Rhinitis2008 Treatment Guidelines

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The diagnosis and management of rhinitis: An updated

practice parameter

Chief Editors: Dana V. Wallace, MD, and Mark S. Dykewicz, MD

Co-Editors:David I. Bernstein, MD, Joann Blessing-Moore, MD, Linda Cox, MD, David A. Khan, MD,

David M. Lang, MD, Richard A. Nicklas, MD, John Oppenheimer, MD, Jay M. Portnoy, MD,

Christopher C. Randolph, MD,Diane Schuller, MD, Sheldon L. Spector, MD, andStephen A. Tilles,MD

These parameters were developed by the Joint Task Force on Practice

Parameters, representing the American Academy of Allergy, Asthma &

Immunology; the American College of Allergy, Asthma and Immunology;

and the Joint Council of Allergy, Asthma and Immunology.

The American Academy of Allergy, Asthma & Immunology (AAAAI) and

the American College of Allergy, Asthma and Immunology (ACAAI) have

jointly accepted responsibility for establishing The diagnosis and

Management of Rhinitis: An Updated Practice Parameter. This is a

complete and comprehensive document at the current time. The medical

environment is a changing environment, and not all recommendations willbe appropriate for all patients. Because this document incorporated the

efforts of many participants, no single individual, including those who

served on the Joint Task Force, is authorized to provide an official AAAAI

or ACAAI interpretation of these practice parameters. Any request for

information about or an interpretation of these practice parameters by the

AAAAI or ACAAI should be directed to the Executive Offices of the

AAAAI, the ACAAI, and the Joint Council of Allergy, Asthma and

Immunology. These parameters are not designed for use by

pharmaceutical companies in drug promotion.

Published practice parameters of the Joint Task Force on

Practice Parameters for Allergy and Immunology include

the following:

1. Practice parameters for the diagnosis and treatment ofasthma. J Allergy Clin Immunol 1995;96(suppl):S707-S870.

2. Practice parameters for allergy diagnostic testing. Ann Al-lergy 1995;75:543-625.

3. Practice parameters for the diagnosis and management ofimmunodeficiency. Ann Allergy 1996;76:282-94.

4. Practice parameters for allergen immunotherapy. J AllergyClin Immunol 1996;98:1001-11.

5. Disease management of atopic dermatitis: a practice param-eter. Ann Allergy 1997;79:197-211.

6. The diagnosis and management of anaphylaxis. J AllergyClin Immunol 1998;101(suppl):S465-S528.

7. Algorithm for the diagnosis and management of asthma: a

practice parameter update. Ann Allergy 1998;81:415-20.8. Diagnosis and management of rhinitis: parameter docu-

ments of the Joint Task Force on Practice Parameters inAllergy, Asthma and Immunology. Ann Allergy 1998;81(suppl):S463-S518.

9. Parameters for the diagnosis and management of sinusitis. JAllergy Clin Immunol 1998;102(suppl):S107-S144.

10. Stinging insect hypersensitivity: a practice parameter. J Al-lergy Clin Immunol 1999;103:963-80.

11. Disease management of drug hypersensitivity: a practice pa-rameter. Ann Allergy 1999;83(suppl):S665-S700.

12. Diagnosis and management of urticaria: a practice parame-ter. Ann Allergy 2000;85(suppl):S521-S544.

13. Allergen immunotherapy: a practice parameter. Ann Allergy2003;90(suppl):S1-S540.

14. Symptom severity assessment of allergic rhinitis, part I. AnnAllergy 2003;91:105-14.

Disclosure of potential conflict of interest: D. V. Wallace is on the speakers bureau for

Schering-Plough, Aventis, Pfizer, and Merck and is on the advisory board for

AstraZeneca. M. S. Dykewicz has consulting arrangements with AstraZeneca, Glaxo-

SmithKline, McNeil, Medpointe/Meda, Merck, Novartis/Genentech, Schering-

Plough, and Teva;has received research support from AstraZeneca, GlaxoSmithKline,

Novartis/Genentech, and Schering-Plough; and is on the speakers bureau for AstraZe-

neca, GlaxoSmithKline, and Merck. D. I. Bernstein has research contracts with Glaxo-

SmithKline, AstraZeneca, Schering-Plough, Novartis, and Greer; is on the speakers

bureaufor Sanofi andTeva; andis on theadvisorypanelfor Schering-Plough.J. Bless-

ing-Moore has received research support from AstraZeneca and Novartis and is on thespeakers bureau for Schering-Plough, Merck, AstraZeneca, Teva, Novartis-Genen-

tech, and Sepracor. L. Cox has consulting arrangements with Stallergenes, Greer, No-

vartis/Genentech, Planet Technology, and Schering-Plough and is on the speakers

bureau for Novartis/Genentech and AstraZeneca. D. A. Khan has received research

support from AstraZeneca and is on the speakers bureau for Merck and GlaxoSmith-

Kline. D. M. Lang has consulting arrangements with, has received research support

from, and is on the speakers bureau for GlaxoSmithKline, AstraZeneca, Sanofi-Aven-

tis, Merck, Novartis/Genentech, Venus, Dey, and Schering-Plough. J. Oppenheimer

has consulting arrangements with, has received research support from, and is on the

speakers bureau for AstraZeneca, GlaxoSmithKline, Sepracor, Apeiron, Merck,

and Schering-Plough. J. M. Portnoy has consulting arrangements with Glaxo-

SmithKline, Sanofi-Aventis, and Greer; has received research support from Clorox;

and is on the speakers bureau for Merck, Schering-Plough, Sanofi-Aventis, AstraZe-

neca, and GlaxoSmithKline. S. L. Spector has consulting arrangements with Merck,

Novartis, Genentech, Critical Therapeutics, and AstraZeneca; has received research

support from Merck, Genentech, Schering-Plough, and AstraZeneca; and is on the

speakers bureau for Merck, Novartis, Genentech, Critical Therapeutics, Schering-

Plough, and AstraZeneca. S. A. Tilles has consulting arrangements with GlaxoSmith-

Kline and Schering-Plough and has received research support from Meda, Alcon, and

Schering-Plough. F. Baroody has consulting arrangementswith GlaxoSmithKline; has

received research support from GlaxoSmithKline and Alcon; and is on the speakers

bureau for Merck and GlaxoSmithKline. G. Rachelefsky has consulting arrangements

with AstraZeneca, Schering-Plough, Merck, and Medpoint and is on the speakers bu-

reau for AstraZeneca, Schering-Plough, Merck, Medpoint, and Genentech. R. Setti-

pane has consulting arrangements with GlaxoSmithKline and Alcon; has received

research support from Alcon, Medpoint, GlaxoSmithKline, and Schering-Plough;and is on the speakers bureau for Sanofi-Aventis, UCB, AstraZeneca, GlaxoSmith-

Kline, Alcon, and Genentech. D. Skoner has consulting arrangements with Merck;

has received research support from AstraZeneca, Sanofi-Aventis, GlaxoSmithKline,

Novartis, Merck, and Greer Laboratories; and is on the speakers bureau for Astra-

Zeneca, Sanofi-Aventis, GlaxoSmithKline, Merck, Schering-Plough, and Novartis.

S. Stoloff has consulting arrangements with GlaxoSmithKline, AstraZeneca, Alcon,

Schering-Plough, Novartis, Genentech, Aventis, Teva, and Dey; is on the speakers

bureau for GlaxoSmithKline and AstraZeneca; and has served as an expert witness

for GlaxoSmithKline. The other authors have declared that they have no conflict of

interest.

Reprint requests: Joint Council of Allergy, Asthma and Immunology, 50 N Brockway St,

#3-3, Palatine, IL 60067.

J Allergy Clin Immunol 2008;122:S1-84.

0091-6749/$34.00

2008 American Academy of Allergy, Asthma & Immunology

doi:10.1016/j.jaci.2008.06.003

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15. Disease management of atopic dermatitis: an updated prac-tice parameter. Ann Allergy 2004;93(suppl):S1-S21.

16. Stinging insect hypersensitivity: a practice parameter up-date. J Allergy Clin Immunol 2004;114;4:869-86.

17. The diagnosis and management of anaphylaxis: an updatedpractice parameter. J Allergy Clin Immunol 2005;115(suppl):S483-S523.

18. Practice parameter for the diagnosis and management of pri-mary immunodeficiency. Ann Allergy2005;94(suppl):S1-S63.

19. Attaining optimal asthma control: a practice parameter. J Al-lergy Clin Immunol 2005;116(suppl):S3-S11.

20. The diagnosis and management of sinusitis: a practice pa-rameter update. J Allergy Clin Immunol 2006;116(suppl):S13-S47.

21. Food allergy: a practice parameter. Ann Allergy 2006;96(suppl):S1-S68.

22. Contact dermatitis: a practice parameter. Ann Allergy 2006;97(suppl):S1-S37.

23. Allergen immunotherapy: a practice parameter second up-date. J Allergy Clin Immunol 2007;120(suppl):S25-S85.

24. Allergy diagnostic testing: an updated practice parameter.Ann Allergy 2008;100(suppl):S1-S148.

These parameters are also available on the internet at http://www.jcaai.org.

CONTRIBUTORSThe Joint Task Force has made a concerted effort to acknowl-

edge all contributors to this parameter. If any contributors havebeen excluded inadvertently, the Task Force will ensure thatappropriate recognition of such contributions is madesubsequently.

