospasm (EIB) is caused by a loss

of heat, water, or both from the airways during exercisedue to increased ventilation and inhalation of cool, dry airrelative to the air within the lungs.

❑ EIB usually begins during exercise and peaks 5 to 10minutes after stopping exercise.

❑ Exercise may be the only cause of asthma for somepatients.♦ These patients should be monitored regularly because

EIB is often a marker of inadequate asthmamanagement.

❑ Symptoms may spontaneously resolve within 1 hour afterexercise.

❑ A warm-up period before exercise may help.❑ If asthma symptoms occur regularly with usual activities

or exercise, increasing (or adding) daily long-term controlmedication(s) may be warranted.

❑ Appropriate long-term control therapy, especially with anti-inflammatory medications, may help reduce exercise-induced symptoms.

Treatment forexercise-inducedasthma:

Minutes beforeexercise to takemedication:

Preventssymptoms forapproximately:

Short-actinginhaled beta2-agonist (2 to 4puffs)

5 to 30 (besttaken justbeforeexercising)

2 to 3 hours

Cromolyn sodiumor nedocromilsodium (2 to 4puffs)

5 to 30 (besttaken justbeforeexercising)

1 to 2 hours

Long-actinginhaled beta2-agonist (2 puffsfor MDI, 1 puff forDPI)

At least 30 10 to 12 hourswith intermittentuse (withcontinuous use,protective effectlasts for less than8 hours)

Leukotrienemodifier

At least 120 Up to 24 hours,depending onmedication

Exercise-inducedsymptoms should beanticipated in ALLpatients with asthma.

Teachers and coachesneed to be notified ifa child has exercise-induced symptoms.They should be toldthat the child canparticipate inactivities, but mayneed inhaledmedication before the activity.

84 Asthma

Preventing “anticipated” episodes of asthmasymptoms (other than exercise):

❑ When the patient understands and recognizes theaggravating factors that increase asthma symptoms, it ispossible to prevent or at least minimize episodes ofsymptoms due to “anticipated exposures” to the factor.

Cold (dry) air ❑ Short-acting inhaled beta2-agonist; cromolyn sodium;or nedocromil sodium shortly(5 to 30 minutes) before goingout in the cold.

❑ Cover nose and mouth witha scarf on cold or windy days.

For “anticipated”symptoms upon exposure to:

Treat with:

Allergens (e.g.,animal dander,pollens)

❑ Cromolyn sodium ornedocromil sodium shortly (5 to 30 minutes) before ananticipated exposure.

❑ Regular use of a long-termcontrol medication may reducethe likelihood of allergen-induced symptoms.

Treating asthma symptoms due to viral upperrespiratory infections (URIs):

❑ Patient should begin regular PEF monitoring at URI onset.

❑ For mild symptoms not associated with a decline inpeak flow rate, a short-acting inhaled beta2-agonist(every 4 to 6 hours for 24 hours, longer with clinicianconsult) may be sufficient to control the symptoms.♦ For recurrent URIs, when this therapy needs to be

repeated more frequently than every 6 weeks, aseasonal increase in (or starting) long-term controltherapy (usually cromolyn sodium for young children;inhaled corticosteroids for other patients) may benecessary.

Managing the patientwith seasonalsymptoms:❑ Start or increase daily

long-term controltherapy 2 to 4 weeksbefore the season.

❑ Gradually decrease(or stop) daily long-term control therapy2 to 4 weeks afterseason.

❑ If symptoms areassociated withseasonal allergicrhinitis or seasonalexacerbations ofperennial allergicrhinitis, treat allergicrhinitis symptomsaggressively.

Exacerbations ofasthma symptoms(coughing, wheezing,difficulty breathing,chest tightness) arecommon with viraland other respiratoryinfections.

85Asthma

❑ For symptoms associated with a decline in PEF into theyellow zone (per the patient’s action plan), use a short-acting inhaled beta2-agonist, consider doubling theinhaled corticosteroid dose for 7 to 10 days.♦ If patient does not respond or PEF decreases into the

red zone, add a short (3- to 10-day) course of oralcorticosteroid.

❑ If the patient has a history of severe recurrentexacerbations with URIs, consider initiating a short (3- to 10-day) course of oral corticosteroid at the firstsign of URI.

Treating the child with asthma:

Administering asthma medications to infants and childrencan be challenging.❑ Medications to treat asthma in children may be given by

inhalation or orally (as tablets or liquids).♦ The inhaled route is generally preferred because:

⇒ Higher concentrations can be delivered moreeffectively 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 thedevice(s) used for inhaled medications).

❑ The ability of individual children to use different devicesfor inhaled medications may vary considerably.

Appropriate long-termcontrol therapyduring the viralrespiratory seasonmay reduce thefrequency and severityof virus-inducedsymptoms.

Using an MDI witha spacer/holdingchamber may beeasier than usingan MDI alone.❑ Trigger one puff from

MDI into spacer/holdingchamber for eachinhalation.

❑ Some young childrenmay be able to use anMDI with spacer/holding chamber and facemask.♦ If a facemask is

used, allow 3 to 5inhalations for eachpuff triggered fromthe MDI.

Primary prevention of asthma(preventing initial development) mayalter its course.❑ Minimize exposure to dust mites, tobacco

smoke, animal dander, cockroach allergens.♦ 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 earlyintroduction of allergenic foods may reduceeczema and food sensitization (see Volume 3:Food Reactions, page 69), but have not beenshown to reduce the prevalence of asthma.

86 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 consultationor comanagement should be considered for childrenbeing given daily medication.

❑ Carefully monitor the response to medication:♦ Treat the wheeze for 4 to 8 weeks.♦ If there is no clear response, stop treatment.♦ 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. ♦ When there are reactions after ingesting food,

the most common causes are milk, peanuts, soy,wheat, eggs.

❑ Reducing exposure to viral respiratory infections maybe important for the difficult-to-manage wheezer.

❑ Nebulizer therapy with facemask may be preferred foradministering cromolyn sodium and for short-actingbeta2-agonists during exacerbations.

❑ Short-acting beta2-agonists are available as liquids, but:♦ The onset of action is slower than when given by

inhalation (approximately 30 minutes for the liquidas compared to several minutes for inhalation).

♦ Adverse effects (e.g., tremor, irritability) aremore likely.

❑ Drugs administered by MDI may be given usinga spacer/holding chamber and facemask.♦ The administered dose will be variable and may

require extra dosing.♦ Actuate one dose at a time in the device. ♦ 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/holdingchamber, a nebulizer or MDI plus spacer/holdingchamber with facemask may be required.

How do you givemedication to infantsand young children?❑ Use a metered dose

inhaler with aspacer/holding chamberplus a facemask.

❑ Use a nebulizer.❑ Use a liquid.Liquid albuterol does nothave as rapid an onset ofaction as inhaledalbuterol, a considerationfor treating exacerbations.

Many children havemultiple caregivers.

All homes andcaregivers shouldhave medications,devices, and amanagement planfor how and whento use them.

87Asthma

School-age Children❑ Inhaled medications are preferred.❑ MDIs, DPIs, and nebulizers may be used.

♦ The child should be able to produce the necessaryeffort and coordination needed for the specific device.

❑ All inhaled corticosteroids by MDI should be used witha spacer/holding chamber.

❑ Some children carry their short-acting beta2-agonist MDI without a spacer/holding chamber. This isacceptable if the child has demonstrated goodtechnique.

❑ Consultation with an asthma specialist is recommendedfor children with moderate and severe persistentasthma.

❑ A consult may be considered for young children withmild 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.

Viral upperrespiratory infectionsare a key precipitatingfactor of asthmasymptoms in youngchildren.

Working withteenagers can bechallenging. Theymay: ❑ View treatment as

infringing on theirindependence.

❑ Fail to recognize thedanger of poorlycontrolled asthma.

❑ Respond best to peersand to peer idols. Usingknown personalitieswho themselves haveasthma and using teensupport groups can bevery effective.

❑ Parents need to stayinvolved.

❑ Consultation with an asthma specialist isrecommended for children with moderateand severe persistent asthma.

❑ A consult may be considered for children with mildpersistent asthma.

88 Asthma

❑ Ask the adolescent about smoking, exposure to tobaccosmoke, and possible drug use.

❑ Encourage exercise and physical activity. Asthma shouldnot be an excuse for not participating in physicaleducation 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 workplaceexposures.

❑ Consider nonadherence if the teen is not doing well.

The child’s schedule and giving asthmamedications:❑ Provide an action plan for handling exacerbations,

including the clinician’s recommendation regarding self-administration of medication and plans to ensureprompt, reliable access to medications.

❑ If possible, schedule long-term control medications sothat they are not taken at school, even if this results inuneven dosing intervals.♦ However, some children benefit from close

supervision of therapy. For these children, givingmedication at school, under the supervision of aschool health professional, is recommended.

❑ It may be helpful for some younger children to have acompressor-driven nebulizer available at their school ordaycare facility.

Asthma, inhaled corticosteroids, and linear growth.❑ A reduction in growth velocity in children or

adolescents may occur as a result of inadequate controlof chronic diseases such as asthma or from the use ofcorticosteroids of treatment. Overall, however, theavailable cumulative data in children suggest that,although low-to-medium doses of inhaledcorticosteroids may have the potential of decreasinggrowth velocity, the effects are small, nonprogressive,and may be reversible. When high doses of inhaledcorticosteroids are necessary to achieve satisfactoryasthma control, the use of adjunctive long-term controltherapy should be instituted to reduce the dose ofinhaled corticosteroids and thus minimize possibledose-related long-term effects on growth. Physiciansshould monitor the growth of children and adolescentstaking corticosteroids by any route and weigh thebenefits of corticosteroid therapy and asthma controlagainst the possibility of growth suppression or delay ifa child’s or an adolescent’s growth appears slowed.

Special concerns of theadolescent include:❑ Effects of medications on

appearance (height,weight, acne), ability toexercise, menses.

❑ Taking medications inpublic.

❑ Peer pressure.

Reliable, prompt accessto asthma medication isessential during the day.❑ The child, caregivers,

teachers, and schoolnurses should understandthis.

❑ Older children should beallowed to carry and self-administer quick-reliefmedications, with clinicianand parent approval.

Poorly controlledasthma may delaygrowth.

The potential risks ofinhaled corticosteroidsare well-balanced bytheir benefits.

89Asthma

Managing asthma in the elderly:

❑ Because of the high prevalence of other obstructivelung diseases (e.g., chronic bronchitis, emphysema)among the elderly, it is important to determine theextent of reversible airflow obstruction.♦ Evaluate carefully. The precise cause of severe airflow

obstruction can be difficult to identify in olderpatients.

♦ A 2- to 3-week trial of therapy with oral corticosteroidscan help detect the presence of significant reversibilityof airway disease. Long-term control asthmamedication can then be offered.

❑ Medication side effects may be increased in the elderlypatient.♦ Airway response to bronchodilators may change with

age, although this is not clearly established.♦ Older patients, especially those with pre-existing

ischemic heart disease, may be more sensitive tobeta2-agonist side effects, including tremor andtachycardia.

♦ Theophylline clearance is reduced in the elderlypatient, causing increased blood levels oftheophylline. ⇒ Age is an independent risk factor for developing

life-threatening events from iatrogenic chronictheophylline overdose.

❑ There is increased potential for drug interactions due tothe increased use of medications in this age group.♦ 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 bonemineral content. ♦ Elderly patients may be at greater risk due to pre-

existing osteoporosis, changes in estrogen levelsaffecting calcium utilization, and a sedentary lifestyle.

Medication sideeffects may beincreased in theelderly patient, andmay require a changein the asthmamedication plan.

Inadequatelycontrolling asthmamay unnecessarilylimit the patient’smobility and activities.

Medications to treatother diseases mayexacerbate asthma;adjustments may needto be made. Consider:❑ Aspirin and

nonsteroidalanti-inflammatoryagents for treatingarthritis.

❑ Nonselective beta-blockers for treatinghypertension and/orarrhythmias.

❑ Beta-blockers foundin some eye drops usedto treat glaucoma.

90 Asthma

♦ Concurrent treatment with calcium supplementsand vitamin D, and estrogen replacement whenappropriate, are recommended.

❑ At very high doses, inhaled corticosteroids may increasethe risk of cataracts and may increase intraocularpressure.

Older patients may be at greater risk for bone loss due to corticosteroidtherapy. ❑ Before starting treatment, evaluate risk with

bone densitometry for patients using moderateto high doses.

❑ Consider regular risk assessments every12 to 18 months during treatment.

The benefits of this approach have not beenevaluated in clinical trials.

Managing the pregnant patient with asthma:

❑ Poorly controlled asthma during pregnancy can resultin increased perinatal mortality, increased prematurity,and low birth weight.

❑ Maintaining sufficient lung function and bloodoxygenation to ensure adequate oxygen supplyto the fetus is essential.

❑ For most medications used to treat asthma and rhinitis,there are little data to suggest an increased risk to thefetus.

❑ Treating asthma is paramount. All long-term controlmedications and short-acting inhaled beta2-agonistsappear to be safe in pregnancy.

❑ Medications with some possibility of risk to thefetus include:♦ Decongestants (other than pseudoephedrine)♦ Antibiotics (tetracycline, sulfonamides,

and ciprofloxacin) ♦ Live virus vaccines♦ Iodides♦ Brompheniramine♦ Epinephrine

For more informationon asthma in olderpatients, see theNational AsthmaEducation PreventionProgram WorkingGroup Report:Considerations forDiagnosing andManaging Asthma inthe Elderly (NHLBI1996).

Poorly controlledasthma duringpregnancy increasesthe risk of:❑ Perinatal mortality❑ Prematurity❑ Low birth weight

All long-term controlmedications andshort-acting inhaledbeta2-agonists appearto be safe inpregnancy.

For more informationon asthma andpregnancy, seeExecutive Summary:Management ofAsthma DuringPregnancy (NHLBI1992).

91Asthma

Managing bronchopulmonary aspergillosis in thepatient with asthma:

❑ Patients with asthma are susceptible to colonization byfungi, especially bronchopulmonary aspergillosis.

❑ Aspergillosis causes an immune reaction that isaccompanied by:♦ Pulmonary infiltrate♦ Peripheral eosinophilia♦ Rise in total serum IgE♦ Worsening asthma

❑ Treat with prolonged (many months) and taperingprednisone.

❑ If aspergillosis is suspected or confirmed, referral to anasthma specialist is indicated.

Managing work-aggravated asthma andoccupational asthma:

❑ Occupational asthma is suggested by a correlationbetween asthma symptoms and the workplace. ♦ 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 withan assessment of the workplace environment. ♦ Peak flow monitoring may be helpful in some cases. ♦ Occupational asthma is suggested by a correlation

between asthma symptoms and work, withimprovement when away from work for several days.

♦ The patient may fail to recognize the workrelationship because symptoms often begin severalhours after exposure.

♦ Objective documentation of changes in airwayfunction with workplace exposure is important inestablishing the diagnosis.

❑ Early recognition and control of exposures areimportant in occupational-induced asthma becausethe likelihood of complete resolution of symptomsdecreases with time of continuous exposure.

Patients with asthmaare susceptible tocolonization byfungi, especiallybronchopulmonaryaspergillosis.

Asthma symptoms thatimprove when awayfrom work suggestoccupational asthma.

Some tips formanaging work-aggravated andoccupational asthma:❑ Work with onsite

healthcare providersand/or managers/supervisors.

❑ Discuss avoidance,ventilation, respiratoryprotection, a smoke-freeenvironment.

❑ Minimize (ideally, avoidcompletely) exposureto aggravating agent(s).

92 Asthma

Some examples of compounds causing occupational asthma:

Animals Farmers; laboratory personnel

Allergen Occupation

Arthropods Farmers; laboratory personnel

Shellfish and fish Shellfish farmers and processors

Wood and vegetableproducts

Carpenters; woodworkers; grain handlers; bakers; foodprocess workers; printers

Enzymes Bakers; detergent industry workers; nurses;pharmaceutical employees; plastics workers

Pharmaceuticals Pharmaceutical workers; pharmacists

Amines Shellac, rubber, lacquer handlers; photographers;solderers; fur dyers; chemists; chemical manufacturers

Anhydrides Paint, plastic, plastics, electronics, epoxy resin, chemicalmanufacturers

Diisocyanates Polyurethane, plastics, varnish, foam, foundry, rubbermanufacturers; spray painters

Fluxes Electronics workers; metal joiners

Metals and metal salts Pot room, hard metal, electroplating workers; printers;tanners; diamond polishers; platinum refiners; hardmetal grinders; solderers; locksmiths

Other chemicals Chemical, reactive dye, resin, plastics, glovemanufacturers; meat wrappers; chemical packaging;refrigeration, textile industry, healthcare workers;hairdressers

Newman L. Occupational Asthma. Clinics in Chest Medicine. 1995; 16:621-636.