CHIEF EDITORJOINT TASK FORCE

Dana V. Wallace, MDAssistant Clinical ProfessorNova Southeastern UniversityDavie, Fla

CHIEF EDITORPARAMETER WORKGROUP

CHAIRMark S. Dykewicz, MD

Professor of Internal MedicineChief, Section of Allergy and Clinical Immunology, Division

of ImmunobiologyDirector, Allergy and Immunology Fellowship ProgramSaint Louis University School of Medicine

St Louis, Mo

TASK FORCE REVIEWERSDavid I. Bernstein, MD

Professor of Clinical Medicine and Environmental HealthDivision of Allergy/ImmunologyUniversity of Cincinnati College of MedicineCincinnati, OhioI. Leonard Bernstein, MD

Clinical Professor of Medicine and Environmental HealthUniversity of Cincinnati College of MedicineCincinnati, OhioJoann Blessing-Moore, MD

Clinical Associate Professor of Medicine and Pediatrics

Stanford University Medical CenterDepartment of ImmunologyPalo Alto, CalifLinda Cox, MD

Assistant Clinical Professor of MedicineNova Southeastern University College of Osteopathic MedicineDavie, Fla

David A. Khan, MDAssociate Professor of Internal MedicineUniversity of Texas Southwestern Medical CenterDallas, TexDavid M. Lang, MD

Head, Allergy/Immunology SectionDivision of MedicineDirector, Allergy and Immunology Fellowship Training

ProgramCleveland Clinic FoundationCleveland, OhioRichard A. Nicklas, MD

Clinical Professor of Medicine

George Washington Medical CenterWashington, DCJohn Oppenheimer, MD

Department of Internal MedicineNew Jersey Medical SchoolPulmonary and Allergy AssociatesMorristown, NJJay M. Portnoy, MD

Chief, Section of Allergy, Asthma and ImmunologyChildrens Mercy HospitalProfessor of PediatricsUniversity of MissouriKansas City School of MedicineKansas City, MoChristopher C. Randolph, MD

Clinical Professor of PediatricsYale Affiliated HospitalsCenter for Allergy, Asthma, and ImmunologyWaterbury, ConnDiane E. Schuller, MD

Professor of PediatricsPennsylvania State University Milton S. Hershey Medical

CollegeHershey, PaSheldon L. Spector, MD

Clinical Professor of MedicineUniversity of CaliforniaLos Angeles School of MedicineLos Angeles, Calif

Stephen A. Tilles, MDClinical Assistant Professor of MedicineUniversity of Washington School of MedicineRedmond, Wash

ASSIGNED REVIEWERSKathleen R. May, MD

Allegany Allergy and AsthmaCumberland, MdTravis A. Miller, MD

University of MichiganCapital Allergy and Respiratory Disease Center

Sacramento, Calif

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Howard M. Druce, MD, FAAAAI

Clinical Associate Professor of MedicineUniversity HospitalMorris Plains, NJ

PARAMETER WORKGROUP MEMBERSFaud M. Baroody, MD

Professor of OtolaryngologyHead and Neck Surgery andPediatrics

Pritzker School of MedicineUniversity of ChicagoChicago, IllJonathan A. Bernstein, MD

Professor of MedicineDivision of Immunology/Allergy SectionDepartment of Internal MedicineUniversity of Cincinnati College of MedicineCincinnati, OhioTimothy J. Craig, DO

Professor of Medicine, Pediatrics and Graduate Studies

Pennsylvania State UniversityHershey, PaJohn W. Georgitis, MD

LaFayette ClinicFayetteville, NCRuby Pawankar, MD, PhD

Professor of MedicineDivision of Rhinology and AllergyDepartment of OtolaryngologyNippon Medical SchoolTokyo, JapanGary S. Rachelefsky, MD

Clinical Professor of Allergy and Immunology

Center for Asthma, Allergy and Respiratory DiseasesUniversity of CaliforniaLos Angeles Medical CenterLos Angeles, CalifRussell A. Settipane, MD

Clinical Associate Professor of MedicineBrown University Medical SchoolProvidence, RIDavid P. Skoner, MD

Professor of PediatricsDrexel University College of MedicineDirector, Division of Allergy, Asthma and ImmunologyAllegheny General HospitalPittsburgh, PaStuart W. Stoloff, MD

Clinical Professor of Family and Community MedicineUniversity of Nevada School of MedicineReno, Nev

Classification of recommendations and evidence

Category of evidence

Ia. Evidence from meta-analysis of randomized controlled trialsIb. Evidence from at least 1 randomized controlled trialIIa. Evidence from at least 1 controlled study withoutrandomizationIIb. Evidence from at least 1 other type of quasi-experimentalstudyIII. Evidence from nonexperimental descriptive studies, such as

comparative studies

IV. Evidence from expert committee reports or opinions orclinical experience of respected authorities, or both

LB Evidence from laboratory-based studies.NR Not rated.

Strength of Recommendation

A Directly based on category I evidence

B Directly based on category II evidence or extrapolated recom-mendation from category I evidenceC Directly based on category III evidence or extrapolated recom-mendation from category I or II evidenceD Directly based on category IV evidence or extrapolated rec-ommendation from category I, II, or III evidence

Note: The Summary Statements that are associated with

the sections of the Preface and Exective Summary are

Indicated inside the brackets.

PREFACE [SUMMARY STATEMENTS 8, 9, 13]Rhinitis, as defined for the purposes of this document, is

characterized by 1 or more of the following nasal symptoms:

congestion, rhinorrhea (anterior and posterior), sneezing, anditching. Rhinitis is usually associated with inflammation, but someforms of rhinitis such as vasomotor rhinitis or atrophic rhinitis arenot predominantly inflammatory.

Rhinitis is a significant cause of widespread morbidity, medicaltreatment costs, reduced work productivity, and lost school days.Although sometimes mistakenly viewed as a trivial disease,symptoms of allergic and nonallergic rhinitis may significantlyaffect a patients quality of life and can be associated withconditions such as fatigue, headache, cognitive impairment, andsleep disturbance. Appropriate management of rhinitis may be animportant component in effective management of coexisting orcomplicating respiratory conditions, such as asthma, sinusitis, and

sleep apnea. The financial burden to society for allergic rhinitis issubstantial. The total direct ($7.3 billion) and indirect costs ($4.28billion, including loss of productivity) estimated in the UnitedStates for 2002 were $11.58 billion.1

Allergic rhinitis affects between 10% and 30% of all adults andas many as 40% of children.2,3-6 In most studies, the ratio of aller-gic to pure nonallergic rhinitis is 3:1.2 Preliminary data suggestthat 44% to 87% of patients with rhinitis may have mixed rhinitis,a combination of allergic and nonallergic rhinitis.2,7 Worldwide,the prevalence of allergic rhinitis continues to increase.

The objective of Diagnosis and Management of Rhinitis: AnUpdated Practice Parameter is to improve the care of patientsby providing the practicing physician with an evidence-based

approach by reviewing data in the medical literature and

Diagnosis and management of rhinitis: An updatedpractice parameter

Preface S3Abbreviations S4

Collation of Summary Statements S4Executive Summary S9Annotations S27Summary Statements with discussion S32References S65


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incorporating this evidence into development of this guideline.While giving an overview of all categories of rhinitis, theparameter will focus on the diagnosis and treatment of allergicrhinitis. Using the 1998 practice parameter on Diagnosis andManagement of Rhinitis8 as the basis, the working draft of thisupdated rhinitis practice parameter was prepared by a work groupchaired by Mark S. Dykewicz, MD, and was revised and edited by

the Joint Task Force on Practice Parameters under the leadershipof Dana V. Wallace, MD. Preparation of this draft included a re-view of the recent medical literature using a variety of search en-gines such as PubMed. Published clinical studies were rated bycategory of evidence and used to establish the strength of the rec-ommendations, as defined in the preamble to this parameter. Theparameter was then reviewed by experts on rhinitis selected by thesponsoring organizations of the American Academy of Allergy,Asthma & Immunology and the American College of Allergy,Asthma, and Immunology. Based on this process, this parameterrepresents an evidence-based document.

Components and organization of this parameterThe Diagnosis and Management of Rhinitis: An Updated

Practice Parameter contains an annotated algorithm that presentsthe major decision points for the appropriate evaluation andtreatment of patients with suspected rhinitis. This is followed by acollation of Summary Statements, which represent key points inthe evaluation and management of this condition. Tables thatprovide clinically useful information in a concise format precede

the body of the practice parameter, which provides a referencednarrative discussion of each Summary Statement. The gradedreferences and figures complete the document. The ExecutiveSummary emphasizes the key updates since the 1998 rhinitisparameter (Box).

To obtain the maximum value from this practice parameter inthe most time-efficient manner, the clinician should review the

Executive Summary, annotated algorithm, Summary Statements,and tables because these arecreated to provide the key information.Thetext and gradedreferences provide thefoundation on which theJoint Task Force formulated and graded the Summary Statements.

ABBREVIATIONSACE: Angiotensin-converting enzymeAERD: Aspirin-exacerbated respiratory diseaseARIA: Allergic Rhinitis and its Impact on AsthmaBHR: Bronchial hyperresponsivenessCF: Cystic fibrosisCNS: Central nervous systemCSF: Cerebral spinal fluidCT: Computed tomographycysLT: Cysteinyl leukotrieneECP: Eosinophilic cationic proteinFDA: US Food and Drug AdministrationHEPA: High-efficiency particulate airIOC: International Olympic CommitteeIOP: Intraocular pressureLT: LeukotrieneLTRA: Leukotriene receptor antagonistMRI: Magnetic resonance imagingNARES: Nonallergic rhinitis with eosinophilia syndromeNSAID: Nonsteroidal anti-inflammatory drugOA: Occupational asthma

OME: Otitis media with effusionOSAS: Obstructive sleep apnea syndromeOTC: Over-the-counterPCD: Primary ciliary dyskinesiaPRN: When necessary (from Latin pro re nata)QOL: Quality of lifeRFVTR: Radiofrequency volumetric tissue reductionRQLQ: Rhinoconjunctivitis Quality of Life QuestionnaireRUDS: Reactive upper-airways dysfunction syndromeSIT: Specific immunotherapySPT: Skin prick testUSOC: US Olympic Committee

COLLATION OF SUMMARY STATEMENTS

Definition and classification of rhinitis

1. Rhinitis is characterized by 1 or more of the followingsymptoms: nasal congestion, rhinorrhea (anterior and poste-rior), sneezing, and itching. D