Occupational exposures may increaseasthma symptoms and/or precipitateasthma exacerbations

93Asthma

Component 4. Education for aPartnership in Asthma Care

Take a proactive approach to asthmaeducation. Form a partnership with thepatient (and family).The educational tips included in the Patient Educationchapter of Volume 1 are appropriate for the patient withasthma (see Volume 1: Patient Education, page 71). Belowfind 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 educationalmessages.

❑ Regularly teach and review:♦ Basic asthma facts.♦ Roles of medications.♦ Device and monitoring skills.♦ Environmental control measures.♦ When and how to take rescue actions.

❑ Provide written action plans for managing exacerbations.

To take medicationscorrectly, patientswith asthma (andtheir families andcaregivers) neededucation. ❑ Education is time-

consuming, but willimprove adherencewith therapy.

94 Asthma

What can you and your staff do in a singleasthma visit?

❑ Document the patient’s (and family’s) concerns.❑ Review the medications: How often are you using your

long-term control medicine? …your quick-reliefmedicine?

❑ Review self-management skills: Show me how you useyour inhaler. …your peak flow meter.

❑ Repeat the important messages: Asthma can becontrolled. Our goal is for you to participate inwhatever activities you’d like.

❑ Help with problem solving: What makes it easier for youto remember to take your medications? …to avoid yourcausal or aggravating factors?

Focus on what is doable to improve adherence withasthma therapy.

❑ Keep therapy simple.♦ Limit medications.♦ Limit doses.♦ Meet the patient’s schedule.

❑ Establish priorities.❑ Write an action plan.❑ Enlist family and peer support.

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.

Be aware of culturaldifferences, e.g.:❑ In some Latino

populations, asthma is viewed as a “cold”illness, amenable to“hot” treatments.Suggest that asthmamedications be takenwith hot tea, hot water,or broth.

❑ In some Asianpopulations, oralmedications arepreferred.

Open andunrestrictedcommunication (withthe patient, family,caregiver) is essentialto successful asthmamanagement. ❑ Encourage the patient to

discuss any concernsand expectations.

❑ Resolution of anxiety isan important treatmentgoal and will increaseadherence to all aspectsof the treatment plan.

95Asthma

Provide clear and accurate informationabout 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 aswhen symptoms occur.

All patients with persistent asthmashould have 2 asthma care plans:❑ A DAILY MANAGEMENT PLAN describing

regular medications and measures to keep asthmaunder control.

❑ AN ACTION PLAN describing actions to takewhen asthma worsens, including:♦ What medications to take.♦ When to contact the clinician and/or when to

go to the emergency room.

Over-the-counter MDIsshould be avoidedbecause they:❑ Are not as effective

as prescriptionshort-acting inhaledbeta2-agonists.

❑ May have side effectsat lower doses.

❑ May unnecessarily delayseeking medical care.

All patients with asthmaneed an inhaled short-acting beta2-agonist for prompt relief ofsymptoms.

Give patient and/orcaregiver(s) a writteneasy-to-understandmanagement plandescribing how tomanage exacerbations,what medications touse, and how to usethem.

96 Asthma

Some examples of delivery of asthma education by cliniciansduring patient care visits*:Recommendations for initial visit:

What is asthma? A chroniclung disease. The airwaysare very sensitive. Theybecome inflamed andnarrow; breathing becomesdifficult.Two types of medicines areneeded:❑ Long-term control:

medicines that preventsymptoms, often byreducing inflammation.

❑ Quick-relief: short-actingbronchodilator relaxesmuscles around airways.

Bring all medicines to everyappointment.When to seek medicaladvice. Provide appropriatetelephone number.

“What worries you mostabout your asthma?”“What do you want toaccomplish at this visit?”“What do you want to beable to do that you can’t donow because of yourasthma?”“What do you expect fromtreatment?”“What medicines have youtried?”“What other questions doyou have for me today?”

Inhaler technique (seepage 93) andspacer/holding chamber.Check performance.Self-monitoring skills tiedto action plan:❑ Recognize intensity and

frequency of asthmasymptoms.

❑ Review the signs ofdeterioration and theneed to re-evaluatetherapy:♦ Waking at night with

asthma.♦ Increased medication

use.♦ Decreased activity

tolerance.Use of an asthmamanagement plan(see page 98).

Assessment questionsfocus on: concerns,goals of therapy, qualityof life, expectations

Teach information insimple language

Teach and demonstrateskills

Recommendations for first follow-up visit (2 to 4 weeks or sooner asneeded):

Use of two types ofmedicines. Remind patientto bring all medicines andthe peak flow meter toevery appointment forreview.Self-evaluation of progressin asthma control usingsymptoms and peak flow asa guide.

Ask relevant questions fromprevious visit and also ask:“What medicines are youtaking?”“How and when are youtaking them?”“What problems have youhad using your medicines?”“Please show me how youuse your inhaledmedicines?”

Use of an asthmamanagement plan (seepage 98). Review and adjustas needed.Peak flow monitoring (seepages 40 to 41) and dailydiary recording.Correct inhaler andspacer/holding chambertechnique.

*Taken from the Practical Guide for the Diagnosis and Management of Asthma, based on the Expert PanelReport 2: Guidelines for the Diagnosis and Management of Asthma.

97Asthma

Recommendations for second follow-up visit:

Relevant environmentalcontrol/avoidance strategies(see page 51).❑ How to identify and

control home, work, orschool exposures thatcan cause or worsenasthma.

❑ How to avoid cigarettesmoke (active andpassive).

Review all medicines andreview and interpret peakflow and symptom scoresfrom daily diary.

Ask relevant questions fromprevious visits and also ask:“Have you noticed anythingin your home, work, orschool that makes yourasthma worse?”“Describe for me how youknow when to call yourdoctor or go to the hospitalfor asthma care.”“What questions do youhave about the actionplan?” “Can we make iteasier?”“Are your medicines causingyou any problems?”

Inhaler/spacer/holdingchamber technique.Peak flow monitoringtechnique.Review use of action plan.Confirm that patient knowswhat to do if asthma getsworse.

Recommendations for all subsequent visits:

Review and reinforce all:❑ Educational messages.❑ Environmental control

strategies at home, work,or school.

❑ Medicines.Review and interpret peakflow and symptom scoresfrom daily diary.

Ask relevant questions fromprevious visits and also ask:“Have you tried to controlthings that make yourasthma worse?”“Please show how you useyour inhaled medicines.”

Inhaler/spacer/holdingchamber technique.Peak flow monitoringtechnique.Review use of action plan.Confirm that patient knowswhat to do if asthma getsworse. Periodically reviewand adjust written actionplan.

Assessment questionsfocus on: concerns,goals of therapy, qualityof life, expectations

Teach information insimple language

Teach and demonstrateskills

Asthm

a Sample Asthma Management Planfor 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):

2 or 4 puffs 5 to 30 minutes before exercise

Medicine How much to take When to take it

YELLOW ZONE:Asthma is getting worse• Cough, wheeze, chest tightness or shortness of breath,

OR• 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)

Add Quick-Relief medicine – and keep taking your GREEN ZONE medicine:

(short-acting beta2-agonist)

If your symptoms (and peak flow, if used) return to GREEN ZONE after 1 hour of abovetreatment:

FIRST

If your symptoms (and peak flow, if used) do not return to GREEN ZONE after 1 hour ofabove treatment:


Add: mg per day for (3-10) days.(oral corticosteroid)

SECOND

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 ZoneORPeak flow: to

(< 50% of my best peak flow)

Take the quick-relief medicine every 4 hours for 1 to 2 days.Double the dose of your inhaled corticosteroid for (7-10) days.

Call the doctor before/ within hours after taking the oral corticosteroid.

Take this medicine:


(oral corticosteroid)

2 or 4 puffs or Nebulizer

mg.

Then call your doctor NOW. Go to the hospital or call for an ambulance if:• You are still in the red zone after 15 minutes AND• You have not reached your doctor.

DANGER SIGNS.• Trouble walking and talking due to shortness of breath• Lips or fingernails are blue

• Take 4 or 6 puffs of your quick-relief medicine AND• Go to the hospital or call for an ambulance ( ) NOW!

Take: 2 or 4 puffs or Nebulizer

98

The child with asthmacan function normallyat school.

Be aware of commonschool problems facedby the student withasthma:❑ Absences due to asthma

symptoms or to doctorvisits.

❑ Avoidance of schoolor activities.

❑ Not taking medicationsbecause it is bothersometo go to the health office.

❑ Side effects that interferewith performance orconcentration.

Students with asthmaneed to have promptand easy access to theirmedications. Theyshould be permitted tocarry and use theirmedication, withphysician and parentapproval.

Some schools do nothave full-time nurses.The action plan must beunderstandable for useby health aides or officepersonnel.

Asthma and the School Since school is the child’s home away from home, it is oneof the most important environments to safeguard. Theclinician should work closely with school personnel to helpthem understand asthma, its impact, and how to meet thespecial needs of children with asthma.

Teachers, coaches, and school health personnelneed to know:

❑ The early warning signs of an asthma episode.❑ How to treat an asthma episode, including:

♦ What medications are used.♦ How the medications are used.♦ When to contact the clinician or emergency room.

❑ What medications the student uses.♦ Common side effects of asthma medications that

warrant communication with the parents and/orclinician: nervousness, nausea, drowsiness, jitteriness,hyperactivity.

❑ How to help the child with asthma follow his/hermanagement plan at school.♦ What causal and aggravating factors are associated with

the student’s asthma.♦ How the student premedicates to prevent exercise-

induced symptoms (and symptoms from other“anticipated” exposures; e.g., allergens, cold air).

♦ How to minimize exposure to causal and aggravatingfactors (e.g., allergens, strong odors) in the classroomand school environment that can worsen the student’sasthma.

❑ Whether the student has clinician and parent approval tocarry and use his/her inhaler(s).

❑ Phone numbers for the clinician, the parents, and theemergency room.

❑ How to use devices to deliver asthma medications,spacers/holding chambers.

❑ How to use a peak flow meter (if appropriate).

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.

99Asthma

100 Asthma

How asthma-friendly is your school?Children with asthma need proper support at school to keep their asthma undercontrol and to be fully active. Use the questions below to find out how well theschool assists children with asthma:

1. Is the school free of tobacco smoke all of the time, including during school-sponsored events?

2. Does the school maintain good indoor air quality? Does it reduce or eliminateallergens 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 strongodors 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 regularlyavailable to the school to help write plans and give guidance for students withasthma about medicines, physical education, and field trips?

4. Can children take medicines at school as recommended by their doctor andparents? May children carry their own asthma medicines?

5. Does the school have an emergency plan for taking care of a child with a severeasthma 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, andasthma medicines? Does someone teach all students about asthma and how tohelp a classmate who has it?

7. Do students have good options for fully and safely participating in physicaleducation class and recess? (For example, do students have access to theirmedicine before exercise? Can they choose modified or alternative activitieswhen medically necessary?)

If the answer to any question is no, students may be facing obstacles to asthmacontrol. Asthma out of control can hinder a student’s attendance, participation, andprogress in school. School staff, health professionals, and parents can work togetherto remove obstacles and to promote students’ health and education.

101Asthma

Student Asthma Action Card

ID Photo

Name: Grade: Age:

Teacher: Room:

Address:

Emergency Phone Contact #1:Relationship PhoneName

Emergency Phone Contact #2:Relationship PhoneName

Physician Student Sees for Asthma:

Other Physician: Ph:

Ph:

Daily Asthma Management PlanIdentify the things which start an asthma episode (check each that applies to the student).

Exercise

Respiratory infections

Change in temperature

Animals

Food

Strong odors or fumes

Chalk dust

Carpets in the room

Pollens Molds

Other

Comments:

Control of School Environment(List any environmental control measures, premedications, and/or dietary restrictions thatthe student needs to prevent an asthma episode.)

Peak Flow MonitoringPersonal Best Peak Flow Number:

Monitoring Times:

Daily Medication PlanName Amount When to Use

School Asthma Management Plan

*Developed by the Asthma and Allergy Foundation of America (AAFA); Endorsed by National Asthma Educationand Prevention Program (NAEPP)

1.2.3.4.

Parent/Guardian Name: Ph (H):

Ph (W):

Parent/Guardian Name: Ph (H):

Ph (W):

Asthma

It is my opinion that should not carry his/her inhaled medicationby him/herself.

Emergency PlanEmergency action is necessary when the student has symptoms such as

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:

School Asthma Management Plan (continued)

or has a peak flow reading of .

Emergency Asthma MedicationsName Amount When to Use

Comments/Special Instructions

I have instructed (name) in the proper wayto use his/her medications. It is my professional opinion that he/she should be allowed tocarry and use that medication by him/herself.

For Inhaled Medications

Physician Signature

Parent Signature

Date

Date

√ No improvement 15-20 minutes after initial treatmentwith 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 can’t start activity again.

√ Lips or fingernails are gray or blue.

} IF THIS HAPPENS,GET EMERGENCYHELP NOW!

1.2.3.4.

102

Asthma

Abramson MJ, Puy RM, Weiner JM. Isallergen immunotherapy effective inasthma? A meta-analysis of randomizedcontrolled trials. Am J Respir Crit Care Med1995; 151: 969-974.

Adinoff AD, Rosloniec DM, McCall LL,Nelson HS. Immediate skin test reactivityto Food and Drug Administration-approvedstandardized extracts. J Allergy ClinImmunol 1990; 86: 766-774.

Agudo A, Bardagi S, Romero PV, GonzalezCA. Exercise-induced airways narrowingand exposure to environmental tobaccosmoke in schoolchildren. Am J Epidemiol1994; 140: 409-417.

American Academy of Allergy andImmunology Board of Directors. Guidelinesto minimize the risk from systemic reactionscaused by immunotherapy with allergenicextracts J Allergy Clin Immunol 1994; 93: 811-812.

Arshad SH, Hide DW. Effect of environmentfactors on the development of allergicdisorders in infancy. J Allergy Clin Immunol1992: 90: 235-241.

ATS Update: Future directions for researchon diseases of the lung. Am J Respir CritCare Med 1998; 158: 320-334.

Bakdaia L. An educational approach tosuccessful management of childhoodasthma as a chronic illness. J Ped Nursing1996; 11: 335-336.

Beeber SJ. Parental smoking and childhoodasthma. J Pediatr Healthcare 1996; 10: 58-62.

Bell TD, Chai H, Berlow B, Daniels G.Immunization with killed influenza virus inchildren with chronic asthma. Chest 1978;73: 140-145.

Bernard-Bonnin AC, Stachenko S, Bonin D,Charette C, Rousseau E. Self-managementteaching programs and morbidity ofpediatric asthma. A meta-analysis. J AllergyClin Immunol 1995; 96: 34-41.

Bjornsson E, Norback D, Janson C, et al.Asthmatic symptoms and indoor levels ofmicroorganisms and house-dust mites. ClinExp Allergy 1995; 25: 423-431.

Bosley CM, Fosbury JA, GM Cochrane. Thepsychological factors associated with poorcompliance with treatment in asthma. EurRespir J 1995; 8: 899-904.

Brazil K, McLean L, Abbey D, Musselman C. The influence of health education onfamily management of childhood asthma.Patient Education and Counseling 1997; 30: 107-118.

Busse WW, Banks-Schlegel SP, Larsen GL.Effects of growth and development on lungfunction: models for study of childhoodasthma. Am J Respir Crit Care Med 1997;156: 314-319.

Busse WW, Lemanske RF Jr., Stark JM,Calhoun WJ. The role of respiratoryinfections in asthma. In: Holgate ST, AustenKF, Lichtenstein LM, Kay AB (eds). Asthma:Physiology, Immunopharmacology, andTreatment. Vol 4. London: Academic Press,1993: 345-353.