Differential diagnosis of rhinitis and associated

conditions

2. Rhinitis should be classified by etiology as allergic or non-allergic and differentiated from conditions that mimic symp-

toms of rhinitis. C

Key updates

The following is a list of key updates discussed in thisdocument:

d Pharmacologic products introduced since publication of

the 1998 Diagnosis and Management of Rhinitis: Com-plete Guidelinesd More defined positioning of agents (eg, leukotriene recep-

tor antagonists) in management based on more recentevidence

d Introduction of episodic as a term to describe rhinitis eli-cited by sporadic exposures to inhalant aeroallergens, andimplications for treatment

d Use of certain agentsthat is, intranasal corticoste-roidson an as-needed basis

d Emphasis on recognizing comorbidities of allergic rhinitis(AR), such as asthma, sinusitis, and obstructive sleep ap-nea, and conducting appropriate studies, such as pulmo-nary function testing and sleep apnea studies

d Evidence on using combination therapy, specifically leuko-triene receptor antagonists, with antihistamines

d Need to consider the benefits versus recently raised safetyconcerns about oral decongestants before their use in chil-dren below age 6 years

d Recommendation of considering second-generation anti-histamines as safe agents for use during pregnancy

d Use of intranasal corticosteroids for symptoms of allergicconjunctivitis associated with rhinitis

d Consideration of using a Rhinitis Action Pland Emerging diagnostic and surgical procedures, such as

acoustic rhinometry and radiofrequency volumetric tissuereduction


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3. Symptoms of allergic rhinitis may occur only duringspecific seasons, may be perennial without seasonal exacer-bation, may be perennial with seasonal exacerbations, ormay occur episodically after specific aeroallergen expo-sures. C

4. Episodic allergic rhinitis is a new rhinitis category that de-notes allergic nasal symptoms elicited by sporadic exposures

to inhalant aeroallergens. D5. The severity of allergic rhinitis ranges from mild and inter-

mittent to seriously debilitating. D6. Although there is no generally accepted method of grading

the severity of rhinitis, the clinician may want to considera graphic rating scale. D

7. Mixed rhinitis (combined allergic and nonallergic rhinitis) isnoted in approximately 44% to 87% of patients with allergicrhinitis and is more common than either pure allergic rhinitisor nonallergic rhinitis. C

Burden and epidemiology of rhinitis

8. Allergic rhinitis affects 30 to 60 million people in the UnitedStates annually, including 10% to 30% of adults and asmany as 40% of children. C

9. Risk factors for allergic rhinitis include (1) family history ofatopy, (2) serum IgE >100 IU/mL before age 6 years, (3)higher socioeconomic class, and (4) presence of a positiveallergy skin prick test (SPT). C

10. The influence of early childhood exposure to infections, an-imals, and secondary tobacco smoke on the development ofatopy and allergic rhinitis is still unknown. C

11. Aeroallergen sensitization may occur within the first 2 yearsof life. C

12. The cost of treating allergic rhinitis and indirect costs relatedto loss of workplace productivity resulting from the diseaseare substantial. Rhinitis is also a significant cause of lost

work and school days. C

Allergic rhinitisPathogenesis

13. The symptoms of allergic rhinitis result from a complexallergen-driven mucosal inflammation caused by interplaybetween resident and infiltrating inflammatory cells anda number of vasoactive and proinflammatory mediators,including cytokines. Sensory nerve activation, plasmaleakage, and congestion of venous sinusoids also contrib-ute. C

14. Allergic rhinitis may be characterized by early-phase andlate-phase responses. Each type of response is characterized

by sneezing, congestion, and rhinorrhea, but congestion pre-dominates in the late phase. C

Seasonal and perennial allergic rhinitis

15. Seasonal allergic rhinitis is caused by an IgE-mediated reac-tion to seasonal aeroallergens. The length of seasonal expo-sure to these allergens is dependent on geographic locationand climatic conditions. C

16. Perennial allergic rhinitis is caused by an IgE-mediatedreaction to perennial environmental aeroallergens. Thesemay include dust mites, molds, animal allergens, or certainoccupational allergens, as well as pollen in areas where pol-

len is prevalent perennially. C

Associated allergic conjunctivitis

17. Allergic rhinitis is often accompanied by symptoms of aller-gic conjunctivitis. C

18. Many treatments used for allergic rhinitis can benefit associ-ated symptoms of allergic conjunctivitis, and a variety oftopical ophthalmic agents is useful for specific treatmentof associated ocular symptoms. A

19. Intranasal corticosteroids, oral antihistamines, and intranasalantihistamines have similar effectiveness in relieving oculareye symptoms associated with rhinitis. A

Nonallergic rhinitis syndromes

20. Nonallergic rhinitis is characterized by periodic or perennialsymptoms of rhinitis that are not a result of IgE-dependentevents. Examples of nonallergic rhinitis are infectious rhini-tis, vasomotor rhinitis, and the nonallergic rhinitis with eo-sinophilia syndrome (NARES). C

Vasomotor rhinitis21. Vasomotor rhinitis (idiopathic rhinitis) accounts for a heter-

ogeneous group of patients with chronic nasal symptomsthat are not immunologic or infectious in origin and is usu-ally not associated with nasal eosinophilia. D

Rhinitis from foods and alcohol

22. Rhinitis may occur after ingestion of foods or alcoholic pro-ducts. This may be a result of vagally mediated mechanisms,nasal vasodilation, food allergy, and/or other undefinedmechanisms. Food allergy is a rare cause of rhinitis withoutassociated gastrointestinal, dermatologic, or systemic mani-festations. B

Infectious rhinitis

23. Infectious rhinitis and rhinosinusitis may be acute orchronic. Acute infectious rhinitis is usually a result of 1 ofa large number of viruses, but secondary bacterial infectionwith sinus involvement may be a complication. Symptomsof acute infectious rhinosinusitis include nasal congestion,mucopurulent nasal discharge, pain and pressure, headache,olfactory disturbance, postnasal drainage, and cough. C

24. Viral infections account for as many as 98% of acute infec-tious rhinitis and the majority of rhinitis symptoms in theyoung child. Routine nasopharyngeal cultures when bacte-rial infections are suspected do not add diagnostic value. C

NARES

25. NARES is characterized by nasal eosinophils in patientswho have perennial symptoms and occasionally reducedsense of smell. These patients often lack evidence of allergicdisease as demonstrated by absence of positive skin testsand/or specific IgE antibodies in the serum. C

Occupational rhinitis

26. Occupational rhinitis is rhinitis arising in response to air-borne substances in the workplace, which may be mediated

by allergic or nonallergic factors, such as laboratory animal



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antigen, grain, wood dusts, chemicals, and irritants. It oftencoexists with occupational asthma (OA). C

Hormonal rhinitis

27. Causes of hormonal rhinitis include pregnancy and men-strual cyclerelated rhinitis. Pregnancy rhinitis, when pre-

sent, is associated with significant nasal congestion, startsafter the second month of pregnancy, and usually disappearswithin 2 weeks after delivery. C

Drug-induced rhinitis

28. Drug-induced rhinitis may be caused by a number ofmedications, including angiotensin-converting enzyme(ACE) inhibitors, phosphodiesterase-5selective inhibitors,phentolamine, a-receptor antagonists, aspirin, and othernonsteroidal anti-inflammatory drugs (NSAIDs). Rhinitismedicamentosa is a syndrome of rebound nasal congestionthat follows the overuse of intranasal a-adrenergic decon-gestants or cocaine. C

Atrophic rhinitis

29. Treatment of primary and secondary atrophic rhinitis in-volves reducing crusting and alleviating the foul odor bycontinuous nasal hygiene, such as nasal lavage and crust de-bridement, and the use of topical and/or systemic antibioticswhen purulent secretions or an acute infection is present. C

Conditions that mimic rhinitisNasal polyps

30. Nasal polyps may occur in conjunction with chronic rhinitisor sinusitis and may contribute significantly to the patientssymptoms. Nasal polyps should always be considered in thedifferential diagnosis of patients who present with invariantnasal congestion and/or anosmia and its sequelae. Allergy asa cause of nasal polyps has not been established, but nasalpolyps may occur in conjunction with allergic rhinitis. C

Anatomic abnormalities

31. Signs and symptoms suggestive of rhinitis can be producedby other conditions, including nasal septal deviation, tu-mors, and hypertrophy of the nasal turbinates. C

32. In infants and young children, nasal congestion or obstruc-

tion can result from structural problems, such as cleft palateand adenoidal hypertrophy, or functional problems, such aslaryngopharyngeal reflux. D

Cerebral spinal fluid rhinorrhea

33. Refractory clear rhinorrhea may be a result of cerebral spinalfluid (CSF) leak, which is often caused by trauma or recentsurgery. B

Ciliary dysfunction

34. Ciliary dysfunction can be primary (primary ciliary dyskine-sia; PCD) or secondary (eg, viral infection) and may contrib-

ute to recurrent rhinitis and sinus infections. C

Evaluation and diagnostic studiesHistory

35. An effective evaluation of the patient with rhinitis often in-cludes the following: a determination of the pattern, chronic-ity, and seasonality of nasal and related symptoms (or lackthereof); response to medications; presence of coexistingconditions; occupational exposure; and a detailed environ-

mental history and identification of precipitating factors. D36. Evaluation of rhinitis therapy should include assessment of

quality of life (QOL). C

Physical examination

37. A physical examination of all organ systems potentially af-fected by allergies with emphasis on the upper respiratorytract should be performed in patients with a history of rhini-tis. The nasal examination supports but does not definitelyestablish the diagnosis of rhinitis. D

Testing for specific IgE antibodySkin testing

38. Determination of specific IgE, preferably by skin testing, isindicated to provide evidence of an allergic basis for thepatients symptoms, to confirm or exclude suspected causesof the patients symptoms, or to assess the sensitivity to aspecific allergen for avoidance measures and/or allergenimmunotherapy. B

39. Skin tests are the preferred tests for the diagnosis of IgE-me-diated sensitivity. The number of skin tests and the allergensselected for skin testing should be determined on the basis ofthe patients age, history, environment, and living situation,such as area of the country, occupation, and activities. D

In vitro assays for specific IgE

40. The precise sensitivity of specific IgE immunoassays com-pared with skin prick/puncture tests is approximately 70%to 75%. Immunoassays have similar sensitivity to skin testsin identifying those patients with nasal symptoms elicited af-ter natural or controlled allergen challenge tests. C

41. Interpretation of specific IgE immunoassays may be con-founded by variables such as potency of allergens boundto solid support systems, cross-reactive proteins and glyco-epitopes, specific IgG antibodies in the test serum, andhigh total IgE. D

Special diagnostic techniques

42. In selected cases, special techniques such as fiber optic nasalendoscopy and/or rhinomanometry may be useful in evaluatingpatients presenting with rhinitis symptoms. These tests may re-quire special expertise for performance and interpretation. Pa-tients with nasal disease require appropriate examination forassociated diseases, such as sinusitis and otitis media. B

43. Nasal smears for eosinophils are not necessary for routineuse in diagnosing allergic rhinitis when the diagnosis isclearly supported by the history, physical examination, andspecific IgE diagnostic studies but may be a useful adjunct

when the diagnosis of allergic rhinitis is in question. C


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44. Although the saccharin test for mucociliary clearance hasbeen relied on as a clinical screening test, it cannot be reliedon for a definitive diagnosis of mucociliary dysfunction. C

45. Nasal biopsy may be indicated when determining whether alesion is neoplastic or granulomatous or if there is an abnor-mality in the ultrastructure of cilia. C

46. The measurement of total IgE and IgG subclasses for the di-

agnosis of allergic rhinitis has limited value and should notbe routinely performed. C

47. The presence ofb-2-transferrin in the nasal secretions is asensitive method of confirming cerebral spinal fluid rhinor-rhea. B

Special testing considerations in children

48. In children with rhinitis, the use of immune studies, sweattest, sinus computed tomography (CT), and nasal endoscopymay be indicated when they are suspected to have comorbidconditions such as immune deficiency, cystic fibrosis (CF),and chronic sinusitis. C

Testing for comorbid conditions

49. A formal evaluation for obstructive sleep apnea may be con-sidered in children and adults presenting with chronic rhini-tis and other risk factors associated with sleep-disorderedbreathing. C

50. Pulmonary function tests should be considered in patientswith rhinitis to assess the possibility that asthma might bepresent. D

Tests without diagnostic validity

51. There is no evidence that the following procedures havediagnostic validity for allergic rhinitis: cytotoxic tests,provocation-neutralization, electrodermal testing, appliedkinesiology, iridology, and hair analysis. B (see AllergyDiagnostic Testing: An Updated Practice Parameter9)

Management of rhinitisEnvironmental control measures

52. The most common allergic triggers for rhinitis include pol-lens, fungi, dust mites, furry animals, and insect emanations.B

53. The types of pollen responsible for rhinitis symptoms varywidely with locale, climate, and introduced plantings. B

54. Highly pollen-allergic individuals should limit exposure tothe outdoors when high pollen counts are present. B

55. Fungi are ubiquitous organisms, many of which produceclinically important allergens. B

56. Reduction of indoor fungal exposure involves removal ofmoisture sources, replacement of contamination materials,and the use of dilute bleach solutions on nonporous surfaces.D

57. Clinically effective dust mite avoidance requires a combina-tion of humidity control, dust mite covers for bedding, high-efficiency particulate air (HEPA) vacuuming of carpeting,

and the use of acaricides. B

58. Avoidance is the most effective way to manage animal sen-sitivity. D

59. Cockroaches are a significant cause of nasal allergy, partic-ularly in inner-city populations. C

60. The best treatment for rhinitis triggered by irritants, such astobacco smoke and formaldehyde, is avoidance. B

Pharmacologic therapyOral antihistamines

61. Second-generation antihistamines are generally preferredover first-generation antihistamines for the treatment ofallergic rhinitis. First-generation antihistamines have signif-icant potential to cause sedation, performance impairment,and anticholinergic effects. Although occasionally advanta-geous (eg, sleep induction when taken at bedtime or areduction in rhinorrhea), these properties are usually unde-sirable and are potentially dangerous. Second-generationantihistamines have less or no tendency to cause these

effects. B62. Before prescribing or recommending a first-generation anti-

histamine, the physician should ensure that the patientunderstands both the potential for adverse effects and theavailability of alternative antihistamines with a lower likeli-hood of adverse effects. D

63. There are important differences among the second-genera-tion antihistamines in regard to their sedative properties: fex-ofenadine, loratadine, and desloratadine do not causesedation at recommended doses; loratadine and deslorata-dine may cause sedation at doses exceeding the recommen-ded dose; cetirizine and intranasal azelastine may causesedation at recommended doses. A

64. Among the newer, nonsedating antihistamines, no singleagent has been conclusively found to achieve superior over-all response rates. C

Intranasal antihistamines

65. Intranasal antihistamines may be considered for use as first-line treatment for allergic and nonallergic rhinitis. A

66. Intranasal antihistamines are efficacious and equal to or su-perior to oral second-generation antihistamines for treatmentof seasonal allergic rhinitis. A

67. Because systemic absorption occurs, currently available in-tranasal antihistamines have been associated with sedation

and can inhibit skin test reactions. A68. Intranasal antihistamines have been associated with a clini-cally significant effect on nasal congestion. A

69. Intranasal antihistamines are generally less effective than in-tranasal corticosteroids for treatment of allergic rhinitis. A

Oral and topical decongestants

70. Oral decongestants, such as pseudoephedrine and phenyl-ephrine, are a-adrenergic agonists that can reduce nasal con-gestion but can result in side effects such as insomnia,irritability, and palpitations. A

71. Oral and topical decongestants agents should be used with

caution in older adults and young children, and in patients



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of any age who have a history of cardiac arrhythmia, anginapectoris, cerebrovascular disease, hypertension, bladderneck obstruction, glaucoma, or hyperthyroidism. C

72. Topical decongestants can be considered for short-term andpossibly for intermittent or episodic therapy of nasal conges-tion, but are inappropriate for regular daily use because ofthe risk for the development of rhinitis medicamentosa. C

Over-the-counter cough and cold medications for youngchildren

73. The efficacy of cold and cough medications for symptomatictreatment of upper respiratory tract infections has not beenestablished for children younger than 6 years. Because ofthe potential toxicity of these medications, the use of theseover-the-counter (OTC) drugs generally should be avoidedin all children below 6 years of age. A

Intranasal corticosteroids

74. Intranasal corticosteroids are the most effective medicationclass for controlling symptoms of allergic rhinitis. A

75. In most studies, intranasal corticosteroids have been shownto be more effective than the combined use of an antihista-mine and leukotriene (LT) antagonist in the treatment of sea-sonal allergic rhinitis. A

76. Intranasal corticosteroids may provide significant relief ofsymptoms of seasonal allergic rhinitis when used not onlyon a regular basis but also on an as-needed basis. B How-ever, as-needed use may not be as effective as continuoususe of intranasal corticosteroids. D

77. When comparing the available intranasal corticosteroids, theoverall clinical response does not appear to vary signifi-cantly between products irrespective of the differences in

topical potency, lipid solubility, and binding affinity. C78. Intranasal corticosteroids may be useful in the treatment of

some forms of nonallergic rhinitis. A79. Intranasal corticosteroids when given in recommended

doses are not generally associated with clinically significantsystemic side effects. A

80. Although local side effects are typically minimal with theuse of intranasal corticosteroids, nasal irritation and bleedingmay occur. Nasal septal perforation is rarely reported. B

Oral corticosteroids

81. A short course (5-7 days) of oral corticosteroids may be ap-

propriate for the treatment of very severe or intractable nasalsymptoms or to treat significant nasal polyposis. However,single administration of parenteral corticosteroids is discour-aged and recurrent administration of parenteral corticoste-roids is contraindicated because of greater potential forlong-term corticosteroid side effects. D

Intranasal cromolyn

82. Intranasal cromolyn sodium is effective in some patients forprevention and treatment of allergic rhinitis and is associatedwith minimal side effects. It is less effective in most patientsthan corticosteroids and has not been adequately studied in

comparison with LT antagonists and antihistamines. A

Intranasal anticholinergics

83. Intranasal anticholinergics may effectively reduce rhinorrheabut have no effect on other nasal symptoms. Although sideeffects are minimal, dryness of the nasal membranes mayoccur. A

84. The concomitant use of ipratropium bromide nasal spray andan intranasal corticosteroid is more effective than adminis-

tration of either drug alone in the treatment of rhinorrheawithout any increased incidence of adverse events. A

Oral anti-LT agents

85. Oral anti-LT agents alone, or in combination with antihista-mines, have proven to be useful in the treatment of allergicrhinitis. A

Omalizumab

86. Omalizumab has demonstrated efficacy in AR; however, ithas US Food and Drug Administration (FDA) approval for

use only in allergic asthma. A

Nasal saline

87. There is evidence that topical saline is beneficial in the treat-ment of the symptoms of chronic rhinorrhea and rhinosinusi-tis when used as a sole modality or for adjunctive treatment. A

Allergen immunotherapy

88. Allergen immunotherapy is effective for the treatment ofallergic rhinitis. A

89. Allergen immunotherapy should be considered for patients

with allergic rhinitis who have demonstrable evidence ofspecific IgE antibodies to clinically relevant allergens, andits use depends on the degree to which symptoms can be re-duced by avoidance and medication, the amount and type ofmedication required to control symptoms, and the adverseeffects of medications. A

90. Allergen immunotherapy may prevent the development ofnew allergen sensitizations and reduce the risk for the futuredevelopment of asthma in patients with allergic rhinitis. B

Surgery

91. Although there is no surgical treatment for allergic rhinitis,surgery may be indicated in the management of comorbidconditions, such as nasal obstruction from severe nasalseptal deviation or inferior turbinate hypertrophy, adenoidalhypertrophy, or refractory sinusitis and complicationsthereof. C

Management decisions

92. Management and monitoring of rhinitis should be individu-alized and based on the spectrum, duration, and severity ofsymptoms; physical examination findings; comorbidities;age of the patient; and patient preferences using both step-

up and step-down approaches. C


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93. Effective allergic rhinitis management requires the develop-ment of a physician/patient/family partnership, avoidance ofenvironmental triggers, and the appropriate use of prescribedtherapeutic interventions. C