Busse WW. Respiratory infections: their role in airway responsiveness and thepathogenesis of asthma. J Allergy ClinImmunol 1990; 85: 671-683.

Calls RS, Smith TF, Morris E, Chapman MD,Platts-Mills TAE. Risk factors for asthma ininner city children. J Pediatr 1992; 121: 862-866.

Centers for Disease Control and Prevention.Prevention and control of influenza.Recommendations of the AdvisoryCommittee on Immunization Practices(ACIP). MMWR 1993; 42(No. RR-6): 1-14.

Chande VT, Exum V. Follow-up phone calls after an emergency department visit.Pediatrics 1994; 93: 513-514.

Chen Y, Rennie DC, Dosman JA. Influence of environmental tobacco smoke on asthmain nonallergic and allergic children.Epidemiology 1996; 7: 536-539.

Childhood Asthma – all that wheezes is not inflammation (editorial). Clinical ExpAllergy 1997; 27: 991-994.

Christiansen SC, Martin SB, Schleicher NC,et al. Evaluation of a school-based asthmaeducation program for inner-city children. J Allergy Clin Immunol 1997; 100: 613-617.

References

103Asthma

Asthma

Christiansen SC, Martin SB, Schleicher NC, et al. Exposure and sensitization toenvironmental allergen of predominantlyHispanic children with asthma in San Diego’sinner city. J Allergy Clin Immunol 1996; 98:288-294.

Cockcroft DW. Airway hyperresponsiveness:therapeutic implications. Ann Allergy 1987; 59: 405-414.

Corrigan CJ, Kay AB. The roles ofinflammatory cells in the pathogenesis ofasthma and of chronic obstructivepulmonary disease. Am Rev Respir Dis 1991; 143: 1165-1168.

Cote J, Golding J, Barnes G, Boulet LP.Educating the educators: How to improveteaching about asthma. Chest 1994; 106:S242-247.

Cuijpers CE, Swaen GM, Wesseling G,Sturmans F, Wouters EF. Adverse effects of theindoor environment on respiratory health inprimary school children. Environ Research1995; 68: 11-23.

D’Souza W, Crane J, Burgess C, et al.Community-based asthma care: trial of a"credit card" asthma self-management plan.Eur Respir J 1994; 7: 1260-1265.

deBlay F, Chapman MD, Platts-Mills TAE.Airborne cat allergen (Fel d1):Environmental control with the cat in situ.Am Rev Respir Dis 1991; 143: 1334-1339.

deBlay F, Heymann PW, Chapman MD,Platts-Mills TAE. Airborne dust miteallergens: Comparison of group II allergenswith group I mite allergen and cat-allergenFel d1. J Allergy Clin Immunol 1991; 88: 919-926.

Djukanovic R. Brochoscopy as a researchtool for the study of asthma pathogenesis and effects of antiasthma drugs. J Allergy Clin Immunol 1996; 98: S41-45.

Dobbs LG. Aveoli and airways: possibleinteractions in the pathogenesis of asthma.Am J Respir Crit Care Med 1994; 150: S31-32.

Doi S, Murayama N, Inoue T, et al. CD4 T-lymphocyte activation is associated with peakexpiratory flow variability in childhoodasthma. J Allergy Clin Immunol 1996; 97:955-962.

Dolen WK. Asthma as an inflammatorydisease: implications for management. J AmBoard Fam Practice 1996; 9: 182-191.

Doull IJ, Holgate ST. Asthma: earlypredisposing factors. Brit Medical Bulletin1997; 53: 71-80.

Eggleston PA. Allergen-specificimmunotherapy in childhood asthma. Curr Opinion Pediatr 1997; 9: 582-584.

Ellingson AR, LeDoux RA, Vendanthan PK,Weber RW. The prevalence ofDermatophagoides mite allergen in Coloradohomes utilizing central evaporative coolers. J Allergy Clin Immunol 1995; 96: 473-479.

Fabbri L, Caramori G, Beghe B, Ciaccia A.Role of leukotrienes in asthma pathogenesis.Mon Arch Chest Dis 1996; 51: 548-555.

Farber HJ, Wattigney W, Berenson G. Trendsin asthma prevalence: the Bogalusa HeartStudy. Ann Allergy Asthma Immunol 1997; 78: 265-269.

Feldman CH, Clark NM, Evans D. The role of health education in medical managementof asthma. Some program applications. ClinRev Allergy 1987; 14: 267-79.

Fisher EB, Sussman LK, Arfken C, et al.Targeting high risk groups. Neighborhoodorganization for pediatric asthmamanagement in the neighborhood asthmacoalition. Chest 1994; 106: S248-259.

Forrest CB, Simpson L, MB; Clancy C, Childhealth services research: Challenges andopportunities. J Am Med Assoc 1997; 277: 1787-1793.

Frederick JM, Warner JO, Jessop WJ, EnanderI, Warner JA. Effect of a bed covering systemin children with asthma and house-dust mitehypersensitivity. Eur Respir J 1997; 10: 361-366.

Frischer T, Kuehr J, Meinert R, et al. Maternalsmoking in early childhood: a risk factor forbronchial responsiveness to exercise inprimary-school children. J Pediatr 1992; 121: 17-22.

Galli SJ. Complexity and redundancy in thepathogenesis of asthma: reassessing the rolesof mast cells and T cells. J Exp Med 1997;186: 343-347.

104

Asthma

Garrison RA, Robertson LD, Koehn RD, Wynn SR. Effect of heating-ventilation-airconditioning system sanitation on airbornefungal populations in residentialenvironments. Ann Allergy 1993; 71: 548-556.

Gemson DH, Ashford AR, Dickey LL, et al.Putting prevention into practice. Impact of amultifaceted physician education program onpreventive services in the inner city. ArchIntern Med 1995; 155: 2210-2216.

Gern JE, Schroth MK, Lemanske RF.Childhood asthma. Older children andadolescents. Clinics Chest Med 1995; 16: 657-670.

Gibson PG, Wlodarczyk JW, Hensley MF, et al.Epidemiological association of airwayinflammation with asthma symptoms andairway hyperresponsiveness in childhood. Am J Respir Crit Care Med 1998; 158: 36-41.

Greco PJ, Eisenberg JM. Changing physicians’practices. N Engl J Med 1993; 329: 1271-1273.

Greineder DK, Loane KC, Parks P. Reductionin resource utilization by an asthma outreachprogram. Arch Pediatr Adolesc Med 1995; 149: 415-420.

Harris JR, Magnus P, Samuelsen SO, Tambs K.No evidence for effects of family environmenton asthma. A retrospective Study ofNorwegian twins. Am J Respir Crit Care Med1997; 156: 43-49.

Henderson WR Jr. Eicosanoids and platelet-activating factor in allergic respiratorydiseases. Am Rev Respir Dis 1991; 143: S86-90.

Henderson WR Jr. The role of leukotrienes in inflammation. Ann Intern Med 1994; 121: 684-697.

Heymann PW, Rakes GP, Hogan AG, et al.Assessment of eosinophils, viruses and IgEantibody in wheezing infants and children.Internat Arch Allergy Appl Immunol 1995;107: 380-382.

Holgate ST, Hardy C, Robinson C, Agius RM,Howarth PH. The mast cell as a primaryeffector cell in the pathogenesis of asthma.J Allergy Clin Immunol 1986; 77: 274-282.

Holt PG. Early acquisition of sensitization inchildhood 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 andwheezing in public schools children:association with maternal smoking duringpregnancy. Ann Allergy Asthma Immunol1997; 79: 80-87.

Ingram JM, Sporik R, Rose G, et al.Quantitative assessment of exposure to dog(Can f1) and cat (Fel d1) allergens: Relationto sensitization and asthma among childrenliving in Los Alamos, New Mexico. J AllergyClin Immunol 1995; 96: 449-456.

James JM, Bernhisel-Broadbent J, SampsonHA. Respiratory reactions provoked bydouble-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 asthmain adult life. BMJ 1994; 309: 90-93.

Joos GF, Germonpre PR, Kips JC, PelemanRA, Pauwels RA. Sensory neuropeptides andthe human lower airways: present state futuredirections. Eur Respir J 1994; 7: 1161-1171.

Kang BC, Johnson J, Veres-Thorner C. Atopicprofile of inner-city asthma with acooperative analysis on the cockroach-sensitive 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 withasthma: the National Cooperative Inner-CityAsthma Study. Pediatr Pulmonol 1997; 24: 253-262.

Kay J, Mortimer MJ, Jaron AG. Do bothpaternal and maternal smoking influence theprevalence of childhood asthma? A study intothe prevalence of asthma in children and theeffects of parental smoking. J Asthma 1995; 32: 47-55.

Kelloway JS, Wyatt RA, Adlis SA. Comparisonof patients’ compliance with prescribed oraland inhaled asthma medications. Arch InternMed 1994; 154: 1349-1352.

105

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Kemp T, Pearce N, Fitzharris P, et al. Is infantimmunization a risk factor for childhoodasthma or allergy? Epidemiology 1997;91: 45-55.

Kesten S, Szalai J, Dzyngel B. Air quality andthe frequency of emergency room visits forasthma. Ann Allergy Clin Immunol 1995; 74: 269-273.

Klucka CV, Ownby DR, Green J, Zoratti E. Catshedding of Fel d1 is not reduced bywashings, 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 childrenassociated with fine particulate matter.Environmental Research 1993; 63: 26-38.

Krahn M. Issues in the cost-effectiveness ofasthma education. Chest 1994; 106; S264-269.

Kroegel C, Virchow JC Jr., Luttmann W,Walker C, Warner JA. Pulmonary immunecells in health and disease: the eosinophilleucocyte. Eur Respir J 1994; 7: 519-543.

Kropfelder L, Winkestein M. A casemanagement 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 factorfor early and late onset of asthma and forpersistence of asthmatic signs in children. J Allergy Clin Immunol 1995; 95: 655-662.

Kumar A, Busse W. Airway inflammation inasthma. Scientific Am Sci Med 1995: 38-47.

Laitinen A, Laitinen LA. Airway morphology:Epithelium/basement membrane. Am JRespir Crit Care Med 1994; 150: S14-17.

Lang DM, Sherman MS, Polansky M.Guidelines and realities of asthmamanagement. The Philadelphia Story. Arch Intern Med 1997; 157: 1193-1200.

Lieu TA, Quesenberry CP, Capra AM, et al.Outpatient management practices associatedwith reduced risk of pediatric asthmahospitalization and emergency departmentvisits. Pediatrics 1997; 100: 334-341.

Litner TJ, Brame KA. The effects of season,climate and air conditioning on theprevalence of Dermtophagoides miteallergens in household dust. J Allergy ClinImmunol 1993; 91: 862-867.

Lozano P, Fishman P, VonKorff M, Hecht J.Healthcare utilization and cost amongchildren with asthma who were enrolled in ahealth maintenance organization. Pediatrics1997; 99: 757-764.

Mahr TA, Evans R. Allergist influence onasthma care. Ann Allergy 1993; 71: 115-120.

Martinez FD. Viral infections and thedevelopment of asthma. Am J Respir CritCare 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 don’t know it? Am Rev Respir Dis1992; 146: 1376-7.

Moore R, Khan A, Burton F. Long-actinginhaled beta2-agaonists in asthma therapy.Chest 1998; 113: 1095-1108.

Mullins J, White J, Davies BH. Circadianperiodicity of grass pollen. Ann Allergy 1986; 57: 371-374.

Munzenberger PJ. Improving adherence inpatients with asthma. Am Pharmacy 1993; NS33: 32-36.

National Heart Lung and Blood Institute.National Asthma Education and PreventionProgram. Expert panel report 2: guidelinesfor the diagnosis and management ofasthma. April 1997: NIH Pudlication 97-4051.

National Heart Lung and Blood InstituteReport of the Working Group on Asthma andPregnancy: Management of Asthma DuringPregnancy. September 1993; NIH Publication93-3279.

Nelson HS, Fernandez-Caldas E. Prevalenceof house-dust mites in the rocky mountainstates. Ann Allergy Asthma Immunol 1995;75: 337-339.

Nelson HS, Hirsch SR, Ohman JL, et al.Recommendations for the use of residentialair cleaning devices in the treatment ofallergic respiratory diseases. J Allergy ClinImmunol 1988; 82: 661-669.

106

Asthma

Nelson Jr Rp, DiNicolo R, Fernandez-CaldasE, et al. Allergen-specific IgE levels and miteallergen exposure in children with acuteasthma first seen in an emergencydepartment and in nonasthmatic controlsubjects. J Allergy Clin Immunol 1996; 98: 258-263.

Newacheck PW, Stoddard JJ, Hughes DC,Pearl M. Health insurance and access toprimary care for children. N Engl J Med1998; 339: 513-519.

Newman, L. Occupational asthma: Diagnosis,management, and prevention. Clinics ChestMed 1995; 16: 621-636.

O’Byrne, PM. Leukotrienes in thepathogenesis of asthma. Chest 1997; 111: S27-34.

O’Byrne, PM. Treatment of mild asthma.Lancet 1997; 349: 818.

O’Hollaren MT, Ynginger JW, Offord KP, et al.Pulmonary function changes in childrenassociated with fine particulate matter. NEngl J Med 1991; 324: 3559-3563.

O’Hollaren MT, Yunginger JW, Offord KP, et al.Exposure to an aeroallergen as a possibleprecipitating factor in respiratory arrest inyoung patients with asthma. N Engl J Med1991; 324: 359-363.

Ostro BD, Lipsett MJ, Mann JK, Braxton-Owens H, White MC. Air pollution andasthma exacerbations among African-American children in Los Angeles. InhalToxicol 1995; 7: 711-722.

Peat JK, Toelle BG, Gray EJ, et al. Prevalenceand severity of childhood asthma and allergicsensitization in seven climatic regions of NewSouth Wales. Med J Austr 1995; 163: 22-26.

Peat JK, Tovey E, Mellins CM, Leeder SR,Woolcock AJ. Importance of house-dust miteand Alternaria allergens in childhoodasthma: An epidemiological study in twoclimatic regions of Australia. Clin Exp Allergy1993; 23: 812-820.

Peat JK, Tovey E, Toelle BG, et al. House-dustmite allergens: A major risk factor forchildhood asthma in Australia. Am J RespirCrit Care Med 1996; 153: 141-146.

Peroni DG, Boner AL, Vallone G, Antolini I,Warner JO. Effective allergen avoidance athigh altitude reduces allergen-inducedbronchial hyperresponsiveness. Am J RespirCrit Care Med 1994; 149: 1442-1446.

Physicians’ Desk Reference. 53rd ed. Oradell,NJ: Medical Economics Company, Inc; 1999.

Platts-Mills TAE, Sporik R, Ingram JM,Honsinger R. Dog and cat allergen andasthma among school children in LosAlamos, New Mexico, USA: Altitude 7,200feet. Int Arch Allergy Immunol 1995; 107: 301-303.

Platts-Mills TAE, Tovey ER, Mitchell EB, etal. Reduction of bronchial hyperreactivityduring prolonged allergen avoidance. Lancet1982; 2: 675-678.

Pullan CR, Hey EN. Wheezing, asthma, andpulmonary dysfunction 10 years afterinfection with respiratory syncytial virus ininfancy. Brit Med J 1982; 284: 1655-1669.

Rachelefsky G. Childhood asthma andallergic rhinitis: the role of leukotrienes. J Pediatrics 1997; 131: 348-355.

Reismann RE, Mauriello PM, Davis GB,Georgitis JW, DeMasi JM. A double-blindstudy of the effectiveness of a high-efficiencyparticulate air (HEPA) filter in the treatmentof patients with perennial allergic rhinitisand asthma. J Allergy Clin Immunol 1990;85: 1050-1057.

Riportella-Muller R, Selby-Harrington ML,Richardson LA, et al. Barriers to the use ofpreventive healthcare services for children.Public Health Reports 1996; 111: 71-77.

Romieu I, Meneses F, Sienra-Monge JJ, et al.Effects of urban air pollutants on emergencyvisits for childhood asthma in Mexico City.Am J Epidemiol 1995; 141: 546-553.