Education of patient and caretakers

94. Education is a key element in promoting adherence and op-timizing treatment outcomes in allergic rhinitis. D

Major comorbid conditions

95. Patients with allergic rhinitis are at increased risk for the de-velopment of asthma. A

96. Treatment of allergic rhinitis may improve asthma control inpatients with coexisting allergic rhinitis and asthma. B

97. There is no established cause-and-effect relationship of rhi-nitis with recurrent otitis media and otitis media with effu-sion (OME). C

Special considerationsPregnancy

98. When selecting medications for treating rhinitis in preg-nancy, the clinician might consider the FDA risk categoriesthat are based largely on animal data and limited humanstudies. However, it is also beneficial to review human co-hort and case-control studies as well as birth registry databefore reaching a decision. C

99. The most critical time for concern about potential congenitalmalformation because of medication use is the first trimes-ter, when organogenesis is occurring. D

100. A sufficient amount of human observational data has nowbeen accumulated to demonstrate safety for second-gener-ation as well as first-generation antihistamines. C

101. Oral decongestants should be avoided during the first tri-mester. Topical decongestants when used on a short-termbasis may have a better safety profile than oral agents forfirst trimester use. C

102. Sodium cromolyn is a safe treatment for allergic rhinitisduring pregnancy. C

103. Montelukast is a safe treatment for allergic rhinitis duringpregnancy. C

104. Intranasal corticosteroids may be used in the treatment ofnasal symptoms during pregnancy because of their safetyand efficacy profile. C

105. Immunotherapy for allergic rhinitis may be continued dur-ing pregnancy but without dose escalation. C

Elderly patients

106. Rhinitis in the elderly may be caused by types of rhinitiscommon in other age groups but may also be influencedby age-related physiologic changes such as cholinergic hy-peractivity, anatomic changes, and medications taken forother medical conditions. C

Athletes

107. Athletic performance can be affected by rhinorrhea andchronic or rebound nasal congestion. Rhinitis medication

for the competitive athlete must be a US Olympic

Committee (USOC) and/or International Olympic Commit-tee (IOC)approved product and should be one that doesnot adversely affect performance. C

Consultation with an allergist/immunologist

108. Allergist/immunologist care improves patient outcomes;

however, consultation/referral services are often under-used. C

109. Consultation with an allergist/immunologist should be con-sidered for patients with rhinitis who have inadequatelycontrolled symptoms, a reduced QOL and/or ability tofunction, adverse reactions to medications, a desire to iden-tify the allergens to which they are sensitized and to receiveadvice on environmental control, or comorbid conditionssuch as asthma and recurrent sinusitis, or when allergenimmunotherapy is a consideration. C

EXECUTIVE SUMMARYDefinition of rhinitis [Summary Statement 1]

Rhinitis is characterized by 1 or more of the followingsymptoms: nasal congestion, rhinorrhea (anterior and posterior),sneezing, and itching. Rhinitis is usually associated with inflam-mation, but some forms of rhinitis such as vasomotor rhinitis oratrophic rhinitis are not predominantly inflammatory. Rhinitisfrequently is accompanied by symptoms involving the eyes, ears,and throat.

Classification and differential diagnosis of rhinitis

and associated conditions [Summary Statements

2-7]Rhinitis is classified as allergic or nonallergic, but not all types

of rhinitis can be easily separated into one of these categories. Forexample, occupational rhinitis has been classified separately fromallergic and nonallergic because it may have components of bothallergic and nonallergic rhinitis. Conditions that mimic symptomsof rhinitis include nasal polyps, cerebrospinal fluid rhinorrhea,ciliary dyskinesia syndrome, and structural/mechanical factors,such as deviated septum and pharyngonasal reflux (Tables Iand II).

There is no generally accepted method of grading rhinitisseverity. In an attempt to do this, an international working group(Allergic Rhinitis and its Impact on Asthma [ARIA])9 has pro-

posed a classification for allergic rhinitis that placed patientsinto 1 of 4 categories: (1) mild intermittent, (2) mild persistent,(3) moderate/severe intermittent, and (4) moderate/severe persis-tent.10 This classification system discarded the terms seasonalandperennial, emphasizing that an aeroallergen (eg, grass pollen) thatoccurs seasonally in one region may be detected throughout theyear in another geographical area. The ARIA definition of mildrhinitis may be a useful comparative reference point for other se-verity grading schemes; this states that none of the following itemsis present: sleep disturbance; impairment of daily activities, lei-sure, and/or sport; impairment of school or work; and symptomspresent but not troublesome.11 This updated parameter supportsthe concept thatmore severe rhinitis is defined as more symptoms

or interference with QOL, because data show that it may not be



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possible to separate patients into moderate and severe cate-gories.12 A modified 7-point visual analog (graphic rating) scalefor grading severity of nasal and nonnasal symptoms of allergicrhinitis and the effects of this disorder on the QOL has been devel-oped (but not validated) and published by the Joint Task Force onPractice Parameters and is included, with minor modification, inFigs 1-4.13

In this document, the Joint Task Force retains and uses theterms seasonaland perennialin classifying patients with allergicrhinitis. These traditional descriptive terms are clinically usefuland allow for accurate categorization of the vast majority of pa-tients as having seasonal, perennial, or perennial allergic rhinitiswith seasonal exacerbations. It has become well recognized thatthe traditional seasonal/perennial and ARIA schemes define dif-ferent patient populations.12 This parameter introduces the termepisodic allergic rhinitis, denoting allergic nasal symptoms eli-cited by sporadic exposures to inhalant aeroallergens that arenot usually encountered in the patients indoor or outdoor envi-ronment, such as while visiting a farm where there is exposureto horses or while visiting a home with pets when a patient has

no pet exposure in their own home or work environments.

Allergic rhinitis: Risk factors and presentation [Summary

Statements 8-17]Risk factors for allergic rhinitis

Risk factors for allergic rhinitis include (1) family history ofatopy, (2) serum IgE >100 IU/mL before age 6 years, (3) highersocioeconomic class, and (4) the presence of a positive allergy

SPT.

4,14-16

The influence of early childhood exposure to infections

TABLE I. Types of rhinitis

I Allergic rhinitis

A Seasonal

B Perennial

C Episodic

II Nonallergic rhinitis

A Vasomotor rhinitis

1 Irritant triggered (eg, chlorine)2 Cold air

3 Exercise (eg, running)

4 Undetermined or poorly defined triggers

B Gustatory rhinitis

C Infectious

1 Acute

2 Chronic

D NARES

III Occupational rhinitis

A Caused by protein and chemical allergens, IgE-mediated

B Caused by chemical respiratory sensitizers, immune mechanism

uncertain

C Work-aggravated rhinitis

IV Other rhinitis syndromes

A Hormonally induced1 Pregnancy rhinitis

2 Menstrual cycle related

B Drug-induced

1 Rhinitis medicamentosa

2 Oral contraceptives

3 Antihypertensives and cardiovascular agents

4 Aspirin/NSAIDs

5 Other drugs

C Atrophic rhinitis

D Rhinitis associated with inflammatory-immunologic disorders

1 Granulomatous infections

2 Wegener granulomatosis

3 Sarcoidosis

4 Midline granuloma

5 Churg-Strauss

6 Relapsing polychondritis

7 Amyloidosis

TABLE II. Differential diagnosis of rhinitis

Conditions that may mimic symptoms of rhinitis

A Nasal polyps

B Structural/mechanical factors

1 Deviated septum/septal wall anomalies

2 Adenoidal hypertrophy

3 Trauma

4 Foreign bodies5 Nasal tumors

a Benign

b Malignant

6 Choanal atresia

7 Cleft palate

8 Pharyngonasal reflux

9 Acromegaly (excess growth hormone)

C Cerebrospinal fluid rhinorrhea

D Ciliary dyskinesia syndrome

FIG 1. Assessment of nasal symptom severity.


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(thehygiene hypothesis),animals, and secondary tobacco smoke onthe development of atopy and allergic rhinitis is still unknown.17-24

Presentation of allergic rhinitisIn childhood, allergic rhinitis is more frequent in boys, but in

adults, it is more frequent in women. Children with a bilateralfamily history of atopy may develop symptoms more frequently andat a younger age than those with a unilateral family history.6,25

Aeroallergen sensitization rarely begins before 6 months of age26

but may start between 6 months and 2 years of life.27 Infants bornto atopic families are sensitized to pollen aeroallergens more fre-quently than to indoor aeroallergens in the first year of life.27

Seasonal allergic rhinitis symptoms generally do not develop until2 to 7 years ofage.28-30 Food ingestion rarely causes allergic rhinitisin infants, children, or adults unless there are associated gastrointes-tinal, dermatologic, or systemic manifestations. The prevalence ofseasonal allergic rhinitis is higher in children and adolescents,whereas perennialallergicrhinitishas a higherprevalence in adults.31

Early-phase and late-phase responses in allergic rhinitis

As in patients with asthma, early-phase and late-phase re-sponses may be seen in allergic rhinitis. Both the early-phase andlate-phase responses in allergic rhinitis are characterized bysymptoms of sneezing, rhinorrhea, and nasal congestion.However, nasal congestion is predominantly a late-phase re-sponse. Mediators released from eosinophils during the late

phase contribute to tissue damage.

32,33

Pretreatment with

glucocorticoids effectively reduces eosinophils and the releaseof cytokines during the late-phase response.34-36

When allergen challenges are given repeatedly, the amountof allergen required to induce an immediate response decreases.This priming effect is thought to be a result of the release ofinflammatory mediators from effector cells during ongoing,prolonged allergen exposure and repeated late-phase responses.

Consequently, at the end of a pollen season, symptoms may de-cline at a slower rate than the pollen count. Therefore, it is impor-tant to know the full spectrum of aeroallergens to which the patientresponds as well as seasonal variations in symptoms. Initiatinganti-inflammatory therapy before pollen season or before anyrepetitive aeroallergen exposure, as indicated, will modify thelate-phase response that is associated with the priming effect.