Romieu I, Meseses F, Ruiz S, et al. Effects ofair pollution on the respiratory health ofasthmatic children living in Mexico City. Am J Respir Crit Care Med. 1996; 383: 247-250.

Rosenstreich DL, Eggleston P, Kattan M, et al.The role of cockroach allergy and exposureto cockroach allergen in causing morbidityamong inner-city children with asthma. NEngl J Med 1997; 336: 1356-1363.

107

Asthma

Ross S, Godden DJ, Abdalla M, et al. Outcomeof wheeze in childhood: the influence ofatopy. Eur Respir J 1995; 8: 2081-2087.

Sampson HA, Mendelson L, Rosen JP. Fataland near fatal anaphylactic reactions to foodin children and adolescents. N Engl J Med1992; 327: 380-384.

Sbarbaro JA, Steiner JF. Noncompliance withmedications: vintage wine in new (pill)bottles. Ann Allergy 1991; 66: 273-275.

Schaubel D, Johansen H, Dutta M, et al.Neonatal characteristics as risk factors forpreschool asthma. J Asthma 1996; 33: 255-264.

Schmitzberger R, Rhomberg K, Buchele H, et al. Effects of air pollution on therespiratory tract of children. PediatrPulmunol 1993; 15: 68-74.

Schwartz D, Torres KA, Addison T, et al. Aframework for healthcare policy in theUnited States. Am J Respir Crit Care Med1997; 156: 1011-1015.

Sears MR, Burrows B, Flannery EM,Herbison GP, Holdaway MD. Atopy inchildhood. I. Gender and allergen-relatedrisks for development of hay fever andasthma. Clin Exp Allergy 1993; 23: 949-956.

Sears MR, Herbison GP, Holdaway MD, et al.The relative risks of sensitivity to grass pollen,house-dust mite, and cat dander in thedevelopment of childhood asthma. Clin ExpAllergy 1989; 19: 419-424.

Sears MR, Holdaway MD, Flannery EM,Herbison GP, Silva PA. Parental and neonatalrisk factors for atopy, airwayhyperresponsiveness, and asthma. Arch DisChild 1996; 75: 392-398.

Sears MR. Epidemiology of childhoodasthma. Lancet 1997; 350: 1015-1020.

Sears MR. Risk factors for airwayhyperresponsiveness in childhood asthma.Ped Pulmonol 1995; 11: 42-43.

Sennhauser FH, Kuhni CE. Prevalence ofrespiratory symptoms in Swiss children: Isbronchial asthma really more prevalent inboys? Pediatr Pulmonol 1995; 19: 161-166.

Sigman K, Mazer B. Immunotherapy forchildhood asthma: is there a rationale for itsuse? Ann Allergy Asthma Immunol 1996; 76: 299-305.

Smith RD, Rooks R. The diurnal variation ofairborne ragweed pollen as determined by acontinuous recording particle sampler andimplications of the study. J Allergy 1954; 25: 36-45.

Solomon WR. A volumetric study of winterfungus prevalence in the air of Midwesternhomes. J Allergy Clin Immunol 1976; 57: 46-55.

Soyseth V, Kongerud J, Boe J. Postnatalmaternal smoking increases prevalence ofasthma but not of bronchialhyperresponsiveness or atopy in theirchildren. Chest 1995; 107: 389-394.

Spiers, R. CFC-free inhalers. Lancet 1997;349: 364.

Sporik R, Holgate ST, Platts-Mills TAE,Cogswell JJ. Exposure to house-dust miteallergen (Der pI) and the development ofasthma in childhood. A prospective study. N Eng J Med 1990; 323: 502-507.

Sporik R, Platts-Mills TA. Epidemiology of dust-mite related disease. Exp ApplAcarology 1992; 16: 141-151.

Sterk PJ. Virus-induced airwayhyperresponsiveness in man. Eur Respir J1993; 6: 894-902.

Swanson DP. Damp housing and childhoodasthma: Validation of reporting of symptoms.Brit Med J 1988; 297: 1223-1226.

Swanson MN, Thompson PE. Managingasthma causes in school. Ped Nursing 1994;20: 181-184.

Taylor WR, Newacheck PW. Impact ofchildhood asthma on health. Pediatrics 1992; 90: 657-662.

Verhoeff AP, van Strien RT, van Wijnen JH,Brunekreef B. Damp housing and childhoodrespiratory symptoms: The role ofsensitization to dust mites and molds. Am J Epidemiol 1995; 141: 103-110.

Vollmer WM, O’Hollaren M, Ettinger KM, etal. Specialty differences in the managementof asthma. A cross-sectional assessment ofallergists’ patients and generalists’ patients ina large HMO. Arch Intern Med 1997; 157: 1201-1208.

Von Mutius E. Progression of allergy andasthma through childhood to adolescence.Thorax 1996; 51: S3-6.

108

Asthma

Warner JA, Kroegel C. Pulmonary immunecells in health and disease: mast cells andbasophils. Eur Respir J 1994; 7: 1326-1341.

Watson WT, Becker AB, Simons FE. Treatmentof allergic rhinitis with intranasalcorticosteroids in patients with mild asthma:Effect on lower airway responsiveness. JAllergy Clin Immunol 1993; 91: 97-101.

Weiss K, Gergen P, Hodgson T. An economicevaluation of asthma in the United States. N Engl J Med 1992; 326: 862-866.

Weiss ST. Diet as a risk factor for asthma.Ciba Foundation Symposium 1997; 206: 244-257.

Wieringa MH, Weyler JJ, VanBastelaer FJ, etal. Higher asthma occurrence in an urbanthan a suburban area: Role of house-dustmite skin allergy. Eur Respir J 1997; 10: 1460-1466.

Woloshin S, Bickell NA, Schwartz LM, Gany F, Welch HG. Language barriers in medicinein the United States. J Am Med Assoc 1995;273: 724-728.

Woodcock, A. Use of spacers with metereddose inhalers. Lancet 1997; 349: 446.

Woodfolk JA, Hayden ML, Couture N, Platts-Mills TAE. Clinical treatment of carpetsto reduce allergen: Comparison of the effectsof tannic acid and other treatments onproteins derived from dust mites and cats. J Allergy Clin Immunol 1995; 96: 325-333.

Woodfolk JA, Luczynska CM, de Blay F,Chapman MD, Platts-Mills TAE. The effect of vacuum cleaners on the concentration andparticle size distribution of airborne catallergen. J Allergy Clin Immunol 1993; 91:829-837.

Zeiger RS, Heller S, Mellon MH, et al.Facilitated referral to asthma specialistreduces relapses in asthma emergency roomvisits. J Allergy Clin Immunol 1991; 87: 1160-1168.

Zeiger RS. Dietary manipulations in infantsand their mothers and the natural course ofatopic disease. Pediatr Allergy Immunol 1994; 5: 33-43.

Zock JP, Burnekreef B, Hazebroek-Kampschreur AA, Roosjen CW. House-dustmite allergen in bedroom floor dust andrespiratory health of children with asthmaticsymptoms. Eur Respir J 1994; 7: 1254-1259.

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Atopic Dermatitis

❑ Atopic dermatitis is a chronic or recurrent atopicinflammatory skin disease that:

♦ Generally begins in the first few years of life.

♦ May be the initial clinical manifestation of anallergic predisposition, usually preceding allergicrhinitis and asthma.

❑ The etiology of atopic dermatitis is generallyunknown.

♦ There is a high frequency of elevated serum IgElevels, but the exact role of IgE in thepathogenesis of atopic dermatitis is not clear.

♦ Approximately 85% of atopic dermatitis patientshave elevated IgE levels with positive immediateskin tests.

❑ In some patients, particularly young children,allergy to food or aeroallergens contributes to thedisease.

❑ Atopic dermatitis may present at any age, butusually has an onset in childhood.

♦ Approximately 50% of patients develop symptomsin the first year of life.

♦ Another 30% develop symptoms between theages of 1 and 5 years.

❑ The characteristic symptoms of atopic dermatitisare intense pruritus and skin reactivity.

♦ Scratching may be intermittent during the day.

♦ Scratching is usually worse in the early eveningand at night.

⇒ Disruption of normal sleep patterns iscommon.

Atopic Dermatitis

Atopic dermatitis issometimes referred toas the “itch thatrashes.”

Atopic dermatitis maybe the initial clinicalmanifestation of anallergicpredisposition,usually precedingallergic rhinitis andasthma. ❑ More than 50% of

atopic dermatitispatients developasthma.

❑ Approximately 75% ofatopic dermatitispatients develop allergicrhinitis.

The prevalence ofatopic dermatitis inchildren is increasing. ❑ Up to 10% to 15% of the

population are affectedby atopic dermatitisduring childhood.

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❑ Certain foods may exacerbate rashes in somepatients, particularly children. (See Volume 3:Food Reactions, page 69)

♦ Skin testing and oral challenges may be necessaryto confirm allergies.

♦ Common foods causing symptoms include eggs,peanuts, and milk.

⇒ Eliminating these foods may amelioratesymptoms in allergic patients.

CausalFactors

FoodsEnvironment

PathogensTemperature

Stress

AtopicIndividual

+ IgE +

Mast cell derived:Histamine

Leukotrienes

Inflammatory Cells and Mediators

Eosinophil derived:Leukotrienes

Major Basic ProteinsPeptides

InflammationPruritis

Acute DermatitisChronic Dermatitis

Atopic Dermatitis

Atopic dermatitis involves a complexinflammatory process associated withlocal activation of lymphocytes,monocytes/macrophages, eosinophils,and mast cells.

▼

▼

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❑ Some patients develop symptoms when exposed toaeroallergens, especially house dust mites andanimal danders.

♦ Avoiding aeroallergens may improve symptoms insensitive patients.

❑ Ocular complications associated with atopicdermatitis:

♦ Atopic keratoconjunctivitis, frequently associatedwith eyelid dermatitis and blepharitis.

♦ Keratoconus from persistent rubbing of the eyes.

❑ Characteristic symptoms of atopic dermatitis areintense pruritus and skin reactivity.

♦ Scratching may be intermittent during the day.

♦ Scratching is usually worse in the early eveningand at night.

♦ Disruption of normal sleep patterns is common.

Atopic Dermatitis

Flaring atopic dermatitiswith severe pruritus and

multiple excoriations. Photo provided by

Anthony Gaspari, M.D.,University of Rochester.

❑ Patients with atopic dermatitis often developrecurrent bacterial, fungal, and viral skin infections,which may lead to difficulty in controlling thedisease.

♦ Decreased cellular immunity and increased skinhyperactivity is related to susceptibility of skin toinfections.

♦ Secondary skin infection is common in all agegroups.

♦ Common bacterial infections includestaphylococci and streptococci.

⇒ Bacterial infection is suggested by:

•Honey-colored crusting

•Extensive serous weeping

•Folliculitis

•Pyoderma

♦ Fungal infections include Trichophyton rubrumand Pityrosporum ovale.

♦ Viral infections include herpes simplex, warts,and molluscum contagiosum.

❑ Altered barrier function, especially during acuteepisodes of atopic dermatitis increases:

♦ Transepidermal water loss.

♦ Absorption of medicaments, allergens, andirritants.

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Infantile eczemacomplicated byeczema herpeticumin gluteal cleft. Photo provided byAnthony Gaspari, M.D.,University of Rochester.

Atopic Dermatitis

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Diagnosing the Patient with AtopicDermatitis Medical History❑ A detailed and accurate history is critical to the proper

diagnosis of atopic dermatitis and its successfultreatment.

❑ Consider:♦ Assessment of the pruritic nature of the skin rash. ♦ Age of onset.♦ Family history of allergic diseases.♦ Distribution and characteristics of the skin rash.

❑ Pattern and duration of symptoms:♦ Chronicity♦ Relapsing nature♦ Seasonal variation

❑ Assessment of casual factors:♦ Environmental exposures♦ Food hypersensitivity

❑ Presence of other allergic diseases, particularly:♦ Asthma♦ Rhinitis♦ Conjunctivitis

❑ Presence of other conditions:♦ Eye complications♦ Ichthyosis cluster

⇒ Dry skin⇒ Keratosis pilaris (rough hair follicles)⇒ Follicular prominences ⇒ Hyperlinear palms⇒ Icthyosis vulgaris

Atopic Dermatitis

Patients with atopicdermatitis often haveconcomitant medicalproblems, particularlyasthma, allergicrhinitis, andconjunctivitis.

Adult atopic dermatitiswith ichthyosis vulgaris

skin changes.Photo provided by


116 Atopic Dermatitis

Patient Distribution Characteristics

Infants Facial and Exudative (oozing,Extensor surfaces weeping)

Older Flexural Lichenified (dry)children;adults

Distribution of lesions of atopic dermatitisin older children and adults:

During severe exacerbations, the lesions may becomemore generalized.

Older Children

Adults

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Ask the patient about what causessymptoms, such as:❑ Allergens

♦ Environmental allergens (e.g., pollens, dogs,cats, dust mites)

♦ Foods ♦ Personal care products ♦ Medications

❑ Chemical irritants ♦ Acids, alkali♦ Solvents♦ Plastics♦ Smoke

❑ Physical irritants♦ Scratchy clothing♦ Occlusive clothing♦ Scratching or vigorous scrubbing♦ Extremes of environmental temperature

or humidity⇒ Sweating ⇒ Extreme dryness

♦ Hot water❑ Internal changes

♦ Infection♦ Emotional stress♦ Hormonal changes associated with

menstruation or pregnancy

Physical Examination❑ 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.

Atopic Dermatitis

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Characteristics of atopic dermatitislesions:❑ Acute lesions/eczema

♦ Intensely pruritic♦ Erythematous papules and vesicles over

erythematous skin♦ Frequently associated with extensive

excoriations and erosions♦ Accompanied by a serous exudate

❑ Subacute lesions♦ Erythema♦ Excoriation♦ Scaling

❑ Chronic lesions♦ Thickened skin plaques♦ Fibrotic papules (lichen simplex chronicus)♦ Accentuated skin markings (lichenification)

❑ The morphology and distribution of lesions changewith age and/or ethnicity.♦ Infants and young children:

⇒ Erythematous lesions.⇒ Scaling eruptions on

scalp, face, ears, trunkand extensor surfaces.

Chronic drylichenifieddermatitis inchild withatopic dermatitis. Photo provided byAnthony Gaspari, M.D.,University of Rochester.

Atopic Dermatitis

Hand dermatitis in a 5-year oldwith atopic dermatitis.

Photo provided by Anthony Gaspari,M.D., University of Rochester.

119

♦ Older children and adults: ⇒ Popliteal and antecubital fossae, neck, intragluteal

creases, wrists, ankles.

❑ African-Americans:♦ Erythema (redness) may be difficult to appreciate

because of underlying pigmentation.♦ Pigment changes (hyper- or hypo-pigmentation) may

be prominent.

❑ Common dermatoses of infancy should be differentiatedfrom atopic dermatitis:♦ Seborrheic dermatitis♦ Diaper dermatitis♦ Diaper dermatitis with

Candida

This exudative dermatitis (eczema)is typical with infantile atopic

dermatitis. Photo provided by Anthony Gaspari, M.D.,

University of Rochester.

Chronic atopicdermatitis may beassociated with pigmentchanges in African-Americans.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 thepublisher Mosby.

Atopic Dermatitis

Flexural eczema inteenager with

secondary impetigo. Photo provided by


120

Distinguishing features of seborrheic andatopic dermatitis in infancy:

Family history

Age of onset

Distribution

Lesions

Pruritus

Laboratory

Prognosis

Skin reactivity

Feature SeborrheicDermatitis

AtopicDermatitis

Usually none

Usually under2 months

Scalp; face andneck; any flexures,especiallygenitoanal; inolder child,eyebrows, eyelids

Erythema withgreasy, yellowishscales; sharplydemarcatedflexural lesions

Minimal

Eosinophiliaabsent; negativeskin tests

Usually clear in3 to 4 weeks, up to2 months; noassociated defects

Normal

History of atopicdisease

Usually over2 months

Cheeks, forehead,scalp, extensorsurfaces of limbs(flexuralinvolvement inolder patients)

Erythema, papules,vesicles; no scales(may be crusted);tapering edges;fine scalyappearance

Severe (a hallmarkof disease)

Eosinophilia;positive skin tests,elevated IgE

Prolonged course;high incidence ofassociated allergicrhinitis and asthma

Whitedermatographism

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)

Atopic Dermatitis

Common clinicalfeatures of atopicdermatitis:❑ Pruritus

❑ Facial and extensorinvolvement in infantsand children

❑ Flexural lichenificationin adults

❑ Chronic or chronicallyrelapsing dermatitis

❑ Personal or familyhistory of atopic disease

Source: Hanifin JM, Rajka G. Acta Derm Venerol 1980; 92: 44-47.

Common dermatosesof infancy should bedifferentiated fromatopic dermatitis:❑ Seborrheic dermatitis

❑ Diaper dermatitis

❑ Diaper dermatitis withCandida

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Diagnostic Testing❑ Skin tests or in vitro tests for specific allergens must be

interpreted cautiously. ♦ Skin tests have a high rate of false-positive

(i.e., clinically insignificant) results.♦ 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:

♦ Used only for a limited period of time (10 to 14 days)?♦ Monitored for outcomes closely?

❑ Blinded oral challenges may be useful in identifyingfood allergens.♦ Oral food challenges should be supervised by an

allergy/immunology specialist.❑ For more information, see Volume 3: Food Reactions,

page 77.

Atopic Dermatitis

Food-sensitive patientswho respond to thebasic elimination dietshould be referred toan allergy/immunologyspecialist in a timelymanner.

Elimination diets are therapeutic trialsand should be supervised by anallergy/immunology specialist. They may fail if the patient:❑ Does not receive adequate education before

starting.♦ 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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Targeted elimination diet:❑ Foods eliminated based on results from specific

IgE tests (e.g., skin tests or in vitro tests) or froma suggestive history given by patient and/orparent.♦ 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.

Atopic Dermatitis

Avoid factors that cause symptoms.

Use appropriate medications.

1 Evaluate for immunotherapy.

Educate and follow-up.2

34

Food-sensitivepatients who respondto targeted foodelimination dietsshould:❑ Continue the diet.

❑ Avoid overzealousrestriction of non-implicated foods.

❑ Have weight (andheight) monitoredregularly.

❑ Be re-evaluated or every4 to 6 months.

❑ Consider seeing adietitian for educationand help in managingtheir diet.

Goals of treatment foratopic dermatitis:❑ Relieve symptoms.

❑ Reduce cutaneousinflammation.

❑ Enhance skin hydration.

❑ Remove “flare factors”(e.g., infections,exposure to irritants).

Nonpharmacologictheraphy is importantfor treating atopicdermatitis.

Managing the Patient with AtopicDermatitisFour general principles of allergymanagement:

Avoid factors that cause symptoms.Avoiding causal factors can decreasesymptoms, prevent exacerbations, andreduce the need for medications.

❑ All patients should:♦ Avoid common irritants (e.g., some soaps, detergents,

chemicals, abrasive or heavy clothing, extremes oftemperature and humidity).

♦ Keep fingernails trimmed short to minimize skintrauma from scratching.

♦ Cover hands when sleeping (e.g., cotton gloves,socks).

♦ Control emotional stress which can exacerbatepruritus and dermatitis.

1

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Help the patient learn how to reduceemotional stress.❑ Patients may respond to stress with increased

itching and scratching.❑ Psychological evaluation or counseling should

be considered for patients who have difficultywith emotional or psychological problems thataggravate symptoms.

Atopic Dermatitis

Long-term trialelimination dietsshould be avoided.❑ Regular monitoring of

weight and height (inchildren) is essential.

Avoiding causalfactors can:❑ Prevent exacerbations.

❑ Reduce the need formedications.

❑ Decrease symptoms.

Dust mite eliminationmay be helpful forsome patients withatopic dermatitis.

Patients with atopicdermatitis may beespecially sensitiveabout theirappearance.

❑ Food sensitive patients who respond to targeted foodelimination diets should:♦ Continue the diet.♦ Avoid overzealous restriction of nonimplicated foods.♦ Have weight (and height) monitored regularly.♦ Be re-evaluated every 4 to 6 months.♦ Consider seeing a dietitian for education and help in

managing their diet. ♦ Use vitamin and mineral supplements, if needed.

Skin care is important for palliation ofsymptoms.❑ The patient should:

♦ Hydrate the skin with proper use of emollients ortopical hydrating agents.

♦ Avoid skin care products containing perfumes anddyes (e.g., bubble baths, bath oils, alcohol-containing“baby wipes”).

♦ Rinse clothing thoroughly after washing to removedetergent and soap residue.

♦ Avoid fabric softeners (liquids and dryer sheets). ♦ Wear soft cotton clothing next to the skin.♦ Avoid irritating fabrics (e.g., wool, nylon).

124

♦ Take daily baths (showers are permissible for patientswith 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.

♦ Avoid products containing urea, lactic acid, or otheralpha-hydroxy acids if skin is inflamed.

♦ Use a humidifier, if needed, for dry skin during wintermonths.

❑ Natural sunlight can be beneficial for patients withatopic dermatitis, but caution the patient about:♦ Sunburn and other potential adverse effects of

sunlight. ♦ Exacerbation of symptoms by high heat and humidity.

❑ Phototherapy with ultraviolet A and/or B or PUVA(psoralen plus ultraviolet A) may be helpful foradolescents and adults with chronic recalcitrant disease.♦ Consider administration under the direction of a

dermatologist.

Atopic Dermatitis

Localized hydration by wet dressingsmay be helpful.❑ Recommended for severely affected or

chronically involved areas of dermatitisrefractory to conventional skin care.

❑ Physiologic saline or Domeboro’s solution(i.e., calcium acetate, aluminum sulfateastringent) may be helpful for exudative and/orcrusted 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.

125

Use appropriate medications toalleviate and prevent the patient'ssymptoms.

CorticosteroidsTopical Corticosteroids

❑ Topical corticosteroid preparations, due to their anti-inflammatory actions, are the key treatment for lesionsassociated with atopic dermatitis.

❑ Use in conjunction with emollients to help promotehydration of the epidermis.

❑ When using a topical corticosteroid:♦ Use the least potent agent that gives control.♦ Switch to a less potent agent when control is

achieved.♦ Remember that certain areas (face, genitalia, axillae)

are especially susceptible to local side effects.♦ Avoid using agents in Groups I through III on children

under 14 years of age.❑ Topical corticosteroids may:

♦ Interfere with wound healing.♦ Mask infection.♦ Exacerbate infection.

Local side effects of topical corticosteroid therapy:

Atrophy Irritation Perioral dermatitis

Burning Itching Purpura

Contact Striae Rosaceaformdermatitis dermatitis

Hypopigmentation Telangiectasia

Systemic side effects with topical corticosteroidsare rare, but may include:

Adrenal suppression Iatrogenic Cushing’s Syndrome

Cataracts Increased intraocular pressure

Growth retardation

Atopic Dermatitis

Medications used totreat Atomic Dermatitis:❑ Corticosteroids❑ Antihistamines ❑ Antibiotics❑ Antiviral agents

General considerationsfor using a topicalcorticosteroid:❑ For total body treatment

start with Groups IV or V.

❑ May use Group VII ordiluted Group VI on face.

❑ For spot (exacerbation)treatments, use GroupsIV or V.

❑ If the patient fails torespond, refer to aspecialist for consultationand/or comanagement.

Side effects are directlyrelated to the potencyrating of thecorticosteroid and theextent of use.Use of topical corticosteroidswith an occlusive dressingmay facilitate absorptionand increase the potentialfor side effects.Consultation with aspecialist is recommended.

2

126

Some suggestions for using topicalcorticosteroids:❑ 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 onchronic 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 forinitial treatment of nonfacial, nonskinfold areas. ♦ Switch to less potent agents after several days.

❑ Once symptoms are in remission, an emollientalone may be sufficient for many patients.

❑ Avoid occlusive dressings with topicalcorticosteroids because of the potential risk ofincreased absorption and/or skin infection.

Atopic Dermatitis

Topical Immunosuppressants

Adults Children

Elidel® 1% cream(pimecrolimus)Protopic®

0.03% ointment0.1% ointment(tacrolimus)

apply 2 times a day

apply 2 times a dayeither dose

>2 yrs of age apply 2times a day>2 yrs of age apply0.03% ointment 2times a day

127Atopic Dermatitis

Topical corticosteroids with potency rankings based onvasoconstrictor assays:

Group VII: Group VI Group V Group IVLeast Potent

Hydrocortisonehydrochloride 1.0%, 2.5% (cream,lotion, ointment)Hydrocortisoneacetate 1.0%, 2.5% (cream, lotion, ointment)Pramoxine hydro-chloride 1.0% (cream, lotion,ointment)

Alclometasonedipropionate 0.05% (cream,ointment)Betamethasonevalerate 0.1%(lotion)Desonide 0.05%(cream)Fluocinoloneacetonide 0.01%(cream, solution)

Betamethasonedipropionate 0.05% (lotion)Betamethasone valerate 0.1% (cream)Fluocinolone aceto-nide 0.025% (cream)Fluticasone propio-nate 0.05% (cream)Flurandrenolide0.05% (cream)Hydrocortisone valerate 0.2% (cream)Prednicarbate 0.1%(cream)

Hydrocortisonevalerate 0.2%(ointment)Flurandrenolide0.05% (ointment)Fluocinoloneacetonide 0.025%(ointment)Mometasonefuroate 0.1%(cream)Triamcinoloneacetonide 0.1%(cream)

Least Potent Moderately Potent ▼

Group III Group II Group I: Most Potent

Amcinonide 0.1% (cream,lotion)Betamethasone dipro-pionate 0.05% (cream)Betamethasone valerate0.1% (ointment)Desoximetasone 0.05%(cream)Diflorasone diacetate 0.05% (cream)Fluocinonide 0.05% (cream)Halcinonide 0.1%(ointment, solution)Triamcinolone acetonide0.1% (ointment)

Use after consultation withspecialist

Most likely to cause side effects.Use only for short periods of timeand on areas that are lichenified.DO NOT USE on face, diaperarea, genitalia, axillae. Use afterconsultation with specialist.

Amcinonide 0.1%(ointment)Betamethasone dipro-pionate 0.05% (ointment)Desoximetasone 0.05%(gel)Fluocinonide 0.05% (gel,ointment, solution)Halcinonide 0.1% (cream)Mometasone furoate 0.1% (ointment)

Betamethasone dipropio-nate 0.05% augmented(cream, ointment)Clobetasol propionate0.05% (cream, ointment)Halobetasol propionate0.05% (cream, ointment)

Group VII agents are least likely to cause long-term side effects. Group I agents are most likely to cause long-term side effects.

Moderately Potent Most Potent ▼

128

Commonly used topical corticosteroids:

Aclovate® Alclometasone diproprionate VI

Aristocort® Triamcinolone acetonide III, IV, VI

Cordran® Flurandrenolide IV, V

Cutivate®* Fluticasone propionate III, V

Cyclocort® Amcinonide II, III

Diprolene® Betamethasone diproprionate I, II

Diprosone® Betamethasone diproprionate III

Elocon® Mometasone furoate II, IV

Florone® Diflorisone diacetate II, III

Halog® Halcinonide II, III

Hytone® Hydrocortisone VII

Kenalog® Triamcinolone acetonide IV, V, VI

Lidex® Fluocinonide II, III

Locoid® Hydrocortisone butyrate V

Locortan® Flumethasone plvolate VI

Maxiflor® Diflorasone diacetate II, III

Maxlvate® Betamethasone diproprionate II, III

Pramosone® Hydrocortisone acetate, VIIpramoxine HCL

Psorcon® Difiorasone discatate I

Synalar® Fluocinolone acetonide IV, V, VI

Temovate® Clobetasol propionate I

Topicort® Desoximetason II, III

Tridesilon® Desonide V, VI

Ultravate® Halobetasol propionate I

Valisone® Betamethasone valerate III, V, V

Westcort® Hydrocortisone valerate V

Brand name Generic name Group

*Cream (0.05%) approved for atopic dermatitis in infants 3 months of age or older.

Atopic Dermatitis

Stoughton RB. Vasocanstrictor assay-specific applications. In:MaibachHI, Surber G (eds). Topical Steroids. Basel, Switzerland:Darger 1992: 42-53.

129

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 theirsymptoms after discontinuing oral corticosteroids.

❑ Avoid use in children, if possible.

Oral Antihistamines❑ Should be used to control pruritus, especially at night.

❑ Older agents, such as hydroxyzine are highly effective, but areassociated with increased sedation.

♦ Use as single dose before bedtime (1 to 2 mg/kg, up to 75mg).

❑ Newer nonsedating (or less-sedating) antihistamines shouldbe considered when sedation or impairment of performanceor cognitive function is an issue.

♦ Dosages of the nonsedating antihistamines are generallyhigher 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 occasionalphotosensitivity.

❑ 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

Atopic Dermatitis

Typical dailyprednisone dosageschedule for moderateflare:Adults: 0.5 to 1 mg/kg,tapering over 3 to 10 daysdepending on severity.

Children: 0.5 to 1 mg/kg,tapering over 3 to 5 daysdepending on severity.

❑ Avoid recurrent use oforal corticosteroids.

❑ If patient isnonresponsive followingthe course ofcorticosteroid, considerreferral to anallergy/immunology ordermatology specialist.

130

Special Considerations for Treating AtopicDermatitisAntibiotics

❑ Indicated when the patient has a secondary bacterialinfection.

❑ Macrolide antibiotics (e.g., erythromycin) are usuallybeneficial.

❑ For patients with macrolide-resistant Staphylococcusaureus, a penicillinase-resistant penicillin (dicloxacillin,oxacillin, or cloxacillin) maybe preferred.

❑ First-generation cephalosporins (cephalexin, cefadroxil)are effective against both staphylococci andstreptococci.

Atopic Dermatitis

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 yearsold).

❑ Targeted elimination diet (under specialistconsultation).

❑ Course of oral corticosteroids:♦ Prednisone (0.5 to 1.0 mg/kg) with tapering

over 2 to 3 weeks.❑ Consider referral for consultation and/or

comanagement with specialist.

131

Antiviral Agents

❑ Systemic acyclovir is recommended for superinfectionwith 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 indermatophyte-infected patients.

Evalute for immunotherapy.

❑ Allergen immunotherapy is not indicated for thetreatment of atopic dermatitis.

❑ Well-controlled studies are still required to determinethe role of allergen immunotherapy in the treatment ofatopic dermatitis.

❑ Allergen immunotherapy may be indicated foraccompanying allergic rhinitis or asthma.

Education and regular follow-upare important.

The educational tips included in Volume 1: PatientEducation, page 71, are appropriate for the patient withatopic dermatitis.

Atopic Dermatitis

4

Allergenimmunotherapy is notindicated for thetreatment of atopicdermatitis. Well-controlled studies arestill required to determinethe role of allergenimmunotherapy in thetreatment of atopicdermatitis.

3

132

❑ Skin tests❑ Targeted elimination diets❑ Identification of causal factors❑ Test interpretation❑ DBPCFC (double-blind, placebo-controlled,

food challenge)

Atopic Dermatitis

Consider referral forpatients with: ❑ Coexisting asthma,

allergic rhinitis, orallergic conjunctivitis

❑ Impaired quality of life(lost work days, lostschool days, sleepdisturbance)

❑ Poorly controlledpruritus

❑ Psychosocialcomplications

Consultation and/or comanagementwith an allergy/immunology specialistfor assistance in diagnosis andmanagement is recommended for:

❑ Patients failing to respond to treatment withtopical corticosteroids or antihistamines

❑ Complications❑ Severe or persistent disease:

♦ Patient requiring long-term or frequent useof potent topical corticosteroids (e.g., Groups< III, see pages 127)

♦ 20% general skin involvement or 10% skininvolvement affecting eyelids, hands,intertriginous areas, and not responsive tofirst-line therapy

♦ Hospitalized patient♦ Recurrent infections♦ Erythroderma or extensive exfoliation

❑ Assistance with diagnosis and management❑ Patient education

Referral to an allergy/immunologyand/or dermatology specialist isrecommended for:

133

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.

DON’T:❑ 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. ♦ Avoid sunscreens containing irritating ingredients.

❑ Swimming may be good, but shower immediately afterto rinse off chlorine. ♦ Apply skin lubricant.