Allergic conjunctivitis [Summary Statements 17-19]Oral antihistamines, intranasal antihistamines, oral anti-LT

agents, intranasal corticosteroids, and allergen immunotherapyaretreatments for allergic rhinitis that havebeen reportedto relieveassociated ocular allergy symptoms in controlled trials.37-52 In sys-

tematic reviews of randomized controlled studies, intranasal

FIG 2. Assessment of non-nasal symptom severity.

FIG 3. Global assessment of nasal and non-nasal symptom severity.

FIG 4. Assessment of quality of life.



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corticosteroids compared with oral antihistamines53,54 and intra-nasal corticosteroids compared with intranasal antihistamines46

were not significantly different in relieving eye symptoms.Use of cold compresses and irrigation with saline solution or

artificial tears has been advocated to relieve mild symptoms ofallergic conjunctivitis. Topical ophthalmic agents are indicatedfor specific treatment of itching or symptoms of allergic conjunc-

tivitis. Vasoconstrictors are indicated for relief of ocular redness,although they do not reduce the allergic response. Prolonged useof ocular decongestants may lead to rebound hyperemia, whichis often referred to as conjunctivitis medicamentosa.55 Use lim-ited to 10 days does not appear to induce this condition.56 Thecombination of an ocular antihistamine and a vasoconstrictorworks better than either agent alone.57 Mast cell stabilizers, alsoapproved for vernal and atopic keratoconjunctivitis, have a slowonset of action and may require several days of treatment beforeoptimal symptom relief is achieved,58 making them more suitablefor prophylactic or longer-term treatment of chronic ocular aller-gies than for acute symptom relief. Topical NSAIDs reduce pros-taglandin production involved in mediating ocular allergy.59

Multiple-action agents possess both antihistamine and mast cellstabilizer activities, generally have onset of action within 30 min-utes, and are suitable for acute and long-term treatment of allergicconjunctivitis symptoms. Ocular corticosteroids should be re-served for more severe symptoms of allergic conjunctivitis con-sidering that the ocular side effects from their use can threatenvision because of the increased risk of cataract formation, elevatedintraocular pressure (IOP), and secondary infections. The modi-fied steroid loteprednol is indicated for the temporary relief ofsymptoms and signs of seasonal allergic conjunctivitis and has agreatly reduced risk of causing increased IOP compared withmany other ocular corticosteroids.60-64

Vasomotor rhinitis [Summary Statements 20-22]

Vasomotor rhinitis, a type of nonallergic rhinitis, may beepisodic or perennial.7 The exact pathophysiology of vasomotorrhinitis has never been established, and for this reason, it is oftenclassified as idiopathic rhinitis.9 When rhinorrhea is the predom-inant symptom, there appears to be enhanced cholinergic glandularsecretory activity based on the fact that atropinelike agents effec-tively reduce secretions.65 Gustatory rhinitis (rhinitis symptomsassociated with eating) is a form of nonallergic rhinitis felt to bevagally mediated that may respond to intranasal anticholinergicagents.66 Patients with predominant nasal congestion may have no-ciceptive neurons that have heightened sensitivity to stimuli such astemperature change, airborne irritants, foods (especially hot andspicy foods), alcoholic beverages, cold dry air, and exercise.67-70

Temperature change has also been noted to increase symptomsand the inflammatory nasal response in patients with allergicrhinitis.71

Acute infectious rhinitis [Summary Statements 23, 24]Acute viral upper respiratory infections are the most common

predisposing factor for bacterial sinusitis, accounting for 90% to98% of all episodes of sinusitis in children and adults.72-76 In un-complicated cases of viral rhinitis, a 7-day to 10-day observationperiod for spontaneous resolution of symptoms is recommendedbefore prescribing antibiotics.77 Acute bacterial rhinosinusitis isusually associated with a viral upper respiratory infection and ischaracterized by symptoms persisting beyond the usual 7-day to10-day duration of a viral infection. Careful consideration of the

need for antimicrobial use is increasingly important because

antibiotic use has been causally related to the development of bac-terial drug resistance.78-82 Furthermore, the administration of an-timicrobials increases the carriage of antimicrobial-resistantstrains of certain bacterial pathogens, such as Streptococcus pneu-monia, especially in children. 78,79,83,84 Although it is generallybelieved that atopic children experience more episodes of acuteotitis media and acute sinusitis compared with nonallergic chil-

dren, this has not been firmly established.77,85,86

Differentiatingallergic rhinitis from infectious rhinosinusitis or adenoiditis maybe difficult, especially in children, because the symptoms overlapand even purulent nasal drainage may be present in noninfectiousrhinitis.

Acute and chronic sinusitis [Summary Statements 23, 24]Distinguishing noninfectious perennial rhinitis from acute and

chronic sinusitis can be difficult because many symptoms, such asmucosal erythema, increased pharyngeal secretions, olfactorydisturbance, cough, nasal congestion, and headache, are found inboth types of rhinitis. Although nasal cytology may be useful indifferentiating infectious from noninfectious nasal and/or sinusdisease, the clinical value, particularly for the diagnosisofallergicrhinitis, is limited by low specificity and sensitivity.87-91 For ex-ample, neutrophils may be present not only in acute and chronicsinusitis but also in conjunction with eosinophils in patientswith allergic rhinitis who also have an acute infection process.92

Cultures of the nasopharynx without visualization in childrenwith rhinitis is of no value because pathogenic bacteria, as partof the normal flora, have been recovered in as many as 92% ofasymptomatic healthy children.93 In adults, endoscopicallydirected middle meatus cultures have given promising results indiagnosing acute bacterial sinusitis.94-97

Nonallergic rhinitis with eosinophilia syndrome [Summary

Statement 25]

Patients with NARES have paroxysmal exacerbations ofsymptoms, including sneezing, profuse watery rhinorrhea, nasalpruritus, nasal congestion, and occasionalanosmia. These patientsare typically middle-age. The prevalence in the general populationis unknown. NARES is characterized by large numbers (incon-sistently defined as >5% to >20%) of eosinophils on nasalsmear.98-102 The etiology is unknown. In some patients, NARESmay precede the development of nasal polyposis and aspirin sen-sitivity.103 Patients with NARES are at increased risk for the de-velopment of obstructive sleep apnea.104

Occupational rhinitis [Summary Statement 26]Occupational rhinitis may be triggered by allergic factors, such

as laboratory animal antigen and psyllium,105,106 or irritant

factors, such as chemicals, grain dust, and ozone.107-109

Allergicoccupational rhinitis frequently coexists with OA.110 Irritantexposures elicit neutrophilic inflammation in the nasal mu-cosa,107-109 whereas allergic exposures are associated with eosin-ophils, basophils, eosinophilic cationic protein (ECP), andtryptase in the nasal lavage.111-113 However, immunologic mech-anisms may also be important in the response to chemical sensi-tizers, such as acid anhydrides, where both neutrophils andeosinophils are increased in nasal lavage fluid of workers with se-rum specific IgE to the relevant anhydride-human serum albumin(HSA) antigen.114 The prevalence of occupational rhinitis isessentially 100% among workers with OA who are sensitized tohigh-molecular-weight proteins, whereas only 50% of those

with OA caused by chemicals have been identified with


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work-related rhinitis.110 Atopy and intensity of exposure are riskfactors for developing occupational rhinitis.115 An asymptomaticlatency period of exposure lasting weeks to years often precedeswork-related symptoms.105,116 Symptoms are temporally relatedto exposure at work and often improve away from the workplace.The diagnostic validity of nasal allergen challenge for occupa-tional allergens has not been evaluated.112,114 Optimal manage-

ment is avoidance of the occupational trigger, but avoidance ofnonoccupational allergens that contribute to the nasal symptomsis also recommended. Chronic pharmacologic therapy as usedfor allergic and nonallergic rhinitis can be instituted. In general,there is insufficient evidence to support the efficacy of immuno-therapy for IgE-dependent occupational rhinitis, and it is inappro-priate to use immunotherapy to treat occupational rhinitis causedby low-molecular-weight chemical allergens.117

Pregnancy and menstrual cycle rhinitis [Summary Statement

27]Symptoms of rhinitis during pregnancy and at the time of

patients menstrual cycles have long been considered to be

hormonally induced. The most common causes of nasal symp-toms during pregnancy are allergic rhinitis, sinusitis, rhinitismedicamentosa, and vasomotor rhinitis. Symptoms of allergicrhinitis increase in 1/3 of pregnant patients,118 perhaps attributedto nasal vascular pooling caused by vascular dilatation and in-creased blood volume.119 A type of rhinitis unique to the pregnantpatient is vasomotor rhinitis of pregnancy or pregnancy rhini-tis. Pregnancy rhinitis had been defined as rhinitis without an in-fectious, allergic, or medication-related cause that starts before thelast 6 weeks of pregnancy (corresponding to 34 weeks gestation),persists until delivery, and resolves completely within 2 weeks af-ter delivery.120 When pregnancy rhinitis causes snoring, it mayeven be a factor in the development of pre-eclampsia.121

Although it is assumed that hormonal changes contribute to this

condition, there is no convincing evidence.120 There may bean as-sociation of nasal congestion with ovulation and the rise in serumestrogen during the normal menstrual cycle in some women.122

Drug-induced rhinitis [Summary Statement 28]Drug-induced rhinitis may be caused by ACE inhibitors,123

a-receptorantagonists used in the treatment of benign prostatichy-pertrophy,124 and phosphodiesterase-5 selective inhibitors used fortreatment of erectile dysfunction.125 There is no direct evidencethat the current combined oral contraceptive pills cause nasalsymptoms.126 Aspirin and other NSAIDs may produce rhinorrheaas an isolated symptom or as part of aspirin-exacerbated respiratorydisease (AERD), formerly termed Samters triad.127,128

Rhinitis medicamentosa [Summary Statement 28]Rhinitis medicamentosa may develop after the repetitive and

prolonged use of topical a-adrenergic nasal decongestant sprayssuch as oxymetazoline and phenylephrine. The recreational use ofcocaine may result in a rhinitis medicamentosalike state.129,130

Benzalkonium chloride in vasoconstrictor spray products, whenused for 30 days or more, may augment local pathologic ef-fects.131,132 Patients may develop rebound congestion, tachyphy-laxis, reduced mucociliary clearance because of loss of ciliatedepithelial cells,133 and on rare occasions, nasal septal perfora-tion.134 The pathophysiology of this condition is not understood.Treatment of rhinitis medicamentosa consists of suspending the

use of topical decongestants and administering intranasal

corticosteroids to control symptoms while allowing the reboundeffects of the nasal decongestantspray to resolve. At times, a shortcourse of oral corticosteroids may be needed to control the pa-tients symptoms while the effects of the nasal decongestant spraydissipate.129,135 Once the rhinitis medicamentosa is treated, thepatient should be evaluated for an underlying condition, such asallergic rhinitis.

Atrophic rhinitis [Summary Statement 29]Primary (idiopathic) atrophic rhinitis is a chronic condition

characterized by progressive atrophy of the nasal mucosa, nasalcrusting, nasal dryness (caused by atrophy of glandular cells), andfetor.136,137 The nasal cavities appear abnormally wide on exam-ination, and there is absence of identifiable turbinates on sinus CT,referred to as the empty nose syndrome.138 Secondary atrophicrhinitis is most commonly a resultof chronic sinusitis or excessivesurgery to the nasal turbinates.138 Although saline irrigation is themainstay of treatment, topical or systemic antibiotics are indicatedwith the appearance of purulent nasal secretions.139,140

Conditions that mimic rhinitisConditions that mimic rhinitis must be considered in thedifferential diagnosis of nasal symptoms.

Nasal polyps [Summary Statement 30]Nasal polyps may coexist with allergic rhinitis; however, allergy

as a cause of nasal polyps has not been established. Nasal polypshaveaprevalenceof2%to4%141-143 and usually occur after age 40years.143 Although previous studies showed a 2:1 male to femaleprevalence of nasal polyps,142,144,145 a recent large populationstudy showed no sex preference.143 AERD, previously referredto as the aspirin triad, consists of nasal polyps, acetylsalicylicacid intolerance, and asthma, and is recognized in 13% to 40%of patients with nasal polyposis.146,147 Eosinophils are a consistent

finding in nasal polyp tissue. When nasalpolypsare associated withasthma, there is hypersecretion of cysteinyl LTs (cysLTs).148 Oralsteroids may be required in severe nasal polyposis to reduce polypsize, improve airflow, and allow for effective topical medicationdelivery. A short course of oral steroids followed by maintenanceuse of intranasal corticosteroidadministered twicedaily shouldfol-low.149,150,151 Subjective improvement has been observed whenLT modifiers are administered in addition to intranasal corticoste-roids.152,153 One study demonstrated that after surgery, reoccur-rence rates and rescue medication requirements were the same inpatients treated postoperatively with montelukast or beclometha-sone.154 In some adult patients with nasal polyps and AERD, aspi-rin desensitization followed by long-term daily aspirin treatmenthas successively reduced the need for removal of nasal polypsand systemic corticosteroids.155-157

Anatomic abnormalities and cerebral spinal fluid rhinorrhea[Summary Statements 31-33]

Nasal septal deviation and turbinate hypertrophy may lead topostnasal drip or nasal obstruction. Unilateral obstruction, espe-cially when associated with bleeding, hyposmia or anosmia, pain,and otalgia, should alert one to the possibility of a tumor.158,159

Clear rhinorrhea, even in the absence oftrauma or recent surgery,may rarely be a result of a CSF leak.160 Nasal symptoms, particu-larly congestion, may be noted in infants and children with pharyn-gonasal reflux resulting from prematurity, neuromuscular disease,or cleft palate.161In infants and children, the mostcommon acquired

anatomic cause of nasal obstruction is adenoidal hypertrophy.



Wallace et al S13


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Ciliary dysfunction syndromes [Summary Statement 34]Ciliary dysfunction syndromes cause ineffective mucociliary

clearance and include (1) PCD162 (also known as immotile-ciliasyndrome), a rare genetic disorder, and (2) secondary ciliary dys-function,163,164 a more common condition caused by acute orchronic infections, multiple sinus surgeries, or irritant rhinitis.In PCD, the clinical history may include recurrent sinusitis, otitis,rhinitis, chronic cough, nasal polyposis, atypical asthma that is un-

responsive to therapy, and bronchiectasis.165

Approximately 50%of subjects with PCD are affected by situs inversus (Kartagenersyndrome). Whereas screening diagnostic tests for mucociliaryclearance use saccharine166 or Teflon (DuPont) tagged particles,definitive diagnosis requires biopsy and examination by electronmicroscopy.167-169 After an infection, resolution of secondary cil-iary dysfunction and cytopathic epithelial damage may requireweeks.163,164,170-172 An adverse effect of tobacco smokeon muco-ciliary clearance in the upper airways in healthy smokers has notbeen established.173,174

Evaluation and diagnostic studies in patients with

rhinitis

History [Summary Statements 35, 36]A thorough allergic history remains the best diagnostic tool

available. The history will include the patients chief concerns andsymptoms and often includes the pattern, chronicity, seasonality,and triggers of nasal and related symptoms, family history, currentmedications, response to previous treatment modalities, presenceof coexisting conditions, occupational exposure, and a detailedenvironmental history. Questions relating symptoms to pollen andanimal exposure have been shown to have positive predictivevalue for diagnosing allergic rhinitis.175 In addition to upper res-piratory symptoms, it is important to determine the effect of rhini-tis on QOL, including symptoms of fatigue, sleep disturbances,learning and attention problems, and absenteeism and presenteeism

(present but with impaired function) at work and/or school.

176-179

The psychological ramifications of untreated allergic rhinitis canlead to low self-esteem, shyness, depression, and anxiety.180

Recent findings that the sexual QOL is affected by seasonal aller-

gic rhinitis and that appropriate treatment improves the patients

sexual functioning emphasizes that allergic rhinitis is an underap-

preciated disease with systemic effects.181 As evidence of the dis-

parities between patients and physicians perspectives of allergic

rhinitis, the symptom severity and the reduced work, home, and

social functioning, as indicators of QOL, are often underrecog-nized and inadequately treated by the patients physician.182

The effect of rhinitis on QOL has been measured using bothgeneric and disease-specific questionnaires (Tables III and IV).

Using generic QOL questionnaires, it has been shown that adults

with moderate to severe perennial rhinitis and moderate to severe

asthma have equal functional impairment.183,184 On the other

hand, disease-specific QOL questionnaires, including those spe-

cific for rhinitis, describe disease-associated problems more accu-

rately and seem to be more responsive to measuring the change

with therapeutic interventions. Although both the generic and dis-

ease-specific QOL questionnaires are often used in research trials,

their sensitivity and precision for usewith individualpatients have

not been determined.185-190

Physical examination [Summary Statement 37]The physical examination (Table V) of all organ systems poten-

tially affected by allergies should be performed in all patients with

a history of rhinitis. Emphasis should be on the upper respiratory

tract, but the examiner should carefully look for accompanying

otitis191 or eustachian tube dysfunction,192 chronic sinusitis, nasal

polyps, conjunctivitis, asthma,193 and atopic dermatitis. If the pa-

tient is asymptomatic or mildly symptomatic at the time of the

physical examination, there may be minimal or no findings even

with a history suggestive of rhinitis.The nasal and oropharyngeal examination may be accom-

plished with a nasal speculum with appropriate lighting, otoscope

TABLE III. Representative generic QOL questionnaires

Questionnaire Web site for information Cost for noncommercial use Reference

Generic QOL adult

Short Form 36

(Versions 1 and 2)

http://www.rand.org/health/surveys_tools/mos/

mos_core_36item_survey.htmll

Free http://www.rand.org/health/surveys_tools/mos/

mos_core_36item.html

625-627

SF-12 (Versions 1 and 2) http://www.medal.org/Visitor/www/active/ch1/

ch1.aspx

http://www.qualitymetric.com/products/license/ 628

Health Utilities Index

Mark 2 and 3 (HUI2

and 3)

http://www.healthutilities.com/hui2.htm http://

www.hqlo.com/content/1/1/54

Contact http://www.healthutilities.com/aplcnform.htm 629, 630

Nottingham Health Profile http://www.cebp.nl/media/m83.pdf http://www.medal.org/visitor/www/Active/ch1/

ch1.07/ch1.07.01.aspx

631-633

Functional Status

Questionnaire

http://www.jasonprogram.org/Articles/

fun_status_question.pdf

http://www.jasonprogram.org/Articles/

fun_status_question.pdf

634

Duke Health Profile http://www.outcomes-trust.org/instruments.htm

More info: [email protected]

Free single use with permission $155 master http://

www.outcomes-trust.org/instruments.htm

635

Generic QOL child

CHQ PF-50 http://www.qualitymetric.com/products/chq.aspx http://www.qualitymetric.com/products/license/ 636

CHQ PF-28 http://www.epa.state.oh.us/dapc/atu/AppendixA.pdf http://www.qualitymetric.com/products/license/ 637

SF-10 http://www.qualitymetric.com/products/chq.asqx http://www.qualitymetric.com/products/license/ 638

Pediatric Quality of Life

Inventory (PedsQL)

http://www.mapi-research.fr/t_03_serv_

dist_Cduse_pedsql.htm

Free Single Copy http://www.mapi-research.fr/

t_03_serv_dist_ReviewPedsQLGenericsf.htm

639-642

Health Utilities Index

Mark 2 and 3 (HUI2 & 3)

http://www.healthutilities.com/hui2.htm http://

www.hqlo.com/content/1/1/54

Contact http://www.healthutilities.com/aplcnform.htm 629, 630

Questionnaires have been validated for research groups but not for an individual.