Atopic Dermatitis

Boguniewicz m, Leung DYM. AtopicDermatitis. In Middleton E, Reed CE, EllisEF, et al (eds). Allergy Principles andPractice, St Louis, MO: Mosby, 5th edition1998: 1123-1134.

Brehler R, Hildebrand A, Luger TA. Recentdevelopments in the treatment of atopiceczema. J Am Acad Dermatol 1997; 36:983-994.

Cooper KD. Atopic dermatitis: recent trendsin pathogenesis and therapy. J InvestDermatol 1994; 102: 128-137.

David TJ, Patel L, Ewing CI, Stanton RHJ.Dietary regimens for atopic dermatitis inchildhood. J Royal Soc Med 1997; 90: S9-14.

Finlay AY. Measurement of diseaseactivity 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 managementof atopic dermatitis. Clin Exp Allergy 1995;25: 799-806.

Graham-Brown R. Managing adults withatopic dermatitis. Dermatologic Clinics1996; 14: 531-537.

Halbert AR, Weston WL, Morelli JG. Atopicdermatitis: is it an allergic disease? J AmAcad Dermatol 1995; 33: 1008-1018.

Hanifin JM, Klas PA. The spectrum ofcutaneous patch-test reactions in patientswith atopic dermatitis. Clin Rev AllergyImmunol 1996; 14: 225-240.

Hannuksela M, Kalimo K, Lammintausta K,et al. Dose ranging study: cetirizine in thetreatment of atopic dermatitis in adults.Ann Allergy 1993; 70: 127-133.

Li JT, Bernstein IL, Berger WE, et al. Diseasemanagement of atopic dermatitis: A practiceparameter. Ann Allergy Asthma Immunol1997; 79: 197-204.

Landow K. Atopic dermatitis: currentconcepts support old therapies and spur newones. Postgrad Med 1997; 101: 101-118.

Leung DYM. Atopic dermatitis:immunobiology and treatment with immunemodulators. Clin Exp Immunol 1997; 107:S25-30.

Leung DYM. Atopic dermatitis: the skin asa window into the pathogenesis of chronicallergic diseases. J Allergy Clin Immunol1995; 96: 302-318.

Linna O, Kokkonen J, Lahtela P, et al.Ten-year prognosis for generalized infantileeczema. 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 andgeneralists: management of childhoodatopic dermatitis. Arch Dermatol 1996;132: 1047-1052.

Reynolds NJ. Recent advances in atopicdermatitis. J Royal College PhysiciansLondon 1997; 31: 241-245.

Ring J, Brockow K, Abeck D. Thetherapeutic concept of "patientmanagement" in atopic eczema.Allergy 1996; 51: 206-215.

Romeo SP. Atopic dermatitis: the itch thatrashes. Ped Nursing 1995; 21: 157-163.

Roth HL. Atopic dermatitis. In: Conn HF.Conn’s 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 thepathogenesis of atopic dermatitis. J RoyalSoc Med 1997; 90: S2-8.

Sampson HA. The immunopathogenic roleof 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 skinof normal infants and infants with atopicdermatitis. J Am Acad Dermatol 1987; 17:988-997.

References

134 Atopic Dermatitis

135

Schultz Larsen F. the epidemiology of atopicdermatitis. Monograph Allergy 1993; 31:9-28.

Singleton JK. Pediatric dermatoses: threecommon skin disruptions in infancy.Nurse Practitioner 1997; 22: 32-50.

Stoughton RB. Vasoconstrictor assay-specific applications. In: Maibach HI,Surber C, (eds.) Topical Steroids. Basel,Switzerland: Darger 1992: 42-53.

Williams HC. On the definition andepidemiology of atopic dermatitis.Dermatol Clinics 1995; 13: 649-657.

Working Group on Atopic Dermatitis.Disease management of atopic dermatitis:a practice parameter. Ann Allergy AsthmaImmunol 1997; 79: 197-211.

Atopic Dermatitis

Associated Disease:Rhinosinusitis 137

Associated Disease:Rhinosinusitis

hinosinusitis is an inflammation of the paranasalsinuses that occurs with rhinitis. It:

❑ Rarely occurs in the absence of nasal inflammation. ❑ Is common in patients with perennial rhinitis.

Classification of RhinosinusitisAcute Rhinosinusitis❑ Is a common infection.❑ Lasts for up to 3 weeks.❑ Often follows a viral upper respiratory infection (URI).

♦ If URI symptoms worsen after 5 days, or persist after7 days, then acute rhinosinusitis should be suspected.

♦ The incidence of acute, infectious rhinosinusitis mayincrease with seasonal allergic rhinitis.

♦ Some young children may develop an acute episodewith high fever, purulent nasal discharge, and toxicity.

Recurrent Acute Rhinosinusitis❑ 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 bypersistent symptoms of acute rhinosinusitis lastinglonger than 3 months.

♦ A lack of response to treatment.♦ A positive imaging study.

❑ May have superimposed bouts of acute rhinosinusitis.

R


Rhinosinusitis:❑ Rarely occurs in the

absence of nasalinflammation.

❑ Frequently occurs inpatients with perennialrhinitis.

Acute rhinosinusitis isa common infectionthat often follows aviral upperrespiratory infection.Consider acuterhinosinusitis if URIsymptoms:❑ Worsen after 5 days

or

❑ Persist after 7 days

138

❑ Common causes: ♦ Infection (i.e., infectious rhinosinusitis)♦ Mechanical obstruction♦ Obstruction due to an allergic process♦ Primary eosinophilic inflammation of nasal and sinus

mucosa❑ Rare cases may be due to:

♦ An immunologic reaction to a fungal agent.♦ 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 havechronic 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.


Tips to distinguish chronic from acuterhinosinusitis:❑ 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 rhinosinusitisis usually nasal obstruction or discharge.

❑ Chronic cough (particularly during the nightor upon awakening in the morning) is oftena presenting symptom of chronic rhinosinusitis. ♦ In children, it may be the only symptom.

Eosinophilicinflammation of thesinuses may beassociated with asthmaand rhinitis (allergicor nonallergic) andshould bedistinguished fromrhinosinusitis of aninfectious orobstructive nature.


Who is at risk for rhinosinusitis?Clinical and environmental factorsthat predispose an individual toinfectious rhinosinusitis:

Local

More common

Upper respiratoryinfection (usually viral)

Allergic rhinitis

Nonallergic rhinitis

Less common

Overuse of topicaldecongestants

Hypertrophiedadenoids*

Deviatednasal septum

Concha bullosa

Malformeduncinate process

Prominentethmoid bulla

Nasal polyps

Tumors

Foreign bodies*

Swimmingand diving*

Cigarette smoke

Cocaine abuse

Barotrauma

Dental diseases

GERD

Systemic

Immunodeficiency(IgG or IgA)*

Cystic fibrosis*

Bronchiectasis

Immotilecilia syndrome*

Wegener’sgranulomatosis

Acquired immuno-deficiency syndrome*

Immunosuppressivetherapy

Kartagener’ssyndrome

*Particularly apply to children.


140

Diagnosing the Patient withRhinosinusitis❑ In general, the diagnosis of rhinosinusitis is made by

the constellation of symptoms plus confirmatoryphysical findings.

❑ Treatment is initiated on a presumptive basis.

Signs and Symptoms Associated withRhinosinusitisMajor❑ Facial pain and/or pressure*

❑ Facial “fullness”

❑ Nasal obstruction/blockage❑ Nasal discharge/purulence

♦ Discolored postnasal drip❑ Hyposmia/anosmia*

❑ Cough

Minor ❑ Headache*

❑ Fever❑ Halitosis*

❑ Fatigue*

❑ Dental pain*❑ Ear fullness/pain/pressure

*More common in adults.


Allergic rhinitisshould always besuspected, evaluated,and treated.

Differentiating acute infectiousrhinosinusitis from seasonal allergicrhinitis:

Acute Seasonal Allergic Rhinosinusitis Rhinitis

Nasal obstruction/ Itchy, runny nosecongestion

Pressure with pain Paroxysmal sneezing

Thick, discolored Thin, waterynasal discharge nasal discharge

Fever Seasonal symptoms

Cough



Diagnostic ProceduresImaging❑ Imaging is used when the patient has failed to respond

to adequate pharmacotherapy (e.g., chronicrhinosinusitis).

❑ Types of imaging used for chronic or recurrent acuterhinosinusitis:♦ Coronal computerized tomography (CT) scan♦ Sinus x-rays

Ethmoid sinus

Sphenoid sinus

Frontal sinus

Maxillary sinus

The signs and symptoms of rhinosinusitismay reveal which sinus is primarily affected.

Sinus Key Signs and Symptoms

Maxillary Toothache or pain overcheekbone

Ethmoid Medial canthal painor pressure

Periorbital headache

Frontal Severe frontal headache

Frontal tenderness

Sphenoid Severe headache withmultiple locationsor occipital area

142Associated Disease:Rhinosinusitis

Limited Screening Coronal CT Scan

❑ Can identify involved sinuses:♦ Maxillary♦ Frontal♦ Ethmoid♦ Sphenoid

❑ Is not optimal for evaluation of ostiomeatal complex.

Extensive Coronal CT Scan

❑ Use when:♦ Defining pathological changes in the paranasal

sinuses.♦ Surgical intervention is being considered. ♦ Complications are suspected. ♦ Diagnosis is in question.

Plain Sinus X-rays

❑ No longer considered a useful diagnostic modality inrecurrent or chronic rhinosinusitis in adults.

❑ May still be used in some areas that do not havescreening CT scans.

❑ A Waters x-ray may suffice for acute rhinosinusitis.♦ Is an adequate screening procedure in children.

Nasal Endoscopy ❑ Helps to:

♦ Pinpoint the source of purulence within the middlemeatus.

♦ Identify anatomic abnormalities.♦ Guide nasal cultures from the ostiomeatal complex.

Other diagnostic tests may be considered insome circumstances:❑ Identification of allergens to which the patient is

sensitive♦ Tests for specific IgE

❑ Mucociliary clearance measurements❑ Nasal airway assessment

143Associated Disease:

Rhinosinusitis

Tips for diagnosing rhinosinusitis:❑ Failure of symptoms to resolve after a typical

URI is an important clinical clue to thediagnosis of acute rhinosinusitis.♦ Symptoms may be indolent and smoldering.♦ Symptoms may not be considered important

by the patient. ❑ Nasal discharge and post-nasal drip may turn

from clear to yellow or green.♦ Diagnosis is supported by visual confirmation

of purulent discharge from the area of thesinus 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.

Some acute episodes need aggressivetreatment:❑ Acute frontal (or sphenoid) rhinosinusitis

is a potential medical emergency.♦ Severe neurologic complications can occur.

❑ Acute ethmoid rhinosinusitis can progressto subperiosteal abscess formation.

❑ Development of acute visual symptoms mayindicate spread of infection to structures nearthe optic nerve.♦ Requires immediate evaluation by an

otolaryngologist and/or ophthalmologist. ❑ Perinasal cellulitis can lead to cavernous

sinus thrombosis.♦ Follow carefully.

Referral to an otolaryngologic allergyspecialist is recommended.

Rhinosinusitis is acommon cause ofasthma exacerbations.❑ Consider rhinosinusitis

for asthmaexacerbations that donot respond toaggressive treatment.

144

Managing the Patient withInfectious Rhinosinusitis❑ Management of rhinosinusitis includes:

♦ Using appropriate medications.♦ Palliative measures.♦ Surgery, when aggressive medical management

has failed.


Pharmacologic ManagementAntibiotic Therapy❑ Before selecting antibiotic therapy for the treatment of

rhinosinusitis, consider:♦ Local sensitivity patterns. ♦ Potential for resistance.

❑ Common bacterial pathogens in acute rhinosinusitis:♦ Streptococcus pneumoniae♦ Haemophilus influenzae♦ Moraxella catarrhalis (primarily in children)♦ Streptococcal species

Initial choice of antibiotic for an isolated episodeof acute rhinosinusitis:

❑ Amoxicillin or trimethoprim/sulfamethoxazole(TMP/SMX) in adults and erythromycinethylsuccinate/sulfisoxazole acetyl in children, may beeffective, inexpensive, and well tolerated. ♦ Erythromycin and ceflacor are generally not effective

in the treatment of rhinosinusitis. ♦ CDC estimates that 25% of S. pneumoniae infections

are resistant to TMP/SMX.⇒ Significant resistance is also seen with cefixime.

♦ Resistance to amoxicillin and cefaclor are common.❑ Local sensitivity patterns that are associated with high

prevalence of resistance may justify the use of otherantibiotics.

❑ Assess response to treatment after 3 to 5 days, andchange antibiotic if needed.

Management goals:❑ Control infection.

❑ Reduce tissue edema.

❑ Facilitate drainage.

❑ Maintain patency ofostia.

❑ Break pathological cycleleading to chronicrhinosinusitis.

Common bacterialpathogens in acuterhinosinusitis:❑ Streptococcus

pneumoniae

❑ Haemophilus influenzae

❑ Moraxella catarrhalis(primarily in children)

❑ Streptococcal species

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.

145

Choice of antibiotic for repeated episodes of acuteor recurrent rhinosinusitis:

❑ The choice of antibiotic depends on the: ♦ Suspected bacteria ♦ Local sensitivity patterns♦ Patient’s 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 penicillinand 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.

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

Use intranasalcorticosteroids forthe patient with:❑ Chronic rhinosinusitis.

❑ Recurrentrhinosinusitis.

Avoid prolonged useof topicaldecongestants.

146

Oral Mucolytics❑ May help to:

♦ Thin discharge♦ Promote drainage♦ Assist resolution

❑ Clinical effectiveness is uncertain.


Surgery❑ Surgery for chronic or recurrent acute rhinosinusitis is

generally reserved for patients for whom appropriateaggressive medical management has failed.

❑ The goals of surgery are to:♦ Reduce recurrences of rhinosinusitis.♦ Remove obstruction(s) to sinus drainage

(e.g., anatomical abnormalities, polyps).♦ Alleviate acute complications

❑ Indications for surgery:♦ Bilateral extensive and massive obstructive nasal

polyposis with complications.♦ Complications of adult rhinosinusitis, including:

⇒ Pott’s puffy tumor⇒ Brain abscess⇒ Meningitis

♦ Complications of childhood rhinosinusitis (e.g., meningitis).

♦ Chronic adult rhinosinusitis with mucocele ormucopyocele formation.

♦ Invasive or allergic fungal rhinosinusitis. ♦ Tumor(s) of nasal cavity and paranasal sinuses.♦ Cerebrospinal fluid rhinorrhea.

Consider surgerywhen appropriatemedical managementof rhinosinusitis hasfailed.


Rhinosinusitis

Specific Considerations for TreatingRhinosinusitisAcute Rhinosinusitis❑ Length of treatment is typically 10 to 14 days.

♦ Patient should be symptom-free for 7 days.♦ Treatment for up to 21 days is sometimes necessary.

Recurrent Acute Rhinosinusitis❑ Length of treatment is typically 10 to 14 days.

♦ Patient should be symptom-free for 7 days.♦ Treatment for up to 21 days is sometimes necessary.

❑ Recurrent acute rhinosinusitis is a more commonproblem in children.

❑ Long-term use of intranasal corticosteroidsmay be helpful.

❑ Consider referral to an allergy/immunology or anotolaryngologic allergy specialist:♦ For an adult who has had more than 4 episodes

in 12 months.♦ For a child who has had 3 or more episodes in

6 months, or 5 or more episodes in 12 months.

Subacute (Persisting Acute) Rhinosinusitis ❑ Treat like recurrent acute rhinosinusitis.

For recurrent acuterhinosinusitis,consider referral toan allergy/immunology or anotolaryngologicallergy specialist for the:❑ Adult who has had

more than 4 episodesin 12 months.

❑ Child who has had3 or more episodes in6 months, or 5 ormore episodes in12 months.

Acute, recurrentacute, and subacute(persisting acute)rhinosinusitis aretypically treated for10 to 14 days. ❑ Patient should be

symptom-free for 7days.

❑ Treatment for up to21 days is sometimesnecessary.

When should surgery be considered?❑ Persistently opacified maxillary sinus requiring

therapeutic or diagnostic intervention.❑ Complications from adenoidal enlargement

(e.g., sleep disturbance, eustachian tubedysfunction, rhinosinusitis).

❑ Nasal septal deviation and/or other nasalanatomical abnormalities (e.g., concha bullosa).

❑ Difficult-to-control asthma and the presence ofchronic rhinosinusitis.

❑ Presence of chronic infectious rhinosinusitis.❑ Subperiosteal orbital abscess.

148

Chronic Infectious Rhinosinusitis❑ If unresponsive, broaden antibiotic coverage.

♦ In adults, consider: ⇒ Ciprofloxacin (no anaerobic coverage)⇒ Levofloxacin⇒ Adding metronidazole to cover anaerobic

organisms♦ In children consider:

⇒ Clindamycin⇒ Adding metronidazole to cover anaerobic

organisms❑ Treat for up to 4 to 6 weeks.

♦ If symptoms do not improve, consider referral to anallergy/immunology or an otolaryngologic allergyspecialist.

❑ Consider topical intranasal corticosteroids. ♦ A short course of oral corticosteroids may be helpful,

unless contraindicated. ❑ Have patient use nasal irrigation with bulb pik.


Additional ManagementConsiderations for the AllergicRhinosinusitis Patient❑ Treat concomitant rhinitis.❑ Determine allergens to which the patient is sensitive. ❑ Educate the patient about allergen and irritant

avoidance techniques and general self-managementskills.

❑ Consider immunotherapy. ❑ Referral to an allergy/immunology or an otolaryngologic

allergy specialist is recommended.

Chronic infectiousrhinosinusitis mayneed up to 6 weeks ofantibiotic treatment.

Consider:❑ Topical intranasal

corticosteroids.

❑ A short course of oralcorticosteroids, unlesscontraindicated.

❑ Nasal irrigation withbulb pik.

❑ Referral to anallergy/immunologyor an otolaryngologicallergy specialist ifsymptoms do notimprove.

Four generalprinciples formanaging allergicdiseases1. Avoid factors that cause

symptoms.

2. Use appropriate medications.

3. Evaluate for immunotheropy.

4. Educate and follow-up.

Managing allergic rhinitis can improverhinosinusitis and asthma symptoms.


Rhinosinusitis

More than 50% of moderate to severeasthmatics have chronicrhinosinusitis. ❑ In the asthma patient, the eosinophilic

inflammation often involves the sinuses aswell as the nose and bronchi.

❑ Clinical evidence of infection is often absent,except during acute purulent episodes.

Special Considerations for TreatingRhinosinusitis in Children❑ The diagnosis of rhinosinusitis is often missed in

children.♦ Children may be diagnosed with concurrent otitis

media, but not treated long enough to cure the sinuscomponent of the infection. ⇒ This can result in subacute disease.

❑ Rhinosinusitis is a common reason for asthmaexacerbations.♦ May be a silent reason for exacerbations that respond

poorly to aggressive therapy, including oralcorticosteroids.

In asthmatic patientswith appropriatesymptoms or who arenot responding totherapy, consider asuperimposed acuterhinosinusitisinfection.❑ Upper airway symptoms

may not be reported bythe patient.

❑ Treatment of infectiousrhinosinusitis frequentlyimproves asthmasymptoms.

The diagnosis ofrhinosinusitis is oftenmissed in children.

Aspirin and NSAID sensitivities arecommon in adult nonallergicrhinosinusitis patients, especiallythose who have nasal polyps. ❑ This is referred to as “Samter’s Triad.”

❑ Primary treatment is avoidance of aspirin andNSAID products, though some patientsdemonstrate improvement with oral aspirindesensitization.

150

❑ The most common symptoms of rhinosinusitis inchildren are:♦ Cough ♦ Rhinorrhea

❑ It is relatively uncommon to hear complaints of:♦ Sinus pressure♦ Headache♦ Facial pain♦ Tooth pain

❑ Rhinosinusitis may be a manifestation ofimmunodeficiency. ♦ Consider referral for a thorough immune evaluation

for patients with recalcitrant disease. ♦ 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:♦ Adenoid hyperplasia♦ Swimming/diving♦ Passive tobacco smoke exposure

❑ Long-term use of intranasal corticosteroids may behelpful in children with recurrent rhinosinusitis. ♦ Patients should be seen at frequent (3 to 6 months)

intervals for:⇒ Evaluation of the nasal mucosa.⇒ Assessment of growth rate.

♦ Dosage should be tapered to the least amount that iseffective.


The most commonsymptoms ofrhinosinusitis inchildren are:❑ Cough

❑ Rhinorrhea

It is relativelyuncommon forchildren to complain of:❑ Sinus pressure

❑ Headache

❑ Facial pain

❑ Tooth pain


Rhinosinusitis

❑ The condition or its treatment interferes withthe patient’s performance causing significantloss of school or work on a chronic or recurrentbasis.

❑ The patient’s quality of life is significantlyaffected 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 immunologictesting.

❑ There is need for complex pharmacology, suchas with antibiotic allergies or resistantpathogens.

❑ Allergic fungal rhinosinusitis is present.

When is referral to an otolaryngologicallergy specialist preferred? ❑ When anatomical defects exist which obstruct

the sinus outflow track, including theostiomeatal complex and adenoidal tissues, andare thought to be contributing to recurrent orchronic rhinosinusitis.

❑ When nasal polyps obstruct the sinus drainageand persist despite appropriate medicaltreatment.

❑ For biopsy of the nasal mucosa to rule outgranulomatous disease, neoplasms, ciliarydyskinesia, or fungal infections.

❑ When maxillary antral puncture is required fordiagnosis and/or treatment.

❑ For recurrent rhinosinusitis associated withmiddle ear disease.

❑ If adenoidectomy is being considered.

Consider referral to an allergy/immunology or an otolaryngologicallergy specialist for consultationand/or comanagement when:

Associated Disease:Rhinosinusitis152

Anand VK, Osguthorpe JD, Rice D. Surgicalmanagement of adult rhinosinusitis.Otolaryngol Head Neck Surg 1997; 117:S50-52.

Arjmand EM, Lusk RP. Management ofrecurrent 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. Allergicrhinosinusitis 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.Who’ll benefit from endoscopic sinussurgery? Patient Care, June 1996: 178-196.

Derebery MJ. Otolaryngic allergy.Otolaryngol Clin North Am 1993; 26:593-611.

deShazo RD, Swain RE. Diagnostic criteriafor allergic fungal sinusitis. J Allergy ClinImmunol 1995; 96: 24-35.

Dohlman AW. Role of antibiotic andnon-antibiotic therapy in the treatmentof 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. What’s causingyour patient’s rhinosinusitis? J Respir Dis1997; 18: 321-334.

Gungor A, Corey JP. Pediatric sinusitis:a literature review with emphasis on therole of allergy. Otolaryngol Head NeckSurg 1997; 116: 4-15.

Joint task force on practice parameters.Parameters for the diagnosis andmanagement of sinusitis. J Allergy ClinImmunol 1998; 102: S107-144.

Kaliner MA. Allergy care in the nextmillennium: guidelines for the specialty.J Allergy Clin Immunol 1997; 99: 729-734.

Kaliner MA. Human Host defense andsinusitis. In: Gershen ME, Incaudo GA(eds). Diseases of the sinuses. New Jersey:Humana Press. 1996: 53-60.

Kaliner MA. Medical management ofsinusitis. Am J Med Sci 1998; 316:21-28.

Kaliner MA, Osguthorpe JD, Fireman P,et al. Sinusitis: bench to bedside. J AllergyClin Immunol 1997; 99: S829-848.

Karlsson G, Holmberg K. Does allergicrhinitis predispose to sinusitis? ActaOtolaryngol (Stockh) 1994; 515: S26-29.

Mackay IS, Durham SR. The classificationand 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 rhinosinusitisdefined. Otolaryngol Head Neck Surg 1997;117: S1-7.

Mabry RL. Allergic and infectiverhinosinusitis: differential diagnosis andinterrelationship. Otolaryngol Head NeckSurg 1994; 111: 335-339.

McNally PA, White MV, Kaliner MA. Sinusitisin an allergist’s office: analysis of 200consecutive cases. Allergy AsthmaProceedings 1997; 18: 169-175.

Nelson HS. Diagnosis and management ofsevere asthma in the adult. In: Szefler SJ,Leung DY (eds.) Severe asthmapathogenesis and clinical management.New York: Marcel Dekker, 1996: 397-419.

Parsons DS. Chronic sinusitis: a medicalor surgical disease ? Otolaryngol Clin NorthAm 1996; 29: 1-9.

Parsons DS, Wald ER. Otitis media andsinusitis: similar diseases. Otolaryngol ClinNorth Am 1996; 29: 11-25.

Reuler J, Lucas L, Kumar K. Sinusitis: areview for generalists. West J Med 1995; 163:40-48.

References



Rhinosinusitis

Rowe-Jones JM. The link between the noseand lung, perennial rhinitis and asthma -is it the same disease? Allergy 1997; 52:S20-28.

Senior BA, Kennedy DW. Managementof sinusitis in the asthmatic patient.Ann Allergy Asthma Immunol 1996; 77:6-19.

Shapiro GG, Rachelefsky GS. Introductionand definition of sinusitis. J Allergy ClinImmunol 1992; 90: 417-418.

Slavin RG. Nasal polyps and sinusitis.J Am Med Assoc 1997; 278: 1849-1854.

Spector S. Overview of comorbidassociations of allergic rhinitis. J AllergyClin Immunol 1997; 99: S773-780.

Weinberg EA, Brodsky L, Brody A, PizzutoM, Stiner H. Clinical classification as a guideto treatment of sinusitis in children.Laryngoscope 1997; 107: 241-246.

155

Associated Disease:Chronic or RecurrentOtitis Media

titis media can be an acute or chronic inflammation of the middle ear.

❑ The patient may experience recurrent acuteepisodes (recurrent otitis media).

❑ May be attributed to eustachian tube dysfunctionand accumulation of serous or purulent fluid inthe middle ear cavity.

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

❑ Often associated with rhinitis.

❑ May be of infectious and/or allergic causation.

❑ It may be:

♦ Acute

♦ Recurrent acute

♦ With effusion

♦ Chronic with effusion

Associated Disease:Chronic or Recurrent Otitis Media

O

Characteristic Signs and Symptoms❑ The earliest signs of acute otitis media are ear pain and

discomfort. ♦ The patient may be irritable.♦ The child may pull on the affected ear. ♦ Infant may fail to feed.

❑ Snoring, mouth-breathing, or nasal obstruction maysuggest adenoidal obstruction.

❑ Hearing loss may or may not be present. ❑ Nonspecific signs associated with otitis media:

♦ Fever ♦ Anorexia♦ Headache ♦ Vomiting♦ Apathy ♦ Diarrhea

Otitis media is themost commonchildhood diseaserequiring physiciancare.

Otitis media isclassified as:❑ Acute otitis media

❑ Recurrent acute otitismedia

❑ Otitis media witheffusion

❑ Chronic otitis mediawith effusion

Children withpersistent otitis mediawith effusion orrecurrent otitis mediaoften experience aconductive hearingloss with the potentialfor defects in speechand languagedevelopment andschool performance.

156Associated Disease:Chronic or Recurrent Otitis Media

Natural History of Otitis MediaRisk factors for otitis media:

❑ Allergy plays a role in recurrent or chronic otitis media. ♦ As many as 50% of children older than 3 years with

chronic otitis media have confirmed allergic rhinitis. ♦ 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.♦ 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.

♦ Interactions between viruses and allergens and theirrespective immune/inflammatory responses maypredispose to development of otitis media.

As many as 50% ofchildren older than3 years with chronicotitis media haveconfirmed allergicrhinitis.

Viral upper respiratoryinfection

Allergic rhinitis

Eustachian tubedysfunction

Cigarette smokeexposure

Age (< 1 yr)

Race (American Indians)

Sinusitis

Cilia dysfunction

Male sex

Immunodeficiency

Fall/winter season

Genetic predisposition

Daycare

Siblings

Adenoidal enlargement

Cleft palate


Chronic or Recurrent Otitis Media

Eustachian tube dysfunction, middle earnegative pressure, and/or nasalinflammation (e.g., allergy, URI) cancontribute to otitis media development.

Diagnosing the Patient withOtitis Media❑ A detailed medical history and physical examination

using a pneumatic otoscope are usually sufficient toestablish the diagnosis.

❑ Consider:♦ Duration of symptoms♦ When symptoms occur♦ Previous history of and treatment for ear disease♦ Family history of atopic disease♦ Presence of associated allergic disease

(e.g., allergic rhinitis)♦ Environmental history to identify allergic or irritant

causal factors♦ Information on the other risk factors such as:

⇒ Daycare⇒ Bottle feeding while lying down⇒ Smoking in household

Eustachian tubedysfunction, a keycontributing factor tootitis media, iscommon in infantsand younger childrenbecause:❑ The eustachian tube has

less cartilage support.

❑ The eustachian tube isless angulated.

❑ The tensor veli palatinimuscle is less efficient.

Recurrent otitis mediaor otitis media witheffusion: ❑ ≥ 3 episodes in

6 months or

❑ ≥ 4 episodes in12 months

Orientation, short length, andpatency of child's eustachiantube causes decreasedprotective function.

1

Nasal secretionsenter middleear througheustachian tube.

2

Secretions createobstruction, causinginflammationand dysfunction.

3

Adult Child

158

❑ Evaluate for underlying factors prior to initiatingpreventative treatments:♦ Allergy♦ Rhinosinusitis♦ Hypertrophic adenoids♦ Immunodeficiency♦ Food intolerance reaction

⇒ Based on anecdotal evidence⇒ Requires further clinical investigation


Normal tympanic membrane. Reprinted from Bull TR.Examination of the ear. In: Bull TR(ed). Color atlas of ENT diagnosis.London: Year Book MedicalPublishers, Inc; 1974: 12-13. Bypermission of publisher Mosby.

Acute otitis media. Reprinted from Bull TR. Thetympanic membrane and middle ear.In: Bull TR (ed). Color atlas of ENTdiagnosis. London: Year BookMedical Publishers, Inc; 1974: 92-93.By permission of publisher Mosby.

Otitis media with effusion. Reprinted from Bull TR. Thetympanic membrane and middle ear.In: Bull TR (ed). Color atlas of ENTdiagnosis. London: Year BookMedical Publishers, Inc; 1974: 84-85.By permission of publisher Mosby.

History and physicalexamination using apneumatic otoscopeare usually sufficientto establish thediagnosis of otitismedia.

159

Does the patient need further allergyevaluation? 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.♦ Interfere with normal activities.♦ 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 OtitisMediaPreventive Therapies❑ Use to treat recurrent otitis media

♦ Prophylactic antibiotic ♦ Tympanostomy tube insertion with or without

adenoidectomy

A flanged Teflon® tube (grommet)may be used to prevent middle earfluid recurrence. Reprinted from Bull TR. The tympanicmembrane and middle ear. In: Bull TR(ed). Color atlas of ENT diagnosis.London: Year Book Medical Publishers,Inc; 1974: 88-89. By permission ofpublisher Mosby.

Inserted tube ventilates themiddle ear. Reprinted from Bull TR. Thetympanic membrane and middle ear.In: Bull TR (ed). Color atlas of ENTdiagnosis. London: Year BookMedical Publishers, Inc; 1974: 88-89.By permission of publisher Mosby.

Four generalprinciples of allergymanagement1. Avoid factors that cause

symptoms.

2. Use appropriatemedications.

3. Evaluate forimmunotherapy.

4. Educate and follow-up.

160

Therapeutic Treatments❑ When otitis media is associated with allergic rhinitis,

control of allergic rhinitis frequently results in theresolution of otitis media.

❑ If associated allergic rhinitis is documented, intensiveallergy therapy is indicated. Consider:♦ Allergen avoidance♦ Antihistamine therapy♦ Intranasal corticosteroids and/or occasional short

courses of oral corticosteroids may be useful forreducing inflammation and eustachian tubeobstruction

♦ Intranasal cromolyn sodium♦ Allergen immunotherapy

❑ Decongestants are widely used to treat the associatedeustachian tube dysfunction, but their clinical efficacyhas not been established.


Otitis media is multifactorial in nature.The best therapeutic results forchronic or complicated problems areoften obtained when the patient ismanaged by a coordinated effortinvolving the primary care provider,otolaryngologic allergy specialist and/orallergy/immunology specialist.