AUGUST 2008

S14 Wallace et al
http://www.rand.org/health/surveys_tools/mos/mos_core_36item_survey.htmllhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item_survey.htmllhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item.htmlhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item.htmlhttp://www.medal.org/Visitor/www/active/ch1/ch1.aspxhttp://www.medal.org/Visitor/www/active/ch1/ch1.aspxhttp://www.qualitymetric.com/products/licensehttp://www.healthutilities.com/hui2.htmhttp://www.hqlo.com/content/1/1/54http://www.hqlo.com/content/1/1/54http://www.healthutilities.com/aplcnform.htmhttp://www.cebp.nl/media/m83.pdfhttp://www.medal.org/visitor/www/Active/ch1/ch1.07/ch1.07.01.aspxhttp://www.medal.org/visitor/www/Active/ch1/ch1.07/ch1.07.01.aspxhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.outcomes-trust.org/instruments.htmmailto:[email protected]://www.outcomes-trust.org/instruments.htmhttp://www.outcomes-trust.org/instruments.htmhttp://www.qualitymetric.com/products/chq.aspxhttp://www.qualitymetric.com/products/licensehttp://www.epa.state.oh.us/dapc/atu/AppendixA.pdfhttp://www.qualitymetric.com/products/licensehttp://www.qualitymetric.com/products/chq.asqxhttp://www.qualitymetric.com/products/licensehttp://www.mapi-research.fr/t_03_serv_dist_Cduse_pedsql.htmhttp://www.mapi-research.fr/t_03_serv_dist_Cduse_pedsql.htmhttp://www.mapi-research.fr/t_03_serv_dist_ReviewPedsQLGenericsf.htmhttp://www.mapi-research.fr/t_03_serv_dist_ReviewPedsQLGenericsf.htmhttp://www.healthutilities.com/hui2.htmhttp://www.hqlo.com/content/1/1/54http://www.hqlo.com/content/1/1/54http://www.healthutilities.com/aplcnform.htmhttp://www.healthutilities.com/aplcnform.htmhttp://www.hqlo.com/content/1/1/54http://www.hqlo.com/content/1/1/54http://www.healthutilities.com/hui2.htmhttp://www.mapi-research.fr/t_03_serv_dist_ReviewPedsQLGenericsf.htmhttp://www.mapi-research.fr/t_03_serv_dist_ReviewPedsQLGenericsf.htmhttp://www.mapi-research.fr/t_03_serv_dist_Cduse_pedsql.htmhttp://www.mapi-research.fr/t_03_serv_dist_Cduse_pedsql.htmhttp://www.qualitymetric.com/products/licensehttp://www.qualitymetric.com/products/chq.asqxhttp://www.qualitymetric.com/products/licensehttp://www.epa.state.oh.us/dapc/atu/AppendixA.pdfhttp://www.qualitymetric.com/products/licensehttp://www.qualitymetric.com/products/chq.aspxhttp://www.outcomes-trust.org/instruments.htmhttp://www.outcomes-trust.org/instruments.htmmailto:[email protected]://www.outcomes-trust.org/instruments.htmhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.jasonprogram.org/Articles/fun_status_question.pdfhttp://www.medal.org/visitor/www/Active/ch1/ch1.07/ch1.07.01.aspxhttp://www.medal.org/visitor/www/Active/ch1/ch1.07/ch1.07.01.aspxhttp://www.cebp.nl/media/m83.pdfhttp://www.healthutilities.com/aplcnform.htmhttp://www.hqlo.com/content/1/1/54http://www.hqlo.com/content/1/1/54http://www.healthutilities.com/hui2.htmhttp://www.qualitymetric.com/products/licensehttp://www.medal.org/Visitor/www/active/ch1/ch1.aspxhttp://www.medal.org/Visitor/www/active/ch1/ch1.aspxhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item.htmlhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item.htmlhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item_survey.htmllhttp://www.rand.org/health/surveys_tools/mos/mos_core_36item_survey.htmll


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with nasal adapter, indirect mirror, and/or rigid or flexiblenasopharyngoscope, based on the expertise of the examiner and/or the assessment needs.194 If after applying a topical deconges-tant there is a reduction of turbinate mucosaedema, this may assistin delineating mucosal versus bony hypertrophy and in differenti-ating severely edematous mucosa from nasal polyps. A pneumatic

otoscope is used to assess tympanic membrane mobility. At times,an impedance tympanometer is also needed to assess the tympanicmembrane mobility and the presence or absence of fluid, espe-cially in children.

Many typical allergic findings are supportive of but not specificfor allergic rhinitis.195 Mucosal appearance may not distinguishbetween allergic and nonallergic noninfectious rhinitis or even in-fectious rhinitis, because hyperemia, for example, may be presentwith all 3. Likewise, classic allergic shiners are reported in 38%of nonatopic individuals.196

Testing for specific IgE [Summary Statements 38-41]Determination of specific IgE, preferably by skin testing, is

indicated to (1) provide evidence of an allergic basis for the

patients symptoms, (2) confirm suspected causes of the patientssymptoms, or (3) assess the sensitivity to a specific allergen foravoidance measures and/or allergen immunotherapy.197,198 Thenumber of skin tests and the allergens selected for skin testingshould be determined on the basis of the patients age, history,and environment and living situation, such as area of the country,

occupation, and activities.9

The precise sensitivity of specific IgEimmunoassays compared with skin prick/puncture tests can varywith the technique used, from less than 50% to greater than 90%,with the average 70% to 75%.199-209 Similar sensitivity has beenreported when these immunoassays are compared with symptomsinduced after natural or controlled challengethat is, nasal provo-cation challenge. The simplicity, ease,and rapidity of performance,low cost, and high sensitivity make skin testing preferable to in vi-tro testing for determining the presence of specific IgE antibodiesin patients with rhinitis. However, specific IgE immunoassays maybe preferable to skin testing in certain clinical situations, such asextensive skin disease, skin test suppressive therapy (for example,antihistamines) that cannot be discontinued, or uncooperative

patients, or when the history suggests an unusually high risk of

TABLE IV. Representative rhinitis QOL questionnaires

Questionnaire Web site for information Cost of noncommercial use Reference

Rhinitis QOL adult

RQLQ http://www.qoltech.co.uk/

Rhinocon.htm#rqlq#rqlq

Free request: [email protected] 643-645

Standardized Rhinoconjunctivitis Quality

of Life Questionnaire

http://www.qoltech.co.uk/Rhinocon.htm#rqlqs Free request: [email protected] 646

Mini Rhinoconjunctivitis Quality of

Life Questionnaire

http://www.qoltech.co.uk/

Rhinocon.htm#minirqlq

Free request: [email protected] 647

Nocturnal Rhinoconjunctivitis Quality of

Life Questionnaire

http://www.qoltech.co.uk/Rhinocon.htm#noct Free request: [email protected] 648

Rhinitis Quality of Life Questionnaire http://www.qoltech.co.uk/Rhinocon.htm#rhinqlq Free request: [email protected] 649

Rhinitis Symptom Utility Index 650

Rhinitis QOL pediatric and adolescent

Paediatric Rhinoconjunctivitis Quality of

Life Questionnaire


PaedRhinocon.htm#prqlq

Free, request: [email protected] 651

Adolescent Rhinoconjunctivitis Quality

of Life Questionnaire


PaedRhinocon.htm#arqlq

Free, request: [email protected] 652

Questionnaires have been validated for research groups but not for an individual.

TABLE V. Physical examination of patient presenting with symptoms compatible with rhinitis

Vital signs including weight and height should be recorded in all patients.

General observations: facial pallor, elongated facies, preferred mouth breathing, and any evidence of systemic disease.

Eyes: Excessive lacrimation, erythema and swelling of the bulbar and/or palpebral conjunctiva, cobblestoning of the tarsal conjunctiva, swelling or dermatitis of

outer eyelids, Dennie-Morgan lines, or venous stasis below the lower eyelids (allergic shiners).

Nose: Reduced patency of nasal valve; alar collapse; transverse external crease; external deformity such as saddle nose; sepal deviation or perforation, spurs,

ulcers, perforation, prominent vessels, or excoriation; nasal turbinate hypertrophy, edema, pallor or erythema, and crusting; discharge (amount, color,

consistency), and nasal polyps. The presence of tumors or foreign bodies should be noted.

Ears: Tympanic membrane dullness, erythema, retraction, perforation, reduced or increased mobility, and air-fluid levels.

Oropharynx: Halitosis, dental malocclusion, high arched palate, tonsillar or adenoidal hypertrophy. Observe for malocclusion or high arched palate associated

with chronic mouth breathing, tonsillar hypertrophy, cobblestoning of the oropharyngeal wall, pharyngeal postnasal discharge, temporomandibular joint pain

or clicking with occlusion, furrowing, coating, or ulceration of tongue or buccal mucosa.

Neck: Lymphadenopathy, thyroid enlargement, or tenderness.

Chest: Signs of asthma. Chest wall deformity or tenderness, abnormal percussion, egophony, audible wheezing, or abnormal or diminished sounds by

auscultation.Abdomen: Tenderness, distension, masses, or enlargement of liver or spleen.

Skin: Rashes, especially eczematous or urticarial (distribution and description), or dermatographism.

Other organ systems when history or general observation indicate these should be included.

Note: This list is not intended to be totally inclusive. Elements of the examination that will assist in the differential diagnosis of rhinitis or that may indicate complications of treatment

are included. Documentation of presence or absence of these elements should be considered.



Wallace et al S15
http://www.qoltech.co.uk/Rhinocon.htm#rqlq#rqlqhttp://www.qoltech.co.uk/Rhinocon.htm#rqlq#rqlqmailto:[email protected]://www.qoltech.co.uk/Rhinocon.htm#rqlqsmailto:[email protected]://www.qoltech.co.uk/Rhinocon.htm#minirqlqhttp://www.qoltech.co.uk/Rhinocon.htm#minirqlqmailto:[email protected]://www.qoltech.co.uk/Rhinocon.htm#noctmailto:[email protected]://www.qoltech.co.uk/Rhinocon.htm#rhinqlqmailto:[email protected]://www.qoltech.co.uk/PaedRhinocon.htm#prqlqhttp://www.qoltech.co.uk/PaedRhinocon.htm#prqlqmailto:[email protected]://www.qoltech.co.uk/PaedRhinocon.htm#arqlqhttp://www.qoltech.co.uk/PaedRhinocon.htm#arqlqmailto:[email protected]:[email protected]://www.qoltech.co.uk/PaedRhinoc

Documents

Rhinitis2008 Treatment Guidelines