Early treatment ofotitis media isimportant. Children with persistentotitis media with effusionor recurrent otitis mediaoften experienceconductive hearing losswith the potential forspeech defects affecting:

❑ Language development

❑ School performance

When otitis media isassociated withallergic rhinitis,control of allergicrhinitis frequentlyresults in theresolution of otitismedia.

Consider referral to an allergy/immunology specialist orotolaryngologic allergy specialist for consultation or comanagement,particularly for chronic or complicatedcases.

Bernstein JM. The role of IgE-mediatedhypersensitivity in the development of otitismedia with effusion: a review. OtolaryngolHead Neck Surg 1993; 109: 611-20.

Bernstein JM, Doyle WJ. Role of IgE-mediated hypersensitivity in otitis mediawith effusion: pathophysiologicconsiderations. Ann Otol Rhinol Laryngol1994; 103: 15-19.

Bernstein JM. Role of allergy in Eustachiantube blockage and otitis media witheffusion: a review. Otolaryngol Head NeckSurg 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 tubedysfunction: connection to allergic rhinitis.J Allergy Clin Immunol 1997; 99: S787-797.

Fireman P. Otitis media and its relation toallergic rhinitis. Allergy Asthma Proc 1997;18: 135-143.

Lieberman PL, Blaiss MS. Allergic diseasesof the eye and ear. In: Patterson R,Grammer LC, Greenberger PA (eds). AllergicDiseases - Diagnosis and Management, 5thed. Philadelphia: Lippincott-Raven, 1997;223-251.

Mattucci KF, Greenfield BJ. Middle eareffusion: allergy relationships. ENT 1995;74: 752-758.

Parsons DS, Wald ER. Otitis media andsinusitis: similar diseases. OtolaryngolClin 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, 5thed. St. Louis, MO: Mosby 1998: 1036-1049.

Spector SL. Overview of comorbidassociations of allergic rhinitis. J AllergyClin Immunol 1997; 99: S773-780.

Wald ER. Otitis media. In: Conn HF. Conn’scurrent therapy. Philadelphia, 1998:208-210.

References


Chronic or Recurrent Otitis Media

Resource Organizations 163

Allergy and Asthma Network/Mothers of Asthmatics, Inc.2751 Prosperity Ave., Suite 150Fairfax, VA 22030Phone: (800) 878-4403www.aanma.org

American Academy of Allergy,Asthma and Immunology611 East Wells StreetMilwaukee, WI 53202(800) 822-ASMA or (414) 272-6071www.aaaai.org

American Academy of Pediatrics141 Northwest Point BoulevardElk Grove Village, IL 60007-1098(800) 433-9016 or (847) 228-5005www.aap.org

American Associationfor Respiratory Care11030 Ables LaneDallas, TX 75229(972) 243-2272www.aarc.org

American College of Allergy, Asthmaand Immunology85 West Algonquin Road, Suite 550Arlington Heights, IL 60005(800) 842-7777 or (847) 427-1200www.acaai.org

The American Lung AssociationFor the affiliate nearest you,call (800) LUNG USAwww.lungusa.org

Asthma and Allergy Foundationof America1125 Fifteenth St, N.W., Suite 502Washington, DC 20005Phone: (800) 7-ASTHMAwww.aafa.org

Centers for Disease Control andPrevention1600 Clifton Rd.Atlanta, GA 30333(800) 311-3435

The Food Allergy Network10400 Eaton Pl., Suite 107Fairfax, VA 22030Phone: 1-800-929-4040www.foodallergy.org

Healthy Kids: The Key to BasicsEducational Planning for Studentswith Chronic Health Conditions79 Elmore StreetNewton, MA 02459-1137(617) 965-9637E-mail: [email protected]

Immune Deficiency Foundation25 W. Chesapeake Ave., Suite 206Towson, MD 21204Phone: (800) 296-4433www.primaryimmune.org

National Heart, Lungand Blood Institute(National Asthma Educationand Prevention Program)P.O. Box 30105Bethesda, MD 20824Phone: (301) 251-1222www.nhlbi.nih.org

National Institute of Allergyand Infectious DiseasesBuilding 31, Room 7A-50National Institutes of HealthBethesda, MD 20892Phone: (301) 496-5717www.niaid.nih.gov

Resource OrganizationsContact the organizations listed below for information andhelpful ideas.

Resource Organizations164

U.S. Department of EducationOffice for Civil Rights,Customer Service TeamMary E. Switzer Building330 C Street, S.W.Washington, DC 20202-1328(800) 421-3481 or (202) 205-5413www.ed.gov/offices/OCR

U.S. Environmental Protection AgencyIndoor Environments Division401 M Street, S.W. (6604J)Washington, DC 20460(202) 233-9370Indoor Air QualityInformation Clearinghouse(800) 438-4318www.epa.gov/iaq

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AAAAI: American Academy of Allergy, Asthma and Immunology.

Airway wall “remodeling”: structural changes that are unlikely to bereversible, resulting from continued inflammation observed in chronic asthma.Permanent changes include continued loss of epithelial cells, deposition ofsubbasement membrane collagen, and increased muscle mass and bloodvessels.

Allergen immunotherapy (allergy vaccine therapy): a form of long-termtherapy consisting of repeated, controlled administration of specific allergensto patients with IgE-mediated conditions to reduce disease severity fromnatural exposure to these allergens.

Allergen: the source of an allergy-producing substance, the allergy-producingsubstance itself, or one or more of the specific proteins that make up thesubstance and provoke the immune response, including IgE antibodies. Theyare 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 immuneresponses (including IgE responses), following repeated contact with usuallyharmless substances such as pollen, mold spores, animal dander, dust, foods,insect venoms, and drugs; include diseases of the atopic diathesis as well asdiseases which may have an allergic component.

Allergy: an acquired potential to develop immunologically mediated adversereactions to normally innocuous substances upon re-exposure to thesensitizing allergen (including IgE antibody responses to allergens), causing therelease of inflammatory mediators.

Anaphylactoid reaction: an immediate systemic reaction that mimicsanaphylaxis 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 beenpreviously exposed. It has many etiologies, resulting from immune-mediated(i.e., IgE-mediated) rapid release of potent mediators from tissue mast cells andperipheral blood basophils. The reaction occurs rapidly and often dramatically,and is usually unanticipated. Signs and symptoms arise systemically and mayinclude 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 amedical emergency! See also exercise-induced anaphylaxis, anaphylactoidreaction, and idiopathic anaphylactic/anaphylactiod reactions.

Glossary

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Angioedema: swelling in the deep cutaneous layer, but the skin may appearnormal.

Antihistamines: drugs that inhibit allergy symptoms by blocking the actions ofhistamine at the H1 receptor. Older sedating antihistamines cause drowsinessand/or loss of concentration and may affect psychomotor performance.Nonsedating antihistamines have poor penetration of the CNS, resulting in nosedative or psychomotor adverse effects.

Asthma: is a chronic inflammatory disease of the airways characterized byairway obstruction, which is at least partially reversible with or withoutmedication, and manifests increased bronchial responsiveness to a variety ofstimuli.

Atopic dermatitis: is a chronic or recurrent atopic inflammatory skin diseasethat usually begins in the first few years of life. It is often the initial clinicalmanifestation of an atopic predisposition, with many children later developingasthma 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 witha 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-actingquick relief, long-term 12-hour control, and for preventing exercise-inducedbronchospasm. The bronchial smooth muscle relaxes in response to beta2-adrenergic receptor stimulation.

Chlorofluorocarbon (CFC): propellant used in MDIs to deliver inhaledasthma medications. Other propellants (HFA-134) will be replacing CFCs in thefuture because CFCs deplete the ozone layer.

Conjunctivitis: a group of ocular disorders that result in inflammation of theconjunctiva. May be of allergic or nonallergic origin.

Contact dermatitis: refers to a broad range of reactions resulting from thedirect contact of an exogenous agent (allergen or irritant) with the surface ofthe skin.

Corticosteroids: medications related to cortisone with anti-inflammatoryeffects 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 anti-inflammatory agents.

DBPCFC: double-blind, placebo-controlled food challenge. Considered the“gold standard” for diagnosing food allergies.

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Decongestants: are sympathomimetic drugs that relieve symptoms of nasalcongestion or blockage by constricting the capacitance vessels in the turbinates.

Desensitization: a medical procedure utilized to reduce or eliminatesensitivity to certain drugs. Desensitization for IgE-mediated drug reactions isachieved by administering progressive doses of the drug until a full therapeuticdose is clinically tolerated. Indicated for patients with established drug allergywhere no substitute for the responsible drug is available and treatment isessential. Desensitization for non-IgE-mediated drug reactions is successful foraspirin and NSAIDs.

Domeboro’s solution: calcium acetate, aluminum sulfate astringent used todry oozing dermatitis.

Dry-powder inhaler (DPI): delivery mechanism without propellant forinhaled asthma medications that are in powdered form.

Early phase reaction (immediate hypersensitivity reaction): animmunological reaction that occurs within minutes of subsequent exposure ofthe IgE antibody to the allergen in sensitized individuals. With repeat exposureof allergen, multiple IgE-FcεR-complexes are cross-linked resulting in immediatehypersensitivity reactions (i.e., mast cells degranulate releasing histamine,leukotrienes, cytokines, and proteases).

Eczema: is an inflammatory disease of the skin with lesions that can beerythematous, 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 oftime (10 to 14 days) to evaluate the patient. Specific foods may be eliminated(e.g., targeted elimination diet) or basic/severe elimination diet protocols maybe utilized in more complicated situations.

Epicutaneous (patch) testing: a form of allergy skin testing that identifies orconfirms suspected T-cell-mediated, delayed hypersensitivity, contact allergensin contact eczematous dermatitis.

Exercise-induced anaphylactic/anaphylactoid reactions: a generalizedreaction 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 thelungs caused by a loss of heat, water, or both from the airways during exercisedue to increased ventilation and inhalation of cool, dry air relative to the airwithin the lungs.

FDA: Food and Drug Administration.

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Food allergy: a group of disorders characterized by immunologic responses tospecific food proteins. Any food may cause a food allergic reaction. Theprevalence is greatest in the fist few years of life and declines over the firstdecade.

Hepa-filters: high efficiency particulate air filter.

Idiopathic anaphylactic/anaphylactoid reactions: a generalized reactionthat is diagnosed by exclusion when neither a causative allergen nor physicalfactor can be identified.

Immediate local reaction: describes an insect sting reaction and issometimes referred to as the “normal reaction.” Presents as pain, erythema,itching, and swelling at the sting site. It is a transient response that usuallydisappears within several hours.

In vitro: refers to a lab test (e.g., ELISA) to diagnose allergens that a person issensitized to.

Ipratropium bromide: used as adjunct therapy to bronchodilators in thetreatment of acute asthma exacerbations. Affects are primarily due toanticholinergic action on bronchial smooth muscle. Also used to controlrhinorrhea in a patient with nonallergic rhinitis.

Large local reaction: describes an insect sting reaction that displays extensiveswelling and erythema, extending from the sting site over a large area and ofteninvolves most of an extremity. Swelling often peaks within 48 hours and may lastas long as 7 to 10 days. Occasionally, fatigue, low-grade fever, and nauseaaccompany the reaction.

Late phase reaction: an immunological reaction that begins 2 to 4 hoursfollowing exposure to allergen and can last for 24 hours before subsiding.Inflammatory leukocytes (e.g., neutrophils, basophils, eosinophils) are involvedbut the late response is primarily mediated by eosinophils in atopic individuals.These inflammatory cells release cytokines and chemokines during theresponse.

Latex allergy: an allergic response to the proteins in natural latex rubber or tothe additives used in processing latex.

Leukotriene modifiers: a group of drugs that may be used as long-termcontrol medications for the treatment of mild persistent asthma. May beconsidered as alternative therapy to low doses of inhaled corticosteroids in mildpersistent asthma, but the position of leukotriene modifiers in therapy has notbeen fully established.

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Long-term control medications: drugs that are taken daily on a long-termbasis to achieve and maintain control of persistent asthma. Examples includeinhaled corticosteroids, long-acting bronchodilators (e.g., beta2-agonists), plusother long-term control medications (e.g., methylxanthines [theophylline],leukotriene pathway modifiers).

Mast cell stabilizer: a group of drugs that exhibit anti-inflammatoryproperties (e.g., cromolyn sodium, nedocromil sodium). The mechanism ofaction of these drugs remains uncertain.

Metered-dose inhaler (MDI): propellant-driven delivery mechanism forinhalation 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 immunesystem but can be important cofactors for developing allergic reactions.

Oral allergy syndrome: a self-limiting condition associated with the ingestionof 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 isnot as sensitive as FEV1 for diagnosing airflow obstruction; primarily ameasurement of large airway function. Peak flow meters are designed asmonitoring, not diagnostic, tools.

Prick/puncture test: are a test used to confirm hypersensitivity to a widevariety of allergens, the most convenient and specific method for detecting IgEantibodies.

Primary prevention: focuses on blocking sensitization and development ofIgE-mediated response.

Quick-relief medications: a group of drugs that give prompt relief ofbronchoconstriction and accompanying acute asthma symptoms: coughing,wheezing, shortness of breath or rapid breathing, chest tightness. Examplesincluding short acting beta2-agonists and anticholinergics.

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Rhinitis: inflammation of the mucous membranes of the nose with symptomsof sneezing, itching, nasal discharge, and congestion. The etiology can beallergic, nonallergic, or both. Seasonal allergic rhinitis is an IgE-mediatedreaction of the nasal mucosa to one or more seasonal allergens. Perennialallergic rhinitis is an IgE-mediated reaction to allergens that show little or noseasonal variation. It is persistent, chronic, and generally less severe thanseasonal.

Rhinosinusitis: is an inflammation of the paranasal sinuses that occurs withrhinitis. It rarely appears in the absence of nasal inflammation, commonlyoccurring in patients with perennial allergic and nonallergic rhinitis and inpatients with moderate to severe asthma. Acute rhinosinusitis is a commoninfection that lasts for up to 3 weeks and often follows a viral upper respiratorytract infection. Suspect if symptoms worsen after 5 days or persist after 7 days.Recurrent acute rhinosinusitis is characterized by four or more episodes ofacute rhinosinusitis per year separated by at least 8 weeks of symptom-freeintervals. Subacute (persisting acute) rhinosinusitis lasts between 3 weeks and3 months. Chronic rhinosinusitis is a complex of symptoms associated withinflammation of the sinuses characterized by persistent symptoms of acuterhinosinusitis 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 smoothmuscle, resulting in bronchodilation usually within 5 to 10 minutes ofadministration. They are most effective medication for relieving acutebronchospasm, and are the therapy of choice for relieving acute symptoms andpreventing exercise-induced bronchospasm. Using more than two times perweek, other than for prevention of exercise-induced asthma, is an indicator forinitiating or increasing anti-inflammatory therapy. Increasing use indicatesinadequate control of asthma and the need to intensify long-term controltherapy.

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 thegeography/community. For example, the Asthma section (Volume 2) uses theterm “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 orpulmonologist or, occasionally, other physicians with experience in asthmamanagement developed through additional training and experience. Similarcomplexities exist in identifying specialists for management of such diseases asatopic dermatitis, rhinosinusitis, otitis media, conjunctivitis, urticaria andangioedema, and contact dermatitis. Therefore, consultation or comanagementis recommended, as appropriate, with the type of specialist determined by thereferring healthcare provider and taking into account the patient’s healthinsurance coverage and the healthcare resources available in the community.

Spirometry (FEV1): pulmonary measurements made with a spirometer toevaluate airway obstruction, and if so, whether it is reversible with abronchodilator. It is mandatory to diagnose and characterize asthma severity.

Targeted elimination diet: an elimination diet with foods eliminated basedon results from specific IgE tests (e.g., skin tests or in vitro tests) or from asuggestive 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 displaysbronchodilation, respiratory stimulation, and may attenuate airwayhyperreactivity.

Treating through: continuing drug treatment in the presence of a suspectedallergic 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 disorderthat usually lasts for a few days. Chronic urticaria lasts longer than 6 weeks.

1Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma: Clinical PracticeGuidelines. NIH Publication No. 97-4051, page 10.

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